Na tvaham kaamaye raajyam

Na svargam na punarbhavam

Kaamaye dukkhataptaanam

praaneenam aartinaashanam

Neither do I crave for land, nor heaven, nor rebirth.

All I want is to relieve the distress of the diseased and

the maimed

1
 This CD has been created for the students of
Cardiothoracic and vascular surgery in order to present
them with the proper perspective as regards preparing
for the examination as well as for proper management
of the cardiac cases later in their career.
Important points in theory and practicals have
been culled from various books and from the
experience of knowledgeable national and international
faculty members to present in summary, all which is
important and frequently asked in the examinations. It
also contains a valuable question bank spanning the
last ten years.
This does not obviate the need for text book
reading. This is only a restructuring and compilation of
existing knowledge & material in order to facilitate the
thought process in the student.
It is hoped that this CD will help the student
become and continue to remain a good cardiothoracic
surgeon.

2
PRACTICAL GUIDE FOR THE STUDENT
Version 2.0

Compiled & Written

BY
Dr. Trushar Gajjar MS, DNB CTVS, FIACS
Additional Senior Consultant
Department of CTVS
Sri Sathya Sai Institute of Higher Medical
Sciences- Prasanthigram (Puttaparthi)

3
 INDEX

CASE PRESENTATION 5
Congenital 5
Valvular 143
Others 228
VIVA VOCE 248
Chest X rays 248
Echocardiograhy 507
Angiography & Cardiac Catheterisation 617
Operations 648
Cardiovascular medications 658
Instruments 688
History & contributions of surgeons 762
History of Cardiac Surgery 779
Cardiac Intensive Care Unit Management 782
QUESTION BANK 808
HOW TO WRITE THEORY ANSWER?
(SAMPLES) 837

4
 CASE PRESENTATION
CONGENITAL HEART DISEASE
Atrial Septal Defect

# What is your Diagnosis?

CAHD, L-R Shunt at atrial level with pulmonary hypertension in Sinus rhythm
without CCF, TEE or IE in NYHA Class II Probably Atrial Septal defect
# Why Atrial septal defect?
Young female patient relatively asymptomatic with poor growth & occasional
palpitation on exertion, on examination Raised JVP withProminent a wave, left
parasternal heave, Wide fixed split S2 at pulmonary area with gr 2/6Mid
diastolic murmur at tricuspid area & Gr 3/6 ejection systolic murmur at
pulmonary area.
# What other symptoms ASD can have?
- Poor Growth
- Recurrent LRTI
- Palpitation
- Dyspnoea on exertion
- Easy fatigability
- Cyanosis
# Why palpitation in ASD?
- Due to systolic contraction of dilated RV.
- Atrial arrhythmia
# Dyspnoea in ASD
- Pulmonary hypertension
- CCF
- Atrial arrhythmia
# Cyanosis in ASD
- Eisenmengerization

5
- RV failure
- Selective drainage of IVC into LA
- Common atrium
- TAPVC
# Why URTI in ASD?
- Massive blood flow increases lung water
- Compression of bronchioles
# What is the hallmark of L-R Shunt at atrial level?
- Flow murmur (gr<3/6) at tricuspid area
- Wide fixed split 2nd heart sound
# What are the lesions producing L-R Shunt at atrial level?
Group 1- Ejection systolic murmur at LPSB
- ASD
- PAPVC
Group 2- Continuous murmur
- RSOV-RA
- Aorta-RA tunnel
Group 3- Continuous murmur
- Coronary RA fistula
- Coronary CS fistula
# Whatare normal split/wide split /wide & variable split /wide& fixed split
/Reverse split of S2?
- Normal split S2 split in inspiration, both components heard in inspiration,
A2-P2 30 seconds.
- Wide split Both the components of S2 heard in expiration & in standing
position (Can be heard in paediatric patient in supine position)
- Wide & variable split- Split increases during inspiration & reduces during
expiration
Causes
- Early A2 MR/VSD/Constrictive pericarditis
6
- Late P2- RBBB/LV ectopics/LV pacemaker
- Wide & fixed split- No change with respiration, Interval between two
components remains fixed
Causes
- ASD
- PAPVC
- RVF
- Massive acute pulmonary embolism
Mechanism in ASD
Wide - due to increased pulmonary hangout interval (prolonged RV ejection)
Fixed as the septal defect equalizes LA & RA pressures throughout
respiratory cycle.
- Reverse split- Split becomes wider in expiration & standing position
Due to
- Late A2- AS/ HOCM/PDA/LBBB/RV pacing/RV ectopics/Systemic
hypertension
- Early P2- WPW (B) syndrome
# ASD with variable split S2
- ASD SV
- ASD with AF
# S2 in Eisenmengers syndrome
- VSD Single loud S2
- PDA- Close split S2
- ASD- Narrow split S2
# ASD with soft P2 with Cyanosis
- Large ASD
- Massive shunt > 4:1
- PS with R-L Shunt
# D/D of ASD-clinically
- PAPVC with intact IAS
7
- TAPVC with anaemia
# Natural history of ASD
< 3mm defects: mostly close by 18 months (they are mostly PFOs)
3- 5mm & 5- 8mm defects: 80% of the defects shall close (by 8 years)
> 8 mm defects: have little chances of closing spontaneously
Survival pattern is lesser than normal
die by 27 years
die by 36 years
# Signs of significant ASD shunt
- If diastolic murmur across the TV- Qp/Qs > 1.5-2/ 1
- Severity of PAH is not on loudness of P2 but on the A2-P2 interval & absence
of murmur across the TV
# Distribution of various ASDs.
- Os secundum= 75%
- Os primum= 15%
- Sinus venosus= 10%
# Commonest associated anomalies in ASD.
In Os secundum= MV prolapsed
In Os primum= MR
In sinus venosus= PAPVC
# Obligatory ASD
- Tricuspid atresia
- TAPVC
# Syndromes associated with ASD
- Sinus venosus
- Scimitar syndrome
- Barlows syndrome- MVP with chordal rupture
- Lutembachers syndrome
- Marfans syndrome
- Turners syndrome
8
 - Noonans syndrome
- Holt-Oram syndrome
# CxR in ASD
- Small aortic knuckle
- Prominent MA
- RV Contour
- Pulmonary plethora
# What will be the difference on CxR between intracardiac & Extra cardiac
shunts?
- Intracardiac shunt- ASD/VSD
- Extracardiac shunt PDA/AP window
- Great vessels enlarged in case of extra cardiac shunt
# ASD with huge heart
- ASD with MR
- ASD with other shunts
- ASD with CCF
- Common atrium
# Characteristic X-ray appearance of ASD
- TOF- Boot shaped heart
- ASD clenched fist / Jug handle appearance
# Large aorta in a patient with ASD
- Systemic hypertension
- PDA
- Associated AV disease
# Why in ASD is PA more prominent as compared to a VSD?
In an ASD, the PVR is lesser elevated. Post births the PVR regresses & hence
the PA thins out & becomes more susceptible to dilatation.
In VSD/ PDA, the wall thickness remains the same as the PVR regresses slowly
& partially, hence resulting in a less complaint artery.

9
# ECG characteristics of ASD
- RAD
- RAE
- RBBB
- RVH (RVVO)
# Difficult to differentiate ASD with PAH
- RAD/RAE/RBBB/RVH will be present in PAH also
- qR pattern in V1 is the only diagnostic sign of PAH.
# Which ECG signs will help in management?
- Axis- LAD in ASD OP
- P wave Inverted in II/III/aVF ASD SV
# LAD in ASD
- ASD OP
- Common atrium
- AV canal defect
# What do you want to know on Echo?
- Confirm Diagnosis
- Size of ASD
- Type of ASD
- Pulmonary veins & systemic veins
- Valves
- RVSP
- RVOT
- LV/RV function
# Echo diagnosis of ASD
Direct proof
- Septal drop out in Sub costal view / Apical 4 chamber view
- ASD OS- Drop out at mid atrial septum
- ASD OP Defect in lower atrial septum
- ASD SV Defect in posterosuperior septum
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- ASD CS- Communication at the level of the orifice of CS
- Turbulence in RA region of ASD
- Colour Doppler
Indirect proof
- Paradoxical septal motion
- Increased dimension of RA & RV
# Clinically ASD but on Echo no ASD
- Fenestrated ASD
- Small ASD
- TAPVC
# DD of ASD on Echo
- Pectus excavatum
- Straight back syndrome
- Mild PS
- Ebstein Anomaly
- PPH
# Types of paradoxical IVS movement
- Type A Normal movement
- Type B IVS moves anteriorly during systole
- Type C Fibrillatory movement of IVS
# Paradoxical IVS movement seen in
- TR
- Pulmonary hypertension
- Constrictive pericarditis
- After open heart surgery
# LSVC is suspected
- Left prominent JVP
- Shadow on left side of the heart on X-ray
- Echo dilated CS
- On table- absent innominate vein, small RSVC, LSVC seen, dilated CS
11
# Associated anomalies to be reported on Echo
- PS, PAH, PAPVC, LSVC, Mitral valve, other shunt
# Cause of MR in ASD?
- Paradoxical IVS motion-papillary muscle dysfunction
- Venturie effect
- As a part of Lutembachers syndrome
- Primum ASD
# ASD P2 normal/soft with mild duskiness
- Cardiac TAPVC with mild PAH
- Common atrium
- Massive shunt adequate oxygenation not occurs
- Unroofed CS
- Large ASD with mixing
- IVC type of ASD with streaming effect
# Complications of ASD.
- Eisemengerization
- Paradoxical embolism
- Arrhythmias
# When to label as PFO
When at classical site & size less than 3- 5mm diameter
# Significance of PFO
- Paradoxical embolism during pregnancy (& other DVTs)
- For deep sea divers during decompression (embolism)
# Characteristics of familial ASD are
- Male= female
- Associated with prolonged PR
- Sudden death known
# Signs of significant ASD shunt
- If diastolic murmur across the TV- Qp/Qs > 1.5-2/ 1

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- Severity of PH is not on loudness of P2 but on the A2-P2 interval & absence of
murmur across the TV
# ASD with large heart
- TAPVC
- Lutembachers syndrome
# D/D of ASD-clinically
- PAPVC with intact IAS
- TAPVC with anaemia
# Signs of PAH in ASD, on an ECG
- Tall R in V1
- qR in V1
# Contrast echo.
Agitated saline is injected which reaches the RA & is seen as echo contrast. If
an ASD is present, its jet (due to left to right shunt) shall cast a negative
shadow in this echo brightness.
If injected through the left basilic vein, a simultaneous diagnosis of a left SVC
may also be obtained.
# Why in an ASD is the shunt left to right
- RA is more complaint than LA
- TV is larger than MV
- RV is the volume loading ventricle
# In patients with ASD having CTR > 65%.
- Common atrium
- AV canal
- TAPVC
- ASD with MS
- CCF (4th/ 5th decade)
# Clinical D/D between secundum ASD & primum ASD
- Primum ASD is characterized by
- Early age of onset of symptoms
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- Rapid progression of symptoms
- Early onset of complications of ASD & LVF
- Associated MR.
# Indications of Cath in ASD
- ASD presenting early < 4years with CCF
- ASD with PAH
- Age > 40 years for coronary angio
- Device closure
# Cath data in ASD
- Step up at atrial level
- RVSP
- PA pressure
- RA mean pressure
- L-R Shunt pre & post O2
- PA saturation at room air & post O2
- PVRI pre & post O2
- Innominate injection
# Catheter course in ASD
- FV-IVC-RA-RV-PA
- FV-IVC-RA-LA-RSPV
- FV-IVC-RA-SVC-PV if PAPVC present
- FV- IVC- RA-ASD LA-LPV (Pulmonary vein confirmation done as catheter is
outside cardiac shadow)
- FV-IVC-RA-TV-RV-PA-LPA
- FV-IVC-RA-CS (Mid line at diaphragm)-LSVC (above lt. sternoclavicular joint)
# Oximatery in ASD
- Normal SVC saturation- 60-65%
- Normal IVC saturation 75%
- 3SVC + 1 IVC / 4 = Mixed venous saturation

14
- If there is a jump of > 10% in mid RA level compared to the expected mixed
venous saturation- It is important to diagnose it as L-R shunt at atrial level
- This should be always associated with no desaturation at LV level
# Small ASD with high Qp/ Qs is seen in?
- SV ASD
- PAPVC
# Which ASD shunt will never be R-L.
- Lutembachers.
# How much difference of mean pressure between RA & LA is allowed?
3mmHg suggest restrictive ASD
# What is significant step up?
10 % in 1st run
7% in 2nd run
5 % in 3rd run
Carried forward to RV & MPA
# Innominate vein saturation is 84%
- Lt. PAPVC/TAPVC
# In case of ASD when you enter in LV possibilities are
- VSD
- ASD OP
- AV canal defect
# Indication of PA injection in ASD
- Supravalvar, branch PA, peripheral PA stenosis
- To avoid doing lt. Heart cath
- Study Pulmonary venous drainage levo phase
# Surgery not required, for ASD, if
- Qp/ Qs < 1.5/1
- Eisenmengerization
- Age of > 40 years (?)
# Timing of surgery in an ASD
15
- Preferred to wait till 3- 4 years of age.
- Surgery advised if:
Qp/ Qs> 1.5-2/1
PVR should be less than 8 Wood/m2
# Can ASD surgery be performed through a left thoracotomy.
Yes, but only under circulatory arrest (as bicaval cannulation cannot be
performed)
# Right thoracotomy incision for ASD.
Broms incision.
# Why midsternotomy for ASD closure
- Familiarity
- Easier to cross clamp & de air
- Easier to manage surprises- Lt. SVC, MS/MR, TAPVC
# What is a McGoons stitch?
- A W horizontal mattress stitch, which is taken at the inferior angle of the
ASD margin, to include a bite of the LA wall. It is taken as:
- To ensure that the IVC drains into the RA
- Inferior margin is thin walled.
# Post ASD closure what happens to the S2 split.
Wide split (due to RBBB) will persist but the fixed component disappears.
# Care while closing ASD
- Defining inferior margin is more important-In accurate suturing or
incorporation of the Eustachian valve in the lower part of the defect leads IVC
blood to LA.
- IVC narrowing avoided.
- Care of CS & Pulmonary veins
- No deep sutures near anterior margin near CS
- No deep suture on superior surface Cor aorticus NCC.

16
- Where defect is large & low lying with in the mouth of the IVC It is safe to
place semipurstring suture along the lower margin incorporating the inner wall
of LA.
# Closure of ASD, historical techniques.
- Well technique- Gross.
- Button technique
- Baileys atriocavopexy (Donut technique)
- Purse string technique (Sondergard)
- Inflow occlusion.
# How is the inflow occlusion technique performed?
- SVC & IVC are looped
- Patient is cooled to 34C
- 100% oxygen & NaHCO3 is administered.
- SVC/ IVC is clamped
- 2-4 beats to allow the heart to empty
- Aorta & MPA clamped
- RA opened & ASD sutured
- RA incision side clamped
- SVC/IVC de snugged & deairing done thru aorta
- MPA & then aorta declamped
- RA incision sutured
# On opening if no ASD found.
- PA soft straight back syndrome, Pectus excavatum
- PA tense, RA dark PPH
- PA tense & RA pink PAPVC with intact IAS
# Extending the ASD is performed in which conditions?
- MV surgery through IAS
- PAPVC with intact IAS
- Sennings surgery

17
# Material used for ASD closure.
- DVD (Double Valour Dacron)
- Pericardium
- PTFE
- Direct
- RA appendage
- Raw silk (Solomon Victor)
- Fascia lata
# Criteria for direct ASD closure
The LA size should not get compromised post direct closure.
# ASD- material used for closure
Double Valour Dacron patch
Advantage of Dacron
- Good handling characteristics
- Early shunting across the patch allows the left sided chambers to adapt
- Helps in deairing 1st 6 hours
Disadvantage of Dacron in ASD surgery.
- Hemolysis (if MR)
- Clot formation on the LA side.
Gortex
Advantage
- Excellent handling
- Do not crumple & fold
- Hemostatic
Disadvantage
- Costly
Untreated Pericardium-
Advantage
- Smooth surface
- Nonthrombogenic
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- Cheap
- Easily available
Disadvantage
- Poor handling
- Aneurysm formation (collagen tissue disruption)
Treated pericardium- 0.6 % Gluteraldehyde solution for 15-20 minutes
Advantage
- Good handling
- Tough
- Do not form aneurysm
# What is sandwich patch?
Use of Pericardium for left side & Dacron on rt. Side.
# Sathpahys adjustable patch technique
- ASD with Severe PAH
- Flap made in Gortex graft
- Allows shunting when RA pressure increases
# Advantage of treated pericardium
- Good handling characteristics
- Low chances of IE
# Advantages of untreated pericardium
- As it is a live patch, higher in-growth implantation
- Live endothelium is antithrombotic
# Where to obtain Gluteraldehyde in OT?
- Cidex
- Storing solution of bioprosthetic valves
# Site of maximum patch giveaway in an ASD closure
Is at the inferior margin, as the IAS is extremely thin here. Thus the IAS should
be incised till the atrial wall. If not incised, then the sutures should be taken
going thru the RA-LA junction into the LA wall.

19
# When is Dacron not used?
- ASD with MR
- Primum ASD
- ASD with MVR performed
# In ASD, through RA what can be palpated.
- TV- for TR
- ASD- margin, size, strands
- Coronary sinus
- MR
- PVs.
# Historical importance of fascia lata.
- Used for ASD closure
- For tissue valve (By Senning)
# Left SVC into LA-clinically
- MDM across MV
- Soft p2
# Coronary sinus rhythm
Maybe seen in patients with left SVC or SVC type sinus venosus ASD. Here the
SA node is activated & the impulse propagates retrogradely. Hence p axis is
leftward.
# Left SVC is commonly seen in
- Single ventricle
- AV canal
- Tricuspid atresia
- TOF
# Importance of left SVC
- For a bilateral Glenn shunt
- During a left BTS, it shall come in the way
- Transvenous pacing from the left side will be impossible
- Cannulation/ occlusion during CPB
20
- For retrograde cardioplegia
# D/D of left SVC on table
Left superior PV
# Raghibs defect
A condition wherein the left SVC opens into the LA thru multiple openings &
the coronary sinus is absent (due to absence of the roof of the coronary sinus)
# Approaches for ASD closure
- Rt. Thoracotomy
- Lt. Thoracotomy
- Mid line sternotomy
# What will you check after opening the sternum?
- Innominate vein
- LSVC
- PAPVC
- PDA
# How will you Differentiate between Azygos & TPVC?
- Azygos Intrapericardial, Disappears posteriorly
- TAPVC Extra pericardial, Enters the lung
# How will you differentiate between Vertical vein & LSVC?
- Vertical vein- Extrapericardial
- LSVC- Intra pericardial
# SVC cannulation in ASD
- SV ASD
- Associated PAPVC
# SVC cannulation must do in
- TCPC
- Mustard operation
- Senning operation
- Schumacher-king operation of TAPVC

21
# If for SVC cannulation angled cannula is not available
Use smaller size flexible straight cannula
# Cannulation for surgery around SVC-RA junction
- Direct SVC cannulation with angled cannula
- Direct SVC cannulation with smaller sized flexible straight cannula
- Straight cannula through RA retracts the cannula with mayo retractor & work
around the SVC RA junction.
# How will you assess MR/ASD/TR before going on CPB?
- MR - Before cannulating RA for SVC cannulation put Lt. Hand finger in
across ASD & feel for MR.
- ASD Finger through RAA purstring feel for
ASD OS-
Able to feel margin all around
CS anterior & below the ASD margin
ASD OP-
Able to feel only superior margin like crescent.
CS posterior & above the ASD margin
MR jet felt
ASD SV-
Able to feel Lower margin
CS away from the ASD
Able to feel Pulmonary vein openings
- TR Finger through the RAA purstring into RA feel for TR jet.
# LSVC cannulation
- Direct cannulation near LAA.
- Cannulation through CS.
- Keeping sucker In CS
# After going on CPB heart is still full
- SVC/IVC cannula too much in.
- Associated LSVC
22
- Associated PDA
- Kink in venous line
# Various RA incisions
Oblique/ Parallel to AV groove
- All defects of are tackled by this incision
- Cuts the muscle & blood vessels
- Suturing in front of IVC cannula
- Close to AV groove
- ASD SV defect exposure poor
Transverse Incision
- More physiological
- Does not cut the muscle & blood vessels
- Most of the defects accessible through this incision
- Can be extended into LA (Supracardiac TAPVC)
- Thin part of RA mainly in TR
Longitudinal incision
- Longitudinal incision (Sinus venosus part of RA) (Posterior vertical incision)
- Thickest part of RA
- ASD OP & valves difficult to expose
- Upper extension damages SA node artery
# RA opened -Blood coming in RA
- Improper snugging of SVC &IVC cannula
- LSVC
- PDA
- Improperly applied cross clamp
# Indications for direct closure
- PFO
- Slit like ASD with well formed thick margin

23
# Disadvantage of direct closure
- LA size reduces- Chances of going in pulmonary oedema increases if
associated MR/IV fluid given rapidly.
- Distorts Mitral valve annulus
- Tension LA on suture line- cuts through
# ASD cannot be closed directly in
- Following OMC
- MR
- ASD SV Thick muscular margins
- ASD OP
# Arrhythmia following ASD closure
- Nodal rhythm Injury to SA node by SVC snugging
- Sutures around internal pathways
- Sutures near CS-IVC junction
- AV node exposed to ambient temperature
# Low output syndrome
- Mitral valve anomaly is missed
- Small LA
- Severe PAH
- Valvar PS
# Thrill over MPA after ASD closure
- Valvar PS
- Dilated PA
# Indication for enlarging ASD
- Flimsy membrane
- Fenestrated ASD
- ASD OS with other defects
- Visualisation of mitral valve for Repair/replacement
# Indications for creating ASD
- Excision of Myxoma
24
- TAPVC with small ASD
# Indications for creating & leaving the ASD open
- Severe LVF
- PS
- TAPVC
- Tricuspid atresia
# How will you assess PS in ASD on table?
- RV & PA pressure before going on CPB, Gradient > 50mmHg
- After opening RA Assessment of Pulmonary valve
- Sizing pulmonary valve annulus with Hegar according to weight of the patient
by - Kirklins nomogram
# How will you open PA & why?
- Open PA vertically between two stay sutures.
# How will you treat PS?
- By commissurotomy & sizing the PA annulus
- If it is not sufficient do valvectomy & size again
- Still Annulus is not allowing adequate sized Hegar, Put Transannular patch
# TAP will be of same size as TOF?
No
# How will you diagnose SV ASD on table?
- Enlarged SVC & RUPV draining into SVC/SVC-RA junction
- IVC type of SV ASD with PAPVC-
- RIPV in abnormal position
- Not able to go around IVC
# How will you close SV ASD?
- Dissect SVC & loop between RUPV & Azygos
- Cannulate SVC with angled cannula above RUPV draining into SVC
- Open SVC- RA junction & extend the incision into RA
- Check for PFO & Mitral valve
- If ASD is restrictive enlarge it.
25
- Close the ASD with pericardial patch using 5-0 prolene suture
- Take care not to narrow down Pulmonary vein openings & SVC opening
- If ASD patch is bulging, augment the SVC-RA junction with another
pericardial patch
# How will you diagnose ASD OP?
- ECG Left axis deviation
- Echo- ASD OP with cleft & MR, tricuspid & mitral valve at same level
- On table- Feel ASD through RAA purstring
# How will close ASD OP?
- Kirklins technique- Keeping CS on LA side
- McGoons technique- Keeping CS on RA side
# Differentiation between cleft in AML in ASD OP & Commisure in AML
- Cleft chordate goes to two different papillary muscles
- Commissural chordate goes to same papillary muscle
# Important points while closing ASD OP
- Closing cleft with interrupted sutures without narrowing the Mitral opening.
- Taking Interrupted/Continuous sutures on the mitral crest more towards the
mitral valve
- Avoid AV node & bundles by small & superficial needle bites along the crest
- Check for MR.
- Do not create puckering of mitral annulus by ASD sutures.
# WhichCardioplegia will you use?
- Cold blood cardioplegia
# ASD with MVP what will be the cause?
- Lack of support to valve annulus
- Venturie effect
- Change in ventricular geometry
- Diseased Mitral valve

26
# How will you assess MR?
- Before cannulating SVC, put finger in RA through RAA purstring across ASD
& feel for MR
- After opening RA by pushing saline in mitral valve
- TEE
- Transoesophageal phonocardiogram
# How will you treat the case of ASD with MVP?
- Mild MR - ASD closure only
- Moderate / Moderate-severe MR Mitral valve repair with ASD closure.
# How will you diagnose ASD with PDA?
- Enlarged Great vessels
- After going on bypass perfusionist will come to know 1st- Poor venous return
- Heart is full after going on CPB
- If small duct-Continuous return in RV through PA
# How will you treat PDA?
- Put femoral arterial line
- Go on CPB
- Do not cool, keep heart ejecting
- Put LV vent through RUPV to give blood to perfusionist
- Dissect PDA between arch of aorta & bifurcation of PA
- Loop with No1 or No 2 silk
- Down on flows
- Ligate the PDA doubly under low flow
- Check for bleeding
- Back up on flows & check for femoral arterial pressure
# How will you deair the heart in ASD?
- Dearing LA before closing patch-Ask anaesthetist to ventilate & surgeon
should press on the LV
- Root vent- Before releasing the clamp ,put head low, connect root vent, ask
anaesthetist to ventilate, Surgeon should press on the LA ,LAA & LV
27
- RA closure-Heart is beating, Last 2 cm of RA left, Clamp IVC ,Ask perfusionist
to watch for return( Or Ask perfusionist to put volume without clamping the
IVC ),Release the IVC snugger, Allow the RA to deair.
# Indications for Device closure
- Size < 20mm
- Defect size not more than 50% of stated diameter of largest available device
- 4mm away from the important structure such as AV valves, Venacavae,
Pulmonary veins
- Fossa ovalis type of defect
- Absent PAPVC
- Single ASD with well formed margins
- Patient large enough (>8 Kg) to allow femoral vein access with 11 F sheath
# Types of Devices used for ASD closure
- Rashkind Umbrella device
- Amplatzer device
- Clamshell device
# Complications of Device closure
- Embolisation
- Thromboembolism
- Infection
- Failure
- Leak
- Hemolysis
# Post operative pulmonary oedema in ASD
- Small LA/LV
- Underestimated MR
- Fluid overload
- PAPVC closed with patch
- LV dysfunction
- Pump lung
28
- Hemo/Pneumothorax
# Management of Post operative pulmonary oedema
- Diuretics
- Inotropes
- NTG
- Echo for diagnosis
# Post operative Arrhythmia in ASD
- Nodal rhythm
- SA node damage due to SVC cannulation
- Damage to SA nodal artery
- AV nodal block
- Deep stitches at CS
- Enlarging of ASD done
# ASD post operative not coming off bypass
- Check- potassium, acidosis, and temperature.
- Check for:
Poor myocardial protection- Treatment-secondary cardioplegia
Heart block. Treatment-pacing
Mixed/ poor pathology;
MV disease. Treatment- do needful
LV small. Treatment- Inotropes, fenestration
# ASD on follow up
- S2 Wide split may be present because of IRBBB
- IRBBB present
- Soft Ejection systolic murmur present
- Pulmonary artery size decreases over 3-6 months

29
 Ventricular Septal Defect

# What is your Diagnosis?

CAHD, L-R Shunt at Ventricular level, PAH, without CCF, Thromboembolic
episodes or Infective endocarditis Probably Ventricular septal defect.
# What the features suggestive of VSD?
- H/O Recurrent respiratory tract infection
- Parasternal heave present
- Loud & palpable P2
- Pan systolic murmur in left 4th intercostals space
- Mid diastolic murmur of Gr 2/6 at mitral area
# What are the clinical features of PAH?
- Loud & palpable P2
- Parasternal heave
# What are the features of post tricuspid shunt?
- Early age of presentation
- PAH develops early if shunt is not restrictive
- Systolic murmur at shunt level
- Diastolic flow murmur at mitral area
- LV type of apex
- ECG LVH ,LVVO
# Conditions producing shunt at post tricuspid level
- VSD
- RSOV
- Truncus
- APwindow
- PDA
- AV canal with ventricular component
# Why does a VSD present early (as compared to an ASD)
- Intrauterine development of shunt
30
- Volume and pressure over load, not dependent on RV compliance (as in ASD)
# What does an early presentation indicate?
- Large VSD
- Multiple VSDs
- AV canal
- Multiple shunts
# Why does patient have LRTI
- Increased blood flow, hence increased mucus production- hence retention &
infection
-Increased flow, tissue edema & lymphatic stagnation
# What is the definition of LRTI
There is no definition. It is borrowed from the definition of chronic bronchitis
i.e. more than 4-5 episodes per year, diagnosed radiologically and requiring the
attention of a physician.
# What are the other symptoms of increased PBF?
These are mainly due to CCF and are,
- Failure to thrive
-Refusal for feeds
-Suck-rest-suck cycle (frustrated feeds)
-Sweating of forehead
# What are the Cause /mechanism of Excessive sweating in VSD?
L-R shunt- Volume overload of LV- CCF Tendency of increased sweating
# What would you find on examination in such cases?
- Precordial bulge
- Increased Precordial activity
- Harrisons sulcus
# When do you say the patient has failure to thrive?
- Weight below 3rd percentile
- < 80% of ideal weight
# What the features of 21 trisomy?
31
 Epicanthal folds,
Single crease (simian monkey like- crease) on the palm
Thumb alignment (?)
# In Trisomy 21, what are problems that complicate the heart disease?
Multiple level shunts
Primary abnormality in lung (decreased number of alveoli & blood vessels,
leading to early development of PAH)
Due to mental retardation, there is underestimation of symptoms.
Due to upper respiratory abnormality which makes it more prone to infection.
#Classification of VSD by size?
# How is size of VSD described?
With reference to aortic annulus
< 50%- small
50- 75%- moderate
> 75%- large
With reference to echo
< 7mm- small
7- 15 mm- moderate
>15mm- large
# Heath & Edwards classification of pulmonary vascular disease
I Medial hypertrophy only
II Cellular intimal reaction + Medial hypertrophy
III Intimal fibrosis - Medial hypertrophy
IV Plexiform lesions
V Cavernous & angiomatoid lesions
VI Necrotising arteritis
# What is the Natural history of VSD closure?
-Spontaneous closure in 25- 40%.
- 90% of those determined to close shall close by 10 years.

32
# Ways of spontaneous closure of VSD?
- Overgrowth of nearby tissue (while the VSD does not grow, hence closes),
- Septal tricuspid leaflet,
- Aneurysm of IVS,
- RCC/ NCC prolapsing,
- Infective endocarditis.
- Small defects: most (80%) close on their own.
- Moderate VSD: 50% will close or reduce in size, not requiring intervention.
- Large VSD: rarely close
# VSD becoming symptomatic at later age?
- AR (9years)
- Infective endocarditis- AR, PR, myocarditis
- Pneumonia/ LRTI
- Acquired heart disease
- Eisenmengerization (3rd decade)
# What is the peculiarity of Eisenmengerization, clinically?
Cyanosis is faint; clubbing is never more than grade .
# Reasons why a patient with a large VSD, LRTI improves spontaneously?
- Due to decreased pulmonary flow as a result of development of PAH
- Spontaneous closure
- Gasulisation.
# VSD & aortic size relation?
Larger the VSD, smaller the aorta.
# What is the general distribution of VSDs?
- Membranous= 70%,
- Muscular= 20%,
- Sub arterial= 5%,
- Inlet=5%

33
# Surgical definitions:
- Primembranous: a part of the margin (post-sup angle) by the central fibrous
body (CFB)
- Sub aortic: a part of the margin by aortic annulus (below NCC-RCC)
- Inlet: a part of the margin (posterior) by the tricuspid annulus. CFB not a
part of margin
- Inlet muscular: VSD under the sepal leaflet of TV. Muscle between TV
annulus and VSD
- Infundibular / Outlet VSD: VSD in infundibular septum, above crista,
muscle margins all around
- Sub pulmonic: a part of the margin (superior) by the pulmonary annulus.
The rest as in infundibular
- Doubly committed: pulmonary and aortic annulus form its superior and
postero-superior annulus
# What decides the shunt in VSD.
- Size of VSD
- PVR
- SVR
# What are the common anomalies associated with VSD?
- Coarctation of Aorta
- Infundibular stenosis/ valvar pulmonary stenosis
- Left svc
- PDA
# Why in a large VSD there is only LVVO & no RVVO initially?
With a moderate or large VSD, when the LV contracts, it pushes the blood
across the VSD straight into the PA (as the RV is also contracting). The RV
hence acts like a conduit. In diastole, the excess volume reaches LV from the
LA leading to LVVO, while the RV receives normal volume form the RA
# Why you say the patient has a significant L-R shunt?

34
LRTI, pan systolic murmur, flow murmur across the mitral valve, plethora on
chest
x- Ray
LVVO on ECG
# Definition of pansystolic murmur
Murmur beginning with S1. It is same intensity throughout systole
# Which other conditions give rise to PSM?
MR, TR & Gerbode defect
# How do you distinguish the conditions?
TR:
v waves on JVP,
Pulsatile liver,
RV activity,
Murmur along the LSB staring at xiphisternum
MR:
PSM at the apex conducted to axilla.
MR due to prolapse of PML - conducted along the LSB

Gerbode defect:
PSM on rt. sternal border.
JVP out of proportion to PAH
# How, on auscultation type of VSD can be diagnosed?
- Murmur starting at 4th/5th spaces conducted along the LSB- Perimembranous
VSD
- Over precordium - Mid muscular VSD
- 2nd/3rd space - Subpulmonic VSD
# What is effect of PAH on PSM?
The murmur gradually becomes soft and short. An ESM is finally heard due
to dilated pulmonary artery.
# VSD without PAH, but without pansystolic murmur?
35
Small muscular VSD (defect is occluded by the contracting myocardium)
# Prominent aortic knuckle (Large aorta) in a patient with VSD, PAH, on
CXR?
- AR
- Coarctation
- PDA
# What are the features of significant shunt on investigation?
CXR: Large heart, small Ao knuckle, LV contour, plethora
ECG: q in V4, 5, 6, LVVO
Echo: Qp/Qs > 1.5-2/1 as judged on TV and MV flows
LA/aorta ratio > 1.2/1
LVVO appropriate for the age
Cath: jump in Saturation > 7% at ventricular level.
# Gasulisation of VSD
Development of PS in patients with VSD
1st described by Gasul
Gasulisation has highest chance of occurring in VSD with rt. Aortic arch
# D/D between Gasulisation & TOF?
- Gasulisation (Gasul originally described in a 3 year old child
- There is late onset cyanosis
- LV is well developed
- Malaligned VSD is absent
- Predominantly infundibular narrowing
- No aortic override
# Small VSDs pose a threat of infective endocarditis.
Risk of IE Vs morbidity/ mortality of surgery favours no intervention of small/
moderate sized VSD.
But once 1 episode of IE has occurred, surgery should be performed, as
chances of re IE are high.

36
# What will you see on X ray of VSD
- Cardiomegaly
- Prominent Aorta & PA
- LV Contour
- Pulmonary plethora
# Cardiomegaly in VSD
- VSD + AR/PR/TR
- During LRTI
- CCF
# VSD with prominent aortic knuckle
- VSD with PDA
- VSD with AR
- VSD with CoA
- VSD with PS with R-L Shunt with overriding aorta
# Rt. aortic arch in VSD
2% of cases
# What is rt. aortic arch?
When arch arches over the rt. Bronchus is called rt. Aortic arch
# How do you find out rt. Aortic arch?
- Rt. Side of spine descending thoracic aorta
- Tracheal gas indentation
- Occasionally on Barium swallow
- Cath
# What are causes of VSD with CTR > 65%?
- Multiple shunts
- AV canal
# What is the usefulness of ECG in VSD
-ve axis with CCWL s/o AV canal, inlet VSDs
Axis of QRS acc to PAH
q in V4,5,6 s/o LVVO
37
 Katz -Watchel phenomenon ( R=S, R+S=> 35)s/o BVH
# What are the problems of diagnosing PAH on ECG?
Due to LVH, RVH voltages may be masked
Infants: RVH voltage seen due to infantile PAH (which is not related
to VSD)
RAD due to PAH not seen in pts with LAD
# Causes of RHB prominent in VSD
PAH- RV failure
Additional ASD
# Which is the best view to visualize VSD on echo?
- Perimembranous VSD subxiphoid long/short axis view or apical 4
chamber view
- Out let VSD Short / long axis view with lateral angulation of
transducer
- Inlet VSD Subxiphoid long/short axis or apical 4 chamber view
- Central muscular VSD Short axis / apical 4 chamber view
- Marginal defects in apical muscular septum difficult to see Doppler is
useful
# Problems of VSD on Echo?
- Small VSDs can be missed
- VSD seen depending on direction of cut
- May report large VSD when actually small VSD
# When additional Valvar PS is suspected?
Cyanosis, usually mild
Soft P2, additional murmur
RVH forces out of proportion to P2
Doming of valve, gradient across more than 40mm of Hg.
# How L SVC is diagnosed on echo?
Dilated CS (other causes: CCF, TAPVC to CS)
Contrast echo
38
# What are the indications for cardiac catch in VSD?
- Decide operability (pts with severe PAH)
- Severity PS
# Causes of high saturation in SVC?
- Lt PAPVC
- Supracardiac TAPVC
# High sat in IVC & low in SVC?
- Rt. PAPVC
- Scimitar Syndrome
- Infracardiac TAPVC
# IVC saturation is always higher than SVC saturation
Because Kidney & liver do not extract O2.
# Why there is drop in saturation in midRA onwards?
Because of CS opening
# Causes of jump in saturation in RVOT
- Outlet VSD
- Any VSD
- RSOV into RV
- APwindow with PR
# Catheter course in VSD
IVC-RA-RV-MPA-branch PA-normal
IVC-RA-RV-VSD-Aorta-in VSD
# Oximetry in VSD
Step up of Oxygen saturation
RV inlet Inlet VSD & AV canal type of VSD
RV out let Out let VSD
MPA Subpulmonic VSD
# Which VSD you will call restrictive /non restrictive?
Restrictive VSD Pressure gradient > 10mmHg
Non restrictive VSD Pressure gradient < 10mmHg
39
# How will you calculate shunt?
Qp = Vo2 / (PVo2-PAo2) (O2 capacity) L/Min
Qs = Vo2 / (Ao2-MVo2) (O2 capacity) L/Min
Qep = Vo2 / (PVo2-MVo2) (O2 capacity) L/Min

VO2 O2 consumption
5-15 years 110-160 ml/min/m2
0-5 years 160-200 ml/min/m2

PVo2 & Aortic saturations take 100 %( 1)

VO2 =VE (FiO2-FeO2)
VE Expired volume
FiO2- Inspired oxygen
FeO2- Expired oxygen
Or
Use La Farge & Miettinens chart of VO2 based on age, sex, heart rate
O2 capacity = 13.6 x Hb
L-R Shunt = Qp Qep
R-L Shunt = Qs Qep
Net Shunt = L-R Shunt R- L Shunt
# How will you calculate PVR & PVRI?
PVR = Mean PA pressure LA Pressure (PCWP) / Qp
PVRI = PVR x BSA Woods unit
PVRI = PVR x BSA x 80 dynes/sec/cm-5
# How will you calculate Two shunts?
S = Flow (Qs) x a-b/ c-a
S= Shunt, Flow = Qs
a = O2 saturation in shunt receiving chamber
b = O2 saturation in proximal chamber
c = Pulmonary venous saturation
40
S = Previous shunt + Qs x a-b/c-a
# What will you see on X ray of VSD?
- Cardiomegaly
- Prominent Aorta & PA
- LV Contour
- Pulmonary plethora
# Cardiomegaly in VSD
- VSD + AR/PR/TR
- During LRTI
- CCF
# VSD with prominent aortic knuckle
- VSD with PDA
- VSD with AR
- VSD with CoA
- VSD with PS with R-L Shunt with overriding aorta
# What is rt. aortic arch?
When arch arches over the rt. Bronchus is called rt. Aortic arch
# How do you find out rt. Aortic arch?
- Rt. Side of spine descending thoracic aorta
- Tracheal gas indentation
- Occasionally on Barium swallow
- Cath
# What are causes of VSD with CTR > 65%?
- Multiple shunts
- AV canal
# Criteria for inoperability of VSD
- Exertion cyanosis
- Silent precordium
- Palpable P2
- Disappearance of PSM or MDM
41
 - CxR Normal sized heart
Prominent central Pas with peripheral pruning
- ECG RVH with pressure overload/ strain pattern
- Cath
Absence of baseline shunt with very minimal increase in shunt
Shunt < 2:1 Reduce with O2
PVRI > 8WU Not coming down below 7 /6.8 WU after Vasodilators
PAEDP > 40mmHg, PAMean> 60mmHg
# What should be the timing of surgery in VSD?
Preferred as early as possible from point of view of regression of PH
Competence of the centre also should be kept in mind
# Surgery advised if:
Qp/ Qs> 1.5-2/1
PVR should be less than 10 Wood units.m2
# Do you close VSD always?
- No
- Severe PAH & Pulmonary hypertensive crisis Low Cardiac output
develops To improve cardiac output leave VSD open
- Palliative Senning in setting of PAH Create Apical VSD
- In TGA+ IVS+LVOTO Puga Technique & Rastelli operation Create VSD
- IN DORV/ TGA VSD PS with restrictive VSD Enlarge VSD
Anterosuperiorly
# Which associated anomalies are difficult to detect on table
Valvar PS, additional apical muscular VSDs
# What are the various approaches for VSD?
- RA: incision : longitudinal, parallel to AV groove:
For Perimembranous, inlet, inlet muscular VSDs
- RV : incision: longitudinal or transverse on infundibulum:
for Perimembranous, infundibular, Subpulmonic VSDs, if asso. PS-
longitudinal incision
42
 - PA: incision : longitudinal /transverse
For: Subpulmonic and infundibular VSDs
- Aorta: for VSD AR , RSOV into LV : multiple muscular VSDs ( LV side
of septum is smooth ,so better visualization), post MI VSD
# When you close VSD directly?
VSD less than 4mm is closed directly.
Midmuscular VSD
# Why other VSDs are not closed directly?
Perimembranous VSD Conduction tissue comes
Outlet VSD Av valve distortion
Inlet VSD Conduction
# Criteria for device closure of VSD
Moderate small sized VSD
Good surrounding margins
Not near conduction Perimembranous & Inlet VSD
At least 1cm away from the aortic valve
# What are the devices used to close the VSD?
Rashkind umbrella device
Amplatzer device
Clamshell device
# VSD is enlarged in which conditions?
DORV with restrictive VSD
# How do you enlarge VSD?
The anterior margin is excised between aortic valve superiorly and septal-
papillary muscle inferiorly.
# How much do you enlarge?
As large as the out flow i.e. aorta /PA
# What structures can this damage
Septal arteries
# Materials used for VSD closure?
43
- Double Velour Dacron
- Pericardium
- PTFE
# What are the advantages of Dacron
Good needle handling characteristics
# What are the disadvantage of Dacron as a patch.
- Hemolysis
- Clot formation
# What modifications of DVD help in overcoming these problems?
Sauvage filamentous Dacron has smooth one side (for LA) and valoured other
side.
# VSD is not found during surgery?
- See opposite to the jet effect
- Stop left heart vent and check the entry of blood
- Fill up the LV gently
- Detach STL and look at the inlet.
- Apical part of the septum
- Open aorta & see from the LV side
# How will you close VSD from RV Approach?
Transverse Incision at the junction of RV body & infundibulum
Level of incision is at aortic annulus
Cut with 15 blade
Take 1st stitch on papillary muscle of lancisii
Go away from margin at least 5-6 mm
# Why not incision on infundibulum / RV body?
Infundibulum Exposure of VSD difficult
RV Body RV function deteriorates
# Disadvantage of transverse incision
Enters AV groove
If extends laterally Lad gets damaged
44
# How will you close VSD?
Bundle is at risk at the postero-inferior margins of the Perimembranous VSD
It runs parallel with & about 2-3 mm from the tricuspid annulus to the conus
region
Placing suture through the base of the septal tricuspid leaflets till a point 5-6
mm below the defect
Placing sutures precise margin of the defect or 5-6 mm below the edge of the
defect
All stitches parallel to the course of the bundle & no stitch at right angle to it
# How will you check leak in the patch?
Small rt. Angle / nerve hook
Discontinue LV vent Check leak
Inject water through PFO into LV
Examine when heart is beating
# Drugs/ conditions that worsen PAH
- Ketamine, Nitrous oxide
- Hypoxia, hypercarbia, acidosis
- Crying, straining, coughing
# Timing of surgery
Large VSD
Infancy: No surgery if- Coarctation, Swiss cheese
Surgery

Early (if large with uncontrolled CCF) others by 6 months (wait for
spontaneous closure)

If PVR > 4 Woods/ m2, or If PVR < 4 Wood/ m2
PASP > 50% of SBP

Surgery Defer surgery till 12 months
45
Till 1 year of age, a VSD with however high the PVR is operable.
After infancy:
Surgery if:
- PVR < 8 Wood/ m2
- Qp/Qs > 1.5/1
- PVR/ SVR < 0.5/1
- If PVR is > 8 Wood/m2 but falls to < 7 Wood/m2 with Isoprenaline (0.01-
0.1 ug/Kg/min in PA)/ Tolazoline (1 mg/ Kg in PA)

Surgery contraindicated (inoperable) if:

- PVR > 8 Wood/m2 & no fall with Isoprenaline
- Qp/Qs < 1.5/1 which falls to < 1/1 after exercises

Moderate VSD
Symptoms present: Surgery
Asymptomatic/ few symptoms:

If PAP< 50 mm Hg, or If PAP > 50 mm Hg
Qp/Qs < 3/1

Observe till 5 years Surgery

If does not close or significant shunt- surgery
Small VSD
Young patient- no surgery
> 10 years age- individual decision (general consensus is to leave alone)
If IE develops, then medical treatment followed later by surgery or if CCF/
increase in CTR/ AR- surgery.
# Pulmonary hypertensive crisis
Definition
46
It is a phenomenon seen post CPB characterized by a rapid rise in pulmonary
arterial pressure (to even suprasystemic levels) with associated systemic
hypotension, hypoxia & acidosis.
Mechanism
Decrease in prostacyclin/ thromboxane A2 ratio
Platelet activation factor
Endothelin release
Endothelial dysfunction
- Precipitating causes
Acidosis
Hypoxia
Hypercarbia
Endotracheal suctioning
Restlessness
Administration of adrenaline/ high dose of dopamine
Types of crisis?
2 types
Minor- elevation of PAP to/ less than systemic PH
Major- elevation of PAP to suprasystemic PH
Prevention
Phenoxybenzamine: 1 mg/ Kg pre operatively followed post operatively by 0.5-
1 mg/Kg/ dose- 8 hrly doses for 4 weeks.
Use fentanyl instead of morphine
Keep electively ventilated for 24- 48 hrs with a PaCO2 < 30 mm Hg & PaO2 of >
100 mm Hg.
Management
Immediate paralysis with vecuronium, 100% FiO2 ventilation
Maintain PaCO2< 30 mm Hg & PaO2> 100 mm Hg
Fentanyl infusion
If Inotropes required- use Isoprenaline
47
NTG/ SNP/ aminophylline/ tolazoline
Prostacyclin may be used
Gradually decrease FiO2 to 50%
After 24 hours start weaning off
Newer- NO, ECMO/ LVAD
Others:
Continuous PA perfusion during CPB
Flap closure of VSD (controlled fenestration)
Oral Endothelin receptor antagonist- Bosentan
Phosphodiesterase V inhibitor- Sildenefil.
# Dose of NO (Nitric Oxide)
5-20 parts per million (PPM) increase in increments of 5 PPM till 80PPM (Max)
Wean by 5 PPM slowly till 20 PPM see for hemodynamics taper till 5 PPM &
stop
# RA approach:
Cannulation considerations: direct SVC, a posteriorly placed IVC cannula is
helpful in space for incision parallel to AV groove cannula does not obstruct the
view
Venting: through VSD, through PFO/ stab the Fossa ovalis.
# Where do you look for Perimembranous VSD?
In the ATL-STL commissure
# How do you expose this VSD?
- No pad under LV, op-table neutral position
- Retract the STL with a stitch (5- 0/6-0 prolene) towards surgeons right
- Small right-angled retractor retracts the ATL and ATL-STL commissure
towards assistants right
- VSD retractor retracting the inferior margin will further improve the exposure
OR
- Stiff craniotomy suction to retract the inferior margin and suck left heart
through VSD.
48
# WhichPerimembranous VSDs are difficult to view, in this approach?
One with outlet extension
# VSD is partly covered by chordae - how will you manage?
- Needle passes in & out through the same gap
- If suturing is by keeping the patch outside all sutures should be through
the same gap
- Detach the septal leaflet 2-3 mm from the annulus, retract towards ATL, and
suture the VSD
- Detach the chordae, retract towards the RA, and suture the VSD
# How you suture the VSD
Principles:
- Distal to proximal (RA approach the antero-superior margin is sutured first)
- Pulling the previous stitch/bite exposes the next stitch/bite
- Mention continuous /interrupted; prolene/ethibond;pledgetted /
nonpledgeted
# How conduction system is avoided?
- In any Perimembranous VSD (i.e. with any suffix to Perimembranous) the
conduction system is along the postero-inferior margin, i.e. along the
surgeons right side
- Transverse mattress sutures 4 to 5 mm away from the margin OR
passing needle parallel to the conduction bundle
- Suturing to the septal leaflet
# Management of Post Operative heart block
R/o &treat hyperkalemia, acidosis, hypothermia
Pharmacological pacing with Isoprenaline
Electrical pacing: place two wires, 2 to 4 cm apart (so they do not touch each
other) on a healthy anterior RV surface. Wires can be passed through the
myocardium directly, if has a built in needle OR fixed with a 5/6-0 prolene.
Ideally, one of the wires should be on diaphragmatic surface of RV, as to mimic
the progress of the current more naturally.
49
# How do you set a VVI pacemaker?
-Increase the sensitivity till ALL the complexes are sensed. This is done by
reducing qrs voltage
- Value required to sense.
# Set the pacing rate much higher (120beats/min) than the intrinsic rate
(40-50beats /min).
# Increase the output (in ml Amp.) till ALL the pacing impulses are captured.
# RV approach
- Cannulation considerations: nil
- Venting: through VSD, RSPV, PA (distal part of RV incision)
# What are the RV incisions
# Longitudinal: on infundibulum (part of RVOT seen above the aortic annulus
level)
# Midway between LAD and RV branches of RCA, in line with the axis of MPA
# Transverse: between the RV branches and parallel to them.
# How do you choose the incision?
- Longitudinal: when associated RVOT obst. more familiar ( due toTOF
correction) but cuts through the circular infundibular muscle and vessels, inlet
extension difficult to visualise
- Transverse: more physiological, better visualization of posterior margin of
VSD & inlet extension. But associated RVOTobst. Difficult to manage,
particularly if patching is required.
# Where do you look for Perimembranous VSD?
Just below the crista, in the ATL-STL commissure surgeon looks towards
RV inflow thru the incision
# How do you expose this VSD?
- Sponge pad under LV, op-table turned towards the surgeon. incision
retracted with suture.
- VSD retractor in the antero-superior angle of VSD and is pulled towards
patients right shoulder
50
- A small right-angled retractor in the inferior angle of RV incision pulling
towards the diaphragm.
-Three retracting sutures help: 1. at the base of papillary muscle of lancisii, 2.
fibrous body 3. Antero- sup angle
# WhichPerimembranous VSDs are difficult to view, in this approach?
One with inlet extension
# How you suture the VSD
Principles: Distal to proximal (in this approach, postero-inferior margin)
Pulling the previous stitch/bite exposes the next stitch/bite
Mention continuous /interrupted; prolene/ethibond; pledgetted /
nonpledgeted

PATENT DUCTUS ARTERIOSUS

# What is your diagnosis?

CAHD, L-R Shunt at great vessel level, with pulmonary hypertension in Sinus
rhythm without CCF, Thromboembolic episodes & Infective endocarditis,
Probably PDA.
# What is the hallmark of shunt at Great vessel level?
- Continuous murmur
- Flow murmur at Mitral area (< Gr 3/6 MDM)
# What are the causes of continuous murmur?
- PDA - Any age
- AP window - Up to 5 years of age
- ALCAPA - Up to 3-4 years of age
- RSOV - Any age
- VSD -AR - Any age
- Venous hum
- Mammary shuffle
- Coronary arteriovenous fistula
51
- Pulmonary arteriovenous fistula
# Why not AP window?
AP window - Continuous murmur in left 3rd /4th intercostals space.
PDA - Continuous murmur in left 2nd / 3rd intercostals space.
# Why not ASD?
- JVP normal
- No parasternal heave
- No wide fixed split
- No Ejection systolic murmur at left parasternal region
- No MDM at tricuspid area
# Why not VSD?
- JVP normal
- No parasternal heave
- No pan systolic murmur at lt. lower sternal border
# Why not RSOV?
- No history of sudden onset of chest pain/ difficulty in breathing
- No parasternal heave
- Continuous murmur at Left lower parasternal border (RSOV-RV/RVOT)
(Classical train in tunnel /Machinery murmur)
# Why not VSD AR?
PDA - Continuous murmur - starts in systole just after 1st heart sound, peaks
near 2nd heart sound & spills over into Diastole.
Systolic component is heard any where on precordium but diastolic component
is limited to pulmonary area.
VSD AR - Systolo- diastolic murmur
2nd heart sound heard distinctly
Diastolic murmur heard at apex
# What is the characteristic findings in PDA/Why PDA?
- H/O Recurrent respiratory tract infection (RTI)
- H/O failure to thrive
52
- H/O maternal rubella syndrome
O/E -
- JVP Normal
- No parasternal heave
- LV type of apex
- Continuous Gr 4/6 machinery murmur in left infraclavicular area
- Gr 2/6 Mid diastolic murmur at mitral area
# What will be the picture if PAH is severe?
- Only systolic murmur is heard
- P2 will be loud
# Causes of LRTI in L-R Shunt
- Increase PBF - Increase mucus production- retention & infection
- Increased flow Tissue oedema & lymphatic stagnation
# Symptoms of increased PBF
- Failure to thrive
- Repeated RTI
- Refusal to feed
- Suck-rest-suck cycle
- Sweating of forehead
- Pounding of chest noted by parents
- Retarded growth
# What is failure to thrive?
- Weight below 3rd percentile
- <80% of ideal weight
# What is repeated/Recurrent RTI?
> 5-6 episodes/ year diagnosed radiologically & requiring treatment
# What is suck-rest-suck cycle?
- Feeding pattern typical in L-R shunt
- A hungry infant awakens from a fretful sleep, vigorously feeds only to stop
short of satisfaction because of dyspnoea, falls asleep again, exhausted by the
53
effort & awakens shortly thereafter with renewed hunger, only to repeat the
frustrating cycle.
# Why the growth is retarded in L-R shunt?
- Repeated RTI - Increased catabolism
- Decreased systemic output
# Signs of increased pulmonary blood flow on examination
Examination
- Precordial bulge
- Harrisons sulcus
- LV apex
- Prominent PA
ECG
- LVVO
X ray
- Pulmonary plethora
# What are the problems of L- R Shunt?
- RVVO & LVVO (Leading to failure & arrhythmia)
- Pulmonary hypertension
- Regurgitant lesions
# What is maternal Rubella Syndrome?
Caused by Toga virus
Affects mother through droplet infection
Clinically characterised by
- Fever
- Followed by lymphadenopathy
- Followed by generalised rash, starting from the face
Risk of fetal infection is
- During 1st trimester - 100%
- During 2nd trimester, 1st half - 40%
- During 2nd trimester, 2nd half & 3rd trimester - 0%
54
Features in the Fetus are
- General - IUFD, IUGR
- Ocular - Retinopathy, cataract
- Auditory - Nerve deafness
- CVS- PDA (in 30%), hypo plastic PAs, Valvar&Supravalvar PS, branched PA
stenosis, Myocarditis, TOF, ASD, VSD, AS
Next baby is immunised as mother is immunised.
# Possible causes of PAH in PDA
- Increased PBF
- Arteriolar vasoconstriction
- Organic occlusive changes in small arteries
- Increased pulmonary venous pressure from LVF
# Disappearance of continuous murmur in PDA
- Increasing PAH & reversal of shunt
- CHF
- Membrane / valve in the ductus
# Anatomical types of PDA
- Conical - with narrow end towards PA (ideal for device closure)
- Conical - with narrow end towards Aorta (rare)
- Tubular
# Which will be the site of PDA with right aortic arch?
On the right side
Some time on the left side going to the left subclavian artery or even more
distal artery
# Natural history of PDA
- Small - Only & high risk of Infective endocarditis
-Moderate & large - High risk of development of PAH (1/3rd by 30 years & 2/3
rd by 40 years)
# When to say Ductus arteriosus a Patent Ductus arteriosus?
When the ductus arteriosus fails to close spontaneously by 3 months of age
55
# Why PDA presents early?
- Systolic & diastolic overload
- Pressure & Volume overload
# Why close even small PDA?
Risk of Infective endocarditis is high
# Risk of IE in PDA 0.4/100/year
# What is obligatory PDA?
Persistent patency of the ductus after birth is desirable for certain forms of
CCHD is called Obligatory PDA
- PDA is the only source of blood flow to PA - Pulmonary atresia with intact IVS
- PDA is the only source of blood supply to Systemic artery - IAA
- PDA constitutes the only means of bidirectional mixing- TGA with IAS/IVS
Also called duct dependant circulation
# What is the difference between prolonged patency & persistent patency
of ductus?
- Prolong patency - When the process of closure delayed
- Persistent patency - When the closure fails to occur ultimately
# When the ductus will close?
- 1st stage - Functional closure - 10-15 hours of birth - contraction of smooth
muscle in the media
- 2nd stage - Anatomical closure - completed within 2 3- weeks - diffuse
proliferation of intima associated with necrosis of inner layer of the media &
haemorrhage into the wall.
# What are the factors influencing ductal closure?
- Release of vasoactive substances - acetylcholine, bradykinin, endogenous
catecholamine
- Variation in PH
- Oxygen tension (Increasing tension closing the ductus)
- Prostaglandins (PGE1, PGE2)
- Prostacycline (PGI2)
56
Increase in oxygen tension (PAO2) - constrict the ductus
PG - relax it
Ductus is hypersensitive to O2 tension in mature fetus
More sensitive to PG in immature fetus
# What is the angle PDA with aorta?
- Proximal angle - Acute 10-40 degree
- Distal angle- Obtuse 110-160 degree
# What are the complications of PDA?
- RRTI
- CCF
- Calcifications
- Aneurysm
- Rupture
- Eisenmenger's complex
# What is normal pulmonary artery pressure?
Normal PA pressure
15-30 systolic
10-15 diastolic
5-10 mean
# PAH by PA pressure
Systolic Mean
Normal 15-30mmHg 5-10mmHg
Mild 30-45mmHg 20-30mmHg
Moderate 45-75mmHg 30-50mmHg
Severe > 75mmHg > 5-10mmHg
# Classical ECG findings in PDA
- Normal axis
- Sinus rhythm
- LVH
- LV diastolic volume load
57
# What is the criteria of LV diastolic overload?
- Presence of 'q', Tall R wave & Tall T wave in V5-6
# What are the Criteria of LVH from ECG?
A) Scott's criteria
1) Limb leads
- R in I + S in III > 25mm
- R in aVL > 11mm
- R in aVF > 20mm
- S in aVR > 14 mm
2) Precordial leads
- S in V1/2 + R in V5/6 >35mm
- R in V5-6 > 25mm
- R + S in any precordial lead > 45mm
B) Sokolow - Lyon criteria
- S in V1 + R in V5-6 > 35mm
- R in V5-6 > 25mm
C) Cornell Voltage criteria
- Female - R in aVL + S in V3 > 20mm
- Male - R in aVL + S in V3 > 28mm
# What are the criteria of RVH from ECG?
- RAD > 110 degree
- R/S ratio in V1 > 1
Or
- R/S ratio in V6 < 1
- R in V1 = 7mm
Or
- S in V1 = 2mm
- With RBBB - R wave > 10mm in V1
- R in V1 + S in V5-6 > 11mm

58
# What are the ECG criteria of Biventricular hypertrophy?
- Voltage criteria of LVH in precordial leads + RAD in limb leads.
- LVH in left precordial leads + Prominent R wave in rt. precordial leads
- Katz- Watchel phenomenon - Most common in VSD
Equiphasic complexes in two or more limb leads & in mid precordial leads
# What are the characteristic X- ray findings of PDA?
- LA/ LV enlargement
- Enlarged Ascending aorta
- Presence of convex shadow between Aorta & PA
- Pulmonary plethora
- Calcification of duct
# What do you want to know from Echo?
- Confirm diagnosis
- Size of PDA
- Gradient across PDA
- LV volume overload
- Associated lesions like CoA, MR, VSD, ASD, and APW
- Shunt
- Ventricular function
# Indications for cath in PDA
- Border line PAH
- Clinically
o Symptomatic earlier now asymptomatic / minimal symptoms of
L-R shunt
o Only systolic component of murmur present
o Loud P2
o ECG - BVH, no LVVO
o Echo- Large PDA, Bidirectional shunt, smaller gradient
- For Coil /Device closure

59
# What data you want to know from Cath?
- Step up at PA level
- PA pressure.
- L-R Shunt basal & Post O2
- PVRI basal & Post O2
# Classical catheter course of PDA
FV-IVC-RA-RV-PA-PDA-descending aorta
# What are the different treatment modalities of PDA?
Pharmacological closure of PDA
Within one week of birth
Using NSAIDs
Indomethacin: 0.2 mg/ Kg/ dose- 12 hourly dosages x 3
Ibuprofen: 10 mg/ Kg- 1st dose
5 mg/ Kg- 2nd dose
5 mg/ Kg- 3rd dose
(All at interval of 24 hours)
A study from Belgium (NEJM 2000) showed equal rate of ductus closure in
both the groups (Indomethacin Vs ibuprofen) of 70%. However a significant
difference in the incidence of post therapy oliguria (high for Indomethacin)
Device closure of PDA
< 3.5 mm- coil
> 5mm- Amplatzer device
3.5- 5.5mm- any of above
> 1cm Contraindication for Device
Surgical treatment-
- Ligation
- Division & Suturing
- Transfixation
- VATS-clipping

60
# Timing of surgery in a PDA?
- Symptomatic: Immediate closure
-Asymptomatic: Wait till 8 weeks to close. Age for surgical closure is between
6- 12 months
-Signs of inoperability-
- PVR > 8 Wood/m2 & no fall with Oxygen / Isoprenaline
- Qp/Qs < 1.5/1 which falls to < 1/1 after exercises
# Which space you will open?
4th intercostals space
# Which structures will you come across while opening Mediastinal
pleura?
Superior intercostals vein drains into Left brachiocephalic vein
# How to identify PDA?
- Lies just beneath the arch opposite to the left subclavian artery, on the
outer curvature
- The superior intercostals vein crosses over the aorta at the point of PDA
- Aorta is slightly bulbous at that point
- It is conical structure with the base towards aorta
- Recurrent laryngeal nerve winds around it
- Thrill present over the PA.
# How is arch identified?
Trace base of the left subclavian artery medially
# While dissecting the duct which structure will come in your way behind
the duct?
- Ladds band
- Tough in adults
# What suture will you use for ligation?
Ductus silk / Ordinary silk no 2 or 3
# Will you ligate doubly/triply & why?
It depends on surgeons choice
61
I will ligate doubly & if needed for added security triply.
# How will you ligate PDA?
Under controlled hypotensive anaesthesia with no 2 or 3 Silk
With equal pressure with both hands.
# What do you mean by controlled hypotension?
I will ask anaesthetist to reduce the BP to 60mmHg using Magnesium, NTG,
SNP, and Halothane
# Why 60 mmHg only not 40 or 80mmHg?
- At 80mmHg pressure Aorta will be tense & there is a chance of
rupture
- At 40mmHg pressure it will affect the perfusion of the other organs
- 60 mmHg pressure is safe & sufficient to ligate the duct
# Advantage of induced hypotension during ductus surgery?
- Ductus becomes less tense (less chances of tearing)
- PA & aorta fall apart (retraction for looping easy
- Clamping of PDA possible
# Ways of inducing hypotension?
Halothane: easy but myocardial depressant- hypotension and bradycardia
Post op patient drowsy
Sodium nitroprusside quick, messy preparation
Nitro glycerine less efficient than SNP, less messy preparation
Intranasal nifedepine (occasionally) not controllable
Magnesium- Controls rate & BP
# Which end will you ligate 1st& why?
Ligating aortic end 1st followed by pulmonary end because if duct tears there
will be a sufficient length to hold the pulmonary end.
It is not a hard & fast rule but any end can be ligated 1st.
# What you will look/check before ligating duct?
- Clamps on the table
- Thrill over the PDA
62
- BP of 60mmHg
# Confirmation of closure of ductus on ligation?
- Disappearance of thrill
- Absence of murmur over ET tube
- Increased DBP
- TEE
# Complications of PDA surgery?
- Tear of PDA, usually the posterior surface
- Recurrent laryngeal nerve injury- Hoarseness of Voice
- Vagus nerve injury (manifests as resulting in gastric distension) due to
dissection around PDA
- Chylothorax
- Sinus tachycardia
- Systemic hypertension-1st 24-36 hours due to disturbed aortic arch
reflexes
- Recanalisation
- Infection
- Aneurysm formation
# How will you manage the Ductal aneurysm?
Ductal aneurysm forms due to infection
Aneurysm of the pulmonary end treated by excision & repair or
Pneumonectomy
Aneurysm of aortic end-
If small & non leaking Mobilize aorta above & below, Excise the aneurysm &
repair the defect with Patch
If large / leaking aneurysm-On bypass
Mobilize aorta, Total circulatory arrest, Excise & repair with patch
# Causes of intraoperative tear of ductus.
Short & large, aneurysmal ductus
Inflamed ductus
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 Tense ductus
# Site of tear?
Mainly posteriorly
# Management of torn ductus?
- I will put index finger & thumb over the aorta & compress it
- Ask for assistant if not there
- Ask assistant to put his finger & compress
- Ask anaesthetist to replace the volume
- I will loop aorta above & below if not looped
Clamp arch and descending aorta
DeBakey clamps on either ends of ductus (if already dissected)
Divide PDA reapply Cooley clamps
Or
Descending aortic cannulation & RVOT cannulation- on bypass- cool
to 32C
Head low (to avoid air going into arch- cerebral vessels)
Circulatory arrest (or trickle flow)
Divide PDA completely clamp either ends with Cooley clamps restart
the circulation
Or
Clamp the ascending & descending aorta, open the pericardium & clamp the
PA- fibrillate the heart- divide &suture.

# Will you loop aorta for all cases?

For early cases of my life I will loop aorta above & below, as my confidence
increases I will not loop.
# Ductus not able to found?
Large ductus. Inferior margin is confused with the inferior margin of arch
AP window.
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# Borderline case of PDA how will you manage?
- After dissecting & looping PDA
- Note the BP & saturation
- Clamp the PDA
- Observe the BP & Saturation
- If blood pressure falls & saturation drops - do not ligate the PDA
- This can be done in cath lab by blocking the PDA with balloon.
# Contraindications of duct ligation
- Pulmonary vascular disease
- Severe PAH
- Large duct
- Inflamed duct
- Calcific duct
- Aneurysm of the duct
- Short & wide duct
# How will manage infected duct?
- Medical treatment till infection gets controlled
- Antibiotics for 3 months before surgery
- Careful ligation if operation is the only way of controlling the
infection
# PDA is ligated with?
- No 2 or 3 silk
- Ductus silk
- Floss silk
# PDA transfixation with?
- 3/0 silk on atraumatic needle
- Purstring at adventitia with 2/0 silk on atraumatic needle
# How will you do division & suturing of PDA?
- Looping the Aorta above & below
- Looping the PDA
65
- Select the clamps
- Lower the pressure & apply the clamp on the PDA
- 1st on aortic side & Next on PA side
- Aspirate the duct with syringe & needle
- Cut the duct with Potts scissor
- Suture the PA end 1st& then aortic end in two layers
- 1st layer whip stitch & 2nd layer over & over suturing
- Release the clamp
- Check for the hemostasis
# PDA D/S on left heart bypass
Atrio-femoral bypass (LA & Left femoral artery bypass)
Indications-
- Very large & short duct
- Ductal aneurysm
- Atheroma & calcific ductus
# Management of Calcific duct
- On CPB
- Described by Goncalves & Estella & Colleagues, later on ODonovan & Beck
- Median sternotomy
- Aortic & SVC/IVC purstring
- After heparin & Checking ACT on CPB
- Dissect the Aorta & MPA till ductus
- Cool the patient
- Clamp the aorta & give cardioplegia
- Compress the PDA opening by compressing the anterior wall of LPA near -
bifurcation of MPA
- Flows down
- Open the MPA & LPA origin
- Out Fogarty /Foley catheter in PDA

66
- If Pulmonary end is non calcific- take purstring suture around the ductus -
opening & tie or put pledgetted sutures & close the opening
- If pulmonary end is calcific- Put Hemashield/ Gortex patch & close the
opening

COARCTATION OF AORTA

# What is your diagnosis?

My diagnosis is age Male/female patient with obstructive disease of Aorta
Probably Coarctation of Aorta/Interrupted Aortic arch or Aortoarteritis.
# What is Coarctation of Aorta?
Coarctation of aorta indicates a narrowing or stricture in some part of this
vessel between the aortic valve & the aortic bifurcation.
# What is Interrupted aortic arch?
IAA is characterized by total luminal discontinuity between arch /isthmus &
the descending aorta.
# How will you classify IAA?
Celoria & Patton 1955 classified IAA
A Interruption distal to LSCA (Left subclavian artery)
B Interruption between LSCA-LCC (Left common carotid artery)
C Interruption between LCC In nominate artery
# How will you classify Coal?
Embryological classification
Infantile CoA
Adult CoA

Anatomical classification
Preductal CoA
Juxtaductal CoA
Postductal CoA
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# What are the criteria for arch hypoplasia according to site?
- Proximal arch- Between innominate artery & left carotid artery Diameter
<60% of ascending aorta
- Distal arch Between LCC-LSCA Diameter < 50 % of ascending aorta
- Isthmic hypoplasia Between LSCA the ductus insertion Diameter < 40% of
ascending aorta
- Arch diameter < 25% of ascending aorta Extended arch repair required.
# Criteria for hypoplastic arch
- Aortic arch diameter < 50% of ascending aorta
- Arch diameter < LSCA
- Arch diameter < Wt (Kg) + 1mm
# Various theories of CoA developments
- Rudolphs flow theory- CoA develops due to disturbance in the balance of
fetal blood flow through the Aorta & PA because of intracardiac defect. no flow
no grow.
Fallacies Not very convincing for a patient with no intracardiac defects
- Skodas ductal sling theory- Abnormal extension of contractile ductal tissue
into the aorta is a significant factor, Explains development of isolated CoA.
- Kappeteins Neural crest theory- Abnormality of neural crest development
- Clagetts embryonic theory Proximal movement of the left 7th
intersegmental artery (LT.SCA) beyond the junction of 6th aortic arch (Ductus).
- Genetic factors- Turners syndrome (XO).
# How will you classify CoA?
- Infantile CoA-Hypoplasia of the Aortic arch & isthmus
- Adult CoA- Presence of ectopic ductal tissue in the aorta at the aortic
insertion of the ductus
# Causes of hypertension in young
- Coarctation
- Interrupted aortic arch
- Renovascular hypertension
68
- Pheochromocytoma
# Mechanism of Hypertension in CoA
- Narrow segment of aorta Diastolic hypertension
- Abnormal rigidity of the prestenotic aortic wall
- Renin-angiotensin Mechanism
- Abnormal Baroreceptors
# Why cyanosis do not develop in Preductal CoA?
- Pressure in proximal & distal aorta is more than PA( Except in infancy)
- If CoA is not severe
- Flow in the intercostals artery is reversed.
# Cyanosis in CoA
-Toe blue & fingers pink CoA + VSD Eisenmengerization
- Fingers blue & Toe Pink (Reverse Cyanosis) TGA + VSD + CoA with
Eisenmengerization
# What will be the status of aorta above & below the CoA?
- Aorta above CoA
Dilated, Thick walled, increased number of elastic lamellae
- Aorta Below the Coal
Dilated, Thin walled, deficient elastic lamellae
# Multiple CoA
- 2% of cases
- Intermittent claudication
- Two murmur
- Collateral vessels in abdomen & back
# Why claudication is not common in Coarctation?
- Because of well developed, since IU life collaterals
- Coarct may not be severe
- Preductal Coarct
# What are the symptoms of CoA?
- Mostly asymptomatic
69
 - Headache,epistaxis,Dizziness
- Atypical chest pain, Pain around shoulder
- Tendency to cold feet or paresthesia
- Intermittent claudication
- Symptoms due to complications like aortic dissection,aneurysm,bacterial
endocarditis
# Heart failure in CoA is due to?
- Closure of ductus Unprepared LV not coping with load of CoA- Lt. sided
followed by rt. sided failure
- When ductus opens above the CoA Load falls on RV leads to
Pulmonary hypertension RV fails
- Associated intracardiac anomaly precipitates failure
# What is the significance of intermittent claudication?
- Described by Wood in 1956
- Occurs in 5% of cases
- Suggest an additional abdominal CoA or development of occlusive
arterial disease of the terminal aorta or its branches especially in > 50
years
# Collateral circulation in CoA
Described by Bramwell & Morgan Jones (1941)
Main vascular bed involved is
- Scapular & internal mammary group above
- Intercostals vessels below
# Which are the collaterals
@ SCA- IMA- ant. intcostals-posterior int. costal desc.Ao
-Musculophrenic- post intercostals-desc.ao
Inferior phrenic - desc.Ao
@ Sup epigastric-inf. epigastric- ext iliac
@ Vertebral-basilar- ant spinal /post spinal- segmental art post intercostals-
desc.Ao
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@ Dorsal scapular scapular anast. -Posterior perforating branches of
posterior intercostals artery
@ Axillary artery- subscapular to scapular anastomosis
-Lateral thoracic- lateral perforator branches of posterior intercostals-
desc.Ao
@ Mediastinal branches of thyro cervical, costo cervical -
pericardial/mediastinal branches of Aorta directly
# What are the auscultatory findings?
- Coarct murmur: continuous or systolic, interscapular 4th space, on left side
- Collaterals- Gr 2-3/6, continuous, same area but laterally on either side
- ESM of bicuspid Ao valve, PSM of VSD, EDM of AR
# What posture is given to pt as to hear Coarct murmur?
Sitting, kyphotic, arms adducted hands on opposite shoulders (in this
posture scapula move apart & muscles are flattened. So, chest piece is near to
the pathology)
# What are the other evidences of collaterals?
Femoral felt but with delay, palpation of collaterals along the lower margin
of rib in the posture described above
# What is the characteristic physique in CoA?
- Trunk & upper limb well developed
- Lower limbs short & less muscular
# What is radio femoral delay?
- Normally femoral pulse precedes brachial pulse,
- In CoA it always follows
- Delay in femoral is not a delay in arrival of pulse but it is slow rise & delayed
peak.
# Radio femoral delay in congenital heart disease?
- Coarctation
- Interrupted arch

71
# Coarctation without delay?
- PDA
- Well developed collaterals
# What is Campbell & Suzmans sign?
Collaterals are can usually be palpated in the rib spaces posteriorly or along
the border of the scapula with the patient bending forward with arms across
his chest.
# Collaterals usually not seen or felt in young children up to 8 years of
age.
# Absence/delay/feeble pulsation in upper limb arteries
- Left radial artery- with low BP Juxta ductal / Preductal CoA
- Right radial artery anomalous origin of RSCA
# Where do you feel the pulsation of arteries / against which bone?
Dorsalis Pedis Navicular &Cuneiform
Tibialis posterior Calcaneum
Anterior Tibial Lower end of tibia
Popleteal Prone Medial condyle of femur, Supine- Back of tibia
Femoral Head of femur
Radial Lower end of radius
Ulnar Lower end of ulna
Brachial Medial epicondyle of radius
Axillary Head of Humerus
Superficial Temporal Temporal
Facial Arch of Mandible
# Eye signs in CoA
- Corkscrew tortuosity
- Serpentine pulsation
- Normal calibre& regularity
- Haemorrhages, Exudates, papiloedema

72
# How to distinguish congenital Coarctation from acquired Coarctation
clinically?
Congenital: Age (birth to 1-2 decade), collaterals present
Acquired: usually 2nd/3rd decade, no collaterals, other upper half body pulses
may be absent
# How do you distinguish Coarct in adult hood from Leriechs syndrome?
Abdominal aortic pulsations palpable, h/o smoking and other risk factors of
atherosclerosis
# Diagnosis of complete interruption is difficult
Because
- Absence of differential cyanosis
- Hypertension in upper limb uncommon
- Femoral pulses are palpable
# CxR in CoA
- Abnormality of Aortic Knuckle-
Elongated
Absent
Double Dilated SCA above & Post stenotic dilatation below
- Dilated ascending aorta
- Docs sign (1948)-Notching of inferior margin of ribs by enlarged
intercostals arteries
- Site of CoA in lateral view-Sudden forward bulge of the barium filled
oesophagus due to the post stenotic dilatation.
# Who has described rib notching?
Meckel 1827 described enlarged, tortuous intercostals vessels
Rosler 1928 & Rails back & Dock 1929 Emphasized the presence of rib
notching X ray wise.
# What is the typical picture of rib notching on chest x-ray
- Classical sign of CoA

73
- Due to collateral blood flow through dilated, tortuous, pulsatile posterior -
intercostals arteries
- Notches originate in costal grooves rather than on the most inferior rib
margins
- Notches may be single, multiple, shallow, deep, broad, narrow
- Notches typically appear as irregular scalloped area on the under surface of
posterior ribs
- Anterior ribs are spared because the anterior intercostals arteries do not run
in costal grooves
- Rarely the superior margin of a rib is notched by a tortuous, over hanging
intercostal artery that makes contact with the rib below
# Absent rib notching in the Children & old patients
Children up to 6years
Elderly poor collaterals
# Bilateral rib notching
Seen in Post SCA CoA (Usual site of CoA)
# Rib notching up to which ribs?
3rd to 9th rib
1st& 2nd rib & beyond 9th rib not involved intercostal arteries doesnt form
collateral circulation
# Rib notching seen in ribs beyond 9th rib
Abdominal CoA
# Unilateral rib notching
- SCA origin involved in Coarct- Rt. sided rib notching
- SCA distal to CoA-Rt. Sided rib notching
- Anomalous origin of RSCA- Lt. sided
# Retrosternal rib notching is seen
In lateral view
IMA dilated & tortuous forms scalloping on the retro sternum

74
# D/D of rib unilateral notching on X ray:
Coarctation with involvement of Left SCA- no left sided notching
Coarctation with origin of right SCA distal to Coarct- no right sided notching
Classical BT shunt
# D/D of bilateral rib notching?
Coarctation aorta
Multiple neurofibromatosis.
# What is pseudo CoA & How will you differentiate it from CoA?
- PseudoCoA is characterised by buckling or kinking of the aorta in the vicinity
-of the ligamentum arteriosum resulting in elongation, tortuosity & dilatation of
the distal aortic arch & proximal aorta
- Absence of narrowing of aortic lumen
- Absence of gradient
- Absence of systemic hypertension
- Absence of Collateral circulation
- On X-ray 3 Sign present but absence of rib notching.
# What is 3 sign
- Proximal enlargement of aorta
- Aortic constriction
- Post stenotic dilatation
# What is E Sign?
When LSCA & descending aorta indent the barium filled oesophagus
# ECG in CoA
- SR
- LVH
- LVVO - If AR / PDA / VSD
# Echo in CoA
Subcostal view Descending aorta continuous flow
Suprasternal view Arch & descending aorta CoA
Parasternal long axis Asso. VSD
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Basal short axis Bicuspid aortic valve
Doppler-
Acceleration & turbulence at CoA
Pressure Gradient
PDA under estimate the Gradient
# Indirect sign of CoA on Echo
Low origin of subclavian artery suggests Juxtaductal /post ductal CoA.
# Indications of cath in CoA
- Inequality of pulses in upper limb
- Unusual site of CoA murmur
- Undue enlargement of aorta
- To know the proximal & distal extent of the CoA.
# Cath Views in CoA
- Descending aortogram Distal extent of CoA & Abdominal CoA
- Aortogram from Rt. brachial/axillary artery Proximal extent of CoA
- PA gram levophase Proximal CoA If Inequality of pulses & Not able to
go through Axillary/brachial artery
- LVgram- trans-septal approach
- Coronary angiogram- Older patient
- Rt. heart cath- CCF
# How will you manage an infant comes with CHF & Report of CoA?
- Admission in ICU
- Secure Arterial & Venous line
- If required intubate the patient & put on ventilator
- Correct acidosis by sodabicarb
- Ventilator setting to keep Pco2- 50mmHg & Po2 60-80mmHg
- After stabilizing the patient I will confirm the diagnosis with 2D Echo
- If prostaglandin is available I would like to give PGE1 0.05-0.1 mg/Kg/min
IV
- Digitalis & Diuretics
76

Measures fails/Patient is stabilized hemodynamically

I will take up for surgery
I will do resection & End-end anastomosis with 6-0 Polydiaxonone (Interrupted)
/Prolene (Continuous) suture
Or
Subclavian flap plasty
Or
Patch aortoplasty
# What are the markers of failure of medical treatment?
- Increase in LA pressure with digitalis
- Increase in PA pressure
- LV & RV enlargement increases
# Ideal time of surgery of CoA
- Ideal time is 5 years of age- asymptomatic
- Dissection / Aneurysm /Infection Urgent surgery
- Infective Endocarditis- 6 Weeks of antibiotic treatment before surgery
# Contraindication for CoA surgery
- Extreme hypoplasia of ascending aorta
- Involvement of Head & Neck Vessels
- Multiple CoA
# Management of CoA during pregnancy
- Elective surgery after delivery
- Watch for infection & aneurysm formation
- Cover with antibiotics
# Indication for surgery in CoA
- Using Echo, CT scan & Aortography reduction of luminal diameter of 50% at
- the site of CoA
- A resting gradient > 20mmHg
77
# What are the approaches for CoA repair?
- Posterolateral thoracotomy through 4th intercostals space
- Trans-mediastinal approach
# Where will you put arterial line?
- Rt. radial & femoral
- If anomalous origin of RSCA temporal artery
# How will you tackle CoA?
- Dissect ,Clamp ,Cut & ligate with 2-0 chromic catgut
- Do not burn the collaterals
- Open the space at the upper border of lower rib
# Which nerves will come in the way?
- Left recurrent laryngeal nerve
- Vagus nerve
# What is Abbotts artery?
- Anomalous artery described by Abbott
- Collateral vessel originating from posterior wall of the aortic arch or SCA
- Not found in normal subject
- Can be controlled with vessel loop or ligated & divided
# How much distal aortic pressure to be maintained & how?
Distal aortic pressure to be maintained > 45mmHg
By
Avoid use of SNP or vasodilator
Administration of volume expanders
Use of Inotropes
Reduce anaesthetic medicine during aortic clamp
If BP falls < 45mmHg, use of CPB / Shunt
# How will you control BP in CoA?
Pre op Beta blocker
Intra op SNP, NTG
Post op Beta blocker & ACE inhibitors
78
# Various techniques of CoA repair
A) Resection & End-end anastomosis-
Crafoord & Nylin 1944 October (12 year boy & 27 year man)
Technique as described by Willis Potts
Excise narrow segment with direct end-end circumferential
anastomosis of aorta
Aorta needs mobilization to avoid tension on suture line
Suture used are
Silk Continuous suture posteriorly, Interrupted everting
horizontal suture anteriorly
Prolene Continuous suture
PDS Continuous / interrupted suture
Advantage
No prosthetic material
Preserves subclavian & its branches
Removes all abnormal ductal &Coarctation tissue
No turbulent flow
Disadvantage-
Extensive dissection
Possible sacrifice of intercostals
Difficult to control bleeding
High incidence of restenosis
Unclear growth potential
Indication Discrete CoA without significant tubular hypoplasia of the
proximal arch
B) Prosthetic patch Aortoplasty-
Vosschulate-1957-Isthmusplasty procedure
Technique-
Longitudinal incision on CoA extended beyond CoA
Proximally up to LSCA
79
 Disruption of posterior CoA membrane
PTFE/Dacron patch
Advantage-
Avoids extensive dissection
Allows simultaneous enlargement of isthmic hypoplasia
Preserves SCA & its branches
Absence of tension on suture line
Easy control of bleeding
Collaterals were preserved
Disadvantage
Risk of prosthesis
Late aneurysm formation opposite to the patch
Indication
Discrete CoA not responding to Balloon dilatation
Diffuse hypoplasia with elongated arch
Infant in failure- failure of medical treatment
C) Prosthetic interposition graft
Robert Gross 1951 Use of aortic homograft
Morris/Cooley/DeBakey/Crafoord 1960 Dacron graft
Indications
Adult
Associated aneurysm
Complex long segment CoA
Recurrent CoA
Unacceptable gradient after initial repair
Advantage-
Allows complete resection of abnormal tissue
No tension on anastomosis
Disadvantage-
Two anastomosis during clamp period
80
 Possible sacrifice of Collaterals
Difficult to control bleeding
Risk of prosthesis
No possibility for growth
D) Subclavian flap Aortoplasty

Waldhausen & Nahrwald 1966

LSCA dissected & ligated at the origin of vertebral artery & opened
laterally
Coal segment opened & SCA turned down on the opened aorta
Can be used as Reverse SCA flap for distal arch hypoplasia
Advantage
Avoids prosthetic material
Growth potential
Avoids extensive dissection
Allows simultaneous enlargement of isthmic hypoplasia
No tension on suture lien
Easy control of bleeding
Simplicity
Short clamp time
Disadvantage
Sacrifice of subclavian & vertebral artery
Indications
Reverse SCA flap Proximal/distal arch hypoplasia, distal arch
hypoplasia
SCA flap Redo surgery, Neonatal CoA
E) Subclavian artery displacement
Meier-Mendonca technique 1985
Tries to incorporate the adventitia of SCA flap aortoplasty while
eliminating the disadvantage of subclavian artery sacrifice
81
 Cut the SCA & Reanastomose over the open aorta at CoA segment with
wider anastomosis
Advantage
Less mobilization of aorta
Preservation of intercostals arteries
Use of autologous tissue & chance of growth present
Preservation of LSCA
Disadvantage
Pathological structure remains inside
Inapplicable for long tubular stenosis
Tension on suture line present
F) Resection with extended end-end anastomosis
Lansmann & associate
Technique-
Dissection of distal aorta up to diaphragm
Proximal clamp between LSCA & LCC artery
Excision of CoA segment & anastomosis of distal aorta on the
under surface of arch
Advantage
Growth potential
Less chance of recoarctation
Arch repair possible
Disadvantage-
Extensive dissection
Sacrifice of intercostals
Difficult to control bleeding
Indication
Significant tubular hypoplasia in the isthmus or the distal &
proximal portion of arch
Modifications of Technique
82
 Elliot transverse arch hypoplasia Clamp the Carotids &
innominate artery
Zannini radically extended end-end anastomosis through midline
G) Jump graft
From proximal normal segment to distal normal segment
Advantage
Avoids need to clamp aorta completely
Minimal dissection
Disadvantage
Risk of prosthesis
Leaves area of turbulence at native CoA
Risk of infective endocarditis
H) Balloon Angioplasty
Sos et al 1979 used the technique
Indications-
Native CoA in selected infants & major systemic illness
Recoarctation
Complications
Aneurysm formation
# What is Blalock-Park technique?
- Described in 1944
- Division of LSCA with anastomosis to the descending aorta to bypass the
obstruction.
# What is recoarctation?
Systolic arm to leg pressure gradient or measured by Doppler is >/= 20mmHg
# Rate of restenosis in various techniques
Resection & end-end anastomosis 9%
Patch enlargement 42%
Subclavian flap 0%
Subclavian transfer 43%
83
# Complications of CoA
A) Pre op
Rupture of Aorta
Occlusive atheroma
CVA
Intercostal aneurysm
Infective endocarditis
Heart failure
B) Per op / Intra op
Haemorrhage
Recurrent laryngeal nerve injury
Phrenic nerve injury
Declamping syndrome
C) Immediate post op ( Within 24 hours)
Systolic hypertension
Paraplegia
Stroke
D) Late post op ( After 24 hours)
Chylothorax
Abdominal pain (Postcoarctectomy syndrome)
Paradoxical hypertension
Left arm ischemia
E) Chronic
Recoarctation / Stenosis
Aneurysm formation
# Paradoxical hypertension-why paradoxical?
As post relief of Coarctation the BP rises instead of falling.
2 phases are present generally
Early phase: Mainly systolic (within 24 hours)

84
Due to loss of stretch on the Baroreceptors of the aortic bodies/ carotid body
leading to increased catecholamine release.
Late phase: after 2- 4 days, lasts for 2- 4 weeks.
Mainly diastolic.
Associated with higher levels of rennin angiotensin, perhaps a response of
phase I.
# Problems of paradoxical hypertension
- Bleeding
- Mesenteric arteritis causing ischemia
# Prevention of paradoxical hypertension
- Preoperative: blockers
- Post operative: SNP, enalapril, propranolol.
# Causes of persistent post op Hypertension
Abnormalities in
Tone in peripheral vascular beds
LV kinetic state
Baroreceptor sensitivity
Presence of residual stenosis
# What is Postcoarctectomy syndrome?
Also called Mesentric arteritis
Described by Sealy in 1953
Occurs in 2-28% of patient
Almost always associated with paradoxical hypertension
Onset of Abdominal pain on 3rd po day characterized by abdominal pain,
tenderness, Ileus, Vomiting, Fever, Melena, leukocytosis- Progressive bowel
necrosis & death
Mechanism-
Sudden increase in pulsatile blood flow after repair of CoA increased
intra-arterial wall tension in mesenteric artery Intimal damage thrombosis-
Necrotizing arteritis or may develop acute inflammatory changes
85
# How to avoid paraplegia after CoA repair?
Aortic clamp time as short as possible
Careful technical anastomosis so reapplication of the clamp not required
Moderate hypothermia (34-350C)
Maintain high proximal BP
No acidosis
Maintain adequate distal aortic pressure (>40-45mmHg)
# How will you test for chyle?
Add ether to chest tube fluid
If fluid becomes clear fat dissolves
# How will you manage chylothorax?
Medical treatment
Fat free high medium chain triglyceride diet
Surgical Approaches
Side of the operation Lt./Rt.
Bilateral chylothorax Rt. side Thoracic duct is on rt. side of aorta

TETROLOGY OF FALLOT

HISTORY:-
# What is cyanosis?
Cyanosis is a bluish discoloration of the skin and mucous membrane due to an
increased quantity of reduced hemoglobin >5 g per dl or >30% of total Hb and
PaO2 < 85% or due to the presence of abnormal hemoglobin pigments in the
blood perfusing these areas.
# Types of Cyanosis:
Central cyanosis
Peripheral cyanosis
Differential cyanosis
# Causes of cyanosis:
86
In case of Central Cyanosis
A. Decreased arterial oxygen saturation
1. Decreased atmospheric pressure high altitude
2. Impaired pulmonary function
a. alveolar hypoventilation
b. Ventilation perfusion mismatch
c. Impaired oxygen diffusion
3. Anatomic shunts
a. Cyanotic congenital heart disease
b. Pulmonary arteriovenous fistulas
c. Multiple small intrapulmonary shunts
4. Hemoglobin with low affinity for oxygen (Hb)
Central: Causes are-
1) Cardiac-
- Congenital cyanotic
- Eisenmengerization
- CCF
2) Pulmonary-
- COPD
- Bronchiectasis
- Massive collapse & fibrosis
3) High altitude
B. Hemoglobin abnormalities
1. Methemoglobinemia (> 1.5 gm per dl)
a. Hereditary
b. Acquired drugs (nitrates, nitrites, sulphonamides).
2. Sulfhemoglobinemia (> 0.5 gm per dl).
3. Carboxyhemoglobinemia (smokers)

87
The diagnosis of Methemoglobinemia can be suspected, if on exposing the
patients blood to air, it remains brown whereas in cyanosis due to decreased
arterial oxygen saturation, it turns bright red.
In case of Peripheral cyanosis
Reduced cardiac output
Cold exposure
Redistribution of blood flow from extremities
Arterial obstruction
Venous obstruction
Peripheral: Causes are-
1) Cold/ vasoconstriction
2) Shock
3) Increased viscosity of blood
In case of Differential cyanosis
Cyanosis is seen only in the lower limbs PDA with pulmonary hypertension
with right to left shunt.
Cyanosis is seen only in the upper limbs PDA with pulmonary hypertension
with right to left shunt and Transposition of great vessels.
Rarely, in addition to the lower limbs, the left upper limb may also be cyanosed
when the patent ductus opens proximal to the origin of left subclavian artery.
# Intermittent Cyanosis is seen in Ebsteins anomaly.
# Differentiating features between Central and Peripheral Cyanosis:
Features Central Cyanosis Peripheral Cyanosis
Mechanism Right to left shunts or Peripheral stasis
lung disorders
Site Whole body Nail bed, nose tip,
earlobe, extremities
Associations Clubbing Polycythemia
---

88
Extremities Warm Cold
On warming the No Change Disappears
extremities
O2 inhalation Slight improvement No change
Arterial blood gas Low < 85% Normal 85 100 %

# Conditions where cyanosis cannot occur are:

- Severe anemia (Hb< 5 gm %),
- CO poisoning

# In Indians cyanosis is apparent when the O% is < 85%. When < 65%,
intense cyanosis.

# Conditions that can mask cyanosis are:

- Anemia (Hb < 15gm %)
- Dark complexion.
# Conditions where the patient appears blue but there is no cyanosis:
- Sulfhemoglobinemia/ Methemoglobinemia
- Silver poisoning
- Aniline dye workers
- Extreme cold environment
# Onset of cyanosis
At birth
- Pulmonary atresia
- Aortic atresia
- TAPVC
- TGA
- Truncus arteriosus
- Taussig Bing
- Hypoplastic left heart syndrome

89
7 days
- Ebsteins
- Tricuspid atresia- Ia / IIa
- HLHS
> 1 week- < 1 month
- TGA
- TAPVC
- Truncus
- TOF with severe PS
- DORV with severe PS
- Common atrium
> 6 months
- TOF & its variations
- Eisenmengerization
# Causes of late onset of cyanosis.
- TOF with mild PS.
- TOF with good collaterals.
- DORV + VSD + PS.
- ASD + PS.
- Ebstein anomalies
Cyanosis at birth (RV not compliant)
Cyanosis disappears (RV compliant)
Cyanosis Reappears (RV failure).
# Reasons for delay in onset of cyanosis in TOF.
- After closure of PDA.
- Increase activity & need for forward flow.
- Conversion of HbF HbA.
- Cure of relative anaemia.
- Progressive increase in PS.

90
# Cyanosis at birth.
- Tricuspid atresia.
- D Transposition of great arteries.
- Obstructive TAPVC.
- TOF with pulmonary atresia.
- Aortic atresia.
- Truncus arteriosus.
# Causes of cyanosis disappearing in old age.
- Development of fixed RVOT Obstruction - Fibrosis.
- Pt. learns to stop activity & squat.
- Development of Bronchial collaterals.
# Factors precipitating cyanosis
- LRTI
- Exertion
- Ductus thrombosis
- Ductus infective endocarditis
# Types of CNS events in Cyanotics
- Hypoxic brain damage
- Brain abscess- Due to infected thrombus
- Central venous thrombosis- Due to high PCV
# CYANOTIC SPELLS:
Synonym: Hypoxic spell/ paroxysmal hyperpnoea
A typical spell is characterized by a progressive increase in rate & depth of
respiration & culminates in paroxysmal hyperpnoea, deepening of cyanosis,
limpness, syncope & occasionally convulsions or death.
# EEG during a spell is similar to that of an acute hypoxic episode.
# The incidence of cyanotic spells increases after 2-6 months of age due to:
- Replacement of fetal Hb by adult Hb
- More activity of child
- Closure of PDA
91
& decreases after 2 years of age due to:
The os infundibulum getting fixed (fibro tic changes in the infundibulum)
Child has learned as to how to avoid a spell
Collaterals grow
Improved Hb
# Cyanotic spells seen in:
-Tetrology of Fallot
- DORV, VSD, PS
- VSD, PS
- TGA, VSD, PS
- ASD, PS
- TA Ib/IIb
# Triggering factors for a cyanotic spell are:
- Spontaneous
- Crying
- Feeding
- Bowel movements
- Particularly if stress occurs immediately after an infant has waken up from a
long deep sleep.
# Theories of spell are:
Guntheroth & Morgan: presence of a vulnerable respiratory control
mechanism, which is especially sensitive after a prolonged sleep.
It reacts to a sudden increase in cardiac output (occurring due to waking up
from sleep)

Increased venous return

Increased Rt. To Lt. Shunt

Fall in PO2 and rise in PCO2
92

Hyperpnoea

Increased Cardiac output
Wood: There is infundibular spasm due to increased sympathetic activity (this
theory does not explain the spells in pulmonary atresia)
Young: Atrial tachycardia leading to increased Rt. to Lt. Shunt.
Decreased RV diastolic filling due to dehydration.

# Treatment of spell:
- O2 +
- Knee chest position +
- Morphine/ buprenorphine (0.1 mg/ Kg, max up to 0.2 mg/ Kg, not to be
repeated within 4 hrs) +
- NaHCO3- 1-2 meq/Kg/ dose

- IV Propranolol 1 mg/ Kg/ dose, slow IV +/ -
- IV Phenylphrine 1-3 ug/ Kg infusion

- Ketamine 2 to 10 mg/ Kg & Intubation

- BT shunt
- Other options available are:
If duct dependent- PGE1/ duct stenting
If TGA- BAS

# The mortality for an emergency BT shunt is much higher than for an

elective shunt (15% vs. 1%)

# Prevention of cyanotic spell:

- Avoid precipitating cause- e.g. Vasodilators
- Iron supplements
93
- Treat RTI promptly
- Blood letting
- Optimization of propranolol therapy
- Plan surgical management
Squatting Episodes:
# History of squatting for relief of symptoms is hallmark of Tetrology of Fallot.

# Squatting helps by (Mechanism):

- Increasing the SVR by kinking the femoral arteries decreasing the rt. To lt.
Shunt.
- Decreased return of a more deoxygenated blood to the heart from the lower
limbs, by kinking the femoral veins.
- Pushing relatively more oxygenated venous blood from the abdominal viscera
to the heart,
- Relaxation of sympathetic overdrive by resting.
# Squatting equivalents:
3 described by Tausig in 1947:
- Knee chest position
- While sitting on the ground
- Legs folded underneath the body (like a namaz position)
- Lying down.
2 more added to the list by Lurie in 1953:
- Standing with legs crossed
- Parent holding the baby against owns abdomen with the babies LL flexed.
# There are 2 types of squatters;
Rapid- mainly adult, &
Slow
# Usual ways in which spell terminates
- Recovery on squatting
- CNS events develops

94
- Arrest due to acidosis
# Causes of Thromoboembolic episodes in cyanotics
- Infective endocarditis of aortic valve
- Paradoxical embolus from DVT
- Dehydration
# Places which get affected in Infective endocarditis in TOF
- RVOT obstruction
- Pulmonary valve
- Tricuspid valve
# Fallots physiology- (Cyanosis with reduced PBF) conditions included
- TOF, VSD, PS
- DORV, VSD, PS
- C TGA, VSD, PS & d TGA, VSD, PS
- VSD, PS
- ASD, PS
- TA Ib/ IIb
- Single ventricle, PS
- AV canal, PS
# Conditions of cyanosis with increased pulmonary blood flow.
- TAPVC
- Truncus
- Taussig Bing
- TGA
- Common atrium
- Eisenmengerisation
# Transposition physiology
Presence of cyanosis with increased PBF (actually is a misnomer as TGA can be
present with decreased PBF). Includes
- TGA
- TAPVC
95
- Truncus arteriosus
- Tausig Bing
- HLHS
- TA Ic/ IIc
- DORV without PS
- Single ventricle without PS

# Neonatal cyanosis with severe PAH

- Obstructed TAPVC
- Persistent fetal circulation

# Conditions associated with mild cyanosis.

- TAPVC
- Ebsteins
- Common atrium
- Eisenmengerization.
# Conditions known for cyanotic spells
- TOF
- DORV, VSD, PS
- Tricuspid atresia Ib/ IIb
- TGA, PS
# Conditions known for squatting
- TOF
- DORV, VSD, PS
- Tricuspid atresia- Ia/Ib, IIa/IIb
# Syndromes associated with TOF
- Downs syndrome 8%
- Noonan syndrome 1%
- Maternal rubella syndrome
# Explanation of symptom of effort intolerance.
- Reduced oxygen content of blood.

96
- RV failure in cyanotics.
# Dyspnoea in CCHD Due to:
- Gross ventilation- perfusion mismatch (V/Q mismatch).
- On exercise Co2 rich blood passes into Brain, Blood is hypoxemic & acidotic,
leads to Stimulation of respiratory centre.
- Hypoxic spells.
# Hemoptysis in cyanosis:
- Bronchial artery rupture
- Polycythemia
- Infective endocarditis leading to infarction
- Tuberculosis

# Chest pain in a patient with TOF.

- RVH
- Rarely coronary artery crossing between aorta & PA
# Why DIC in TOF
- High Hct leading to relative plasma deficiency
- Hypoxia affecting liver & platelets
All these factors lead to
- Decrease in number of platelets
- Decreased functioning of platelets
- Increased FDP
- Altered WBC function
- Decreased liver clotting factor
# Headache in CCHD.
- Cortical venous thrombosis (due to high Hct)
- Brain abscess
- AV malformation with a bicuspid AV/ Coarctation
- Systemic hypertension
- Embolization

97
# TOF in failure causes.
- Anaemia.
- RV dysfunction due to Polycythemia.
- PR due to absent PV.
- PDA / MAPCAS.
- Infective endocarditis.
- Closing down VSD restrictive VSD.
- Hypertension.
- Adult TOF.
GENERAL EXAMINATION:-
# CLUBBING:
Definition: A selective bulbous enlargement of the distal portion of the digit
due to increased subungal soft tissue.
Both horizontal & transverse curving of the nails enlarges.
Normal angle between the nail & the nail bed is 1800 & is called Lovibond
angle.
The minimum duration required for clubbing to manifest is 2-3 weeks.
Clubbing 1st appears in the index finger.
Clubbing is rare in infancy even if cyanosis is intense.
Clubbing is common in TOF by age of 2-3 years.
Clubbing develops quickly in pulmonary abscess in 2-3 weeks & disappears
quickly when cause is removed.
Grades: 5 grades;
I) Softening of the nail bed
II) Obliteration of angle of nail bed
III) Increase in the curvature of nail- parrot beak
IV) Drum sticks appearance
V) Hypertrophic osteoarthropathy - Swelling in all dimensions with X ray e/o
subperiosteal new bone formation (hypertrophic pulmonary osteoarthropathy)

98
Theories of clubbing:
There is interstitial edema & dilatation of arterioles & capillaries due to;
Neurogenic theory: Vagal stimulation causes vasodilatation & clubbing.
Hormonal theory: GH, PTH, Oestrogen, PG, Bradykinin, Serotonin -Causes
vasodilatation & clubbing
Hypoxia: stimulating opening of AV fistulae to increase blood flow to fingers &
toes
Ferritin: Reduced Ferritin in venous blood escapes oxygenation in the lung &
enters systemic circulation & acts as a stimulant for dilatation of AV
anastomosis & hypertrophy of the terminal phalanx.
Platelet derived growth factor: Released secondary to infection anywhere in
the body also causes vasodilatation & this is the latest & most acceptable
theory for clubbing.
Pseudo clubbing: In hyperparathyroidism, resorption of bone leads to bulging
of finger tips. However the nail curvature is normal.
Causes of clubbing:
@ Congenital / Familial: Congenital hypertrophic pulmonary
osteoarthropathy Pachydermoperiostosis.
@ Acquired:
Unidigit / pandigit
Unilateral / Bilateral
Differential
Unidigit clubbing: Seen in
Topheous gout, Local injury, Sarcoidosis
Unilateral clubbing: Seen in
Aneurysmal dilatation of aorta/subclavian/innominate artery, Brachial AV
fistula, hemiplegia, Pancoast tumour.
Only UL- IV drug abusers
Only LL- in farmers who work bare feet.
Differential clubbing: Seen in
99
PDA with reversal with cyanosis & clubbing occurring in the lower limbs only.
@ Generalized:
Pulmonary- Bronchogenic carcinoma, Metastatic lung cancer, Suppurative
lung disease (brochiectasis, lung abscess, cystic fibrosis, Empyema), Interstitial
lung disease, long standing pulmonary TB, Chronic bronchitis, Mesothelioma,
Neurogenic diaphragmatic tumour, Pulmonary Av malformation, sarcoidosis
Cardiac- Cyanotic CHD, Eisenmengerization, infective endocarditis, Atrial
Myxoma.
Alimentary- ulcerative colitis, crohn's disease, cirrhosis, GI malignancy.
Endocrine- myxedema, acromegaly, Thyrotoxicosis.
Others- idiopathic, hereditary, Syphilis

# Pseudo clubbing: Seen in

- Hansens disease due to resorption of tissue.
- Vinyl chloride worker due to focal tissue reaction to the chemical.
- Leukaemia due to tissue infiltration.
- Hyperparathyroidism due to bone resorption.

# Only clubbing, no cyanosis seen in;

- Infective endocarditis
- Non cardiac etiologies
# Objective signs of clubbing:
- Schamroths window- normal diamond shaped space in between two
approximated nails. Lost in clubbing.
- Lowibonds angle- acute angle formed by the nail bed. Disappears with
clubbing.
# Post operative improvement in clubbing:
Grade 3 or less improves by grade one
Grade 4 & more does not improve.

# Causes of raised JVP in TOF

- TOF with anaemia.
100
- Associated TR/AR/Hypertension.
- Adult TOF.
- Restrictive VSD.
- Shunted TOF/PDA.
- Infective endocarditis

# CCHD with bounding pulsations

- TOF with PA, TOF with AR
- Truncus
- TGA
# Cyanotics presenting with bradycardia
- CCTGA
- Single ventricle
- Drug therapy Propranolol
# Pulmonary Kochs is common in cyanotics- 10% incidence pulmonary
Kochs in TOF.
- Poor pulmonary alveolar perfusion but alveolar ventilation is satisfactory
Very high alveolar oxygen tension in cyanotics.
- Possibility of fall in immunity in this pt.
# Radio femoral delay in TOF.
Ideally should not be mentioned because in TOF ideally there should not be
associated aortic arch anomalies.
However if questioned it is acceptable to say that RF delay was mentioned due
to routine format in long cases.
Radio-femoral delay never occurs in TOF- because with right & left sided
obstruction patient will not survive.

# Causes of Radio-radial delay in TOF

- Classical BT shunt
- Modified BT shunt with kinking / thrombosis of subclavian secondary to
shunt.

101
# Swollen joints in cyanotics
- Hyperuricemia (due to increased RBC turnover)
- Sepsis
- Hemarthrosis

CVS EXAMINATION

# Quiet precordium is on inspection.

# Silent precordium is on auscultation.
# Quiet precordium DD.
- TOF.
- DORV+ VSD + PS.
- Constrictive pericarditis.
- Emphysematous chest.
- Pendulous breast.

# Quiet precordium in TOF is because of large non restrictive VSD & RV

ejects into LV through VSD & not in the PA.

# Active precordium in TOF (same DD for Cardiomegaly in TOF).

- CCF in TOF Anaemia /IE / AR.
- Dilated Aorta Post Shunt / PDA.
- LV dilatation Gross AR / HTN.
- Restrictive VSD.
- Pulmonary thrombosis.
Note Naturally occurring coll. Can never exceed the requirements of heart &
so cardiomegaly & CCF will not occur in TOF due to excessive flow from the
coll.

# Two main causes of precordial activity in TOF

- Failure
- Absent pulmonary valve

102
# LV apex in TOF
- Shunted TOF
- TOF with PDA
- TOF with HTN
- TOF with AR
- TOF with MAPCAS

# Grading of parasternal heave.

I Feel with tip of the only the tip of the finger is very sensitive & pick up
even slight RV activity.
II The medial aspect of the palm of the hand is lifted by RV activity but on
applying pressure the hand can be kept steady.
III The hand moves even after applying pressure.
IV Features of dilated RV.

# Causes of thrill in TOF.

- Mild PS 2nd LICS.
- Interscapular area Coll.
- Restrictive VSD.
- PDA.
- BT shunt.

# Causes of dullness in the 2nd left intercostals space in TOF

- Dilated PA: Due to
- Post stenotic dilatation
- Post shunt
- Absent pulmonary valve syndrome

# Information about TOF which can be decided from murmur.

Harshness/ duration of murmur severity of RVOT obstruction.
As severity murmur in duration in pulmonary atresia there is usually no
murmur audible.
Site of the murmur point to the possible etiology.
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4th ICS best heard & radiating up Infundibular PS.
2nd ICS best heard & radiating up - Valvar PS.

# Other murmurs in TOF.

- Diastolic murmur of AR.
- Collateral murmur Interscapular & Lateral scapular.
- Subcostal murmur of TR RV failure.
- Shunt murmur best heard in same side suprascapular/Deep axilla/ Infra
clavicular.
- PDA.
- Continuous murmur axilla Br PA stenosis.

# Points to say diagnosis as TOF.

- Late onset of cyanosis.
- Pt. surviving into late childhood.
- Severe cyanosis but never in failure (Because of RV hypertrophy, hyperplasia,
Non restrictive VSD).
- JVP not raised.
- Quiet precordium.
- No cardiomegaly.
- Normal apex.
- Single S2.
- ESM pulmonary area softer & shorter on hand grip exercise.

# Pointer to severity to TOF.

Severity degree of RVOT obstruction The only confounding factor is the
presence of coll. circulation. While it is right to say that pt. with severe
cyanosis have severe TOF but it is not right to say that pts with mild cyanosis
have mild RVOT obstruction.
Early age of presentation.
Spells& squatting.
Effort intolerance
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Deep cyanosis.
Grade 4 clubbing.
Murmur already decreased.
Collateral murmur.

# CCHD with split P2.

- TAPVC
- Common atrium
- Ebsteins
- ASD with Eisenmengerization

# Loud S2 in TOF
- Increased blood flow through Aorta.
- Aorta anteriorly placed.
- Dilated aorta.

# Continuous murmur in cyanotics

- Truncus arteriosus
- TOF with PA
- Shunted TOF
- TOF with collaterals
- TOF with PDA

# Additional auscultatory signs in TOF.

Murmurs
- Diastolic murmur of AR.
- Collateral murmur Interscapular & Lateral scapular.
- Subcostal murmur of TR RV failure.
- Shunt murmur best heard in same side suprascapular/Deep axilla/ Infra
clavicular.
- PDA.
- Cont. murmur axilla Br PA stenosis.

105
Clicks
- Aortic - > common, due to blood flow through aorta.
- Pulmonary Valvar PS.

# Clinical DD of TOF
- TOF
- DORV VSD PS
- Single Ventricle PS
- TGA VSD PS
- VSD PS
- ASD PS
- PS VSD

# Clinical differentiation is difficult in

- TOF
- DORV VSD PS
- VSD PS
- PS VSD

INVESTIGATIONS
X RAY CHEST

# What will you expect?

- CTR < 50%
- Pulmonary Bay
- Boot shaped heart
- Pulmonary blood flow
Reduced in TOF,
In Shunted TOF normal/reduced/increased.
Rib notching in shunted TOF
- Contour -
LV type Shunted TOF/TOF with MAPCAS,
RV type Coeur en Sabot/Wooden shoe
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# Causes of rib notching
- TOF with MAPCAS
- Shunted TOF
- Classical BT Shunt
- Coarctation of Aorta
- Interrupted aortic arch
- Schwannoma
# Diagnostic X- Rays in CHD
- Ebsteins: CTR > 60%, RAE, small MPA, narrow pedicle & oligemic lung fields
- Valvar PS with TR: CTR > 60%, RAE, MPA full, narrow pedicle & oligemic lung
fields
- D TGA: egg on side appearance, cardiomegaly, plethora
- Supracardiac TAPVC: figure of 8, cardiomegaly, plethora
- C TGA: L posed aorta
- TOF with APVS: dilated PA with oligemic lung fields, no LV
# Cyanotic heart disease with increased CTR
- TAPVC
- Ebsteins
- Single ventricle
- Truncus
- Av canal defect
# Reason for boot shaped heart in TOF?
Due to absence of LV density.
# Non clinical signs of lt. Sided shunt.
- Rib crowding.
- Synostosis of ribs.
- Callous formation.
- Subperiosteal bone deposition.
- Blunting of CP angle.
- Elevation of diaphragm secondary to injury.
107
# Rt. aortic arch in TOF.
Incidence 25%.
Important to know in deciding Shunt / Cannulation.
# Right aortic arch seen in
- TOF with PA
- Truncus
- TOF
- TA
- Single ventricle
- AP window
# Dilated PA shadow in TOF.
- Collaterals.
- Post shunt.
- Low infundibular obstruction with 3rd chamber.
- Absent pulmonary valve.
# Couer en sabot in TOF.
Incidence 25 30 % / >.
Main causes for boot shaped heart.
@ Absence of LV shadow.
@ Pulmonary baying.
@ Predominantly RV shadow is seen.
# Narrow pedicle on X-ray
- Truncus
- Aortic dilatation- AR/ PDA
- Aortic override- PS, PA
# Box shaped heart in CHD
- Ebsteins
- TAPVC
# Prominent aortic knuckle in TOF
- TOF with AR
108
- TOF with Hypertension
# Prominent right heart border in TOF
- TOF with TR
- TOF with ASD
ECG
# What will you expect?
- RAD
- Axis 90-180
- RAE- Adult TOF
- RVH
- LVH Adult TOF, Shunted TOF/TOF with MAPCAS
- Clockwise loop q in II, III, aVF
- Dominant R in V1, Dominant S in V6
- T inversion Severe RVH
- Early transition in V2- Window effect of VSD / LV forces through VSD
# Differentiate between VSD.PS & PS.VSD
If axis > 135- PS.VSD
If axis < 110- VSD.PS
# ECG in TOF- special
If counter clockwise loop & LAD- AV canal associated
If qR in V1- cTGA
No r in V1 Tricuspid atresia, VSD PS, PS VSD, TOF in failure
# Reasons for well developed LV in TOF are:
- AR
- Good collaterals/ PDA/ shunt
- Adult TOF
- Common AV canal
- VSD is restrictive
# D/D of Fallot physiology on ECG
- TOF: -QRS axis between 90- 150
109
- DORV, TGA: - If > 150
- Tricuspid atresia:-30 to -60 with LVH
- AV canal, Single ventricle: - Left axis deviation with RVH
- Single ventricle: - Right axis deviation without RVH
# ECG in adult TOF
- Due to high RVEDP- RV dilatation leading to tall p in II & V1.
ECHO
# What information do you want from echo?
- VSD - Site, size, number
- RV Infundibular stenosis
- PA MPA, RPA, LPA
- Coronaries
- LV/RV function
- Associated anomalies
# Echo findings of use to surgeons in TOF.
- Size, position & restriction of VSD.
- Type of RVOT obstruction Infundibular / Valvar / supra Valvar.
- Infundibular obstruction,
@ Low OS infundibular RVOT patch not req.
@ Diffuse tubular narrow RVOT patch.
@ Short atretic Infundibulum Approach through PA.
- Pulmonary annulus size.
- MPA size.
- Branch PAs Confluence / stenosis / size.
- Associated anomalies ASD / VSD / PDA / LSVC / Rt. aortic arch.
- Coronary arteries crossing RVOT.
- LV size Normal systolic volume 30 ml / m2.
- LV volume < 60 % normal Poor prognosis.
- Better to do palliative ICR (leave VSD open).
- MV size - < 2SD below normal - Poor prognosis.
110
# VSD position in TOF.
Best in Apical 5 chamber view- show VSD below Aorta.
Other in short axis view VSD positions,
@ Between 12 & 1 o clock position Sub pulmonic VSD- part of margin by
pulmonary annulus.
@ Between 11 & 12 o clock position Sub aortic VSD Part of margin by
aortic annulus.
@ Between 9 & 11 o clock position Perimembranous VSD part of margin
formed by fibrous trigone.
@ Inlet VSD part of margin formed by tricuspid annulus.
# Echo Views in TOF
Parasternal long axis VSD, Aortic over ride.
Parasternal short axis RVOTO, Descending aorta, PA size
Apical 5 chamber view VSD
Apical 4 chamber view Aortic over ride
Subcostal coronal view descending aorta at diaphragm
Suprasternal view PA size
# Incidence of multiple VSD in TOF
2%. Mainly of inlet type (may be missed by a RVOT approach)
# LV size for TOF contraindicating intracardiac repair
LVEDV < 30 ml/m2
LVED (D) < 60% of normal for that weight
MV area < -2 Z
# LV size in TOF- range
Large if diameter > RV
Small if diameter < 3/4th RV
Diminutive if diameter < RV
(All diameters taken transversely at the end of diastolic frame)

111
CATH
# Indications for cath in TOF.
Policy of institution.
Problems/ grey areas in diagnosis,
@ Branch PA stenosis.
@ Coronary crossing RVOT.
@ PA confluence.
@ MAPCAS
# Points to note on cardiac cath.
- Distal RVOT.
- Peripheral PAs.
- Coronary anatomy.
- Collaterals.
# Problems of cath in children.
- Access.
- Hypothermia.
- Hypoglycemia.
- Blood loss.
- DIC.
- Spells induced by catheter in RVOT.
- Contrast (2ml /Kg) dosage is maximum & so it has to be used judiciously &
only relevant anatomy to be delineated.
# Use of coronary angio in TOF
- Prominent conal artery crossing RVOT
- LAD from RCA
- Entire LCA from rt. Side
- Double LAD from LCA & RCA
- Intra pericardial adhesions after previous Waterston Cooley shunt/Central
shunt- To see course of coronary artery

112
# Views in TOF
@ RV gram in lateral view
- Coarsely trabeculated RV followed by PA & Aorta.
- PA anterior to Aorta
- Infundibular stenosis
- LV opacifies through VSD
- Aortic override
- Size of MPA & Aorta
@ RV gram in PA view
- Coarsely trabeculated RV followed by PA & Aorta
- RPA seen very well
- LPA lower lobe branches seen
- LPA upper lobe branch not seen very well
- Aorta is rt. of the PA
- Aortic override
@ RV gram in LAO shallow with cranial tilt (Hepatoclavicular view)
- MPA followed by RPA & LPA
- LPA origin & its branching
@ LV gram in LAO 600
- Smooth walled LV
- Followed by Aorta & RV through a SA VSD
- Aortic over ride
- VSD
@ LCA angio in RAO 300& LAO 600
@ Aortic root shoot in LAO 600
- Aortic opacification
- Coronary artery branching
- AR
# How will you see for Aortic over ride?

113
- LV gram in LAO 60-700
- Draw a line from the center of the aorta downwards
- If lower part of IVS towards LV side 25% override
- If line falls at the Apex of IVS 50 % override
- If line falls on rt.side of the IVS 75% override
- Line totally on the RV side - 100% override
# Catheter course in TOF
Right heart study- RFV->IVC->RA->RV->PA
Left heart study RFA-> Aorta->LV
# Catheter course RV->Aorta possibilities are
- TGA
- AP window
- Pulmonary atresia
- TOF
# Can you make out BT shunt is working by oxymetry PA cannot be
entered.
# Lt. Heart study in TOF
- Coronary
- MAPCAS
- PDA
- AR
- LV gram septum in profile.
# Visualization of PA in TOF
- RV gram
- MAPCAS
- PV wedge injection.
# Methods of assessment of PA size
@ Mc Goon Ratio
Described in 1981. Angiographic ratio.
Piehler & asso. Suggested
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Diameter of RPA & LPA at pre branching level / RPA is measured at the right
border of spine & LPA before its 1st lobar artery.
Divided by Diameter of descending aorta at the Diaphragm level in systole
>2 ideal, >1.5 Acceptable, <0.8 severely restrictive Central PAs
Drawback-Descending aorta at the diaphragm level tends to be narrower in
TOF than normal individual making Mc Goon ratio falsely more favourable.
Fallacies of Mc Goon ratio-
Post stenotic dilatation
Peripheral pulmonary artery Coarctation
PS PAH Situation
TOF with APV syndrome
Mc Goon used his little finger & index finger to size the PA annulus
Little finger if BSA is <1.0 & Index finger if BSA is > 1.4
A little finger = 13mm
Index finger = 17mm
@ Nakata Index
Nakata &Coll. described
By Echo
Cross sectional area of RPA & LPA.
Divided by BSA
Normal value 330+/- 30 mm2/m2
<150 mm2/m2-Diminutive Pas
>100 mm2/m2 ICR in TOF

# Fallacies of Mc Goon/ Nakata?

It does not take into account:
Distal PA stenosis
PA dilatation
@ Kirklins index-
Kirklin, Blackstone &coll. described
Post op PRV: LV - < 0.85 predicted
115
@ Z value Number of standard deviations that the patients pulmonary valve
annulus is away from the mean normal value.
Established by Rowlatt, Rinoldi & Lev
# Points to remember to ask in TOF.
Post shunt
@ Improvement in symptoms.
@ Spells.
@ CCF.
@ Lt. Radial pulse /BP / RR delay.
Hemoptysis
@ Rupture of AP collaterals.
@ Pulmonary infarction.
@ Kochs.
Adult TOF CCF.
# D/D of TOF
VSD, PS:
- Generally late (5-6 years) presentation,
- Mild cyanosis,
- LRTI in early childhood,
- LV apex
PS, VSD:
- Harsh PS murmur with late peaking
DORV, VSD, PS:
- On echo
CTGA, VSD, PS:
- Heart block
- qR in V1
TA IIb:
- No RV inflow pulsations
- No R in V1, V2
116
# Difference between TOF & DORV VSD PS
Morphology DORV TOF
Aortic override >90% 50%
Aorto-mitral continuity Absent Present
Aortic & Pulmonary valve Same level Different level
VSD SA/SP/DC SA
Shunt L-R (Anatomic) R-L
R-L (Physiologic)

MANAGEMENT
MEDICAL
# Drugs in TOF
Iron & Propranolol
# Drugs C/I in TOF
Digoxin- Causes infundibular spasm
Lasix Causes hemoconcentration
Vasodilator precipitates spell
# How does propranolol help in TOF
- Decreasing the infundibular spasm by decreasing the adrenergic drive
- Decreasing HR & thus less chance of SVT
- Shifts the O2 dissociation curve to right
- Unhindered activity leading to increased SVR, hence decreased R-L shunt
# Dosage of propranolol.
1-4 mg/Kg/Day in 3 divided doses.
Dosages as high as 20 mg/ Kg/ Day also have been tried however the
complication rate is very high. During high dose regimen watch for:
Bradycardia
Increase in CTR
Decrease in EF on echo

117
# Optimum propranolol therapy
Till;
HR falls by 25% of the basal HR
No bronchospasm
# Limitation of propranolol treatment during spell
Heart rate
Systolic BP: if SBP falls by more than 20 mm Hg of baseline, then propranolol
administration has to be stopped
# Non surgical treatment in TOF
- Blood letting
- Balloon pulmonary valvotomy
- PDA kept patent by stenting & PGE2
- Embolisation of MAPCAS
- Balloon atrial septostomy
- Laser coring of RVOT
# Intervention in TOF
Pre op:
- Coil embolization of MAPCA
- BPV
- Perforation/ coring of RVOT/ pulmonary. Atresia
Post op:
- Dilatation of BT shunt
- Arrhythmias management
- Management of AV block
- Septostomy
SURGICAL
# Indications for a BT Shunt are
- CCHD not fit for ICR, with severe symptoms
- TOF with pulmonary atresia
- TOF with
118
@ Unresolved spell
@ Age < 6 months with low weight/ failure to thrive/ repeated spells
@ Hypoplastic PA
@ Underdeveloped LV (< 60% of normal)
@ MV annulus < -2 Z
- Institutional criteria for performing an ICR
- TGA with PA banding for later arterial switch
# Palliative procedures for cyanotics from midline
- BT shunt
- Waterston Cooley shunt
- Gazzaniga shunt
- Glenn shunt
- Davidsons shunt (direct anastomosis of MPA to aorta)
- Brocks procedure (infundibulectomy only through a purstring in RVOT)
- Mc Goons procedure (patch widening of the MPA, RPA & LPA)
# Shunts from left lateral thoracotomy
- BT shunt- classical & modified
- Potts shunt
- Benson Roe procedure (anastomosis of LAA to vertical vein for palliation of
TAPVC) - historical
# Palliative surgeries from right thoracotomy
- Right BTS
- Blalock Hanlon atrial septectomy
- Waterston shunt
# Chronology of palliative procedures of CCHD
- Classical BT Shunt: 1944
- Potts shunt: 1946
- Davidsons shunt: 1956
- Glenn shunt: 1958
- Waterston shunt: 1962
119
- Waterston Cooley shunt: 1966
- Gazzaniga shunt: 1976
- Modified BT Shunt: 1981
# Most important points of each shunt
Classical BT Shunt
If on right side then after transaction of the Rt. SCA, it is taken out of the loop
of the right recurrent laryngeal nerve & then anastomosed to RPA.
Take down: dissect posterior to SVC & loop
Modified BT Shunt
On right side mediastinal pleura is opened posterior to SVC & phrenic nerve
Azygous vein is ligated & divided
Takedown:
On the right side: Graft generally lays just posteromedial to SVC, which is
dissected, looped & ligated/ divided.
On the left side: dissect beneath the arch of aorta & above the LPA or open the
left pleura & dissect from the lateral aspect, then dissect for the peel over the
PTFE conduit. A plane (well developed) between the peel & the conduit is
isolated & graft is looped & ligated/ divided.
Waterston shunt:
Shunt between the posterior ascending aorta & anterior LPA thru a right
lateral thoracotomy.
Anastomsis posterior to SVC
Problems of Waterston shunt;
Size of shunt- if small then cyanosis, if large then CCF
Distortion of RPA & preferential flow to one lung
Takedown: on CPB there are 3 ways, either dissect the shunt & loop or loop
RPA & LPA;
Incise the native suture line followed by primary closure of the aorta & patch
plasty of the RPA
Open the aorta & examine from inside (Cooley)
120
Transect aorta & repair RPA
Waterston Cooley shunt:
Anastomosis is done between aorta & RPA, anterior to SVC
Potts shunt:
Between descending aorta & posterior LPA
Problems: are
Increased flow- leading to CCF
Decreased flow- leads to cyanosis
LPA aneurysm
Difficulty in takedown
Takedown: There is high risk of air embolism when descending aorta is opened
hence the technique followed is;
CPB- aortic or femoral arterial
Digital occlusion of the shunt from the outside for preventing pulmonary
flooding & more effective cooling
Circulatory arrest- cross clamp &cardioplegia
Carotids are snared
LPA opened anteriorly & the opening of the shunt is closed with a PTFE patch.
Flow is reinitiated & deairing done( if femoral arterial cannula then deairing is
from cardioplegia needle, if aortic cannula then deairing is from the LPA-
descending thoracic aorta suture line)
# Site of BT Shunt murmur
Classical BT shunt-
Supraclavicular & interscapular region radiating to neck
Modified BT shunt-
Infraclavicular not radiating to the neck
# What is modified rt. BT shunt through Midline?
Innominate artery to RPA shunt through midline.
# Central shunt
- Very small PAs.
121
- Two techniques-
Direct (Gazzaniga shunt) Transect MPA & anastomose distal end to ascending
aorta-Roger Mee tech.
Indirect Gortex tube graft from ascending aorta to MPA (Davidsons shunt)
# TOF PA with PDA, How will you manage?
Do modified BT shunt on the side of PDA & ligate PDA.
# Investigations required prior to carrying out an emergency BT shunt in
a child with unresolved spell
- Hct (SOS bloodletting to obtain Hct of around 65%)
- Platelet function & count
- Echo examination for
@ PA size,
@ PA confluence
@ Side of arch
# Anesthesia during BT Shunt.
- With Ketamine (2- 10 mg/Kg),
- IV line with utmost care (no air injected)

# During BT Shunt what structure may come in front of the LPA?

Lymph node
# During dissection of SCA, damage to which artery is dangerous?
To the vertebral artery as damage to it will cause retraction of the artery into
the vertebral foramen.
# Why modified BT Shunt on the same side as arch
Longer length available of SCA before it branches
Lesser chances of damage to recurrent laryngeal nerve.
# Size of Gortex to be used?
Protocol by age
@ If < 6 months- 4 mm
@ 6mnths to 2 years- 5mm
122
@ 2 to 6 years- 6mm
@ > 6 years- 8mm
Protocol by weight
< 7 Kg- 4mm
7 to 12 Kg- 5mm
12- 20 Kg- 6mm
> 20 kg- 8mm
(However the decision for the size is ultimately based on the size of the SCA)
# Care with Gortex.
- Cut with a sharp knife
- No crushing
- No multiple punctures
# If Gortex is not available for a BT Shunt
- Classical BT Shunt
- Maternal saphenous vein
- Dacron
# What are Gortex sutures.
They are hygroscopic & hence clog the needle holes
# Air removal after a modified BT Shunt
Distal PA & distal SCA- followed by proximal PA & the proximal SCA (never
needle puncture Gortex (as it loses its electronegitivity)
# Why as proximal LPA as possible for BT Shunt
- More equal distribution of blood flow &
- Easy to loop from midline (for later closure during an ICR)
# If LPA is not seen during BT Shunt
- Check dissection
- Open pericardium & anastomose to MPA
- If large MAPCA seen entering hilum- a shunt to the MAPCA
- Close & turn patient to opposite side

123
# Cause of bradycardia on clamping the LPA?
- RPA absent/ osteal stenosis/ hypoplastic/ non confluent
- Isolated left lung ventilation
- Vagus nerve included in the clamp.
# Measures to be taken if bradycardia occurs?
- Check bilateral ventilation
- Allow re-expansion of lung & then start
- Check inclusion of vagus in clamp
- Try side clamping the artery
- BT Shunt to upper lobar artery.
# Management of spells on table under anaesthesia.
- Partially clamp the aorta as it mimics like squatting situation.
- Neosynephrine injection.
# Care of bleeding BT shunt.
- Packing around the anastomosis & wait.
- Protamine can be given Good thrill on graft, when graft is bleeding & not
artery.
# Ways to ensure patency of BT shunt.
- Taking suture under vision
- Inside out suturing of artery.
- Heel toe anastomosis.
- Lie of graft no kinking.
- Technically perfect anastomosis.
# Sign of good shunt functioning
- Graft Sweating
- Thrill over PA
- Hemodynamics
- Improvement in O2 saturation%
- Fall in DBP

124
# Thrill absent after BT shunt.
- Check BP- low BP
- High Hct
- Small SCA (ligate distal SCA)
- Technical cause- Immediate cause.
- Neointimal proliferation.
- Shunt thrombosis.
- Infective endocarditis.
- Patient outgrows the shunt.
# Changes after a BT shunt.
- Symptomatic improvement
- PA-
PA size grows (by 25%)
Increase in annular size (due to increased pressure on the sinus of
valsalva)
All within the first 6 months
- LV develops- normalizes
- Infundibular obstruction worsens
- Hct decreases & coagulation profile normalizes
- Collaterals close
# Patient symptomatic after BT Shunt?
- Patient has outgrown shunt
- Shunt blocked due to
Thrombosis
Neointimal hyperplasia
Infective endocarditis
PA distortion
- Intracardiac cause- AR/ PR
# Ways of closure of shunt
- Dissect on inner side of arch & loop
125
- Ligate SCA
- On CPB, open MPA & suture opening from the inside
# Why symptoms are severe if a BT Shunt gets blocked?
- Infundibular obstruction has become worse
- Collaterals have closed
# Indication for repeat BT shunt
Blocked shunt
# Why not a repeat BT Shunt on the same side?
Due to technical reasons as increased adhesions will be present hence a higher
tendency for bleeding.
# Steps taken during redo
- 1st perform SCA & then PA end
- Ensure adequate heparinization
- Heel first
- Inside out sutures over the artery
# What should not occur post BT Shunt
- Cyanotic spells &
- CCF
# How long does Hct take to normalize post BT Shunt?
Around 15 days.
# Causes of late appearance of cyanosis after BT Shunt are:
- Patient outgrowing shunt
- Increased infundibular spasm
- Infective endocarditis causing PR/ TR
# Disadvantage of a BT Shunt through a thoracotomy
Due to a thoracotomy there is increased collateral formation & may interfere
during and post intracardiac repair if Fontan performed.
# Problems during BT shunt.
- Bradycardia.
- V-P mismatch.
126
- Absent PA on that side.
- Vagal stimulation.
- Spell under anaesthesia.
- Horners syndrome.
- Bleeding.
# Complications BT shunt
Immediate
- Shunt blockage
- Over size/Under size-CCF/ Inadequate perfusion
- Bleeding
- Seroma
- Weeping shunt
- Kinking of shunt
- Necrosis of arm Classical BT shunt
- Diastolic hypotension
- Metabolic acidosis
- Haemorrhagic pulmonary edema
Late
- Pulmonary plethora/Inadequate perfusion
- CCF
- Distortion of PA
- Acquired pulmonary stenosis/pulmonary atresia
- Disparity in arm- Classical BT shunt
- Chylothorx
- Horners syndrome
# Complications of Cyanosis
- Cerebral embolism
- Paradoxical embolism
- Brain abscess
- Infective endocarditis
127
- Iron & folic acid deficiencies
- Repeated hemoptysis
More in older patient
Due to
- Pulmonary infarction
- Pulmonary embolism
- Pulmonary oedema- shunted
- Rupture of collateral vessels
Bleeding due to
- Low fibrinogen
- Low platelets
# Advantage of modified Vs classical BT shunt.
- Decrease chances of distortion of- PA & SCA
- Less dissection
- Blood supply to arm is maintained
# CCF in modified BT Shunt Vs classical BT Shunt
Same incidence; as the flow limiting factor is the subclavian artery.
# Evidence of previous BT Shunt on X-ray?
Of thoracotomy
- Rib crowding
- Synostosis/ callous formation
- Subperiosteal resection
Of dissection
- Elevation of dome of diaphragm
Of shunt
- Normalization of pulmonary vasculature
- MPA prominent
- LV developed
# Reasons for cyanosis disappearing after BT shunts.
- More blood to lungs before oxygenation.
128
- Blood loss during surgery.
- Fall in hematocrit due to no longer stimuli being present.
# Reasons for Blocked BT shunts.
a) Technical reasons
- Narrow anastomosis.
- Bite through posterior wall.
- Graft kinking.
b) Neointimal proliferation at the anastomotic site.
c) Shunt thrombosis.
d) Infective endocarditis of the shunt.
e) Patient outgrows the shunt physiological blockage.
Note When a BT shunt of sufficient size is working than all other minor
collaterals & disappearing & only major collaterals persists.
# Compare morbid effect of various shunt
Modified BT Central Potts shunt WC shunt
shunt
PVOD 1-5% 5years <10% 5 years 50% 5years 6% 5years
CCF Rare Rare 38% 26%
Effect on ICR 4-8% 5-10% 15-60% 29%
Mortality

# Dose of Heparin & Aspirin after shunt

Heparin 10 units/kg/hr on table till 24 hours
Aspirin 5mg/kg daily after 24 hours
# Collateral supply to hand after classical BT shunt
- Superior intercostal artery
- Transverse cervical artery
- Transverse scapular artery
- Subscapular artery
- Suprascapular artery
129
- Circumflex humeral artery
# Indications for ICR in TOF
- Mc Goon ratio >0.7
- Nakata Index >100
- Z value > -3
- LV Volume 60% or more than normal (30 ml/m2)
- Absent peripheral pulmonary coarctation
- No major conal branch crossing RVOT
# Contraindications for ICR TOF.
- Unfavourable PA anatomy in infant
- Multiple VSD in infant
- Coronary artery crossing RVOT in infant
- Hypoplastic LV (LVEDV < 30 ml/m2, MV < -2 Z, Pulmonary annulus < -7 Z)
- Institutional criteria for performing ICR at a particular age & weight
# Definition of obligatory & non obligatory collaterals.
Obligatory collaterals is one when the collateral is the sole supply to a
portion of the lung whereby it cannot be ligated as then the lung become
ischemic.
Non obligatory collaterals is one when the collateral supplies the lung by
joining with the pulmonary artery so that even on ligation the blood supply to
lung is not necessarily jeopardized.
# What is Unifocalisation?
The process of connecting all obligatory collaterals to the main or branch
pulmonary arteries so that the pulmonary arteries form once again the main
blood supply to the lungs is called Unifocalisation of the vasculature.
# Source of collateral blood supply in the TOF.
- Descending aorta.
- Bronchial arteries.
- Arch of aorta.
- PDA.
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- Intercostal vessels + Chest wall.
Opens at,
- Intrapericardial part of PA.
- At the hilum.
- Sole supply of blood to alveoli.
Note Collateral flow will never exceed normal flow & so it is difficult to get flow
murmurs.
# Ideal age for Unifocalisation
3 years (collaterals are large enough)
# MAPCAS 2 classification system.
Robinovitchs classification based on origin
@ Direct origin
Type I Bronchial artery
Type II From Aorta
@ Indirect origin Type III branches of aorta.
Mc Goons classification based on termination
Type I Intra pericardial end side entry into MPA.
Type II Extrapericardial end side entry into Branch PA.
Type III Sole supply to lobe of lung.
Management varies according to the type of MAPCAS.
# Role of angio in MAPCAS.
- Number
- Site.
- Type.
- Flow through MAPCAS.
- Embolisation of MAPCAS.
# Site to look for MAPCAS.
On Rt. side Between Aorta & SVC.
On Lt. Side Posterior pericardium lt. of MPA & LAA.
# How will you manage shunted TOF?
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- Use Hemostat / Trasylol
- Keep warm banked blood ready to tackle the blood loss during sternotomy
- Prepare pericardium
- Take purstring for safety
- Dissect shunt
- Lt side Lt. Pleura
- Rt. Side Between SVC & Aorta, Behind SVC
- Go on CPB, Do not cool, keep ejecting, down on flows
- Ligate / clip the shunt
- LV vent to avoid distension/manage venous return.
# Not able to locate the shunt
- Cool patient
- Clamp
- Vent LV
- Give plegia stab PA
- Open RPA/LPA Block shunt with finger
- Put fogarty /foley catheter
- Close from inside.
# How will you manage TOF with MAPCAS?
Presuming MAPCAS are not supplying major portion of the lung & that side of
the lung is supplied by PA - On the day of surgery embolize the MAPCAS & do
ICR.
OR
Trasylol/Hemostat
Warm banked blood ready
On CPB
LV Vent
Dissect MAPCAS posterior pericardium near Hilum Ligate
# How will you manage TOF with multiple VSD?
TOF with well formed VSD margin
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Amenable to close easily
1+ 1 or 2 VSDs I will close
> 2 or 3 VSDs I will not operate
# TOF with LPA stenosis
- If LPA & MPA hypoplastic Extension of TAP into LPA.
- MPA normal & LPA origin stenosis Rectangular pericardial patch
# Total occlusion of LPA origin
Dissect LPA till hilum
Open LPA till MPA acts like posterior wall
Put pericardial patch as anterior wall of LPA
# LPA cord like till hilum
- Transect LPA
- Dissect till hilum
- Mobilize MPA
- Open LPA & anastomose it as a posterior wall to the lateral wall of MPA
- Put pericardial patch anteriorly
# TOF with RPA stenosis
# RPA excised from MPA
- Enlarge MPA
- Cut open RPA
- Anastomose RPA to the Lateral wall of MPA as posterior wall
- Put pericardial patch anteriorly
# RPA opened Extend incision into MPA, Put pericardial patch anteriorly.
# TOF with bifurcation stenosis
If patient is > 5 year Homograft conduit
OR
Mobilize Aorta, MPA, LPA, RPA
PA incision- into LPA & RPA
Superior edge of both opened artery are sutured together over a distance of
10mm
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OR
Separate patch repair of RPA & extension of TAP into LPA
# Requisites for TOF surgery at your centre.
Age 5 years (Maturity of lung & myocardium) (Not applied now can be done
at early age).
Wt. 10 Kg & above (Not applied now).
Suitable anatomy
@ Suitable sized LPA / RPA.
@ Confluent PA.
@ No branch PA stenosis.
@ No major branch crossing RVOT.
Investigations (Never say routine investigations).
@ X ray chest size of PA can be assessed.
@ Echo & Doppler must.
@ Hb PCV For bypass point of view.
@ Platelet count > 40000 required.
@ Coagulation profile.
@ Angiography not routinely done unless Echo expresses difficulty in
commenting on,
Poor visualisation of the PA.
Turbulence noted in PA but ductus not seen.
Presence of MAPCAS.
Coronaries crossing RVOT.
Confluence.
Branch PA stenosis.
# Anesthesia during ICR TOF.
Induction with:
Ketamine (2- 10 mg/ Kg). Advantages are:
Can be given IM

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Although it has sympathomimetic action & is expected to increase the right to
left shunt but the opposite effect is seen.
(Always give with atropine)
Midazolam (0.2- 0.3 mg/ Kg)
Maintenance with:
Fentanyl & pancuronium.
# Physiologically significant components in TOF.
RVOT obstruction
Dynamic obstruction seen in early part of life < 6 years.
A dynamic obstruction seen > 6 years, due to fibrosis of RVOT.
Malaligned, Non restrictive VSD.
# Bleeding from sternum during opening chest seen in.
Post classical BT shunt Here in order to get adequate length of subclavian
artery all its branches are ligated.
Blood supply to the rt. side is thus changed.
LIMA Inter mammary collaterals (Bleeding during sternotomy).

RIMA

Rt. anterior intercostals

Lateral thoracic artery

Subclavian artery
DIC state.
Adult TOF.

# Which sternotomy bleeds

Post classical BTS.

# Way of tackling this bleed

135
By using
FFP
Blood transfusion
# Indications for complete clearance of Thymus either one side or both
sides.
- Taking down of shunt.
- Dissection of the PDA.
- Accommodation of RVOT conduit.
- LSVC & PAPVC.
- Routinely done.
# Conditions for large pericardial harvest.
Pericardial conduit Extra cardiac Fontan, Rastelli.
Pericardial patch Mustard.
Extent of the patch Phrenic to phrenic & Diaphragm to reflection of
pericardium on the great vessels.
# Instruction to perfusionist TOF.
- Maintain optimum Hb Bloodletting to be done safely.
- Maintain HCT 45 Avoids capillary leak syndrome.
@ On table after induction from IV line.
@ From venous cannulae.
@ On bypass from reservoir.
- Dilution preferentially with colloids Albumin 1st choice, FFP 2nd choice.
- Maintain low perfusion pressure as,
@ All blood goes to collaterals.
@ Due to sudden hemodilution.
- Massive broncho pulmonary return due to collaterals can be harmful
because of,
@ Fills the field.
@ Rewarming the heart.
@ Distension of the heart.
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- Can be prevented by cooling & if required TCA & reducing the flow.
# In a deeply cyanosed child how much Hct should be maintained on
bypass?
45%.
As lower Hct shall lead to capillary leak syndrome
Excessive prime requirement.
# Cause of low pressure on CPB in TOF
Hemodilution
Collaterals
# If excessive LA return
Adjust flows, cool further
Search for PDA
Open pleura, retract lung to visualize the descending thoracic aorta- visualize
any obvious collaterals & tackle
# Approaches for ICRTOF:
RA-PA: Hudspeth
RVOT (longitudinal incision): Lillehei
RVOT (transverse): Gerbode
PA only: Sakornapant Pantpis
RA only: Edmunds, Saxena
# RVOT incision selective points.
Upper margin of RVOT incision:
- Just below the annulus
Lower margin of RVOT incision:
Till the level of the aortic annulus, or
1/3 distance from PA to apex
# Care while excision of the RVOT muscle
Septal side: take care for
- Can create a new VSD
- Damage to papillary muscle to ATL
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- Damage to the 1st septal artery

Parietal side:
- If excess shaved, there will be no margin for suturing
Crista:
- Damage to RCC
- If scissor inserted across the VSD (in case of infundibular atresia- damage to
AV/ VSD may get enlarged.
# Good coring of the RVOT has been done if:
Following structures can be visualized
From PA
- Complete VSD
- Tricuspid valve
- Apex of RV
From RA
- Pulmonary valve
- AV across the VSD.
# How to improve the exposure of VSD in TOF.
In RV approach:
- Stay sutures over RV
- Turn table to left
- Mop beneath the LV
- Adequate excision of the parietal band
- Retractor in VSD
- Visualization improves with suturing
- Start at the anteroinferior margin
In RA approach:
- Stay sutures over the RA & STL
- Additional retractor in the TV
- If required detachment of the STL
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# Dimensions of RVOT patch for reconstruction
The dimensions should be;
Length 1 1/2 times the incision length
Width should be according to Hegar size for particular weight
# Strategy for coronary crossing RVOT.
- If PA size & annulus adequate sized - RA-PA approach (Hudspeth)
- Elective LIMA- LAD anastomosis (Cooley)
- Turn the flap of anterior pulmonary artery to the ventriculotmoy & suture and
additional patch over this PA flap (Van Son)
- Mobilization of the coronary artery & suture patch beneath the lifted coronary
(Boncheck)
- Use of pericardial conduit
- Central shunt
# TOF corrected clamp released but heart is not beating
Rule out & correct
- Hypothermia
- Hyperkalemia
- Acidosis
- Xylocard given/not
- Pacing
- Look for LV distension Put LV vent if needed
# How will you treat hyperkalemia?
- Give glucose insulin (Insulin 0.1unit/Kg with Dext. 25%)
- Calcium Gluconate
- Correct acidosis with sodabicarb
- Inj. Lasix
- Wait for 10-15 minutes
- Repeat potassium again
# Heart is distending what will you do?
- Go upon root vent up to 1 litre.
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- Stab PA & put sucker in PA
- Put LV vent through RSPV.
# How will you put LV vent?
- On CPB
- Take purstring on RSPV-LA junction
- Ask perfusionist to keep some volume in the heart
- Ask anaesthetist to keep lung inflated
- Ask assistant not to suck blood & keep some blood level in pericardium
- Give curvature to the vent
- Stab the RSPV & put the vent
- Direct towards the lt. Hip
- Feel with right hand in the Lt. AV groove
- Remove the stylate & check for the back bleeding
- Connect to the sucker
- Tighten the purstring
# TOF corrected, Heart is beating, But not able to come off CPB
Rule out & correct
- Hypothermia
- Hyperkalemia
- Acidosis
- Urine output
- Residual shunt (RA-PA step up / TEE)
- Residual RVOTO (RV-PA pressure / MPA-RPA pressure / MPA LPA pressure
/ TEE)
- Pulmonary regurgitation (TEE)
Monocusp/bicuspid valve
Homograft conduit
Prosthetic conduit
Prosthetic valve
Still not able to come off CPB
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- Rest the heart for some time on CPB & after maximum support try again to
come off CPB
- Look for pulmonary pathology
Pneumothorax- Open pleura/Put ICD
Consolidation Nebulisation & suction
Secretion- Nebulisation & suction
# What will you look for during this time?
Distension of heart by finger on LV & PA
If heart is not beating perforate patch/create ASD /PFO.
# Incidence of complete heart block post ICR TOF.
Less than 1%
# Incidence of RBBB +/- LAHB post ICR TOF.
20- 25%.
# Reason for LAHB.
If sutures taken in the VSD lie towards LV side.
# Late complications of ICR TOF.
- RVOT restenosis
- PR/TR leading to RV failure
- Arrhythmias
- Aneurysm of RVOT patch
- Calcification of RVOT patch (Dacron, PTFE)
# Causes of RV dysfunction in TOF
Pre op:
- Chronic ischemia (adult TOF)
- Repeated cyanotic spells
Post op:
- CPB & cross clamp
- RV incision
- Damage to coronaries
- PR/TR
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- Large adynamic patch
- Residual VSD
# Post ICR TOF with heart block is of grave prognosis
-RBBB with LAHB (higher chances of sudden death)
# Care of hypertensive RV intraop.
Preop.
- Administration of O2 free radicals
Intra op: by
- Cold blood antegrade cardioplegia
- Aprotinin
- Warm induction
- Avoid large incisions over RVOT
- Avoid PR
Postop:
- Adequate inotropes
# Adult TOF are higher risk for surgery due to
- RVH may lead to RV failure
- Endocardial fibroelastosis
# Post ICR TOF arrhythmias
Ventricular arrhythmias can be detected in 40- 50% of patients, in the
postoperative period, using Holter monitoring.
# Predictors of arrhythmias are:
- Age of surgery
- Moderate/ severe PR
- Ventricular dysfunction
- Prolonged QRS interval (> 180 msec)
- RBBB is common after TOF surgery but complete heart block is rare.

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 VALVULAR HEART DISEASE

# What is dyspnoea?
Abnormally uncomfortable awareness of ones own breathing.
# How will you grade the dyspnoea?
Divided into 5 grades, similar to NYHA classification.
NYHA classification: The New York Heart Association: Have 4 components,
viz; Dyspnoea, palpitations, fatigue & angina.
Presently followed is the 7th edition of NYHA, laid down in 1994
NYHA I: In a patient with heart disease with no limitation of physical activity.
Ordinary physical activity does not cause dyspnoea, palpitations, fatigue or
angina. (More than Accustomed activity)
NYHA II: In a patient with heart disease with mild limitation of physical
activity. Comfortable at rest but ordinary physical activity causes dyspnoea,
palpitations, fatigue or angina. (On accustomed activity)
NYHA III: In a patient with heart disease with moderate limitation of physical
activity. Comfortable at rest but less than ordinary physical activity causes
dyspnoea, palpitations, fatigue or angina. (Less than Accustomed activity)
NYHA IV: In a patient with heart disease with marked limitation of physical
activity. Symptoms present at rest & increase on exertion. (At rest)
NYHA V: In CCF on anti failure medical treatment
# Which other classification systems you know?
1- Canadian cardiovascular society classification CSS - only angina (of)
2- Specific activity scale (of Goldman)- most specific- calculation of
metabolic equivalents (1 MET= 2.5 ml/ Kg/ min)
# What is Orthopnoea?
Dyspnoea in lying down position & relieved in sitting position

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# What is the Mechanism of orthopnoea?
In the recumbent position there is decreased pooling in the lower limbs &
abdomen blood is displaced from extrathoracic compartment to thoracic
compartment
Failure of LV pump to pump blood
Increased pulmonary venous congestion & capillary pressure
Interstitial edema leading to:
1) Decrease in lung compliance +
2) Increase in airway pressure +
3) Ventilation perfusion mismatch.
Dyspnoea.
It occurs rapidly, within1-2 minutes of lying down & is relieved on sitting.
# What is Dyspnoea & Orthopnoea equivalent?
Cough accompanies due to pulmonary congestion.
A non productive cough in CCF is considered as dyspnoea equivalent and n
recumbence is considered as orthopnoea equivalent
# What is Trepopnea?
Dyspnoea occurs only in the left or right lateral decubitus position, most often
in patients with heart disease.
# What is Platypnea?
It is dyspnoea which occurs only in the upright position.
Causes: 1. Left atrial thrombus
2. Left atrial tumors Myxomas
3. Pulmonary arterio-venous fistula.
# What is Paroxysmal Nocturnal Dyspnoea (PND)?
Attacks of dyspnoea which occur at night and awaken the patient from sleep.
It occurs 2-5 hours after the onset of sleep and takes 10-30 minutes for
recovery after assuming the upright posture.

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# What is the mechanism of PND?
Mechanism of PND is similar to that of orthopnea. However, a fall in PaO2 and
a decreased sympathetic support to left ventricular function during sleep also
contribute to the development of PND. It is a symptom of minimal left
ventricular dysfunction.
# Reasons for PND are:
1) Slow absorption of extracellular fluid from the dependent areas &
resultant increase in blood volume
2) Elevation of diaphragm
3) Decrease LV adrenergic support during sleep
4) Depression of respiratory centre during sleep
5) Transient nocturnal arrhythmias.
# What are the causes of PND?
1. Ischemic heart disease
2. Aortic valve disease
3. Hypertension
4. Cardiomyopathy
5. Atrial fibrillation
6. Rarely in mitral disease or atrial tumours.
PND is the earliest symptom of left heart failure.
# Reason for dyspnoea in CCF/ LVF:
1) Pulmonary function depressed increased interstitial fluid decreased
lung compliance increase airway pressure.
2) Respiratory muscle dysfunction.
# What is Hemoptysis?
Definition: Expectoration of blood.
Ranges from streaky sputum to gross hemoptysis.
Types: True- tracheobronchial & alveolar
False- oral/ nasopharyngeal

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# What are the causes of hemoptysis in a patient with MS/ LVF (Paul
Wood 1954)
1) Pulmonary apoplexy/ sudden haemorrhage- profuse, rarely life
threatening, due to rupture of dilated thin walled bronchial veins caused
by acute rise in left atrial pressure. (This is not seen generally due to
chronicity which causes the vein walls to become thick)- stops on own
2) Blood stained sputum associated with PND.
3) Pink frothy sputum seen in pulmonary edema due to rupture of alveolar
capillaries.
4) Pulmonary infarction- due to PA embolism.
5) Following chronic bronchitis due to edematous bronchial mucosa.
# What are the causes of chest pain?
Chest pain may divided into 3 categories-
- ischemic cardiac
- non ischemic cardiac
- non cardiac
Ischemic cardiac:
1) coronary artery disease (decrease supply)
2) LVH/ RVH (increase demand)
Non ischemic cardiac:
1) pericarditis
2) dilatation of the PA
3) dissection of aorta
Non cardiac:
1) Pulmonary embolism
2) Pleural
3) Oesophageal
4) Skeletal
# What is Palpitation?
Awareness of beating of ones own heart.
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Due to following cardiac physiological alterations:
1) change in heart rate
2) change in rhythm &
3) augmentation of contractility
Other causes of palpitations are:
- Thyrotoxicosis
- Hypoglycemia
- Fever
- Drugs
# Palpitations in the first decade of life
1) RHD with vale affection
2) Ebsteins
3) c TGA
# What is Syncope?
An association of
Generalized weakness of muscles with a loss of postural tone
Inability to stand upright &
A loss of consciousness
# What are the cardiac causes of syncope?
Decreased cardiac output:
LVOT obstruction- AS, hypertrophic subaortic stenosis
Obstruction to pulmonary blood flow- severe PS/ pulmonary atresia,
cyanotic spell, pulmonary embolism
Myocardial- massive MI
Pericardial- tamponade
1) Arrhythmias:
- Bradyarrythmias
- Tachyarrhythmia
2) CNS- embolism/ hypoperfusion
- LA thrombus, arch aorta aneurysm with thrombus
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 - LA myxomas
- Vegetations
- Others- carotid artery stenosis, vasovagal, rupture of IC
aneurysm due to hypertension.
# What will you ask for H/O Congestive cardiac failure?
In form of:
Oedema feet & puffiness of face
Distension of abdomen
Pain in the right upper abdomen
Anorexia, nausea & vomiting
Chest pain (15% of cases of CCF) due to RVH
Oliguria & nocturia (due to fluid retention with redistribution at night)
# Who proposed the forward & backward failure theory of CCF
Backward theory- James Hope (1832)
Forward theory- Mackenzie (1913)
# What will you ask for H/O Thromboembolic episode?
Ask for affection to the following organs;
1) CNS- loss of consciousness
- transient (TIA)
- prolonged with neurological deficit
- Convulsions
2) Other organs:
- hematuria
- abdominal pain
- limb pain
- coronary pain
# What are the source of embolism from the heart?
1) Thrombus
2) Vegetations
3) Myxomas
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 4) Paradoxical embolism
5) Plaques (rarely)
Tendency for embolisation is directly related to:
- age,
- size of LAA
- atrial fibrillation
Tendency for embolisation is inversely related to:
- Cardiac output.
# It is usually the fresh clot that embolize (only a minority of patients with h/o
recent TEE have clots found in the LAA)
# 50% of TEE are cerebral & is recurrent/ multiple in 25% of above.
# Commonest cyanotic congenital heart diseases to produce CNS
complications are:
1) Tricuspid atresia- 35% incidence beyond the age of 3- 4 years)
2) TOF
# What is infective endocarditis?
Definition: A microbial infection of the endocardium.
1st stage in the formation of non thrombotic bacterial endocarditis (NBTE)
which gets infected later.
NBTE form over areas of:
- endocardial injury
- turbulence
Areas of affection:
- Tends to occur in high pressure areas thus more on the left
side.
- Areas where the blood flows thru a narrow orifice from
high to low pressure, E.g. distal to a coarctation, VSD on
the RV side, PDA on the PA side.
#Endocarditis is rare in low flow states, e.g. ASD.

149
#Endocarditis occurs more frequently in Regurgitant lesions than stenotic
lesions & is characteristically on the atrial surface of MV & ventricular surface
of AV.
# What are the Clinical features of Infective endocarditis?
1) Constitutional features of infection,
2) Local destruction
3) Embolisation of vegetation leading to
- Infarction
- Infection
4) other area of infection due to persistent bacteraemia
5) Immune reactions.
Thus symptoms of IE are:
- onset after 2 weeks of precipitating event
- gradual onset with mild fever & malaise if the organism is
of low virulence (streptococcus) or acute onset with high
fever if the organism is of high pathogenecity ( staph)
- Fever- low or high is present in all patients with IE.
(#except in elderly, congenital heart disease, fungal IE)
- fever is generally low grade (< 39.4 C)
- arthralgia & arthritis
- symptoms of embolisation are:
- Hematuria
- Hematemesis
- Limb ischemia.
- Worsening of symptoms/ CCF- due to leaflet destruction
# What are the Signs of IE
- Constitutional- fever
- Local destruction resulting in
- new murmur
- change in pre-existing murmur
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 - CCF
- Splenomegaly & petechie 30% of patients with long duration. Petechie are
usually seen on conjunctiva, palate, buccal mucosa, upper extremity.
- Roth spots- over retinal haemorrhages with clear centre.
-Osler nodes- tender nodules on fingers/ toe pads- believed to be due to
deposition of immune complexes
-Jane way lesions- seen in acute endocarditis- are small haemorrhages with
nodular character seen on palm & soles.
-Clubbing- long standing disease.
-Embolization- especially pulmonary emboli are seen with- IV drug abusers
with Rt. sided IE & - Lt. sided IE with Lt. Rt. shunt.
-Mycotic aneurysm
-CNS manifestation- due to embolization& cerebral abscess
-Glomerulonephritis- due to immune complexes & embolisation
D/D:
- Acute rheumatic fever
- Myxomas
# Prophylaxis against IE in a patient with a prosthetic valve
Procedures not requiring antibiotic prophylaxis are
- Dental picking
- Upper GI scopy
- Primary bronchoscopy
- Clean surgery- E.g. Elective caesarean section
- Shedding of primary tooth
- IUCD insertion
For oral/ dental/ upper GI procedures
Regimen I: 3 gm Amoxycillin prior & 1.5 gm Amoxycillin 6 hours post
procedure
Regimen II: 1 gm Erythromycin prior & 500 mg Erythromycin 6 hours post
procedure
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For lower GI/ GUT procedures
Regimen I: IV amoxycillin (3 gm) + IV Genta (1.5 mg/Kg) hour prior to the
procedure & 1.5 gm Amoxycillin 6 hours post procedure.
Regimen II: IV Vancomycin (1 gm) + IV Genta (1.5 mg/Kg) hour prior to the
procedure.
# No prophylaxis is required in which cardiac lesions?
1) ASD- unoperated or operated
2) MV prolapse
3) Coronary artery disease/ post CABG
# Classification of postoperative IE
Early < 60 days postoperative
Late > 60 days postoperative
Early is due to intraoperative or immediate postoperative contamination.
Mechanical > Bioprosthetic > Homograft IE is more in the early period
However in the late period, IE is equal in all the kinds of valves.
# Treatment of IE:
Stretococcus: Penicillin G 6 lac units 6 hourly- 4 weeks +/- Gentaminicn 1.5
mg/ Kg/day
Staph: Vancomycin 15 mg/Kg/dose 12 hrly- 4 weeks +/- Gentamicin 1.5 mg/
Kg/day
# Echo predictors of embolism in a patient with infective endocarditis are:
- (By JACC, 2001) Increased chances are if:
Mobile vegetation
> 10 mm vegetation (if > 15 mm vegetation then chance of embolisation is 80%)
# Prosthetic valve endocarditis: types
Early; within 60 days
Late; after 60 days
Risk of prosthetic valve endocarditis is greatest within the first 6 months after
surgery, especially the first 6 weeks.
< 12 months- organism is usually staph aureus
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> 12 months- organism is usually streptococcus
# Prosthetic valve endocarditis Vs native valve endocarditis
-NVE is largely confined to leaflet. In PVE, the infection commonly extends
beyond the valve ring, into the annulus & Para annular tissue.
# What is the proper/complete treatment of infective endocarditis?
- Minimum Two IV bactericidal antibiotics
- Minimum 4-6 weeks
# Reason for postponing cardiac surgery in a patient with IE, who
otherwise requires surgery for the same are:
1) CNS- acute hemorrhagic stroke (< 10 days)
2) Renal- Acute glomerulonephritis leading to renal failure.
3) Thrombocytopenia
# Indication for surgery in IE
Absolute
1) CCF Moderate/ Severe
2) Uncontrolled infection
Relative
1) >10mm vegetation
2) highly mobile vegetation
3) Embolism
4) Paravalvar extension
5) Continuous fever
# Duration of treatment for IE
If blood culture negative 6 weeks
If blood culture positive post op 6 weeks and then till 3 subsequent blood
cultures are negative
# Characteristics of native valve IE
1) Lt>Rt.,
2) MV>AV
3) Regurgitant> stenotic
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# Commonest area of annular involvement in IE
1) Aortic valve annulus
- between RCC and LCC (can compress on Lt main)
- between RCC and NCC (can cause heart block)
2) Mitral valve annulus posterior
- paravalvar extension is rare in pulmonary and tricuspid valves
# What are the indications of surgery in Active Infective endocarditis?
- Large loose vegetation
- Multiple embolic episodes
- Severe hemodynamic compromise
- Continuous sepsis in spite of treatment
- Paravalvular abscess
# What are the choice of valve in paravalvar abscess?
- Auto graft
- Homograft
- Bioprosthetic valve
# Which is the homograft valve of choice in mitral area?
- Mitral homograft
- Pulmonary homograft- Ross II procedure
# What will you do to the valve after excising?
I will send it for Gram stain & culture.
# What will you ask for H/O Rheumatic fever?
Ask for h/o sore throat followed by fleeting arthritis.
# What is rheumatic fever?
Definition: It is an acute non suppurative immune mediated inflammatory
disease, usually in children, that follows a few weeks after a pharyngitis caused
by group A hemolytic streptococci.
# Reason for increased prevalence in developing nations is not known.
Believed to be due to
- Increased urbanization (due to increased droplet infection)
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 - Overcrowding
There is no role to suggest that nutritional factor has a role in RF.
# Causative agent is group A hemolytic streptococci however in 1/3rd of
the patients there is no h/o sore throat or blood culture yield e/o
streptococcal infection.
# Pathogenesis is not known & is believed to be an immune reaction to
bacterial allergy or autoimmunity.
Aschoff bodies:
- May be seen if cardiac involvement.
- Seen in the myocardium & endocardium (rarely over the valves)
- Most frequently seen in the; IVS & posterior surface of LV/ LA.
- They are discrete lesions, < 1mm diameter, formed by a collection
of round cells, fibroblasts & MN giant cells, surrounded by a zone
of PMN cells & lymphocytes.
- Particularly situated around small blood vessels.
# What are the clinical features of rheumatic fever?
- Symptoms begin usually 2-3 weeks after an episode of acute pharyngitis.

-fever (is always present, except in chorea)

-Fever lasts for 2-3 weeks.
-Other features that may follow are:
1) Arthritis: It is a fleeting arthritis affecting large joints with no residual
deficit. Generally affected joints are;
- knee
- ankle
- elbow
- wrist
Each joint remains inflamed for 1-7 days & complete episode lasts for 3
weeks.
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#Rarely affected joints are:
- shoulder
- hip
- Small joints.
#Rarely a deformity may be left behind- Jaccouds arthritis.

2) Subcutaneous nodules:
#considered pathognomic of rheumatic fever.
They are:
- less than 2 cm diameter
- freely mobile overlying skin
- Site: Over bony prominences especially skull, galae aponeurotica.
For examining for these nodules, ask the patient to squat & keep the elbows on
the knees & wrists folded beneath the chin. Now palpate the shin, extensor
aspect of elbow, occiput & mid back, i.e., over & around the spine & scapula.
3) Erythema marginatum: These are;
- Rapidly evolving small macules papules large circles with
raised & well defined edges which blanch on pressure.
- Disappear within few hours.
- Site; trunk, limbs. Very rare on the face.

4) Chorea (St. Vitus dance): These are;

- Characterized by involuntary, non repetitive, jerky movements
which decrease during sleep and increase with anxiety.
- In children any gender, but post puberty mainly in girls,
- The patient becomes irritable & produces jerky movements,
grimacing involuntarily & has slurred speech.
- Generally seen along with carditis or nodules.
#clinical examination: when child is asked to extend the arms there is tendency
to flexion of wrist & hyperextension of the fingers.
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# Who was St. Vitus?
- St. Vitus was a roman catholic priest who patronized epileptics &
actors
5) Carditis:
It is essentially a pancarditis.
50% of cases of rheumatic fever have carditis.
Endocarditis-
th of patients developing carditis have a new murmur which may
be
- apical pan systolic murmur; due to myocarditis (the commonest
murmur)
- apical mid diastolic murmur, Carrey Coombs murmur,
- PA systolic murmur, due to fever, anemia.
Myocarditis-
- Important feature of myocarditis is progressive dilatation of LA &
LV.
Pericarditis- 2 types
- acute fibrinous
- effusion
(Pericarditis is associated with sever forms of carditis.)
#CCF occurs in 10% of patients with rheumatic carditis.
#Prolongation of PR interval is temporary but may persist for months (reason is
not known)
# Rheumatic fever may lick the joints but certainly bites the heart.
# Rheumatic fever mainly affects the left side of the heart (reason unknown)
# What is Jones criteria?
Original- T. Duckett Jones (Australia) in 1944
Current- 4th edition of Jones criteria, updated in 1992.
The criteria as-

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Major Minor
Carditis Clinical-
- fever
- arthralgia
- h/o rheumatic fever/RHD
Polyatrthritis Investigations-
- Presence of acute phase reactants (CRP, ESR,
leucocytosis)
- PR interval prolongation
Subcutaneous
nodules
Erythema
marginatum
Chorea
# E/o of streptococcal infection, in form of
- ASLO +ve, or
- +ve throat culture, or
- h/o scarlet fever.
#Diagnosis of rheumatic fever by modified Jones criteria is by
- 2 major criteria + e/o streptococcal infection, or
- 1 major & 2 minor criteria + e/o streptococcal infection.
If there is no supporting e/o streptococcal infection then the diagnosis of
rheumatic fever should not be accepted, except in 2 conditions:
- Only signs of chorea, or
- Only signs of carditis.
This is because the infection may have occurred few months back &
hence the antibody titres may have returned to normal.
#In India Polyarthralgia is included as major criteria (in 1994 by Padmavati &
Khanna)

158
#Average duration of rheumatic attack is 3 months. In cases of carditis, it may
progress for nearly 6 months.
#ASLO- described by Todd in 1932.
Normal levels are up to 333 Todd units- in children &
Up to 250 Todd units in adults.
Most specific test for rheumatic fever is AntiDNAase antibody levels.
Normal levels are up to 240 Todd units- in children &
Up to 120 Todd units in adults.
# D/D of streptococcal pharyngitis?
- Viral: characterized by more malaise & rhinitis.
- Other bacterial.
# What is the recurrence ratio of RF?
Risk of recurrence of rheumatic fever is 65% & the risk decreases with time.
# What is WHOs recommendation for sore throat?
WHO recommendations are to treat all sore throat as due to group A
hemolytic streptococci unless proved otherwise.
The prophylaxis involves:
Single injection of 12 lac units Benzathine penicillin (if wt. > 27 Kg) &
Single injection of 6 lac units Benzathine penicillin (if wt. < 27 Kg)
Or
Oral Erythromycin 20 mg/Kg/day for 10 days.
# Treatment of Rheumatic carditis
Is 3 fold
1) Treatment of CCF- bed rest, salt restriction, digoxin, diuretics
2) Treatment of Carditis- Aspirin- 100 mg/kg/day in 8-10 divided doses for
1 month if symptoms persist after few days of starting aspirin add
Prednisolone 1-2 mg/ Kg/ day & reduce aspirin.
3) Treatment of rheumatic fever.
# Incidence of valvar affection of RHD:
MV- 70-80%, MV + AV- 20- 25%,
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Only AV- 5- 8%, TV- 30- 50% (autopsy)
# First auscultatory manifestation of carditis in rheumatic fever.
1) Pansystolic murmur of MR (between Grade 2-4)
Occasionally
2) Carrey Coombs murmur &
3) Flow murmur across the PV
# Prophylaxis against RHD
AHA guidelines (1995) - Dajani et al (Journal- Pediatrics, 1995)
Primary prophylaxis:
Consider all sore throat as streptococcal infection and treat (unless throat swab
proves otherwise. The prophylaxis consists of-
Agent Dose Mode Duration
Benzathine penicillin G 6 lac units for 27 Kg intramuscular Single
12 lac units for > 27 Kg
Penicillin V Children: 250 mg, 2-3 Oral 10 days
(phenoxymethylpenicillin) times daily
Adolescents & adults:
500 mg 2-3 times daily
For those allergic to
penicillin:
Erythromycin 20- 40 mg/ Kg/ day, 2- Oral 10 days
4 times, max 1gm/ day
Estolate 20- 40 mg/ Kg/ day, 2- Oral 10 days
4 times
Ethylsuccinate max 1gm/ day Oral 10 days
40 mg/ Kg/ day, 2-4
Azithromycin times Oral 5 days
max 1gm/ day
500 mg on first day &

160
 later 250 mg/ day for 4
days
Secondary prophylaxis:
3 subgroups of patients
Group Prophylaxis
Rheumatic fever + For 10 years & till at least 40 years
Carditis + of age, with consideration of
Valvular heart disease + lifelong therapy (especially in
endemic areas)
Rheumatic fever + At least for 10 years or into
Carditis + adulthood; whichever is longer
Valvular heart disease -
Rheumatic fever + At least 5 years or till 21 years of
Carditis - age, whichever is longer
Valvular heart disease -

Prophylaxis is by:
Benzathine penicillin: if > 27 Kg- 12 lac units
If 27 Kg- 6 lac units
4 weekly in developed countries
3 weekly in developing countries
Penicillin V 250 mg BD-
Erythromycin 250 mg BD-
Sulphadiazine: 1 gm OD if > 27 Kg
500 mg < 27 Kg
# Potential for vaccine development for rheumatic fever
From IHJ 2002
Vaccine strategies are:
against M protein- due to nearly 93 types, a polyvalent vaccine is required. Also
there is risk of cross reactivity with the heart tissues
161
against bacterial attachment to mucosal surface (against fibronectin binding
protein)
Limitation of an above vaccine project: is a lack of animal model.
# What are the pressure symptoms?
- Hoarseness of voice &
- Dysphagia
# What are the reason for hoarseness: (Otners syndrome)?
Due to compression on the left recurrent laryngeal nerve by
- Dilated LA
- Tracheobronchial LN
- Enlarged PA
- Arch aorta or proximal descending thoracic aortic aneurysm
- Aneurysm of ductal ampulla
# What are the reason for dysphagia?
Due to pressure on esophagus by
- arch/ descending thoracic aortic aneurysm
- aberrant Rt. Subclavian artery- dysphagia lusoria
- LA enlargement
- Rt. Aortic arch
MITRAL STENOSIS

# What is your diagnosis?

My diagnosis is Male/female patient with severe Mitral stenosis with mild
functional TR in sinus rhythm without CCF, Thromboembolic episodes IE in
NYHA class II Probably of Rheumatic etiology.
# Why Mitral stenosis?
- H/O SOB
- H/O Rheumatic fever
- JVP normal
- Pulsus parvus
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 - Tapping apex
- Diastolic shock
- Diastolic thrill
- Heart sounds- Loud S1, Loud P2, OS- may/ may not be present
- Murmur- middaistolic murmur with a presystolic accentuation
heard over the apex, radiating to the axilla, best heard with the bell
of the stethoscope, with the patient in left lateral position & breath
held in expiration & increased on clinching the fists.
# What not TS?
TS- Will have no sign of PH, different site of murmur, increase in murmur on
inspiration
# Why not LA myxoma?
LA myxoma- will have constitutional symptoms, postural syncope, tumor plop,
changing murmur in different position.
# What are the signs of PAH?
Loud P2
Prominent a wave in JVP
# Why do you say Functional TR?
Murmur of Gr 2/6
Absence of TS murmur.
# If murmur is not heard in MS what will you do?
- Make patient walk / Do exercise Auscultate again
- Left lateral decubitus
- Bell of stethoscope
- Breath hold in expiration
# Causes of Thromboembolic episode in SR with MS?
- Transient AF
- Calcific valve
- Infective endocarditis
- LA myxoma
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# Differences between Austin flint murmur & MDM of MS
Austin flint murmur MDM of MS
- Opening snap Absent Present
- Loud S1 Absent Present
- Presystolic
Accentuation Absent Present
# What are the causes of mitral stenosis?
- Rheumatic heart disease
- Congenital Parachute Mitral valve
- Hunters syndrome
- Hurlers syndrome
- Lutembachers syndrome
# What are the differentiation points between OS & LVS3
OS LVS3
High pitched (not palpable) Low pitched (palpable)
Heard best with diaphragm heard best with bell
No change with respiration with expiration
# Reason for loud S1 in MS.
Due to tensing of MV leaflets due to late closure of a fully opened MV.
# Reason for OS.
Due to tensing of MV after it opens in diastole.
# How does a patient of MS improve spontaneously?
Due to;
1) Development of TR
2) Development of PH
3) Development of precapillary stenosis (secondary MS)
# Rheumatic valvulitis produces 3 distinct pathological changes
- Commissural fusion
- Fibrosis of leaflet with stiffening & retraction
- Fusion & shortening of chordae
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# What is normal mean LA pressure/PCWP & which factors affect it?
- Normal mean LA pressure is 10-12 mmHg
- Severity of MS,Cardiac output, Heart rate affects it
# What is Auscultatory Triad in MS?
- Apical diastolic rumble Blood flow through stenotic orifice
- Loud S1 Thickening of Mitral leaflets
- Opening snap
# Earliest rheumatic fever.
- 3 years (Padmavati)
# Earliest rheumatic MS, requiring intervention.
- 6 years (reported by Stanley John, circulation 1983)
# Earliest rheumatic MR, requiring intervention.
- 4 years, Carpentier (Circulation 2001)
# How will assess severity of MS?
A) According to Valve area & Symptoms
Normal Mitral valve area is 4-6cm2
Valve area Symptoms
> 2.5 cm2 None
1.5-2.5cm2 (Mild MS) Dyspnoea on severe exertion
1-1.5cm2(Moderate MS) PND Pulmonary oedema
<1.0 cm2 (Severe/critical MS) Orthopnoea (Class IV)
B) Severity of MS is on A2- OS interval
Mild MS (LAP 15 mm Hg) 0.08- .12 sec
Moderate MS (LAP 20 mm Hg) 0.04- 0.08 sec
Severe MS (LAP 25 mm Hg) 0.04 sec
C) According to gradient across Valve
Normal valve mean gradient is 0 mmHg.
Severity Mean gradient
Mild MS <5 mmHg
Moderate MS 5-15mmHg
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Severe MS > 15mmHg
D) Duration of diastolic murmur is directly proportional to severity.
# Conditions simulating MS
-LA myxoma
- Cortriatriatum
- Ball valve thrombus in LA
- Diastolic flow murmur across normal valve in VSD, PDA, Severe MR
-Carey coombs murmur of mitral valvulitis
# What is the characteristic X ray finding in MS?
- Left atrial enlargement
Double shadow behind the heart
In Rt. Heart border shadow in shadow
- Straightening of left heart border
Due to Prominent PA & LAA
- Splayed carina
- Small Aorta
- Kerleys B line Dense ,short horizontal line seen in Costophrenic
angle Pulmonary venous pressure 20-30mmHg
- Kerleys A line straight, dense lines up to 4 cm length running
towards the hilum Pulmonary venous pressure > 30mmHg
- Mitral valve calcification
- Pulmonary hemosiderosis Parenchyma ossification
# What are the features of pulmonary venous congestion in MS?
- Pulmonary vascular markings
- Upper & lower lobe pulmonary vein congestion
- Peribronchial cuffing
- Pulmonary oedema
- Kerleys A,B,C lines
- Hemosiderosis

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# Barium swallow in RAO view & LA enlargement
I Compression of barium filled oesophagus
II Compression & posterior displacement
III Displacement & increased curvature
# Prominent aortic knuckle in MS
- AR
- HTN
# What will be the ECG findings in MS?
- SR/AF
- Left atrial enlargement P mitrale M shaped P in Lead II
,Biphasic P in V1
- RVH
# RAE in ECG of MS
Associated TR
# ECG correlation with severity of MS.
ECG will reveal the following
1) LAE
2) PAH- RVH with strain pattern
3) RAE
4) Axis (mild: 90- 100, moderate: 100- 110, severe: > 110)
5) Rhythm
# What you would like to see on Echo in MS?
- Morphology of Mitral valve- Pliability ,MVA,Subvalve,MVGr
- Ventricular function
- LA & LAA clot
- Other valves
- Other cardiac anomalies Like ASD,VSD,PDA
# Echo in MS
M Mode: Findings are

167
 1) Due to slow closure of MV in early diastole the EF slope is markedly
diminished
2) Diminished mobility causes a reduced DE amplitude
3) Thickened leaflets
4) Anterior movement of PML
Discrepancy:
- In patients with AS/ AR, with normal MV the EF slope is
diminished- hence it is unreliable & obsolete
- 20% of patients of MS will not have anterior movement of PML
2 D Echo: is the principle means of evaluating valvular pathology in MS
Features are
1) Doming of AML in diastole (due to inability of valve to accommodate all
the blood available for delivery into the LV)
Doppler: Shows
1) Rate of decrease in diastolic flow after E point
2) Accentuation of A wave (absent in atrial fibrillation)
3) Pressure half time (the time required for the peak gradient falls to half)
for valve area.
MVA= 220/ PHT
4) Valve area by continuity equation
A1 x V1= A2 x V2 (A1= AV area, V1= velocity across AV, A2= MV area,
V2= velocity across MV)
A2= [A1 x V1]/V2
(This is provided there is no AR/MR)
# Fallacies of TEE (transesophageal echo) in MS
- Tip of LAA not seen in TEE
- Clot < 1cm not seen
# LA clot not seen on TTE (Tran thoracic echo)
- Density of clot same as blood
- Mildly calcific or organised clot
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# What is LA smoke?
It is echodensites seen due to churning of blood in the dilated LA due to
stagnation, in a patient with MS.
# How will you differentiate smoke from Clot?
- LA clot- It doesnt move or only oscillate
- Smoke Moves like whirl pool from one place to other place
# How will you differentiate smoke from LA myxoma?
- LA myxoma It doesnt move or moves in & out of MV with each
beat
- Smoke _ Moves like whirl pool from one place to other place
# Indications for cath in MS
- No correlation between ECG, Echo & CxR.
- Evaluate PA pressure
- LV systolic function
- AR Status not able to quantitate on Echo
- Age > 40,Angina on exertion for coronary angio

# What are the medical treatment in MS?

- Anti failure measures
- Anticoagulants in AF
- Rheumatic prophylaxis
- Infective endocarditis prophylaxis
# What are the other modalities of treatment?
- Balloon Valvuloplasty ( PBMV/PTMC)
- Surgery ( CMV/CMC,OMC,MVR)
# What are the indications of PBMV?
Pliable, noncalcific valve with mild moderate subvalvar pathology, No MR
Wilkinss Echo score < 8
# Contraindications for PBMV
- Other valve disease/ Coronary artery disease needs surgery
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 - LA/LV thrombus
- Thickened atria septum ( > 4mm)
- Moderate MR
- Calcification of mitral valve
- Recurrent thromboembolic events
# What is Wilkinss score?
Wilkins et. al.s Echo Score for Modality of treatment.

1 2 3 4
Leaflet Rigidity Mobile Valve - - Immobile Valve

Leaflet Thickening Thin - - Sev. Thickening

Valvular Calcification No bright echoes - - Multiple Bright

Subvalvar Disease Sparse echoes - - Multiple Thick
Score
4-8 Young patient with loud OS Excellent candidate for BMV, good long term
result
9-12 Less likely to achieve lasting improvement with BMV, Greater potential
for restenosis, better for OMV/MVR
13 Poor result of Mitral valve repair Usually requires MVR
# Which patients will you send for BMV?
MS with bilateral bronchiectasis
# Paul Woods apoplexy what bleeds?
Veins of Ellis
# During BMV why a pigtail is kept in the aorta?
To avoid damage to the NCC during septal puncture.
# How to calculate size of inoue balloon for BMV
Size of balloon= {height (cm)/ 10} + 10
# Criteria for operating a patient with MS?
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 1) Moderate/ severe MS with Class III or more symptoms.
2) Asymptomatic MS if
- LA clot
- Thromboembolism
- Pulmonary hypertension (PASP > 60 mm Hg)
- RV dysfunction (RVID (D) > 17 mm/m2)
- Critical MS (area < 0.7 cm2)
- ? atrial fibrillation
- hemoptysis
# What are the indications of CMV?
- Same as BMV
- Failure of BMV
- Not able to cross septum
# What are the contraindications of CMV?
- Calcium in the valve
- LA/LAA clot
- MR++
- AR++

# Grade- I AR with MS will you do CMV?

I will see the LV size & rotation If normal Yes
# Grade II AR good /bad for CMV?
Bad
# Grade I AR with OMV/MVR, what are the problems?
- Cooling reduces the heart rate-heart will distend
- During cardioplegia keep hand on the root
- Put Foley catheter across the valve
- May need retrograde plegia
# What are the indications of OMV?
- Calcium in valve
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 - LA/LAA clot
- MR
# What are the approaches for CMV?
- Anterolateral thoracotomy
- Posterolateral thoracotomy
# What care to be taken during induction in MS?
- Do not allow tachycardia-Pulmonary oedema occurs
- Do not give fluid fast even if hypotension develops Pulmonary
oedema occurs
- Intubate only when patient is completely paralysed to avoid
sympathetic stimulation
# Incision taken during the first CMV?
C shaped incision over the anterior chest wall
# If confusion of 4th or 5th space during CMV, which space preferred?
The 5th space, as the crucial part is lifting of the LV apex.
# Where will you open the pericardium in CMV?
Anterior to the Phrenic nerve & vessels
# When approach posterior to phrenic during CMV?
- A posterolateral thoracotomy approach
- Redo CMC
# CMV in pregnancy- outcome?
Ueland, Am J Obst.Gynecol. 1975
514 patients with maternal mortality= 2%, fetal mortality= 8.5%
# Where will you take purstring on the LV?
Between LAD & Diagonal
# How will you stab the LV?
Using No 11 blade, Incision will be parallel to LAD & in the direction of the LV
muscle fibres.

172
# How will you dilate the LV stab?
1st with back of No 11 blade handle & then with No 7 & 8 Hegar dilator
respectively.
# What all things will you see before proceeding for CMV?
- Thrill on LV
- LAA appearance
- Palpate PA
# Where will you take purstring on LA?
On LAA
# How will you take purstring on LAA?
- Clamp the LAA
- Take 4-0 prolene suture & take purstring above the clamp
- Open the LAA & extend the incision with pott's scissor
- Put 4-0 silk stays on both the lips of LAA
- Give thorough wash in LAA
# If LAA is small what will you do?
Take two purstring on LA Pulmonary vein junction
# What all things will you assess after putting finger in LA?
- Mitral leaflet
- Nodularity & calcium
- Commissural fusion
- Mitral valve opening
- MR
# How will you dilate the valve?
- Check & adjust the Tubbs dilator opening
- Put rt. Hand finger into LAA
- Lift the apex with remaining fingers of rt. Hand
- Using Tubbs dilator passed through LV stab
- Pass the dilator across the MV
- Open the dilator perpendicular to leaflets/commissures
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 - Remove the dilator & access the valve opening
# Who was Tubb?
- Oswald Sydney Tubb- Contemporary thoracic surgeon,St.
Bartholomew hospital London
- Invented Tubbs dilator for CMV
# What is finger fracture technique?
Opening the comissures with force of index finger applied over the
commissures.
# Orientation of dilator during CMV?
- Tubbs dilator perpendicular to leaflet/commissures
- Colley- perpendicular to the commissures
- Logan- any direction
# What all things will you look for after opening the valve?
- Valve opened fully/not
- Residual commissural fusion
- MR
- Subvalve apparatus
- Redo CMV will be possible or not
# When you open the LAA clot is present what will you do?
- Soft clot release the clamp allow the clots to come out.
- Ask anaesthetist to compress the carotids at the time of dilatation
of the valve
Or
- Loop carotids & snug before dilating the valve ( possible through
Posterolateral approach)
- Keep extra blood ready
- Do single dilatation rather than multiple / staged dilatation
- Role of fibrillation while cot is being extracted
- If only LAA clot take purstring at the LA-pulmonary vein junction
- Firm clot left insitu abandon the procedure & do OMV.
174
# Causes of clot in SR?
- Low output state
- Intermittent SR
# How the LAA will look if clot is present?
With clot Shrivelled, dull blue in colour
Without clot Pink, tense, glossy
# How will you decide on table which valve is not suitable for CMV?
- Calcium on commissure with eccentric opening
- Calcified cusp
- Commissural calcification
- MR
# While doing CMV LAA tears what will you do?
- If bleeding is more control bleeding 1st then do CMV
- If bleeding is less do CMV 1st then control the bleeding
- Call for the help of assistant
- Ask anaesthetist to arrange for more blood
- Keep finger in the LAA
- Ask assistant to take the purstring around your finger
- Remove the finger & press on the lateral wall of LA
# Causes of tear in LAA?
- Fat female
- Fat laden LAA
- Small LAA
- Small incision as compared to the size of index finger
# While tying the LV purstring it tears what will you do?
- Put finger into the LV opening
- Ask assistant to take purstring around your finger

- Pass a Foleys/ Fogarty catheter into the LV and hitch it up against the tear

175
- Fibrillate the heart & suture

- CPB (complete or left heart only)
# While dilating the valve heart fibrillates what will you do?
- Dilate the valve 1st
- Remove the finger
- Continue massaging the LV till paddles comes
- Defibrillate the heart
- Treat the potassium & acidosis
- Give xylocard
# Post CMV Airway pressure is going up what is the cause?
Post CMV MR
# Management of post CMV Pulmonary oedema
- Put patient on Pressure control mode
- Start Dobutamine
- Check MR by echo, If MR is moderate- severe MVR
- Replace the valve (MVR)
# What are the important points during redo CMV?
- Skin incision larger than previous
- Adequate adhesion release
- Purstring on LA-PV junction
- LV purstring at the same site
# Contraindication for redo CMV
- More subvalvar fusion
- Quality of cusp fusion
- MR
# Post CMV why do OMV but not redo CMV?
1) Difficulty in access- no LAA, adhesion
2) Severe subvalve fusion

176
 (However post CMV, redo CMV has been a common practice & hence can be
debated)
# Post OMV eccentric annuloplasty (at commissures)
Woolers annuloplasty
# Specific points of anesthesia in MS
- Avoid fluid overload
- Avoid tachycardia.
# Brief history of mitral valve surgery?
- Elliot Cuttler- tenotomy knife to cut the AML
- Henry Souttar- first digital palpation of MV (with pt. Having
symptomatic improvement)
- CP Bailey- introduced a curved knife to be entered through the
LAA for cutting the commisures of MV
- Brock- Digital fracture of commissures
- Dubost- transatrial dilators
- Logan & Turner- Transventricular dilators
- Modification of TV dilators by- Beck, Glenn, PK Sen, Cooley, Tubbs
(Tubbs introduced screws for adjustment of opening diameter)
- OMV- CW Lillehei
- Series of OMV- Kay et. al.
- MVR (mechanical valve)- Albert Starr (21st Sept, 1960)
- MVR (homograft)- Senning in 1965
- MVR (bioprosthetic)- Carpentier
# What are the signs of Rheumatic activity on opening the chest?
- Butter cheese appearance of adhesions
- Petechial haemorrhage
- Arrhythmia
- Irritable heart
# What care on table will you take in Post BMV for MVR?
- Loop the SVC & IVC
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 - Snug the SVC & IVC before opening the LA- ASD created during BMV
will suck air & cause air lock.
- Small sized LA & LAA-because of decompression of LA into RA through
ASD
# Why in post CMV is the adhesinolysis is started on the aorta
1) Aorta is anteriorly placed
2) It is thick & easily palpable
3) Adhesion release is easy to start
# How will you do adhesion release in CMV?
- Open pericardium over the aorta
- Put finger in & do boating against the pericardium to create the plane
between RV & pericardium
- Cut pericardium over the finger
- Do sharp dissection only (Avoid blunt dissection with finger)
- Do not give heparin till adhesions are released over the main part
- Release as much adhesions as possible without compromising hemodynamics
- Release Apex & lateral wall on CPB
- Check all over the heart for bleeding & control all bleeding if there before
replacing the valve (It will be difficult to lift the heart post replacement)
# Why normothermic release of adhesions
1) Better myocardial preservation
2) If AR- prevents distension
# Advantages of adhesinolysis
1) Better exposure of the MV
2) Easy of checking MV competence, post OMC/ repair, from LV apex
3) Deairing
4) Defibrillating
5) Pour ice slush around the heart

178
# Extent of adhesinolysis
Till beyond the AV groove, as if the adhesions are not removed there will be
cephalad deviation of the mitral valve
# What are the approaches to mitral valve during MVR?
- LA
- RA-trans septal
- Superior septal
- Roof of LA
- Biatrial RA-LA/Vertical incision
# Approaches to the MV?
Elkins Paraseptal
Barner Combined paraseptal & Superior
Rogue - Hitch pericardium after freeing SVC
Larbalestier -Freeing of Waterstons groove
Brawley- Trans RA septum
Dubost -Trans RA-LA (vertical incision)
Seale -Retract SVC/ disconnect SVC & extend incision upwards into
superior LA
Saxena & Meyer - Through roof of LA
Through LAA
M Yacoub - Through aorta
Batista - Through LV apex
Cooley- Trans aortic
Julien - Transseptal
Cohn Trasseptal extended to opposite side
Smith Transseptal extended to SVC
# What will you do if LA is small?
- Visualisation of mitral valve is difficult
- Table up on rt. Side,

179
 - Lift the rt. Side of the pericardium up
- Turn the table on left side
- Dissect the interatrial groove/Sondergards groove/Waterstons groove
- Extension of the incision behind the SVC & IVC ,Snugging of cavae to be
done
- Put Loop retractor or two small retractors
- Extend the incision on the superior surface of LA after dividing the SVC
High SVC cannulation required
- Trans septal approach
- Biatrial approach
- Trans RA approach
# Where does the IAS open if LA is incised
Inferior end of incision IAS turns posteriorly and to the right
# LA can be retracted with
1) Cooleys retractor
2) Two right angle
3) Loop retractor
4) Carpentier self retaining
# Intraop grading of commissural fusion:
Grade I- Partially fused
Grade II- completely fused but fissure identified
Grade III- densely fused with no delineation
# How will you remove the clot from the LAA?
- Less LAA & heart handling before clamping
- Ask perfusionist to put Arterial line filter
- Hold the clot with sponge holder
- Remove peel from the LAA-Isolate LAA
- Invert appendage
- Take gauze piece & rub in the LAA
- Wash keep outside sucker/rough sucker in field
180
# Where will you start incising the valve?
At 120 clock position
# Why start at the 120 clock position in AML for MVR?
1) It is the most accessible area
2) It is a safe area
3) No subvalvar structure behind it
4) This area is rarely affected by calcification
5) Provides an opportunity to protect the PML
# During an MVR why is the AML incised & excised first
1) At 12o clock position there are no important structures
2) No chordal structure behind the AML
3) Easily accessible
4) Rarely affected by calcification
5) Gives an opportunity for PML preservation
# Why AML is not preserved frequently?
It increases the gradient across the LVOT.
# PML preservation advocated by:
Lillehei (he plicated the PML first and then used it as a neoannulus during the
MVR)
# Techniques of leaflet preservation?
PML tucking- Lillehei
AML & PML plication- Hertzer
AML bulk excision- Rose
Splitting of the AML/PML in centre- Miki
Splitting of the AML according to chordae & then suture that segment to
the respective site on the annulus- Khonsari (modified version- Khonsari
II)
# Advantage of Chordal preservation
- Maintains the geometry of LV
- Preserves the LV function
181
 - Increase EF
- Reduce wall stress
- Increase contractility
# MVR in calcified annulus
- Pre op evaluation
# Coronary angio Circumflex artery
# LV angio Amount & degree of calcium
# TTE/TEE Repair/replacement Extensive leaflet calcium
- Technique
# Excise the leaflet, Soften the annulus with ronger.
# Care to be taken on Posterior annulus not go too deep
# If too much calcium is there, cover the area with pericardium
# Thorough washing of LV cavity
# Interrupted pledgetted sutures
# Indications of MVR in HOCM
- Interventricular septum dimension < 18mm in area of resection
- Atypical septal morphology in which the hypertrophied region lies outside
the field of standard myotomy& myomectomy
- Persistent symptoms & obstruction following an adequate myomectomy
- IHSS with severe MR secondary to organic mitral disease
# Does technique of suturing matters in paravalvular leak
Yes. Continuous technique > incidence. Kirklin Ann Thoracic Surgery 1983.
# Clinically Stuck valve
- Absence of click on Ryles tube/ET tube
- TTE/TEE
- Heart beating on CPB-Distends & stops beating off CPB
# Surgical importance of poor EF
- Work of LV increase after MVR
- Needs good myocardial protection
- Avoid injury to circumflex artery
182
 - Preserve the chordae
# Problem of a high profile valve in the mitral position?
1) LVOT obstruction
2) Hemolysis
3) Increased thromboembolism
# Which valves are high profile valve?
- Starr-Edwards
- Bioprosthetic valve
# Which valves are low profile valves?
- St.Jude
- Medtronic Hall
- Omniscience
- Carbomedics
- TTK Chitra
# Ten commandments of prosthetic heart valves
By Harken
1) It must not propagate emboli
2) It must be chemically inert & not damage blood elements
3) It must close promptly (< 0.05 sec)
4) It must offer no resistance to physiologic flow
5) It must remain closed during the appropriate phase of cardiac cycle
6) It must have lasting physical & geometric features
7) It must be inserted in a physiologic site- generally the normal anatomic
site
8) It must be capable of permanent fixations
9) It must not annoy the patient
10) It must be technically practical to insert.
# Advantage of a built in holder
1) No chance of inserting a valve upside down
2) No damage to disc
183
# Rule for choosing valve size:
- In aortic position choose same size &
- In mitral position choose one size less.
# MVR for MR better or AVR for AR
AVR for AR as
1) In MR, LV is pumping into low pressure LA & post MVR now has to
pump in aorta
2) In MVR, when the valve is excised, a portion of the LV is excised.
3) MR/MS is associated with elevated PAP.
# Antibiotic coated sewing rings
1) Minocycline
2) Rifampicin
# Complication of maze
If close to PV then it may cause PV stenosis
# Medtronic Hall valve 1st implanted in
1977
# St. Jude valve 1st implanted in
1977
# Who invented pyrolytic carbon
Jack Bokros. An engineer, invented pyrolitic carbon for covering uranium
pellets.
It was tried by Dr. Vincent Gott.
Jack Bokros then eliminated the silicone content of pyrolytic carbon
&launched his own valve in 1996 (the Onex valve)
# How to prolong life of bioprosthetic valve
1) Non Gluteraldehyde treatment
2) Reduce BP & heart rate (anti impulse therapy)
3) Immunosuppression
# Who started St. Jude.
Manual Villafona in 1976.
184
# Modifications from the Lillehei Kalke valve
Lillehei Kalke valve St Jude valve
All titanium Pyrolytic carbon
Opening angle= 60% Opening angle= 85%
Pivot mechanism- small More for systolic & diastolic washing
# Clinical trial on the Lillehei Kalke valve
Used only in one patient, died after 24 hours.
# Sutureless valve
Magovern Cromie (Ball in cage) valve. High incidence of heart block.
# 1st pivoting disc valve.
Wada Cutter valve. It was removed from market in 1972 (MV) & 1974 (AV).
# 1st Dura mater allograft
Puig et al, 1971 (Brasil)
# Development of Medtronic Hall valve
Combination of design of Bjork Shiley & Lillehei Kaster, gives rise to Hall
Kaster valve, which was later renamed as the Medtronic Hall valve.
(Hall: Karl Victor Hall, Norway)
# Who was St. Jude
A Jewish saint.
# Valve orientation of tilting disc in mitral position.
If Chordal preservation is not done
- Bjork-Shiley: Greater orifice posteriorly
- Medtronic -Hall: Greater orifice towards IVS (to prevent possibility of
hindrance to disc due to hypertrophied mural side structures.
- TTK Chitra valve Greater orifice posteriorly
- Omnicarbon valve Greater orifice posteriorly
If chordal preservation done
Greater orifice facing anteriorly in all tilting disc valves
# Valve orientation in Bileaflet valve in mitral position?
Anatomic position
185
Antianatomic position
# Who introduced xenografts
Jean Paul Binet, Jean Langlois & Alain Carpentier.
# Who introduced glutaraldehyde
Alain Carpentier
# Who coined the term bioprosthesis
Alain Carpentier (Biologic origin with Prosthetic fate)
# In a Starr Edward valve why is Barium impregnated in silicone.
- Reduce the wear & tear
- Make it radio-opaque
# Who is Hancock
Warren Hancock, Vice President of Edwards laboratories left it& established his
own company & released Hancock valve.
# Care of biological valve on table
- Do not squeeze
- Rinse thoroughly with saline
- No penicillin antibiotics to be used topically (as it may displace the
Gluteraldehyde moiety)
- Keep valve continuously moist
# Why MV bioprosthesis degenerates faster than AV prosthesis.
1) Higher pressure for closure
2) Faster closure
3) Atrial fibrillation (?)
# Early biological valve dysfunction
1) age (children)
2) pregnancy
3) hypertension
4) hyperparathyroidism
# What is Ross II Procedure?
Use of pulmonary autograft in mitral position
186
Inverted top hat position
# Types of LV rupture
Treasures classification
Type I: In the AV groove. Seen in
- Resection of the MV annulus during MVR
- Use of a large size prosthesis
Type II: Base of papillary muscle. Seen in
- Resection of papillary muscle
- Decalcification
- Due to strut of bioprosthetic valves
- Deairing post MVR
- Adhesinolysis
- Site/ extension of LV vent
Type III: In between above two. Seen in as Type II
# Prognosis of LV ruptures
If intraoperative diagnosis- 50% mortality
If post operative diagnosis- 100% mortality
Type I mortality > Type II/ III
# Problems of large LA post CPB
1) Deairing
2) Higher chances of thromboembolism
3) Weaning from ventilator
4) Post operative low Cardiac output
5) Persistence of atrial fibrillation
# Post MVR patient not coming off bypass
1) Poor myocardial protection- ischemia
2) Conduction block
3) Prosthesis dysfunction/ left circumflex artery injury
# Advice on pregnancy post MVR
It depends upon preoperative PH/ LV dysfunction
187
If no PH/ Normal LV- can become pregnant but advised after 6- 12 months
If PH+/ LV dysfunction present- wait for 6- 12 months & then repeat echo &
advice
# Family planning post MVR
Avoid
1) OCP
2) IUCD- infective endocarditis/ bleeding
# Current recommendation for adding aspirin to Warfarin in patients with
prosthetic valves are:
-Given by JACC, 2001
1) TEE in a patient with mechanical valve on warfarin
2) Patient with a mechanical valve with risk factor, viz.
- H/o TEE
- Atrial fibrillation
- Large LA
- LA clot
- > 1 mechanical prosthesis
- CAD
- Ball valve
# Anti thrombotic treatment post prosthetic heart valves
(JACC 1998 recommendations) by McAnulty, Rahimtoola
Warfarin Warfarin Aspirin
(INR 2- (INR 2.5- (80-100
3) 3.5) mg)
Mechanical prosthetic valves
A. First 3 months after +
replacement
B. After 3 months + +
Aortic valve + +

188
 Aortic valve + risk + +
factor + +
Mitral valve
Mitral valve + risk
factor + +

Biological prosthetic valves +

A. First 3 months after + +

replacement +

B. After 3 months + +

Aortic valve
Aortic valve + risk
factor
Mitral valve
Mitral valve + risk
factor

Risk factor: are

- Atrial fibrillation
- LV dysfunction
- Previous thromboembolism
- Hypercoagulable conditions
# INR should be maintained between 2.5 & 3.5 for aortic disk valves & Starr
Edward valves.
# INR between 2.0- 3.0 applicable only for bileaflet valves & Medtronic Hall
valves.
# Antithrombotic therapy in patients requiring non cardiac surgery/
dental care
Usual approach

189
If patient on -Stop 72 hrs before procedure
warfarin -Restart in afternoon on the day of procedure or
after control of active bleeding
-Stop 1 week prior to procedure
If patient on restart the day after procedure or after control of
aspirin active bleeding
Unusual
circumstances -Stop warfarin 72 hours prior to procedure
Very high -Start heparin when INR falls below 2
risk of -Stop heparin 6 hours prior to procedure
thrombosis -Restart heparin within 24 h of procedure &
if off continue until warfarin can be started & INR 2
warfarin -Start heparin as soon after surgery as deemed safe
& maintain PTT as 55- 7- seconds until warfarin
restarted & INR 2
Surgery
complicated -Continue antithrombotic therapy
by
postoperativ
e bleeding
Very low
risk for
bleeding

# Clinical judgement. Consider this approach if recent thromboembolism,

Bjork Shiley valve or 3 risk factors (viz: atrial fibrillation, LV dysfunction,
previous thromboembolism, hypercoagulable conditions & mechanical
prosthesis). One risk factor is sufficient to consider heparin in patients with
mechanical valve in mitral position.
# Heparin can be administered in outpatients basis before & after surgery
190
E.g. Local skin surgery, teeth cleaning, treatment of caries.
# Survival post valve replacement
Survival rates are better for AVR than for MVR/ DVR.
10 year survival, in general, for
AVR = 65%
MVR= 55%
DVR= 55%
-Late mortality is higher for regurgitant lesions.
-Late mortality is higher for rheumatic/ ischemic valve replacement in
comparison with degenerative diseases.
# Mortality distribution post valve replacement
(From surgery for valve- late outcomes-Peter Groves, Heart 2002)
- 60%- cardiac, non valve surgery related (CCF, myocardial infarction,
arrhythmias)
- 20%- valve related
- 20%- non cardiac causes
# Predictors of mortality are:
1) age > 65 years
2) LV dysfunction
3) NYHA 4 at time of surgery
4) Coronary artery disease
5) Ventricular arrhythmias
# Sudden death post valve replacement
Sudden death is defined as death within 1 hour of an event of abrupt onset &
accounts for around 25% of all late deaths following valve replacements.
There are 3 categories of sudden death:
1) Natural disease process: ventricular arrhythmias (AVR > MVR)
2) Related to prosthesis: Thrombosis, TEE, IE, leak, mechanical failure
3) Management failure: IC bleed due to elevated INR
# Changes in PAH post valve replacement
191
The most dramatic regressive changes in PAH occur within the first few days
after surgery & are generally complete 6 months postoperatively.
Full normalization is rarely achieved. Even if the PAPs are normal at rest, an
increase with exertion will be seen suggesting residual irreversible changes.
This leads to a chronic increase in afterload.
# Guidelines for FU after valve surgery
AHA/ACC guidelines 1998
1st FU: should be clinical, ECG & X- ray. Also an echo examination for
documenting prosthesis function, ventricular function & PH- for reference for
future.
# Large RA in TV disease is seen in
1) TS + TR
2) Atrial fibrillation
3) Mean RAP 12 mm Hg
# Significant gradient across the TV, on cath is:
A gradient more than 5 mm Hg.
# Role of tricuspid annuloplasty in functional TR
It has been shown that correcting the MV lesion, without interfering on the TV,
is associated in many patients with persistence or worsening of TR
postoperatively.
Hence TV annuloplasty should be contemplated if
- TR is moderate or severe
- Annular dilatation is > 21 mm/m2.
As in above spontaneous regression in the postoperative period is rare.
# Normal PV area is
2 cm2/m2
# Pulmonary valve stenosis
Valve area Gradient Peak systolic RV pressure
Mild > 1 cm2 < 50 mm Hg < 75 mm Hg
Moderate 0.5- 1 cm2 50 80 mm Hg 75- 100 mm Hg
192
Severe < 0.5 cm2 > 80 mm Hg > 100 mm Hg

MITRAL REGURGITATION
# What is your diagnosis?
My diagnosis is Age, Male/female patient, with severe MR without CCF,
Thromboembolic episodes, or Infective endocarditis in atrial fibrillation with
controlled ventricular rate, NYHA class III, probably of rheumatic etiology.
# Why MR?
- Dyspnoea & palpitation
- Wide pulse pressure
- Hyperdynamic apical impulse which is shifted down ward & out
- Parasternal lift
- Soft S1
- S3 over apex
- P2 loud & S2 widely split (in PAH)
- Systolic thrill over mitral area
- 4/6 Blowing Pansystolic murmur at mitral area radiating to axilla & back
# How will you say it is severe MR?
- Presence of systolic thrill over the apex
- Large LV
- Presence of S3
- Flow MDM at mitral area
# What are the features of Acute & chronic MR?
Acute MR Small heart, pulmonary oedema
Chronic MR Large LV & TR
# Severity of MR on auscultation
- PSM at apex
- Mild PSM in anterior axillary line
- Moderate-PSM at Posterior axillary line
- Severe- PSM at posterior scapular line
193
# Why S1 is loud in MS?
- Less volume of blood in LV Abrupt closure of mitral valve
- Summation of Mitral & tricuspid valve closure
Possibilities of loud S1 in MR?
- Tachycardia
- Thin chest wall
# What is the importance of functional class?
- Treatment modality & decision making
- Post op outcome
- Mortality
# What are the other causes of PSM?
- VSD
- TR
# Why not VSD?
In VSD
- RRTI
- History from childhood
- Parasternal heave present
- P2 loud
- Harsh PSM at left parasternal border
- 2/6 MDM at mitral area
# Why not TR?
In TR
- JVP is raised
- PSM at subxiphoid region
- Liver palpable
# Acute deterioration in a patient with valvular heart disease
- Atrial fibrillation
- IE
- Carditis
194
# Incidence of atrial fibrillation
- In general population: 0.4- 2%
- In > 60 years age group: 10%
# Importance of atrial fibrillation
- Increased morbidity & mortality.
- In MS if atrial fibrillation is present the mortality is increased by 17 times
- In coronary artery disease if atrial fibrillation is present the mortality is
increased by 7 times.
# Orifices of the normal mitral valve are:
- Primary- at the annular level (not affected in RHD)
- Secondary- cuspal level
- Tertiary- chordal level
# Prerequisites for elective cardioversion for atrial fibrillation
The patient should be
- Fasting
- Anesthetized
- Anticoagulated
The shock should coincide with the R wave of the ECG
# Internal cardioversion
If external has failed. The electrodes are placed in the right atrium & coronary
sinus
# Carvallos sign?
To differentiate between TR Vs MR. With inspiration if the loudness of murmur
increases, it is a TR murmur.
# MV disease with a midsystolic murmur.
MV prolapse
# Silent MR.
- Paravalvar leak
- Post myocardial infarction MR
- Obesity
195
 - Emphysematous chest
# What are commissural leaflets.
Sometimes accessory leaflet tissue is present at the commissures of MV,
termed as commissural leaflets. It is functionless.
# What will X- ray show in MR?
- Cardiomegaly
- Left atrial enlargement
- LV apex
- Signs of pulmonary venous hypertension
# Normal CT ratio if patient with MR?
- Acute MR (infective endocarditis, post MI MR, trauma, post
BMV/OMC/CMV)
# What are the X- ray criteria of LA enlargement?
- Straightening of left heart border( Mitralization)
- Double atrial shadow- Reversed 3 sign at right heart border
- Carinal angle > 1100
- Lateral view LA shadow overlapping spine
- Barium swallow LAO view Indentation of oesophagus
# MR with small LA
- Associated ASD
- Acute MR
# Criteria for giant for LA
Kawazoe (Ann Thoracic Surgery 1982)
Echo:
# LV compression- bowing of posterior wall of LV by > 30 mm in the long axis
view
X-Ray:
# Carinal angle > 120
# Left bronchus/ trachea ratio < 0.4
# Right CTR > 0.6
196
Piccoli criteria: LA dimension (AP) on echo > 65mm
# How will you differentiate LA enlargement in MS & MR?
- Small arch of large circle MS
- Large arch of small circle MR
# How will you differentiate the LA from RA in X-ray?
- RA shadow will continue with SVC above & touches diaphragm below
- LA shadow never touches diaphragm
# How will you say calcification is in mitral or aortic valve from X-ray?
- A line drawn from rt. Cardiophrenic angle to Inferior border of LAA
- Calcium above the line Aortic valve
- Calcium below the line Mitral valve
- Fallacies
Below the line but aortic calcification
Ascending aorta aneurysm pushing the aorta down
Calcium extending into LVOT
Ascending aorta calcific
Above the line but mitral calcium
Aneurysm of Mitral valve
# How will you differentiate PAH from PVH on X-ray?
- PVH
Increased pulmonary vascularity
Kerleys lines

- PAH
Increased pulmonary vascularity
Increased end on vessels
Absence of kerleys line
# What will you find in ECG?
- P Mitrale
- LVH with LVVO
197
 - AF/SR
# What do you want on Echo?
- Mitral valve morphology
- Vegetation & Subvalve
- LA & LV dimensions
- LVEF
- MV annulus
- Other valves
# What is normal LA/Ao ratio?
LA/Aorta ratio -1.3/1
# What is normal ejection fraction?
658 %
# When will you find EF 75-80%?
In AR & MR
# Indications for cath in MR?
- Coronary angio ( Age > 40 years)
- Blood culture from particular chamber for Infective endocarditis
# How will you manage the case of severe MR?
Mitral valve repair
- Thin pliable leaflets
- Mild moderate SV pathology
- Young female patient
Mitral valve replacement
- Not possible to repair
MVR + LA reduction
- Large LA > 7cm
MVR with Maze procedure
- Large LA with AF
# LA reduction by various techniques
- LA placation from inside
198
 - Cutting LA strip on the posterior wall
- Cutting LA strip on the rt.side
- Left side maze procedure
- Complete Maze procedure
- Pulmonary vein isolation technique
# Post MVR poor EF
- LV has to work hard
- Poor myocardial protection
- Chordae not preserved
- Injury to circumflex artery
# Advantages of annuloplasty rings
1) Retain shape & size of annulus
2) Keeps tension of suture lines
3) Increases leaflet coaptation
4) Prevents recurrent dilatation of annulus
# Types of annuloplasty rings
2 types- Rigid & Flexible.
(Rigid rings have been shown to interfere with the LV filling & functioning of
the anterolateral segment)
Ring Incomplete Complete
Carpentier Edward Original CE Physio ring
(Baxter) stainless steel- Titanium + velour Dacron
now Titanium Size-22 to 36 (transverse
diameter), 26= 3 cm2 area,
28= 4 cm2 area
Duran (Medtronic) Complete flexible. Titanium
core with silicone felt. Have 3
marks for reference.
Seguin (St. Jude) Semi flexible with

199
 anteroposterior angulation
Tailor (St. Jude) Complete flexible ring.
Silicone with barium
Cosgrove (Baxter) C shaped ring,
with no support
for the anterior
annulus
Annul flex (Sulzer Complete flexible
Carbomedics)
Homemade Stainless steel
wire with a 4
mm PTFE
Endoscopic placement Autologous
pericardium
over a titanium
platform

# Concept of incomplete ring

Only the mural annulus dilates & hence needs to be restored back in shape.
# Concept of circular semi flexible ring.
Anterior portion is rigid- as no change occurs in the transverse diameter during
cardiac cycle
Posterior portion is flexible- allows increase & decrease of the anteroposterior
diameter
AORTIC STENOSIS

# What is your diagnosis?

My diagnosis is age, male/female patient with Severe Aortic stenosis without
CCF, Thromboembolic episodes & Infective endocarditis in SR with NYHA class
II Probably of Rheumatic etiology
200
# Why Aortic stenosis?
- H/O Angina ,Syncope & Dyspnoea
- Slow rising small volume pulse
- Heaving apex beat
- Ejection click
- Carotid thrill present
- Rough 5/6 ejection systolic murmur loudest in the aortic area radiate to
the carotids
# What is the difference between Heaving & hyperdynamic apex beat?
- Heaving
Increase in both amplitude & duration of impulse
LV pressure overload
- Hyperdynamic
Increase in amplitude only
LV Volume overload
# Why valvar AS not Supra /subvalvar AS?
- Presence of ejection click suggest valvar AS
# What is the SAD in AS?
S- Syncope- Life expectancy 3 years
A- Angina- Life expectancy 4 years
D- Dyspnoea- Life expectancy 2 years
# Absence of ejection click in Valvar AS?
Calcific AS
# Silent AS
- AS with CCF
- AS with MS
# Findings of severe AS are:
- Increased harshness of murmur
- Late peaking of murmur
- Soft S2
201
 - Pulsus parvus et tardus
# The sign of severity of AS:
- Late peaking of murmur
# Difference between degenerative & rheumatic AS.
- In degenerative: mainly first involves the cusps
- In rheumatic: mainly first involves the commissures
# Sudden death incidence in AS.
- considered high traditionally however recent studies have shown
that the incidence of sudden death, in AS, is low (provided the
patient is asymptomatic)
# Severity of AS
A) According to S2
- Mild stenosis A2 followed by P2
- Moderate stenosis A2 delayed giving rise to single S2
- Severe stenosis Reverse splitting of S2 ( P2-A2)
B) According to valve area
- Normal aortic valve area is 3- 4cm2
- Mild AS - >1.5cm2
- Moderate AS - >1.0-1.5cm2
- Severe AS - <1.0cm2
- Critical AS - <0.5cm2
C) Long murmur & late peaking up of murmur indicates severe AS
D) According to gradient across aortic valve
Normal gradient is 0mmHg
Mild AS - < 30mmHg
Moderate AS 30-50mmHg
Severe AS > 50 mmHg
E) Presence of S4 & absent A2 indicates severe AS
# Mechanism of Angina in AS?
- 50-70%
202
-Imbalance between coronary blood flow & O2 demand
- Ventricular wall thickness/wall stress/ wall tension- during systole
compression of coronary artery & during diastole- high LVEDP
# Mechanism of syncope in AS?
- 30-50%
- Hypotension
- Faulty Baroreceptors mechanism- vasodilatation
- Arrhythmia
- Obstruction to forward flow Reduced cardiac output
# In AS at which valve area symptoms starts?
1.2-1.5cm2
# What is the significant gradient in AS?
Peak systolic Gradient of > 50mmHg
# Which is the best method to assess AR?
Angiography
# Rate of progression of AS
- Degenerative >> rheumatic
- Jet velocity: 0.3 m/sec/year increase
- Valve area: 0.1 cm2/ year decrease
- Mean transaortic gradient: 7mm Hg/ year increase
# Guidelines for FU of patient of asymptomatic AS (JACC 1998)
- Mild AS: 5 years
- Moderate AS: 2 years
# Outcome of asymptomatic AS;
- Excellent prognosis
- Once symptomatic- prompt surgery
# In severe AS, rate of becoming symptomatic is:
- 40% by 2 years
- 80% by 3 years

203
 (Hence strict FU is required for these patients, but can wait till
symptoms appear)
# Gallaverdin dissociation of AS
Described by Gallaverdin in 1925. In patients with a severe calcific AS, a high
velocity ventricular ejection produces a loud midsystolic murmur in aortic area
& vibrations of the AV during systole creates a soft apical musical murmur.
# Atrial fibrillation in AV disease indicates:
- Coexistent MV disease
- Terminal stage
# CxR in AS
- Small heart
- Enlarged aorta & aortic knuckle
- Calcification
# ECG in AS
- LVH with strain pattern
- LBBB
- Complete heart block if calcium of valve into extends into
conduction tissue
# Prolonged PR interval in a patient with AS.
- Digoxin toxicity
- Calcification/abscess extending into the AV node
- Rheumatic carditis
# Echo in AS
M MODE: shows
1) thickened & immobile leaflets
(M Mode for determining valvar pathology, in AS, is no longer done)
2) LV wall thickness
2 D ECHO:
1) systolic doming

204
 (Systolic doming is the most important 2 D Echo finding of any valvar
stenosis)
DOPPLER
1) pressure gradient across the AV using modified Bernoullis equation
2) AV area by the continuity equation
AV area= [LVOT (area) x LVOT (velocity)]/ AS (velocity)
3) measurement of ejection time
# Severity of AS on echo- JACC 1998
Jet velocity Peak gradient Valve area
Mild < 3m/sec <36 mm Hg >1.5 cm2
Moderate 3-4 m/sec 36- 64 mm Hg 1- 1.5 cm2
Severe > 4 m/sec > 64 mm Hg < 1 cm2
(Area of normal aortic valve= 3- 4 cm2)
# Indications of Cath in AS
- Age > 40
- AS with H/o Angina
# Cath data in AS
- Systolic Gradient between LV & aorta
- AR assessment
- Post stenotic dilatation of aorta
- Coronary angio
# Surgical intervention recommended in AS is
1) Moderate/ severe AS with symptoms- angina/ palpitations/ dyspnoea/
syncope/ presyncope
2) Moderate/ severe AS with ECG e/o ischemia
3) Asymptomatic AS if-
- Decrease in LV systolic function
- Woman with AS, contemplating pregnancy
- Occupation involving increased exertion
- Critical AS ( < 0.6 cm2) in whom symptoms are shortly inevitable
205
 - Other concomitant procedures
- LV Posterior wall thickness > 15 mm
# How will you go on CPB for AVR
Aortic cannula & Two stage Venous cannula
# Why two stage venous cannula?
- Only aortic valve surgery
- Disadvantage Rewarms the heart
# Advantage of one stage venous cannulae in AVR?
- Do not rewarm the heart
- Useful in LV dysfunction
# How will you put retrocannula?
- Purstring on the RA -1 cm away from the AV groove & at the
junction of upper 1/3rd& Lower 2/3rd of AV groove.
- Keep volume in the heart
- Stab & hold the cannula with left hand
- Right hand over the CS near IVC
- Put cannula through RA anterior to two stage venous cannula
- Direct posteriorly
- Once it enters the CS opening direct it towards the left shoulder
- Withdraw the stylate & see for pulsatile black blood coming out
- Connect it to pressure line
- Confirm the trace of it with pressure of 4-5mmHg
# How will you put LV vent?
- After going on CPB
- Do not cool keep heart ejecting
- Take purstring on the RSPV-LA junction
- Keep volume in the heart
- Stab the RSPV & Hold the vent in left hand
- Right hand in the Left Av groove
- Direct the vent towards the left hip
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 - Guide with right hand across the Mitral valve
- Remove the stylate & see for bright red blood ejecting from vent
- Connect to the vent line
# Where will you open the aorta?
- 1.5 cm above the right coronary artery
Or
- Lower border of RPA ( if RCA is not visible in fat)
- Extend the incision
Lt side Aorta-PA groove
Right side Centre of NCC
# Direct ostial plegia, which one 1st Left/right?
- Left 1st
- Because
In front of the eye
LV perfusion is more important for its function
# How will you give left & right plegia?
- Left Coronary plegia-
Angled cannula
Directed towards Assistants leg
- Right coronary plegia-
Ask assistant to retract anterior lip with two forceps
Push RCA from outside using back of the forceps inside
Put the cannula in the ostia
Direction facing towards the sky
# How will you say cardioplegia is going?
- Coronary artery distends Left LAD, Right RCA
- Metal part of the cannula cold
- Heart stops beating
- Blood starts coming out from other coronary

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 - Perfusionists Plegia volume level falls without resistance
# Cardioplegia is not going what are the possibilities?
- Kink in cardioplegia line
- Clamp on cardioplegia line
- Cannula tip is not in ostium
- Cannula tip is touching the wall
- Atherosclerotic ,small artery
# Where will you excise the valve?
- With scissor at RCC-NCC commissure or with No 11 knife at centre
of RCC
- Cut towards RCC-NCC-LCC
- Most upper part of annulus & easily accessible
# What care will you take while cutting the valve?
- Leave 1mm margin
- Avoid damage to AV node ,AML & coronaries
# What care will you take in calcific valve?
- Put tampon in LV cavity
- Cover coronaries with retractor /coronary occluder
- Use of outside suction/rough sucker
- Thorough wash
- Do not excise the calcium too much in to annulus
# Which suture will you use?
2-0 Ethibond non pledgetted suture fro commissures & Colour coded
pledgetted sutures for annulus
# How will you put the sutures in the annulus?
Pledgetts facing aorta (Everting mattress) Suture-
Easy technique
Everts the edge
Pledget removal easy if suture breaks
Narrow downs the orifice area
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Pledgetts facing LV side-
Less number of sutures required
Advantageous in small aortic root
Difficult to retrieve pledgetts if suture breaks
Pledgetts Forms a source for infection/IE.
May give rise to > gradient ( Act as SAM)
Figure of 8 Sutures (Nonpledgetted)-
Fast technique
AR with good annulus
No source of infection
No LVOT gradient
Useful in small annulus
Sutures needs to be put very carefully very close to each other
Chances of paravalvar leak is high
# What is Small aortic root?
Aortic valve has no fibrous annulus
Aortic annulus is the aortoventricular junction where the aortic leaflets are
attached
Diameter of normal aortic annulus ranged from 23-27mm depending on the
patient size
Definition of small aortic root is relative
Aortic annulus of 23 is normal for BSA of 1.5-1.6m2, but small for BSA of
2.0m2.
Based on the hemodynamic data obtained from post op Doppler echo with
AVR, matching the size of the valve to the size of the patient

Body surface area Smallest valve size (mm)

< 1.5 m2 21
1.5-1.7m2 23

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1.7-1.9m2 25
>1.9m2 27

# What are the various methods used for small aortic root?
- Top hat Oblique position of the valve in NCC, sutures from
outside in.
- Nicks Centre of NCC use of hemashield/Gortex/Pericardium ,2-
3 mm enlargement
- Manougian NCC-LCC commissure,5-6 mm enlargement
- Kono Rastan
- Blanks modified technique
- Supraannular patch
- Homograft
- Autograft Ross procedure
# What is Ross procedure?
Use of autologous pulmonary valve for aortic position & use of homograft
/allograft for pulmonary position
# Candidates for Ross procedure
1) Patient between 10- 50 years age
2) Isolated aortic valve pathology
3) Have endocarditis limited to aortic root
4) Athletes/ young individual
# Contraindications to the Ross procedure
1) Extremes of age ( < 1 yr or > 70 yrs)
2) Marfans
3) PV pathology
4) Depressed LV function
5) Multivalvar disease
6) Rheumatic (as shown by Dr. Sampath Kumar, JHVD 1994)

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# Criteria for Ross procedure
There should not be >3mm difference in the size of Aortic & Pulmonary
annulus size
# Injury to the 1st septal artery
1) Ross procedure
2) Morrows procedure (for hypertrophic subaortic stenosis)
3) Vouhes procedure (for hypertrophic subaortic stenosis)
4) Kono Rastan procedure
5) Infundibular resection (septal side) in TOF
# Surgeries where the MPA is transected
1) Arterial switch
2) Extracardiac fontan
3) Kreutzers modification of Fontan
4) Damus Kay Stansel procedure
5) Ross procedure
6) Anastomosis to left main
7) Norwood procedure
# Surgeries where the aorta is transected
1) Aneurysm ascending aorta- for replacement
2) Lecompte manoeuvre
3) Surgery for APVS
4) Arterial switch
5) Ross procedure
6) Takedown of Waterston Cooley shunt
# Damage to artery to SA node
1) TCPA
2) Senning
3) Mustard
4) LA roof approach for MVR
5) Atriocavopexy for SV ASD
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Also in
6) Damage to artery following myocardial infarction

AORTIC REGURGITATION

# What is your diagnosis?

My Diagnosis is age, male/female patient with severe AR without CCF,
thromboembolic episodes, infective endocarditis in SR, NYHA class III, probably
rheumatic etiology
# Why AR?
- H/o Palpitation, Dyspnoea
- Waterhammer pulse &other peripheral signs of AR
- Hyperdynamic apex
- Diastolic thrill (very rare)
- Heart sounds- S1 normal, S2: Loud A2 with narrowing of A2 P2
split, LVS3/S4 may be present
- Murmur- Early diastolic murmur, decrescendo in nature, best
heard over the aortic area, sternum & to the left, radiating to apex,
heard best with the diaphragm of the stethoscope with the patient
sitting, leaning forward & breath held in expiration.
- Austin Flint murmur may be present
- Murmur of functional AS may be present (with/ without a thrill) -
this is the only functional murmur that may be present with a
thrill.
# Difference between Rheumatic AR & Syphilitic AR
Features Rheumatic AR Syphilitic AR
- History Rheumatic fever Syphilis
- Angina < common > common
- A2 Normal & soft Loud, Tambour likes
- Diastolic murmur 3rd LICS 2nd RICS
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- Peripheral signs of AR Not very well marked Very well marked
- Other valve involvementCommon Never present
- VDRL Negative Positive
-X-Ray Calcium in the Valve Calcium in aortic wall
No irregularity Irregularity in
in aortic wall aortic wall
# Difference between Acute & Chronic AR
Features Acute AR Chronic AR
- Onset Early/sudden Late/Insidious
- Pulse pressure Normal Wide
- Systolic pressure Normal Increased
- Diastolic pressure Normal/decreased Markedly reduced
- LV impulse Normal Hyperdynamic
- S1 Soft/absent Normal
- P2 Normal/loud Normal
- S3 Common Uncommon
- AR murmur Short & medium pitch Long, High pitch
- Aortic systolic murmurGrade 3/< Grade 3/>
- Austin flint murmur Absent Present
- Peripheral signs Absent Present
- ECG Normal LV LVH, LVVO
- X-ray Normal LV, PVH LVH, No PVH
# The auscultatory signs of severity of AR
- Length of murmur
- Austin flint murmur
- S3
# Severity of AR
Diastolic pressure
Mild 40-60mmHg
Moderate 20-40mmHg
213
 Severe- <20mmHg
Pulse pressure
Mild 40-60mmHg
Moderate 60-80mmHg
Severe 80-100mmHg
Hills Sign
Mild Difference 20mmHg
Moderate 20-40mmHg
Severe ->60mmHg
All peripheral signs present Sever AR
CxR Cor Bovinum
# What are the Peripheral signs of AR?
Wide pulse pressure.
o Mild= 40- 60 mm Hg
o Moderate= 60- 80 mm Hg
o Severe= > 80 mm Hg
Hills sign- Difference between the systolic BP of LL & UL.
o Mild AR= 20 40 mm Hg difference
o Moderate= 40- 60 mm Hg
o Severe= > 60 mm Hg
Reason for a Hills sign?
Believed to be due to;
o Impaired reading recording due to excessive muscle bulk of thigh
thus requiring higher pressure in the cuff to occlude the artery
o Augmentation of the systolic wave front by wave amplification, as
the it travels into the aorta to the periphery
Alfred de Musset sign (He was a poet) - increased pulsations of the head
& neck vessels.
Lighthouse sign- alternating blanching & perspiration of the forehead,
Landolfes sign- papillary dilatation & contraction
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 Beckers sign- Retinal artery pulsations.
Mullers sign- pulsating uvula
Corrigans sign- dancing carotids
Quinkes sign- pulsatile capillary filling of nail bad on application of
pressure over the nails.
Waterhammer pulse- brisk upstroke, brisk down stroke with high
volume, felt even through a less sensitive area like palm.
Locomotor brachials.
Maynes sign- < in DBP by > 15 mm Hg when BP is measured with arm
hanging & later with arm raised.
Austin Flint murmur- due to
o Regurgitant jet hitting AML,
o The coming together of 2 jets, i.e., AR jet & The LA to LV jet, to
create turbulence,
o Increased LVEDP
o #Even in severe AR an Austin Flint murmur may not be heard due
to calcific AML or an eccentric jet.
Rosenbach sign- liver pulsations,
Gerhardts sign- splenic pulsations,
Duroziez murmur- on auscultation over femoral artery, with pressure a
systolic murmur heard distally & a diastolic murmur proximally
Lincoln sign- toe movements with cardiac contraction,
Traubes sign- pistol shot femorals,
Shileys sign- Pulsating cervix
# What is Marfans syndrome?
Described in 1896 by Antine Marfan.
65-70% is genetic transmission. Caused due to mutation of the FBN1 gene on
chromosome 15.
Organ systems affected are- CVS, Occular, pulmonary, skeletal & skin.

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Diagnostic criteria laid down by Ghent;
1) Skeletal:
Major-
- Pectus excavatum/ carinatum
- Upper segment/ lower segment< 0.8
- Arm span/ height > 1.05
- Walker Murdoch sign (wrist sign)- little finger can go across the opposite
wrist and touch the thumb
- Steinberg sign (thumb sign)- thumb flexed and if it protrudes out of the
medial aspect of the hand, sign is +ve
- Metacarpal index> 8.4 (radiological length of 2,3,4 & 5 metacarpal added
& indexed to the added diameter of them at the centre)
- Scoliosis
- Angle of elbow> 160.
Minor-
- High arched palate- uvula not seen
- Oblong head,
- Endopthalmus
- Down sloping eyes
2 major or 1 major + 2 minor criterion required for the skeletal system to
qualify as a +ve system.
2) Occular:
Major-
- Subluxation of lens (mainly upward- characteristic feature of Marfans)
Minor-
- Flat cornea
- Axial length of globe > 23.5 mm,
- Hypoplastic iris/ ciliary muscle
1 major or 2 minor criterion required for the occular system to
qualify as a +ve system
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3) CVS:
Major-
- Dilatation of ascending aorta (> 40 mm) with/ without AR with dilated
sinuses of valsalva
- Dissection of any portion of the aorta
Minor
- MVP with/ without MR
- Dilatation of MPA > 20 mm without peripheral PA stenosis, in age < 40
years.
1 major or 1 minor criterion required for the CVS system to qualify as a +ve
system
4) Dura:
Major-
- Lumbosacral dural ectasia
Minor- none
1 major criteria required for the dura system to qualify as a +ve system
5) Pulmonary:
Minor only-
- Spontaneous pneumothorax
- Blebs
6) Cutaneous:
Minor only-
- Stretch marks
- Spontaneous hernia
For diagnosis of Marfans;
1) Genetic analysis +ve, 1 system +ve & one criteria of any other system.
2) If genetic analysis not possible, then 2 systems should be +ve & 1 criteria
from a 3rd system.
#CVS manifestations of mar fans are seen generally around 30 years of age.
Rest can manifest at any age.
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 #If root > 40 mm, pregnancy not advised till root replacement.
If root > 45 mm, advised root replacement in all.
#Chance of transmission of Marfans to child is 50%.
# Parasternal & Suprasternal pulsations in aortic valve disease
a) Parasternal
- Post stenotic dilatation of aorta
- Marfans syndrome
b) Suprasternal-Dilatation of arch of aorta
- Dilatation of wall Aneurysm
- Volume overloaded LV- PDA/APW
- Pressure overload-HTN
- Uncoiling of carotids
# Right ventricular activity in Aortic disease
- Pulmonary hypertension
- Additional MV disease
# Systolic murmur in AR
- Organic aortic stenosis
- Functional aortic stenosis
- Associated MR
- VSD
# Characteristics of apex beat are:
Normal- It is characterized by
- Localized to I ICS or < 2.5 cm diameter
- Inside MCL
- Lasting for < 50% systole
- Felt as gentle tap
Tapping- Seen in RVH, It is characterized by
- Just a tap, not lifting finger
- Localized
- Only in early diastole
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 - No paramedical retraction
Hyperdynamic- Seen in LVVO (E.g. AR, PDA, and MR), It is characterized by
- Diffuse, i.e., > 2 ICS or > 5 cm diameter or > 2 finger width
- Ill sustained (< 2/3 rd systole)
- Outside MCL (generally)
- Forcible
Heaving- Seen in LV pressure overload (E.g. AS), it is characterized by
- Diffuse
- Sustained, > 2/3 rd systole
- Forceful
# AR & site of murmur:
If heard best in;
- Erbs area- there is no dilatation of the aortic root- rheumatic
- Aortic area- there is dilatation of the aortic root- Marfans
(connective tissue)
# Clinical detection of acute AR
By presence of;
- Acute onset of symptoms
- Soft S1- due to closure of MV even before the onset of ventricular
systole, due to acute LVVO.
- Absence of peripheral signs of AR
(If there is echo e/o MV preclosure, then the prognosis is grave,
unless immediate surgical intervention is done)
# Importance of Austin Flint murmur?
Suggests that at least moderate AR is present.
# Cause of Austin Flint murmur?
Reasons advocated are;
- AR jet hitting upon the AML hence producing vibrations
- AR jet hitting the jet coming from LA to LV.

219
# AR murmur is never more than Grade III as it is high pitched (& thus no
thrill)
# Syphilitic AR.
-Has the following features;
- Minimum 9 years post primary syphilis
- Congenital syphilis is very rarely affects the AV
- Often associated with coronary osteal narrowing- angina, for
impaired cardioplegia delivery
# Criteria for dilated aortic root are
- Displacement of coronary ostia > 20 mm from the annulus
- Diameter of annulus > 1.5 times normal (in Marfans> 1.34 times;
operate)
# X-ray in AR
- Cor Bovinum- cardiomegaly
- Calcium in ascending aorta Syphilitic AR
- Calcium in valve leaflets Bicuspid aortic valve & Rheumatic AR
# Diagnosis from X-ray in aortic valve disease?
- CorBovinum AR
- Boot shaped heart-Marked dilatation of LV
- Calcification of aortic wall-Associated disease
- Calcification of wall Suggest syphilitic etiology
- Moderate dilatation of ascending aorta-Primary aortic valve disease
- Marked widening of ascending aorta Primary disease of wall
# ECG in AR
LVH with LVVO (q in V5-6)
# Causes of prolonged PR interval?
- Early heart block
Calcific AS
Infective endocarditis
Digoxin toxicity
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 - Carditis
# Echo in AR
M MODE:
1) Fine fluttering of AML
2) Fine fluttering of IVS
(No longer performed)
2 D ECHO:
1) Reverse doming of the AML
COLOR DOPPLER:
1) Size of jet
2) PISA
3) Rate of decline of the AV regurgitant velocity- diastolic decay. (the
rapidity with which the aortic & LV pressures equalize is a function of
the severity of AR)
# Uses of TEE in cardiac surgery
1) Intraoperative:
a) Off pump- for LV dysfunction
b) Area free of plaques for application of cross clamp & side biting
clamp
c) Checking adequacy of MV/ AV repair procedures
d) Completeness of deairing
e) Placement of IABP
f) During Batista
g) TMLR
2) Diagnosis of ASD
3) Balloon guidance during intervention for BAS, dilatation of atrial baffle
4) Diagnosis of clots
5) Dissection
6) Endocarditis
7) Myocardial viability on stress echo
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8) Prosthetic valve dysfunction
9) Congenital echo- especially in adults
Newer uses
10) Diagnosis of aortic arch plaques as a cause for unexplained stoke
11) Catheter ablation guidance
12)3 D echo
# IVS movement on M mode
- Type A into LV during systole Normal
- Type B straightening of IVS in systole
- Type C No movement
B & C are paradoxical movements
# How to calculate the Qp/ Qs on echo?
Q= mean velocity x time x cross-sectional area
# Contraindications to TEE
1) Oesophageal disease
2) GI bleeding
3) Cervical spine injury
# Cath in AR?
- Age > 40 years for coronary angio
- Assess AR status
# Criteria for operating patient with AR.
1) Moderate/ severe AR with NYHA II/III/IV symptoms
2) Asymptomatic AR if
a) LV dysfunction
- LVID (S) > 50mm
- LVID (D) > 70 mm
- LVESV > 60 ml/m2
- LVEDV > 200 ml/m2
- EF < 55%
- Fractional shortening < 27%
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 b) moderate/ severe AR along with CABG
c) acute AR
# Smith criteria:
- Operate AR if:
- CTR > 60%
- LVH on ECG > 60 mm
- Pulse pressure > 100 mm Hg
# Rahimtoulla criteria (rule of 55):
- Conserve AR if
- Age > 55 years
- CTR < 55%
- LVH on ECG < 55mm
- LVID (S) < 55mm
- EF > 50-55%
# Patient of severe AR with a DBP of 30-40 mm Hg?
Due to;
- Acute AR
- Increased LVEDP
- Proximal stenotic lesion (severe MS)- causing vasoconstriction
# Comparison of Hills sign Vs Angiographic AR
Hills sign Angiographic AR
20- 40 mm Hg Grade II+ AR
40- 60 mm Hg Grade III+ AR
> 60 mm Hg Grade IV+ AR

# What is Coanda effect?

Described by Henri Coanda (1930). When a jet stream (of air or water) comes
into contact with a curved surface, it will attach itself to it & follow the curve.
# Contraindications for AVR
- EF < 25%
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 - LV systolic dimension > 55mm
- LV diastolic dimension> 75mm
# Aortic cannulation as distal as possible
# Advantage of single venous cannnula
- Small RA may not have space for 2 cannulae
- More complete drainage
- Retracts the RAA
- Used in CABG/Aneurysm of aorta,AVR
# Disadvantage of single cannula
- Cant use in RSOV,VSD AR,APW
- Rewarming heart
# How much will you do cooling?
- 28 0- Reduces metabolism by 50%
- 180 Reduce metabolism by 20%
# When will you start cooling in AR for AVR?
Just before clamping
Because early cooling will fibrillates heart
# Heart fibrillates in AR at 320
- Hold the LV in hand & massage
- LV vent to be put/Stab LA & put sucker in RSPV
- Cross clamp
# Which aortotomy?
a) Oblique aortotomy
# 1cm away from RCA, incision started from anterior surface of aorta &
carried towards pulmonary artery till aorto pulmonary groove
# Posteriorly at the junction of NCC& LCC
# Advantage
Excellent exposure
Incision can be extended further for aortic root widening procedure
b) Transverse Aortotomy-
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 - At lower margin of RPA
- Advantage
- High profile valve lower lip covers whole valve
- Excellent vision of aortic valve
# Not able to come off CPB
- Check for Temprature, Potassium, Urine
- Valve dysfunction TEE Cool, clamp & redo procedure
Support the heart
Mechanical support- IABP, Mechanical assist device
# Paravalvar leak in AVR
- Etiology
Calcium
Annul prosthetic mismatch
Inadequate suturing technique
- Clinically
Hemolysis
Acute AR Pulmonary oedema
- Diagnosis by Echo
- Treatment-
Minimal AR Leave it
Moderate severe Redo case
# Management of Stuck valve
In Close position Patient will die immediately
In Open position- Acute AR Pulmonary oedema, Hemodynamic changes
Echo diagnostic
Thrombolyse within 6 hours
No improvement in 48 hours
Mechanical valve damage Change it
Thrombus Clear the thrombus
# Causes of sudden death during Balloon valvuloplasty
225
- Complete block of Aortic orifice-No flow
- Embolism of calcium & catheter
- Coronary blocked by catheter
-Rupture of aortic valve
# How will you do DVR?
- Separate SVC & IVC cannulation
- No LV vent
- After clamping the aorta stab the LA 7 vent
- Open Aorta & excise the aortic valve
- Open The LA & excise the Mitral valve
- Wash the cavity
- Put aortic sutures in annulus & valve
- Do not tie the Aortic valve
- Mitral sutures to be put & lower the mitral & tie
- Close the LA
- Lower the aortic valve & close the aorta
# Importance of etiology in surgical consideration?
- Syphilitic etiology-
Expect coronary ostial stenosis
Expect difficulty in suturing of wall
- Marfans-
Expect dissection of ascending aorta
Be ready for Bentall procedure
# Cardioplegia in ostial stenosis?
- Retrograde CP
- Small sized cannula
- Flexible DLP cannula
- Put conduit onto the coronaries for CP
# Gross morphology in rheumatic AR
- Leaflet thickening always suspect RHD
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 - Normal leaflets- Connective tissue disorder /Syphilis
# How will you manage suture line bleeding?
Depends on 3 factors
a) Source of bleeding
- Needle holes Wait till protamine goes
- Dog earing / cut through Take suture
b) Amount of bleeding
- Jet / spurt take suture
- Ooze Wait till protamine
c) Site of bleeding
- Easily accessible - wait till protamine
- Difficult to access- Suture
Two things to be kept in mind while taking suture
- Reduce Blood pressure
- Use pledgetts for suturing
# How will you manage a case of AR +++ & MR++?
- Before going on bypass I would like to see AR & MR by TEE on
table.
- I will look at Mitral valve through Aorta / LA
- I will test the mitral valve by pushing saline in MV
- If MV looks alright
AVR only
While coming of CPB I will take LA pressure by needle in
RSPV/Roof of LA
LAP 12 mmHg I will accept
LAP 12 mmHg I will think of repairing / replacing the MV
I will see MR by TEE while coming off CPB Moderate + MR with
hemodynamic instability ( LAP- 12mmHg) I will repair /replace
MV
# How will you manage a case of AR+++ with MS++?
227
 - I will access the mitral valve on table
- If MV is pliable ,noncalcific I will do OMV with AVR
- If MV is calcific with severe SV fusion- I will do MVR with AVR
OTHERS
AORTO-ARTERITIS

# What is your diagnosis?

My diagnosis is a young female patient with obstructive lesion of the
descending aorta without ischemic changes of lower limb probably
Aortoarteritis / CoA / Atherosclerosis of aorta
# Why aortoarteritis ?
- Young female patient
- Known hypertensive
- With constitutional symptoms
- Fever
- Without signs & symptoms of collateral formation
# Which other history will you ask?
- Headache
- Head vessel involvement Eye symptom
- Celiac& SMA involvement Abdominal pain
- Renal vessel involvement Hypertension, urinary symptoms
- Constitutional symptoms
- Fever
# Why not congenital CoA?
Absence of collaterals

# What are the cardiac lesions in Aortoarteritis?

- Coronary ostial involvement
- Pulmonary artery involvement
- Head neck vessel involvement
228
- Aortic wall involvement
# What is reversed CoA?
When both SCA are involved with / without any other syndrome complexes
Lower limb BP will be higher than upper limb
Called reversed CoA
# Distribution of lesions in Aortoarteritis
Purely stenotic 85%
Purely dilatation 2%
Mixed 13%
# Classification of Takayasus arteritis
A) Takayasus classification
Type I Arch alone
Type II Only descending Aorta
Type III Mixed
Type IV Pulmonary artery
B) Parulkar et al
Type I Arch of Aorta
Type II Thoracic aorta
Type III Abdominal aorta
Type IV Aortic bifurcation
# What are the diagnostic criteria of aortoarteritis?
A) Obligatory Age < 40 years
B) Major Criteria
Lt. & Rt. mid SCA lesion
Presence of characteristic signs & symptoms for at least 1 month
C) Minor Criteria-
Unexplained high ESR
Common carotid tenderness
HTN
AR / Annuloaortic ectasia
229
 Lesions of pulmonary artery
Left mid common carotid lesion
Lesions of distal brachiocephalic trunk
Lesions of descending thoracic aorta
Lesions of abdominal aorta
Bifurcation of aorta involved
Coronary artery lesions in absence of risk factors
Diagnostic
2 Major
1 Major + 2 minor
More than 4 minor
# What is the classical X- ray appearance?
Prominent wide aortic shadow of descending aorta with an irregular, wavy
outline seen in plain X-ray chest & upper abdomen
# What is the Angiographic presentation?
Constricting
Aneurysmal
Diffuse dilatation
Irregularity without dilatation / stenosis
Combination of the above
Total block of the aorta
# Peculiar features of aortoarteritis
Marked adventitial thickening & periaortic adhesions
Excessive intimal thickening leading to constriction
Segmental involvement of the aorta with abrupt changes from normal
abnormal
# Indications for Medical treatment?
Refuse to undergo surgery
Early lesions
Surgery is not possible due to extensive disease
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Surgery contraindicated associated co morbid conditions
# Medical treatment in Aortoarteritis
Antihypertensive
Digitalis
Diuretics
Vasodilators
Anticoagulants
Anti TB drugs
Steroids
# Surgical procedures in Aortoarteritis
- Thromboendartrectomy
- Thoraco-thoracic bypass Supradiaphragmatic disease
- Dorsal aorta (posterior thoraco abdominal bypass)- supra & infra
diaphragmatic lesions
- Ventral aorta (anterior thoraco abdominal bypass)
- Renal artery revascularization (Aorto renal anastomosis)
# Difference between Atherosclerosis & Aorto arteritis
Atherosclerosis Aortoarteritis
Location & character Terminal abdominal Descending & upper
aorta & illiofemoral abdominal aorta
branches
Coronary & cerebral More Less
artery involvement
Renal artery Mouth only Whole arterial tree
Periaortic adhesions & Rarely present Invariably present
matting
# Complications of surgery
False aneurysm
Anastomotic restenosis
Thrombotic blockage of graft
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Gastric fistula
# How will you measure the graft size?
Approximately size of the descending aorta
# Approach
Thoraco abdominal
# What difference you will get on table between Congenital CoA &
Aortoarteritis?
- Paucity / absence of Collaterals
- Mediastinal lymph nodes like bunches of grapes
- Adhesions around aorta
- Onion pill appearance of aorta on cutting
- Tough to suture
# Intervention & stenting of the narrow segment
Restenosis 13.5% after 2-6 months
Complications Dissection, pseudo aneurysm, Hypotension

CONSTRICTIVE PERICARDITIS

# What is your diagnosis?

My diagnosis is ___ Aged Male/Female patient with constrictive physiology
probably constrictive pericarditis
# Why constrictive pericarditis?
- Dyspnoea on exertion
- Ascites
- JVP raised, seen even in sitting position
- Sharp y descent in JVP
- Pulsus paradoxus
- Hepatomegaly
- Normal heart sounds
- CxR pencilling of heart border, pericardial calcifications present
232
- ECG Low voltage QRS axis
# What is constrictive pericarditis?
End result of chronic inflammation & thickening of pericardium, producing
nonexpansile encasement of heart restricting diastolic filling of ventricle
Both parietal & visceral pericardium is involved
Myocardial atrophy often present
# What are the causes of constrictive pericarditis
1) Idiopathic
2) Tuberculosis
3) Dresslers syndrome
4) Radiation
5) Uremia
6) Drug induced- procainamide/ hydralazine
7) Post operative (especially if Betadine washes used- Miller & Mansoor,
Ann Thoracic Surgery 1982, showed a 20 times higher incidence of
postoperative constrictive pericarditis with betadine washes)
All conditions causing acute pericarditis can cause subsequent constrictive
pericarditis except rheumatic carditis.
# What is Kussamauls sign?
Increase in systemic venous pressure during inspiration
Occurs in chronic RVF & Restrictive Cardiomyopathy
In Constrictive pericarditis there is a failure of intrathoracic pressure changes
during respiration to be transmitted to pericardial space& cardiac chambers
In normal subjects & Cardiac tamponade during inspiration systemic venous
& RA pressure falls & venous flow into RA increases
# What is pulsus paradoxus?
> 10mmHg reduction in Blood pressure during inspiration
Due to
- Reduced rt. Sided venous return
- Increased lung capacity
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- Reduced pulmonary venous return
# What will you see on CxR of Constrictive pericarditis?
- CTR Small, Normal or Enlarged (Pericardial effusion, Thickening,
Hypertrophy of chamber)
- SVC enlarged
- LA enlarged
- Calcification- Over rt. Heart chambers & AV groove
- Kerleys lines If LA pressure is > 15-30mmHg
# What is the X-Ray characteristic of Constrictive pericarditis?
- Penciling of heart borders
- Because of disappearance of pericardial fat
# What will ECG show?
- Low voltage QRS complexes
- Generalized T wave inversion or flattening
- P Mitrale LAE
- AF Long standing LAE/Increased LA pressure
- Block pattern Calcium in myocardium
# Echo in CP
M Mode
- Pericardial thickening
- Abrupt posterior motion of IVS in early diastole- Pericardial knock
- Abrupt posterior motion of IVS during atrial systole
- Reduced amplitude of LV posterior wall motion
- Premature pulmonary valve opening due to high RV early diastolic pressure
2D Echo
- Immobile dense appearance of pericardium
- Abrupt displacement of the ventricular septum during early diastolic filling-
Septal bounce
- Prominent early diastolic filling
- Abnormal contour of the junction of LA & LV posterior wall
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- Dilatation of Hepatic Vein & IVC
- Intense & spontaneous contrast in IVC
- Distension of IVC with blunted respiratory fluctuation in diameter- Plethora
Doppler
Increased early diastolic tricuspid flow
Increased hepatic vein flow velocity during inspiration
# Restriction Vs constriction on echo
Restrictive Constrictive
1) Septal bounce - +
2) LV thickness + -
3) EF Decreased Normal
4) Early diastolic Decreased Normal
filling
5) Changes with - +
respiration
# Cath in CP
- Elevation & equalization of End diastolic pressure in all chambers (with in
5mmHg)
- Dip platue of RV pressure trace
- Square root sign
- Prominent y descent of rapid ventricular filling followed by elevated diastolic
platue
# Advantage of Cath in CP
- Diagnosis
- Assess effect of CP on Stroke volume & cardiac output
- Evaluate myocardial systolic function
- Differentiate between CP & RCM
- Exclude compression of coronary arteries & out flow tract
# CT scan in CP
- Pericardial thickening
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- Dilatation of Venacavae
- Deformation of RV
- Increased filling fraction of ventricle in early diastole
- Nonvisualisation of LV postero-lateral wall by Ct suggest myocardial fibrosis
or atrophy predicts poor post pericardiectomy outcome
# MRI in CP
- Pericardial thickening
- Dilatation of Venacavae & hepatic veins
- Narrowing of RV
- Dilatation of RA
# Laboratory Investigation in CP
- Reduced serum Albumin
- Increased Serum Globulin
- Increased Conjugated & unconjugated Billirubin
- Abnormal LFT
# D/D of CP
- SVC obstruction
- Nephrotic syndrome
- Hepatic & intraabdominal disease due to malignancy
- RA hypertension Restrictive cardiomyopathy, TS, TR, Hypertrophic
cardiomyopathy, RA myxoma
# Cath signs of constrictive pericarditis & D/D with restrictive
cardiomyopathy
1) RA mean pressure > 10 mm Hg
- Mild: 10- 15 mm Hg
- Moderate: 15- 20 mm Hg
- Severe: > 20 mm Hg
2) Equalization of diastolic pressures in all the 4 chambers (within 5 mm
Hg)

236
 [In restrictive cardiomyopathy the LVEDP (PCWP) is > 5 mm Hg higher than
the RVEDP]
3) RVEDP > 1/3rd RVESP
[In restrictive cardiomyopathy RVEDP < 1/3rd RVESP]
4) positive square root sign
5) Positive Kussmaul's sign
6) Thickness of pericardium on fluoroscopy > 5 mm
7) Fluid challenge (500- 1000 ml of normal saline over 6-8 minutes) will
lead to persistent elevation in CVP
8) Endocardial biopsy
[In restrictive cardiomyopathy will show an infiltrative pathology]
9) Pulmonary hypertension will be negative
[In restrictive cardiomyopathy will be positive]
10) RV angiography will show blunting of apex (Ballet Dancers shoe)
# Types of pericardiectomy
- Radical: pericardium is removed from all surfaces of the heart & over
intrapericardial major vessels
- Adequate/ total/ extensive: Pericardium over the RV & LV (including
anterolateral & diaphragmatic surfaces) removed but RA, PVs & cavae are left
alone
- Partial: leave the diaphragmatic wall & anterolateral wall
# Pericardiectomy through Lt. Anterolateral thoracotomy
Advantage
- Good exposure of LV inferior & posterior aspect & majority of RV
- Cosmetic
Disadvantage
- Exposure of entire RA/RV & cavae suboptimal
- Resection of pericardium up to rt. phrenic nerve difficult
- Cannulation to be done from femoral artery & vein in emergency
- Post op pain.
237
 - If heart fibrillates difficult to defibrillate

# Pericardiectomy through Median sternotomy

Advantage
- Excellent exposure of cavae,RA,RV & great vessels
- Easy access to CPB
- If heart fibrillates easy to defibrillate if one external paddle is
placed
Disadvantage
- Suboptimal exposure of lateral aspect of LV
- Complete LV freeing difficult
# During pericardiectomy which part of heart will you release 1st& why?
Left ventricle
If RV is released 1st it will push more blood in to noncompliant LV 7 leads to
pulmonary edema.
# When will you start dopamine in pericardiectomy?
Once LV is released
# What is Bird in cage phenomenon in CP
Due to chronic constriction myocardial fibrosis sets in & once the pericardial
constriction is released heart starts distending (Forgets to beat) & fails.
# What is Waffle technique
Criss-cross incisions over the pericardium
Used when pericardium is densely adherent to the heart
# Poor outcome after pericardiectomy
- Radiation induced CP
- High RVEDP
- Pre-op NYHA class IV
- Renal dysfunction (S. Creatinine >2.0mg %)
- Diuretic use Myocardial dysfunction/ atrophy
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# Poor long term outcome
- For malignant disease
- Previous more limited resection

MIDLINE REDO

# Surgery through Midline

Congenital
ASD
VSD
TOF
Pulmonary valvotomy
Central shunt
Acquired -
MVR
OMV
MV repair
AVR
DVR
Thymectomy
Constrictive pericarditis Pericardiectomy
CABG
# Surgery through left thoracotomy
1) CMV
2) Pericardiectomy
3) MIDCAB
4) Potts operation (historical)
5) Benson Roe procedure (historical)
# Surgery through posterolateral thoracotomy

239
 1) BT shunt
2) Coarctation/ descending thoracic aortic procedures
3) PDA surgery
4) MVR (rare)
5) CMV
# Mention all possibilities of pre op conditions
# Describe in patients own words What surgery was done, any reoperation
# Ask about the post operative course
- Extubation, IV fluids, Blood, Support, Oxygen, ICU stay, Hospital stay
# Ask medical treatment on discharge
- Duration of Medical treatment
- Anticoagulation & its duration
- Rheumatic fever & infective endocarditis prophylaxis
# What are the causes of restenosis?
- Rheumatic etiology
- Calcification
- Structural valve degeneration
- Infective endocarditis
# What are the causes of patient coming back?
- Rheumatic involvement of Same/other valves
- Infective endocarditis involvement of same or other valves
- Blocked graft in CABG
- Development of new lesions
- Post BT shunt for total correction
- VSD AR repair with residual VSD/Severe AR
- Mitral repair with severe MR
# From history DD
- Valve
- Congenital
- Coronary
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 - Noncardiac
# On examination
- About scar
- Pulse & Blood pressure
# Post examination possibilities?
- Valve OMV/MV repair/MVR/AVR/DVR
- Other valve
- CABG
- Congenital
# On X-ray prosthetic valve not seen
- OMV
- MV Repair
- Bioprosthetic valve
Like Deka Total plastic strut
Homograft
Autograft
# What other things to see on X-ray?
- Valve-prosthesis
- Other valve calcification
- RAE,RVH,LVH
- On lateral view gap between RV & sternum
# What will you look for in Echo?
- Mechanical / bioprosthetic valve
- Other valve involvement
- Ventricular dimension & function
# Angiography in redo cases?
- Coronary angio
- Post BT shunt
Functioning BT shunt
PA size
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 PA Pressures
MAPCAS
Coronary artery anatomy
# What will you do before surgery in redo MVR?
- I will do chest X-ray lateral view
For distance between sternum & RV
Calcium in other valve
# What are the approaches for Redo MVR?
Midline sternotomy
Rt. Thoracotomy
Paramedian sternotomy
# Advantage & Disadvantage of Various approaches
a) Midline-
Advantage-
Known approach
Good exposure
Cannulation easy
Defibrillation easy
Only one scar
Disadvantage-
Adhesions
Trauma to heart chambers
Bleeding
b) Rt.Thoracotomy
Advantage-
Good exposure
MV exactly in front of eye
Disadvantage-
Cannulation difficult

242
 Cross clamping aorta difficult
Deairing difficult
Defibrillation difficult
Two scars
c) Paramedian sternotomy
Advantage
Same as median sternotomy
Disadvantage
Same as midline sternotomy
Unstable thorax
Sacrifice of IMA
d) Left thoracotomy
Indications
Emergency situation
Severe MR during CMV
Cannulation PA & Aorta
On CPB dissect PA & Aorta
Clamp aorta
Disadvantage
Deairing problem
# IIliac cannulation
Advantage
Less chance of infection
Disadvantage-
Likely to open peritoneum
Close to ureter
Associated ascites difficult exposure
Deeply situated
Previous abdominal surgery difficult exposure

243
# Disadvantage of femoral cannulation
Infection
# Preparation for redo MVR through midline
- Rt. Groin prepared with hip slightly abducted
- Femoral/Iliac artery cannulation
- Use of aprotinin
- Median sternotomy using Oscillating Saw
# What is Aprotinin?
Aprotinin is a natural antifibrinolytic agent
Derived from Bovine lung
Mechanism of action
Inhibits Kallikrein- Inhibits contact protein with induces factor XII
activation
Antifibrinolytic : Binds with && inhibit plasmin & plaminogen
Prevent platelet aggregation & adhesions
Side effects
Anaphylaxis
Renal dysfunction
Dose 1ml= 10000 Kallikrein Inactivated Units (KIU)
Adult Dose
5 ml - Test dose
200ml Loading dose
200ml Pump prime
50 ml/hr Till surgery gets over
Pediatric Dose Half the dose as mentioned above
Contraindication
Allergic reaction
Renal dysfunction
# Which other agent can be used?
E-Aminocaproic acid
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Loading 150 mg/kg
Continuous infusion 10mg/kg
Tranaxemic acid-
Loading 10-20 mg/kg
Continuous infusion 1-2mg/kg
# What all measures to be taken while doing sternotomy in Redo?
- Dissect the Suprasternal notch area & xiphisternal area
- Create a plane behind the sternum with blunt finger dissection
- Use of oscillating saw
- Cut sternal wires & put both the ends on clamp & pull it up ,Cut
the anterior table with saw till you feel grating sensation
- Towel clip to lift the sternum up
- Use forceps to be kept between sternum & heart
- Use of small spreaders to gradually widen the area
- Ask anaesthetist to reduce the BP to 60-70mmHg
- Ask perfusionist to remove blood through arterial line in femoral
artery till Bp comes down to 60-70mmHg
# High risk for reoperations
The Annals of Thoracic surgery, Loop listed following as a high risk in
reoperation
- > One operation
- Ascending aortic aneurysm
- Multiple valve disease or conditions that causes RAE & RVH
- Reoperation in patient with RVOT patch
- Previous mediastinitis with sternal osteomyelitis
# What all structures remains frequently adherent to the sternum?
- SVG- RCA,LIMA & RIMA
- Right ventricle
- Right atrium
- Aorta, aortic graft & aortic aneurysm
245
 - Innominate vein
- Pulmonary artery
- Lung
- Peritoneum
# What are the surgical prophylaxis at Primary CABG in preparation for
reoperation?
- Open pericardium with invertedY
- Avoid exposure of left innominate vein
- Mark bypassable arteries with silk
- Mark IMA on medial side with silk
- Mark SVG origin
- Do not surround ascending aorta with tape
- Avoid intercostals space with wire sterna closure on side of
unharvested IMA
- Route high marginal & ramus grafts through transverse sinus
- Route LIMA graft through pericardial window
- Avoid direct anterior attachment of SVG to aorta
- Cover gastroepiploeic artery with omentum
- Close pericardium & prethymic fat
# How will you remove Bioprosthetic valve?
- Using 15 blade single sweep at one place to remove fibrous tissue from the
cloth of the sewing ring
- With mosquito develop plane between sewing ring & annulus & sweep it
laterally
- Identify the sutures & remove it with nerve hook
- Struts will be present in LV one at 10 o clock position, one at 2 o clock
position & One at 6 o clock position
Remove strut in the same way a sewing ring
Remove additional fibrous tissue & pannus from LV
Thorough wash
246
# Post Lutembacher repair for redo, problems?
- ASD area calcific
# Previous AVR done, Needs now MVR difficult thing?
Anterior annulus
Tough to suture
Suture goes through fibrous tissue & sewing ring of AV
# Which valves will you put in Young female patient & Old male patient?
Young female
Family life completed Mechanical valve
Bioprosthetic family life not completed / Anticoagulants
Contraindicated
Old male
Now put bioprosthesis
Anticoagulants contraindicated
Willing for bioprosthesis
# Redo DVR problem & its solution?
- Cardioplegia retro induction
- Open aorta
- Remove valve
- Antegrade CP
- Other steps routine
# TOF redo for what?
- RVOT obstruction
- PR
# Redo CABG Conduits
Vein Opposite long saphenous, short saphenous
Basillic & cepahlic
Artery- Radial, Gastroepiploic, superior epigastric
RIMA
Prosthetic conduits
247
 VIVA-VOCE
Chest X-rays
Basics:
X-ray history

Wilhelm Conrad RoentgenDiscovers x-ray in 1895.

Projection:

AP v PA - Heart size:

The heart, being an anterior structure within the chest, is magnified by

an AP view.

Magnification is exaggerated further by the shorter distance between the

X-ray source and the patient, often required when acquiring an AP
image.

This leads to a more divergent beam to cover the same anatomical field.

As a rule of thumb, you should never consider the heart size to be

enlarged if the projection used is AP.

248
 If however the heart size is normal on an AP view, then you can say it is
not enlarged.

AP v PA - Scapular edges:

Radiographers will often label a chest X-ray as either PA or AP.

If the image is not labelled, it is usually fair to assume it is a standard PA

view.

If, however, you are not sure, then look at the medial edges of each
scapula.

249
Rotation:

Principles of rotation

The spinous processes of the thoracic vertebrae are in the midline at the
back of the chest.

250
 They should form a vertical line that lies equidistant from the medial
ends of the clavicles, which are at the front of the chest.

Rotation of the patient will lead to off-setting of the spinous processes so

they lie nearer one clavicle than the other.

Rotation and heart size:

Heart size can be assessed accurately with a well-centred posterior-

anterior (PA) chest X-ray.

If the patient is rotated to the left the heart may appear enlarged and if
rotated to the right its size may be underestimated.

251
Inspiration and lung volume:

Chest X-rays are conventionally acquired in the inspiratory phase of the

respiratory cycle.

When interpreting a chest X-ray it is important to recognise if there has

been incomplete inspiration.

252
 If the image is acquired in the expiratory phase, the lungs are relatively
airless and their density is increased.

Also, the raised position of the diaphragm leads to exaggeration of heart

size, and obscuration of the lung bases.

Assessing inspiration:

To assess the degree of inspiration it is conventional to count ribs down

to the diaphragm.

The diaphragm should be intersected by the 5th to 7th anterior ribs in

the mid-clavicular line.

Less is a sign of incomplete inspiration.

While checking for adequate inspiration if patient's lungs are

hyperexpanded (>7th anterior rib intersecting the diaphragm at the mid-
clavicular line).

This is a sign of obstructive airways disease.

253
Penetration:

Penetration is the degree to which X-rays have passed through the body.

Assessment of penetration is traditionally a standard part of assuring

chest X-ray quality.

With modern digital systems over or under penetrated/exposed images

are rarely a problem.

Image data can be 'windowed' to optimise visibility of anatomical

structures.

A well penetrated chest X-ray is one where the vertebrae are just visible
behind the heart.

The left hemidiaphragm should be visible to the edge of the spine.

Loss of the hemidiaphragm contour or of the paravertebral tissue lines

may be due to lung or mediastinal pathology.

254
Image quality:

Mnemonic - RIP - Rest In Peace

Rotation - Spinous processes at midpoint between medial ends of the

clavicles?

Inspiration - 5 to 7 anterior ribs intersecting the diaphragm in the mid-

clavicular line?

Penetration - Spine visible behind the heart?

255
HOW TO APPROACH CARDIAC DIAGNOSIS FROM THE CHEST
RADIOGRAPH

256
 The right mediastinal contour consists of a straight upper vertical border
formed by the SVC and a smooth convex lower cardiac contour formed by
the RA.

Occasionally, a short segment of IVC may be seen where the right atrium
meets the diaphragm.

The normal left mediastinal contour is formed by a series of convexities:

from superior to inferior,

the aortic knob,

the pulmonary trunk, and

the left ventricle abutting the diaphragm.

Rarely, the left atrial appendage can be projected between the pulmonary
trunk and the left ventricle in the normal heart, primarily in young
females.

257
 The shape of the pulmonary trunk segment varies with age and body
habitus.

Most frequently, this segment is only slightly convex; however, it can be

prominent in women 20 to 40 years old and straight or even concave in
older patients and still be within normal limits.

Occasionally, the cardiophrenic junction of the cardiac silhouette is not

formed by the left ventricle but by a fat pad.

Less common is a border-forming fat pad in the right cardiophrenic angle

which should not be confused with a cardiac mass.

Frontal chest radiograph: Normal border forming structures

Left upper border

Left subclavian artery, aortic arch (aortic knob)

Left middle border

Pulmonary trunk , left atrial appendage

Left lower border

Left ventricle

Right upper border

Innominate vein and superior vena cava or

innominate artery and ascending aorta

Right lower border

Right atrium, inferior vena cava

258
Lateral Projection:

It is routine that the patients left side is positioned against the film
cassette to minimize distortion of the heart due to geometric
magnification.

Superiorly, the anterior border Asc.aorta posterior to the retrosternal

air space;

inferiorly, the RV & RV OT abut the sternum and blend into the main
pulmonary artery, which then courses posteriorly to its bifurcation.

The posterior cardiac contour -LA superiorly beneath the carina and the
LV curving inferiorly to the diaphragm, where the straight vertical edge of
the inferior vena cava is often apparent within the thorax as it enters the
right atrium.

259
260
Lateral chest radiograph: normalborder-forming structures

Anterior upper border

Ascending aorta

Anterior lower border

Right ventricle

Posterior upper border

Left atrium and pulmonary veins

Posterior lower border

Left ventricle (sometimes right atrium),

inferior vena cava

HEART SIZE:

The size of the cardiac silhouette has importance, because it may

represent several underlying disease processes.

261
 It may be evaluated subjectively, or by measuring the cardiothoracic ratio
or by volume measurement.

Subjective assessment is the most common method used by the

experienced observer.

Technical factors mentioned previously should always be taken into

consideration.

The cardiothoracic ratio (CTR)the ratio of the transverse cardiac

diameter to the maximal internal diameter of the thorax at the level of
the diaphragm on an upright PA chest radiographcorrects for body size
and magnification produced by slight differences in radiographic
techniques.

In adults, a CTR greater than 0.5 is considered to represent

cardiomegaly.

A CTR > 0.5 with a normal heart size occurs with

Absent pericardium

262
 Pectusexcavatum

Obesity

Poor inspiration

263
264
AORTIC KNOB:

265
 If the aortic knob cannot be identified, congenital abnormalities should
be considered, including

a right-sided arch,

coarctation of the aorta, or

double aortic arch.

In the presence of a right arch the trachea is deviated to the left, and this
sign may be very helpful.

266
267
268
269
Pulmonary artrery:

The normal aortic knob and normal main pulmonary should be

approximately equal in size.

This observation must be based primarily on examining that portion of

the arc of each great artery, which is visible on the frontal radiograph.

270
Left Atrium:

The LA sits just below the angle of the carina, in proximity with the left
bronchus and esophagus; thus, enlargement is readily reflected by the
displacement of these neighboring structures.

Enlargement usually produces a double density behind the right atrial

margin on a frontal projection as the LA bulges out from the
mediastinum into the right lung.

Occasionally, a double density can be seen in the presence of a normal-

sized LA in patients with a prominent right pulmonary venous
confluence.

Additional signs include upward and posterior displacement of the left

main bronchus, resulting in a less acute carinal angle.

271
 Enlargement of the LA appendage initially causes straightening and,
subsequently, a convexity in the upper left cardiac contour.

In the presence of a giant LA, the LA itself may project beyond the RA
and form a portion of the right cardiac contour.

272
 On the lateral projection, LA enlargement can be recognized by posterior
and upward displacement of the left main stem bronchus.

The left atrium itself enlarges upward and posteriorly to form an

increasing convex density

273
274
275
Left Ventricular Enlargement:

Left ventricular enlargement can be due to dilatation or hypertrophy or

both.

The classic appearance of LV hypertrophy on the PA projection is

rounding of the cardiac apex, with downward and lateral displacement
without cardiac enlargement.

LV dilatation causes an increase in the transverse diameter of the heart

and CTR, together with an apparent increase in the length of the left
heart border.

The cardiac apex may be displaced to the extent that it projects below the
diaphragm.

On the lateral projection, dilatation increases the posterior convexity of

the left ventricular contour, which will project behind the edge of the
vertical inferior vena cava.

Causes:

Obstruction to LV emptying or increased afterload

Regurgitant valvular lesions

Dilated cardiomyopathies

LV aneurysms

276
Right Atrial Enlargement:

increased fullness and convexity of the right cardiac contour and

angulation of the junction of the SVC and RA.

There may be associated dilatation of SVC & IVC - widening of the right
superior mediastinum and an additional border in the right
cardiophrenic angle.

On the lateral projection, right atrial dilatation is often difficult to

appreciate.

It causes a filling-in of the retrosternal clear space anteriorly and

superiorly, with the cardiac silhouette extending behind the sternum
more than one-third the way above the cardiophrenic angle, similar to
that seen with right ventricular enlargement.

277
Right Ventricular Enlargement:

The RV enlarges by broadening its triangular shape in the superior and

leftward direction.

With increasing RV enlargement, the entire heart rotates to the left

around its long axis and displaces the LV posteriorly.

This displacement causes increased convexity of the left upper heart

border and elevation of the cardiac apex.

The rotation also makes the pulmonary trunk appear relatively small.

With marked dilatation, the RV may form the left heart border on the PA
projection.

On the lateral projection, the RV extends cranially behind the sternum,

with increased bulk anteriorly.

Pulmonary Blood flow:

278
279
280
281
282
Normal Pulmonary Blood Flow:

The pulmonary arteries and veins extend outward from each hilum in an
orderly branching fashion, with gradual tapering peripherally.

The hilar density is composed of the proximal pulmonary arteries, with

the left hilum normally projecting more cranially than the right one
because of the course of the left pulmonary artery over the left main
bronchus.

In the upper lobes, the veins and arteries are essentially parallel, with
the veins lying lateral to their corresponding arteries.

The major arteries and veins in the lower lung fields cross each other,
with the veins taking a more horizontal course toward the left atrium.

In the upright position, there is increased flow to the base of the lungs
(largely due to the effects of gravity), which causes the lower-lobe vessels
to increase in size.

The pressure differential between the apex and the base of the lung is
approximately 22 mm Hg in adults in the upright position.

283
 The right descending pulmonary artery measures 10 to 15 mm in
diameter in males and 9 to 14 mm in females.

Therefore, position has a marked effect on flow distribution.

Abnormal pulmonary vascularity:

Abnormalities in volume

Increased PBF

Decreased PBF

Abnormalities in distribution

Cephalization

Centralization

Lateralization

Localization

Collateralization

Increased PBF:-

As pulmonary flow increases, the pulmonary vessels, both arteries and

veins, become enlarged.

These enlarged vessels become apparent when pulmonary flow is

approximately twice normal.

The over-circulation pattern may be symmetric or asymmetric.

High-output states with increased circulating blood volume, result in a

symmetric increase in vascularity, as do various congenital defects
characterized by left-to-right shunts .

An asymmetric increase in pulmonary flow may be congenital in origin

(e.g., pulmonary arteriovenous malformation, anomalous origin of a
pulmonary artery) but is more commonly the result of surgical
intervention to create a systemic-to-pulmonary shunt to improve
pulmonary blood flow in the presence of severe pulmonary stenosis or
atresia (e.g., a Blalock-Taussig shunt).

284
Decreased Pulmonary Blood Flow:-

Essentially all the linear shadows in the normal lung fields are due to
pulmonary vasculature.

When flow and, therefore, vessel size are diminished, the lung fields
appear abnormally radiolucent.

Both symmetric and asymmetric patterns of abnormal vascularity can be

observed.

Generalized undercirculation can be due to an obstructive lesion in the

right heart, as in tetralogy of Fallot, pulmonary atresia, right ventricular
tumor, or tricuspid valve atresia.

Small-caliber pulmonary vessels with relatively hyperlucent lungs and a

small heart are evidence of a marked decrease in the circulating blood
volume (e.g., in Addison disease, hemorrhage).

Segmental and asymmetric decreases in pulmonary vascularity are seen

with

pulmonary embolic disease ,

segmental COPD,

partial pneumonectomy, and

branch pulmonary artery stenoses

Abnormalities in Distribution:

An abnormal distribution of PBF (or an abnormal PBF pattern) always

reflects a changed pulmonary vascular resistance, either locally or
diffusely.

Cephalization:-

In the presence of postcapillary pulmonary hypertension (PH),

physiologic disturbances begin when the total intravascular pressure
exceeds the oncotic pressure of the blood.

As a result, fluid leaks out of the vessels and collects in the interstitium
before filling the alveoli.

285
 Alveolar hypoxia has a profound influence on the pulmonary vessels,
causing them to constrict.

Because there is greater alveolar hypoxia in the lung bases than in the
apices, the basilar vessels constrict significantly, forcing the blood to flow
upward.

This phenomenon actually represents a reversal of the normal PBF

pattern: redistribution or cephalization of the pulmonary vascularity.

Cephalization occurs in any of three conditions:

(1) left-sided obstructive lesionseg; MS or AS;

(2) LV failureeg; CAD or cardiomyopathies; and

(3) severe MR even before LV pump failure occurs.

It should be emphasized that unless there is obvious constriction of the

lower-lobe vessels, the diagnosis of cephalization should not be made.

Dilatation of the upper lobe vessels is of secondary importance and can

be found without narrowing of the basilar vessels in a number of entities,
most noticeably left-to-right shunts.

286
Centralization:-

In the presence of precapillary PH, the pulmonary trunk and central

pulmonary arteries dilate, and the distal pulmonary arteries constrict in
a concentric fashion from the periphery of the lung toward the hilum.

This phenomenon is called centralization of the pulmonary vascularity.

It occurs in patients with

primary PH,

Eisenmenger syndrome,

recurrent PTE, and

severe obstructive emphysema

Lateralization:-

Massive unilateral pulmonary embolism can cause a lateralized PBF

pattern.

Because one major pulmonary artery is obstructed, the blood is forced to

flow through the healthy lung only.

287
 The paucity of pulmonary vascularity in the diseased lung with the
obstructed pulmonary artery is termed the Westermark sign.

In the case of congenital valvular PS, a jet effect from the stenotic valve
can cause a lateralized PBF pattern in favor of the left side.

Localization:-

A localized abnormal flow pattern is exemplified by a congenital

pulmonary arteriovenous fistula in a cyanotic child.

288
Collateralization:-

Patients with markedly decreased PBF (eg, severe tetralogy) tend to show
numerous small, tortuous bronchial arterial collaterals in the upper
medial lung zones near their origin from the descending aorta.

The native pulmonary arteries are extremely small, although smooth and
gracefully branching.

289
290
HEART FAILURE:

291
Stage I heart failure Redistribution:-

In a normal chest film with the patient standing erect, the pulmonary
vessels supplying the upper lung fields are smaller and fewer in number
than those supplying the lung bases.

The pulmonary vascular bed has a significant reserve capacity and

recruitment may open previously non-perfused vessels and causes
distension of already perfused vessels.

This results in redistribution of pulmonary blood flow.

First there is equalisation of blood flow and subsequently redistribution

of flow from the lower to the upper lobes.

The term redistribution applies to chest x-rays taken in full inspiration in

the erect position.

292
Artery-to-bronchus ratio:-

Normally the vessels in the upper lobes are smaller than the
accompanying bronchus with a ratio of 0.85.

At the level of the hilum they are equal and in the lower lobes the arteries
are larger with a ratio of 1.35.

When there is redistribution of pulmonary blood flow there will be an

increased artery-to-bronchus ratio in the upper and middle lobes.

This is best visible in the perihilar region.

293
The upper lobe vessels have a diameter > 3 mm (normal 1-2 mm).
Notice the increased artery-to-bronchus ratio at hilar level (arrows).

Stage II - Interstitial edema:-

Stage II of CHF is characterized by fluid leakage into the interlobular and

peribronchialinterstitium as a result of the increased pressure in the
capillaries.

When fluid leaks into the peripheral interlobular septa it is seen as

Kerley B or septal lines.

Kerley-B lines are seen as peripheral short 1-2 cm horizontal lines near
the costophrenic angles.

These lines run perpendicular to the pleura.

294
 KerleysA lines are linear opacities extending from the periphery to the
hila; they are caused by distention of anastomotic channels between
peripheral and central lymphatics.

Kerleys B lines are short horizontal lines situated perpendicularly to the

pleural surface at the lung base; they represent edema of the interlobular
septa.

Kerleys C lines are reticular opacities at the lung base, representing

Kerleys B lines en face.

These radiologic signs and physical findings suggest cardiogenic

pulmonary edema.

295
When fluid leaks into the peribronchovascularinterstitium it is seen as
thickening of the bronchial walls (peribronchial cuffing) and as loss of
definition of these vessels (perihilar haze).

296
There is an increase in the caliber of the pulmonary vessels and they have lost
their definition because they are surrounded by edema.

Stage III - Alveolar edema:-

This stage is characterized by continued fluid leakage into the

interstitium, which cannot be compensated by lymphatic drainage.

This eventually leads to fluid leakage in the alveoli (alveolar edema) and
to leakage into the pleural space (pleural effusion).

The distribution of the alveolar edema can be influenced by:

Gravity: supine or erect position and right or left decubitus

position

Obstructive lung disease, i.e. fluid leakage into the less severe
diseased areas of the lung

297
Cardiothoracic ratio:

An increased cardiac silhouette is almost always the result of

cardiomegaly, but occasionally it is due to pericardial effusion or even fat
deposition.

A CTR of > 50% has a sensitivity of 50% for CHF and a specificity of 75-
80%.

An increase in left ventricular volume of at least 66% is necessary before

it is noticeable on a chest x-ray.

298
Pleural effusion:

Pleural effusion is bilateral in 70% of cases of CHF.

When unilateral, it is slightly more often on the right side than on the left
side.

There has to be at least 175 ml of pleural fluid, before it will be visible on

a PA image as a meniscus in the costophrenic angle.

On a lateral image effusion of > 75 ml can be visible.

If pleural effusion is seen on a supine chest film, it means that there is at

least 500 ml present.

299
Vascular pedicle:

The vascular pedicle is bordered on the right by the superior vena cava
and on the left by the left subclavian artery origin.

The vascular pedicle is an indicator of the intravascular volume.

A vascular pedicle width less than 60 mm on a PA chest radiograph is

seen in 90% of normal chest x-rays.

A vascular pedicle width of more than 85 mm is pathologic in 80% of

cases.

5 mm increase in diameter corresponds to 1 liter increase of

intravascular fluid.

An increase in width of the vascular pedicle is accompanied by an

increased width of the azygos vein.

300
 There are three principal varieties of pulmonary edema: cardiac,
overhydration and increased capillary permeability (ARDS).

The vascular pedicle width (VPW) can help in differentiating these

different forms of pulmonary edema:

Normal VPW: most common in capillary permeability or acute

cardiac failure.

Widened VPW: most common in overhydration/renal failure and

chronic cardiac failure.

Narrowed VPW: most common in capillary permeability.

301
 The VPW may increase due to rotation to the right.

On an AP-view the VPW will increase 20% compared to a PA-view.

302
Dilation of the azygos vein:

This is a sign of increased RA pressure and is usually seen when there is

also an increase in the width of the vascular pedicle.

The diameter of the azygos vein varies according to the positioning.

In the standing position a diameter > 7 mm is most likely abnormal and

a diameter > 10 mm is definitely abnormal.

In a supine patient > 15 mm is abnormal.

An increase of 3 mm in comparison to previous films is suggestive of

fluid overload.

The difference of the azygos diameter on an inspiration film compared to

an expiration film is only 1mm.

This means that the diameter of the azygos is a valuable tool whether or
not there is good inspiration.

303
CARDIAC MALPOSITIONS :

Cardiac malpositions are diagnosed only when either the heart or the
stomach is out of the normal left-sided position.

This definition is crucial in distinguishing an isolated right-sided aortic

arch from a cardiac malposition.

304
Dextrocardia with SitusInversus:

Recently, the term dextrocardia has been used to indicate any congenital
right-sided heart regardless of the position of abdominal viscera.

Dextrocardia with situsinversus indicates the mirror image of normal.

305
 In this situation, the incidence of congenital heart disease is only 5%, a
nine-fold increase over the general population.

The combination of dextrocardia, sinusitis, and bronchiectasis is known

as the Kartagener triad.

Dextrocardia with SitusSolitus:

This represents an anomaly with normal situs but a right-sided heart.

Radiographically, normal situs (situssolitus) is a certainty when both the

aortic knob and the gastric air bubble are on the left side.

Situssolitus also means that both the abdominal viscera and the atria are
in the normal positions.

Under these circumstances, if the ventricles fail to swing from the

primitive right-sided position to the normal left-sided position, abnormal
relationships between the ventricles and the rest of the cardiovascular
structures are bound to develop.

306
 This entity was formerly termed dextroversion.

In patients with dextroversion, the incidence of congenital heart disease

has been estimated at 98%.

More than 80% have congenitally corrected (or L loop) transposition of

great arteries.

The next most commonly associated lesions are a combination of

ventricular septal defect (VSD) and pulmonary stenosis, a tetralogy-like
pathophysiology .

Levocardia with SitusInversus:

This is a mirror image of dextroversion, and it is associated with nearly a

100% incidence of cyanotic congenital cardiac lesions similar to those
seen in dextroversion.

This entity was formerly termed levoversion.

307
 Levocardia with SitusSolitus:

This is entirely normal.

Cardiac Malpositions with SitusAmbiguus:

In this group, the patient's heart can be either left or right sided.

The site is ambiguous because the aortic arch and the stomach are not
on the same side.

Under these circumstances, the patient has either asplenia or

polysplenia syndrome.

Patients with polysplenia syndrome tend to be acyanotic and frequently

survive into adulthood.

308
 The associated lesions are bilateral left-sidedness, interruption of the IVC
with azygos continuation, polysplenia, and a left-to-right shunt, most
frequently an atrioventricular septal defect.

Patients with asplenia tend to be cyanotic and critically ill and die in
infancy.

CONGENITAL HEART DISEASES

TRANSPOSITION OF GREAT ARTERIES:

In the normal anatomy, the aorta is anterior to and at the right of the
pulmonary artery; in TGA, the pulmonary artery is situated to the right
of its normal location and is obscured by the aorta on frontal chest
radiographs.

This malposition, in association with stress-induced thymic atrophy and

hyperinflated lungs, results in the apparent narrowing of the superior
mediastinum on radiographs, the most consistent sign of TGA.

309
 The cardiovascular silhouette varies from normal in the first few days
after birth to enlarged and globular, with the classic appearance
described as an egg on a string

The specific radiologic features are determined by

the extent to which the great arteries are superposed in the plane
of imaging,

the size of the communication between the pulmonary and the

systemic circulation, and

the presence and severity of obstruction to pulmonary flow.

310
TOTAL ANAMOLOUS PULMONARY VENOUS RETURN:

This occurs when the pulmonary veins fail to drain into the left atrium
and instead form an aberrant connection with some other cardiovascular
structure.

Four types of TAPVR are defined.

311
 In type I, the most common of the four (55% of cases), the anomalous
pulmonary veins terminate at the supracardiac level.

On chest radiographs, this cardiovascular anomaly resembles a

snowman or figure of 8

The dilated vertical vein on the left,

The innominate vein on the top, and

The superior vena cava on the right form the head of the snowman;

The body of the snowman is formed by the enlarged right atrium.

Typically, four anomalous pulmonary veins converge directly

behind the left atrium and form a common vein, known as the
vertical vein, that passes anterior to the left pulmonary artery and
the left main bronchus to join the innominate vein

312
Partial Anomalous PulmonaryVenous Return:

The scimitar sign is produced by an anomalous pulmonary vein that

drains any or all of the lobes of the right lung.

The so-called scimitar vein curves outward along the right cardiac
border, usually from the middle of the lung to the cardiophrenic angle,
and usually empties into the inferior vena cava but also may drain into
the portal vein, hepatic vein, or right atrium.

Although the diameter of the scimitar vein depends on whether it drains

the entire right lung or only a portion of it, the diameter generally
increases as the vein descends.

The characteristic appearance of the vein has led to its comparison to a

scimitar, a sword with a curved blade that traditionally was used by
Persian and Turkish warriors.

313
 The scimitar vein is one of the components of scimitar syndrome, which
is characterized by the following additional features:

(a) hypoplasia of the right lung with dextroposition of the heart,

(b) hypoplasia of the right pulmonary artery, and

(c) anomalous arterial supply of the right lower lobe from the abdominal aorta.

Flow through the scimitar vein produces a left-to-right shunt that is

usually hemodynamically insignificant.

Symptoms generally do not occur unless 50% or more of the pulmonary

flow shifts from the left to the right.

Endocardial Cushion Defects:

The gooseneck-shaped deformity in endocardial cushion defect is caused

by a deficiency of both the conus and sinus portions of the
interventricular septum, with narrowing of the left ventricular outflow
tract.

314
 The concavity of the IVS below the mitral valve, along with the elongation
and narrowing of the LVOT, produces a characteristic shape that has
been compared to a sitting goose with an elongated neck on the AP
projection in LV angiography

TETRALOGY OF FALLOT:

On chest radiographs in those affected by this syndrome, the heart has

the shape of a wooden shoe or boot (in French, coeur en sabot) .

This deformity is due to uplifting of the cardiac apex because of right

ventricular hypertrophy and concavity of the main pulmonary artery.

The shadow of the pulmonary arterial trunk is almost invariably absent,

and blood flow to the lungs is usually reduced.

315
COARCTATION OF AORTA:

Two classic radiologic signs associated with aortic coarctation are the
figure-of-three sign and the reverse figure-of-three sign.

The aortic segment affected by coarctation has a shape that resembles

the number 3 on frontal chest radiographs.

The number 3 is formed by dilatation of the left subclavian artery and

aorta proximal to the site of coarctation, indentation of the site, and
dilatation of the aorta distal to the site.

This sign is seen in 50%66% of adults with aortic coarctation.

316
 The reverse figure-of-three sign, a mirror image of the number 3, is
observed on the left anterior oblique view during barium esophagography
in patients with aortic coarctation

317
 Rib notching is absent in 25% of pts. with significant coarctation.

318
319
EBSTEINS ANOMALY:

This is characterized by the downward displacement of the septal leaflets

and posterior leaflets of the tricuspid valve into the inflow portion of the
right ventricle.

This displacement results in the formation of a common right

ventriculoatrial chamber and causes tricuspid regurgitation.

The most consistent imaging feature is RA enlargement; the RA may be

huge and fill the entire right hemithorax.

The LA is normal in size, but the left cardiac contour has a shelved
appearance because of the dilated RVOT.

The aorta is small, and the pulmonary trunk, which normally appears as
a discrete convex bulge, is absent.

This combination of features produces a cardiac silhouette that has been

described as box shaped.

Atrial septal defect:

The salient plain film findings are cardiomegaly, enlargement of the RV,
dilation of MPA, and pulmonary plethora

320
321
GREAT VESSELS :

Pulmonary thromboembolism

322
323
324
VALVULAR HEART DISEASES :

Position of prosthetic valves

325
 A line can be drawn from the left atrial appendage to the point of
intersection of the right atrium and diaphragm.

The aortic valve lies above and the mitral below this line.

On the frontal chest radiograph, cardiac valvular prostheses can be localized

by drawing a longitudinal line through the mid sternal body. Use this line to
bisect the sternum in the sagittal plane and then draw a perpendicular line
dividing the heart horizontally. The aortic valve should overlie the intersection
of these two lines. The mitral valve will lie in the lower left quadrant (the
patients left). The tricuspid valve would lie in the lower right corner (the
patient's right) and the pulmonic valve will lie in the upper left corner (the
patient's left).

326
 On lateral radiograph this line is drawn from the carina to the point
where the sternum is intersected by the left diaphragm.

The location of the cardiac valves is best determined on the lateral

radiograph. A line is drawn on the lateral radiograph from the carina to
the cardiac apex. The pulmonic and aortic valves generally sit above this
line and the tricuspid and mitral valves sit below this line.

327
 A second technique to further localize prosthetic valves involves drawing
a second line which is perpendicular to the patient's upright position
which bisects the cardiac silouette. The aortic valve projects in the upper
quadrant, the mitral valve in the lower quadrant and the tricuspid valve
in the anterior quadrant. The pulmonary valve projects in the superior
portion of the posterior quadrant.

328
329
BALL AND CAGE valve:-

Radiopaque base ring

Radiopaque cage

Three struts for the aortic valve; 4 struts for the mitral or tricuspid valve

Silastic ball impregnated with barium that is mildly radiopaque (but not
in all models)

Monoleaflet valve:-

Medtronic valve-

330
Bjork-Shiley valve-

331
TTK Chitra valve-

332
OMNISCIENCE Valve-

333
St. Jude Bileaflet Valve-

334
335
PERICARDIAL DEFECTS :

Normal pericardium is seldom identified on plain chest radiographs.

It may be visible as a sharp line at the cardiac apex, outlined by

epicardial and mediastinal fat.

Pericardial Effusion:-

A pericardial stripe wider than 2 mm that parallels the lower heart

border, usually in the lateral projection and best identified in the
sternophrenic angle, is diagnostic of a pericardial effusion.

The only clue to a relatively small effusion may be a noticeable change in

heart size compared with that on previous films.

The classic water flask configuration of a large effusion may not be

present, and the appearance of the cardiac silhouette may be identical to
that in DCMP with no significant distortion other than enlargement.

A large heart with a prominent superior vena cava and azygos vein in
combination with decreased pulmonary vasculature should raise the
question of cardiac tamponade.

336
Pericardial Calcification:-

Constrictive pericarditis may occur as the end result of pericarditis and

pericardial effusion of any cause.

Calcification of the pericardium is highly suggestive but not

pathognomonic of constrictive pericarditis.

More than 50% of patients with constrictive pericarditis do not show

calcifications on the plain chest film.

Calcifications are found frequently on the anterior and diaphragmatic

surfaces, but they may be over any part of the heart.

337
Pericardial Defects:-

Congenital or surgical absence of the pericardium may result in changes

in the cardiac contours.

Congenital absence is more commonly left-sided and rarely right-sided.

Partial defects may allow a portion of the heart (usually the left atrial
appendage in congenital defects) to herniate outside the pericardial sac,
with the herniated portion producing a bulge in the contour of the heart.

Complete absence of the pericardium is actually a unilateral defect and

nearly always left-sided.

The heart appears shifted to the left without a shift in the trachea.

The left cardiac contour has an elongated appearance.

The pulmonary artery often appears prominent and sharply defined.

338
 A somewhat similar appearance is seen on the frontal projection when
the heart is rotated because of compression of the chest wall in patients
with pectusexcavatum deformity.

HOW TO APPROACH LUNG DIAGNOSIS FROM THE CHEST RADIOGRAPH

A) Air Fluid Levels

You can encounter air fluid levels in chest x-rays in the following conditions:

Cavitary lung lesions

Loculated empyema

Hydropneumothorax

Esophageal obstruction
339
 Mediastinal abscess

Hydropneumopericardium

Hiatal hernia

Chest wall abscess

Biliary ductal ectasia

1) Air Fluid Level in Front of Diaphragm

Biliary ductal ectasia

2) Air Fluid Level

Across entire hemithorax in PA and

lateral view
Pleural space
Post-pneumonectomy

340
3) Air Fluid Levels

Multiple lung cavities with fluid levels

Projecting over lung field in both PA and lateral view

Other findings include:

Egg shell calcification of lymph nodes

Diaphragmatic pleural calcification

Colon

341
Eventration & Hiatus hernia

Colon in chest
Haustral markings

Other findings include:

Bony mets from prostate cancer

The colon is pulled up following resection of

esophagus.

342
 Air fluid levels in mediastinum

Widening of mediastinum

Note air fluid levels in the anterior mediastinum.

343
Colon Pulled up Following Resection of Esophagus

Radiolucency of mediastinum

344
Note haustral markings in anterior mediastinum

Esophagus

345
Air Fluid Level

In mediastinum in PA view (not seen clearly)

In esophagus (in lateral view below)
Lung cancer with esophageal obstruction

Other findings include:

Loculated effusion
Paratracheal mass
Left hilar mass

346
Air Fluid Level - Cancer Esophagus

In mediastinum in PA view
In esophagus in lateral view

347
Hiatal Hernia

Inhomogeneous cardiac density

Fluid level
Crossing mid-line

Osteoporosis

Retraction of lateral chest

348
Air Fluid Level

Inhomogeneous cardiac density

Retrocardiac density
In mediastinum in PA view
Hiatal hernia

Other findings include:

Pleural fibrosis on right

349
Hiatal Hernia

Note the two air fluid levels; one in the stomach and the other in the
esophagus
Inhomogeneous cardiac density
Crossing midline
Retrocardiac density

350
Lung Abscess

Diffuse Aspiration

Bilateral
Multiple
Fluid level

Cavity

Lung Abscess

Anterior segment of LUL

Atypical location for aspiration lung abscess
Thick wall
Fluid level

See lateral view below.

351
 Anterior segment of LUL

Lung Abscess - Aspiration

Superior segment RLL dense pneumonia

Note the progression below / Cavity / Complete clearance

Alcoholic presented with fever cough and weight loss of 2 weeks duration. Sub
acute onset of pneumonia, typical of anaerobic lung abscess.

352
 Cavitation in pneumonia
Necrotizing pneumonia

Superior segment pneumonia Cavitation

Complete resolution
Most lung abscesses can be cured with antibiotics, postural drainage
and good nutrition.

353
 Lung Abscess

Cavitation of right upper lobe with air

fluid level

Necrotic tissue along the walls

Pseudomonas pneumonia

Necrotizing pneumonia

Lateral view below

B) Pleural space

Pleural Effusion

Massive opacity right hemithorax

No shift of trachea and heart
Smaller right hemithorax
Right heart and diaphragmatic silhouettes are not identifiable

354
 Lateral

Right diaphragm not visible

Diffuse haziness

Air Fluid Level - Cancer Esophagus

In mediastinum in PA view
In esophagus in lateral view
355
 C) Bronchiectasis

Radiologic findings include:

Normal appearing CXR in most

Tubular shadows
Tram line
Gloved fingers
Mucocele
Ring shadows with thickened bronchial walls
Air fluid levels
Watch for dextrocardia
o Immotile cilia syndrome
Diffuse lung fibrosis
o Due to recurrent infections

Bronchiectasis

Left lung atelectasis due to mucus plugging

Mucus plugs suctioned with bronchoscopy
Bronchogram done after bronchoscopy
Saccular bronchiectasis in bronchogram below

356
Bronchiectasis

Multiple bilateral basal air fluid levels

See close up view below.

357
 Left Lower Lobe Atelectasis

Left lower lobe atelectasis

Left hilum pulled down
Retrocardiac tubular densities
(hard to visualize)

Review the bronchogram below.

Saccular Bronchiectasis

D) Calcification

Focal lung lesion: Ghon's complex

Miliary lung calcification
o Histoplasmosis
o Tuberculosis
o Alveolar microlithiasis
o Chicken pox pneumonia
Solitary pulmonary nodule
o Central / Granuloma
o Lamellar / Histoplasmosis
o Pop corn / Hamartoma
o Eccentric / Scar Cancer
Nodes
o Homogenous / TB

358
 o Clumpy / Histoplasmosis
o Egg shell / Silicosis, Sarcoidosis
Tracheal cartilage / Aging
Tumor
o Mediastinal mass / Teratoma
o Healed lymphoma / Mets
Vascular
o Aortic calcification
o Pulmonary artery calcification / Pulmonary hypertension
Pleural
o Visceral / Hemothorax, TB, Empyema
o Parietal / Asbestosis
Subcutaneous calcification
o Cysticercus

Broncholith
Sub segmental atelectasis

Subsegmental atelectasis
Calcified histoplasmosis node
Broncholith obstructing bronchus

359
Broncholith

Lingular pneumonia below

Broncholith in lingular orifice
Calcified histo node

Review films below.

Lingular pneumonia
o Loss of silhouette of left heart
margin
Post obstructive pneumonia

360
 Lingular pneumonia

Post obstructive pneumonia

Silicosis

Egg shell calcification of lymph nodes

Other findings include:

Diaphragmatic pleural calcification

Multiple cavities with fluid levels

Lateral and close up views below.

361
 Multiple cavities with fluid levels

Egg shell calcification of lymph nodes

Histoplasmosis

Calcified nodes
Clumpy calcification
Calcified nodules in lungs

362
Histoplasmosis

Calcified nodes
Calcified nodules in lungs

Popcorn Calcification

Solitary pulmonary nodule

Popcorn calcification
Hamartoma

363
Pleural Calcification

Visceral pleura
Probable old tuberculosis
Note translucent parietal pleura

364
 Visceral pleural calcification

Open drainage with air fluid levels

in pleural space

Silicosis

Diaphragmatic pleural calcification

Other findings include:

Multiple cavities with fluid levels

Egg shell calcification of lymph nodes

365
 Pneumothorax

Air in pleural cavity: no vascular

markings
Lung margin: adherent to chest
wall at one site
Increased density of atelectatic
lung: abnormal lung
Larger right hemithorax

Other findings include:

Calcified diaphragmatic pleural plaque

Cysticercus

Subcutaneous calcified lesions

Other findings include:

Old fractured ribs

Uncoiling of aorta

See below images

366
Solitary Pulmonary Nodule

LUL posterior segment

Gradual increase in size over 10 years
Central calcification
Tuberculoma (not confirmed)

Additional findings include:

Pleural calcification

367
 E) Cavitation

Radiological Criteria

A hole in the lung with a wall, lumen and contents. Focus of increased
density whose central portion has been replaced by air.

The following characteristics help in the differential diagnosis.

Number:

Multiple bilateral cavities would raise suspicion for either branchiogenous or

hematogenous process. You should consider:

Aspiration lung abscess

Septic emboli
Metastatic lesions
Vasculitis (Wegener's)
Coccidioidomycosis, tuberculosis

Single cavity

Primary lung cancer

Post-traumatic lung cyst
Many other diseases

368
Size:

A large cavity encompassing the entire lobe or lung should raise suspicion for
gangrene of lung.

Location:

Classical locations for aspiration lung abscess are superior segment of

the lower lobes and axillary subsegments of anterior and posterior
segments of upper lobes.
Tuberculous cavities are common in superior segments of upper and
lower lobes.
When a cavity in anterior segment is encountered, a strong suspicion for
lung cancer should be raised. TB and aspiration lung abscess are rare in
anterior segments. Cancer lung can occur in any segment.

Wall Thickness:

Thick walls are seen in:

o Lung abscess
o Necrotizing squamous cell lung cancer
o Wegener's granulomatosis
o Blastomycosis
Thin walled cavities are seen in:
o Coccidioidomycosis
o Metastatic cavitating squamous cell carcinoma from the cervix
o M. Kansasii infection
o Congenital or acquired bullae
o Post-traumatic cysts
o Open negative TB

Lining of Wall:

The wall lining is irregular and nodular in lung cancer or shaggy in lung
abscess . The appearance is akin to stalactites and stalagmites.

Contents:

The most common cause for air fluid level is lung abscess. Air fluid levels
can rarely be seen in malignancy and in tuberculous cavities from
rupture of Rasmussen's aneurysm.
A fungous ball should make you consider aspergillosis. A blood clot and
fibrin ball will have the same appearance.

369
 Floating Water Lily: I have never seen this. The collapsed membrane of a
ruptured echinococcal cyst, floats giving this appearance.

Associated Features:

Ipsilateral lymph nodes or lytic lesions of the bone is seen with malignancy.

Evolution of Lesion:

Many times review of old films to assess the evolution of the radiological
appearance of the lesion extremely helpful. Examples

Infected bullae
Aspergilloma
Sub acute necrotizing aspergillosis
Bleeding from Rasmussen's aneurysm in a tuberculous cavity

Etiology:

Cavity can be encountered in practically most lung diseases.

Common diseases and their characteristics include:

Primary Lung Cancer

o Thick wall
o Shaggy lumen
o Eccentric cavitation
Necrotizing Pneumonia
Lung abscess
o Gravity dependant segments
o Thick wall
o Air-fluid levels
Tuberculosis
o Superior segments
o Infiltrate around
o Bilateral
Fungal infections
o Aspergillus
Fungous ball
Sub acute invasive aspergillosis
Metastatic disease
o Thin walled (Squamous cell)
o Thick wall (Adenoma)

Comprehension of the Above Principles:

370
 Rationale for multiple bilateral cavities.
Why does reactivation TB occurs in superior segments?
Why does aspiration lung abscess occur in the superior segment of lower
lobes?
What is the criteria for thick and thin wall ?
What is the pathogenesis of stalactites and stalagmites?
What is crescentic sign?
How do you differentiate between aspergilloma and sub acute necrotizing
aspergillosis?
Does the location of cavity in a density have diagnostic significance?
What is open negative TB?
In metastatic disease, when do you get thin walled cavities and when do
you get thick walled cavities?

Cavity
|Squamous Cell Carcinoma Lung

LUL mass
Thick walled cavity
Eccentric location of cavity

Fluid level

371
Fungous Ball

Long standing cavity

Containing round density (A)
Mobile density
Adjacent pleural reaction (B) - characteristic of aspergilloma

Cavitating Metastasis

372
Multiple Thin Walled Cavities

Cancer Cervix

Lung Cancer / Squamous Cell

Mass density
Anterior segment of LUL
Thick wall cavitation

Lateral view below.

Mass density
Anterior segment of LUL

Cavity
Squamous Cell Carcinoma
373
 Anterior segment of LUL
Thick wall
Fluid level
Full hilum

Left hilar fullness: Nodes

Thin walled Cavity

Squamous Cell Carcinoma Lung

Thick wall
Irregular lumen

Left hilar fullness: Nodes

Old Coccidioidomycosis

374
Cavitating Metastasis
Multiple Thin Walled Cavities
Cancer Cervix

F) Chest Wall
Cervical Rib

375
You identify the rib by the transverse process with which it articulates.
A: Transverse process cervical vertebra: Horizontal
B: Transverse process dorsal vertebra: Upward

Subcutaneous Emphysema

Air outlining pectoral muscles

376
 Air along chest wall
Pneumomediastinum

Patient with lymphangitic metastatic spread.

Extra Pleural Sign

Cancer Lung

Density in periphery
Sharp inner margin
Indistinct outer margin
"Cat under rug" sign
Angle of contact with chest wall
Expanding destructive rib lesion

Paratracheal widening

This is an example of an RUL lesion.

Extra Pleural Sign

Cancer Lung

Density in periphery
Sharp inner margin
Indistinct outer margin
"Cat under rug" sign
Angle of contact with
chest wall
Expanding destructive rib
lesion

Paratracheal widening

This is an example of an RUL lesion.

377
 G) Consolidation

The following are radiological criteria to call a shadow on CXR consolidation:

1. Lobar or Segmental Density: The density should either correspond to

the lobe or lung segment.
2. Air Bronchogram: Presence of air bronchogram would confirm an
alveolar process.
3. No Loss of Lung Volume: Lung volumes increase in early stages of
consolidation. In later stages there can be some amount of loss of lung
volume due to secretions obstructing airways. As a general rule, there is
no significant loss of lung volume in consolidation.

Consolidation / Lingula

Density in left lower lung field

Loss of left heart silhouette
Diaphragmatic silhouette intact
No shift of mediastinum
Blunting of costophrenic angle

Lateral

Lobar density
Oblique fissure not
significantly shifted
Air bronchogram

378
 Consolidation / Left Lower Lobe

Density in left lower lung field

Left heart silhouette intact
Loss of diaphragmatic silhouette
No shift of mediastinum
Blunting of costophrenic angle

Lateral

Lobar density
Oblique fissure not
significantly shifted
Loss of silhouette: Posterior
portion of left diaphragm

Consolidation Left Lower Lobe

Density in left lower lung field

Left heart silhouette intact
Loss of diaphragmatic silhouette
No shift of mediastinum
Pneumatocele

379
 One diaphragm only visible
Lobar density
Oblique fissure not significantly shifted

380
Left Upper Lobe Consolidation

Density in the left upper lung field

Loss of silhouette of left heart margin
Density in the projection of LUL in lateral view
Air bronchogram in PA view
No significant loss of lung volume

381
Lobar Pneumonia Right Middle Lobe

Lateral

Density
Vague density right lower lung
corresponding to
field
RML
Indistinct right cardiac
No loss of lung
silhouette
volume
Intact diaphragmatic silhouette
Air bronchogram
(not demonstrable
in this presentation)

382
 Consolidation Right Middle
Lobe

Density in right middle

lung field
Loss of right cardiac
silhouette
Pulmonary artery overlay
sign
Air bronchogram not
visible in this presentation

Minor movement of fissure

Consolidation Right Upper Lobe / Air Bronchogram

Density in right upper lung field

Lobar density
Loss of ascending aorta silhouette
No shift of mediastinum
Transverse fissure not significantly shifted
Air bronchogram

383
H) Diaphragm

Both hemidiaphragms should be visible in both PA and lateral views.

The right hemidiaphragm is at a higher level due to the congenital
position of the heart, and not due to the liver.
Dome peaks in the center.
Markings representing attachment to the ribs are normal.
Lateral view
o Right diaphragm
Seen in its entirety
Right oblique fissure touching
Projects outside: Phenomenon of beam divergence
o Left diaphragm
Not seen in its entirety because of the heart resting on
diaphragm: Silhouette sign
Stomach bubble under
Left oblique fissure touching

384
"Elevated Diaphragm"

Note pneumoperitoneum
Supradiaphragmatic mass
Can be mistaken for elevated diaphragm

385
 Pellets

Pellets

I) Hyperlucent Lung

Factors
o Vasculature: Decrease
o Air: Excess
o Tissue : Decrease
Bilateral diffuse
o Emphysema
o Asthma
Unilateral
o Swyer James syndrome
o Agenesis of pulmonary artery
o Absent breast or pectoral muscle
o Partial airway obstruction
o Compensatory hyperinflation
Localized
o Bullae
o Westermark's sign : Pulmonary embolus

Agenesis of Left Pulmonary Artery

386
 Missing vascular markings in left lung
Left hilum not seen
Entire cardiac output to right lung

Emphysema

Hyperlucent lung fields

Multiple blebs
Avascular zones
Prominent pulmonary arteries
Radiologic TLC

See lateral view below.

387
Hyperlucent lung fields

AP diameter increased

Flat diaphragms

Multiple blebs

Retrosternal and infracardiac air

Radiologic TLC

Unilateral Hyperlucent Lung

Left Upper Lobe Resection

Left lung hyper lucent

Left hilum pulled up
No abnormal density

388
Unilateral Hyperlucent Lung
Right Upper Lobe Resection

Right lung hyperlucent

Right hilum same level as left hilum
No abnormal density

389
Unilateral Hyperlucent Lung
Peanut in Left Bronchus
Partial Airway Obstruction

Left lung hyperlucent

Left lung stays hyperlucent on expiration
Mediastinal shift with respiration

J) Interstitial Disease

Ground glass appearance

Nodules
Reticular
Honeycombing

390
 Honeycombing

Seen in end stage lung disease

Indicative of diffuse interstitial
fibrosis
Due to bronchiolectasia
Most of the time in bases
Upper lobe distribution seen in
eosinophilic

granuloma

Close up and gross lung specimens

391
Milary Tuberculosis

Interstitial nodules
o Uniform size
o Sharper edges

Silicosis

Miliary nodules
Left subpulmonic effusion

K) Lateral Chest

392
There is valuable information that can be obtained by a chest lateral view. A
few of them are listed below:

Sternum
Vertebral column
Retrosternal space
Localization of lung lesions
Lobes of lungs
Oblique fissures
Tracheoesophageal stripe
Pulmonary artery
Heart
Aorta
Mediastinal masses
Diaphragm
Volume measurements
o SPN
o Radiologic TLC

Pneumonectomy

Opacity left hemithorax

Tracheal shift to left
Cardiac and left diaphragmatic
silhouettes missing
Crowding of ribs

393
One diaphragm in lateral

Density over spine

Right pulmonary artery prominent
Herniation of right lung in anterior mediastinum

394
Mediastinal Lymph Nodes

Extrapleural

Polycyclic margin

Anterior mediastinum

Mediastinal Mass

L) Mass

Mass density can be encountered in lung cancer, benign tumors, sarcoma,

lymphoma, Wegener's and blastomycosis and tuberculoma.

Radiological criteria for a mass lesion are chest lateral and PA views.

Density
Round or oval
Sharp margins
Homogenous density (exception: air bronchogram in lymphoma and
blastomycosis)
No respect for anatomy (in cancer)
Can break down leading to thick walled cavity
May show calcification (histoplasmoma, tuberculoma, hamartoma)

395
Note in a gross cut section a mass which is well demarcated from the adjacent
normal lung. Malignant tumors have infiltrating edges, while benign tumors
are rounded and well circumscribed.

Mass

Round or oval
Sharp margin
Homogenous
No respect for anatomy

Lung Cancer: Large cell

Mass

Round homogenous density

Sharp margins
Medial portion pleural based (acute
angle)

This is a case of squamous cell lung

cancer.

396
Mass

LUL anterior segment

Aortic knob silhouette intact
Round homogenous density
Sharp margin

This is a case of lung cancer.

397
M) Lung Mass / Cancer Lung

The radiological pattern depends on the cell type.

Squamous cell
o Large mass
Cavitation
o Atelectasis with hilar mass
o Lympadenopathy
Large cell
o Large mass
Adenocarcinoma
o Solitary pulmonary nodule
Small cell
o Insignificant lung lesion
o Massive mediastinal adenopathy
Alveolar cell
o Solitary pulmonary nodule
o Pneumonic
o Multicentric
Pancoast tumor
o Apical shadow
o Posterior rib destruction
o Drooping of shoulder / Brachial plexus

398
 Round homogenous density
Sharp margins
Pulmonary artery overlay sign

Mass is present in front of the descending left pulmonary artery

Fluid in Fissure

Phantom Tumor

Pulmonary edema

Fluid in fissure

Biconvex density
In oblique fissure

N) Nodes

Para tracheal Unilateral VS bilateral

399
 Azygous
Anterior mediastinal Bilaterally symmetrical VS asymmetrical
Middle mediastinal
Posterior mediastinal Radiologic signs
AP window nodes
Para vertebral Polycyclic margin
Sub carinal Silhouette sign
Hilar Extra pleural sign
Parenchymatous Clear space between heart and
Internal mammary nodes nodes
Lung field Inhomogeneous cardiac density

AP Window Nodes - Small Cell Cancer

Rapid clearance followed by recurrence

Polycyclic margin

400
AP Window Nodes /Left Hilar Mass

Hilar Nodes

401
 Note bilateral symmetrical hilar nodes and para tracheal nodes.
A clear space between the nodes and heart, identifies the nodes as hilar.

Sarcoidosis
Alveolar Form

Symmetrical hilar nodes

Mediastinal nodes
Multiple bilateral mass densities with alveolar features

Soft coalescing

Internal Mammary Nodes

Cancer Breast

402
 Film below precedes 4 years
Note absent breast on right
Right lower lung field increased radio lucency
Polycyclic margin: Lymph nodes
Extrapleural

Lung Cancer

RUL primary lesion

Para tracheal nodes

403
"Potato" Nodes
Sarcoidosis

Bilateral symmetrical hilar nodes

Clear space between hilar nodes and heart
AP window nodes
Paratracheal nodes
RLL alveolar lung infiltrate

O) Pleural Effusion

404
Fluid accumulates in the pleural space.

Irrespective of the nature of fluid, radiologically they will look similar.

Radiological criteria are:

Density Massive
In dependent portion Unilateral VS bilateral
o Costophrenic angle in PA view Sub pulmonic
o Anterior and posterior portions Loculated
of gutter in lateral view Supine position
o Along sides in lateral Lateral decubitus position
decubitus position
o Along posteriorly in supine
position, giving diffuse
haziness on the side of
effusion
Silhouette of upper limit of density
o Upper margin high in axilla in
PA view
o Upper margin high interiorly
and posteriorly in lateral view
Blunting of costophrenic angle
Lack of identifiable diaphragm
(silhouette sign principle).

Pleural Effusion

Homogenous density
Meniscus maximum in axilla
Loss of cardiophrenic angle
Loss of diaphragmatic and right
cardiac silhouette

Loculated Pleural Effusion

405
Empyema

Pleural effusion

Air fluid level

Loss of right diaphragmatic and cardiac silhouettes

Loculation evident in lateral

Supine film

Loss of fluid level

Loculated Pleural Effusion

Empyema

Haziness of right hemithorax

Density not corresponding to lobar
anatomy
Diaphragmatic and cardiac silhouettes
intact
Lateral film below
o Loculated fluid overlying vertebral
column

Loculated fluid overlying vertebral column

406
Empyema

Haziness of left hemithorax

Loss of diaphragmatic and cardiac silhouettes
Chest wall edema

Pleural Effusion

Homogenous density
Loculated
Loss of cardiophrenic angle

Loss of lateral portion of diaphragmatic

silhouette

407
Pleural Effusion

Massive opacity right hemithorax

No shift of trachea and heart
Smaller right hemithorax
Right heart and diaphragmatic silhouettes are not identifiable

Lateral

Right diaphragm not visible

Diffuse haziness

Pleural Effusion Massive

Multiple Myeloma

Plasmacytomas

Unilateral homogenous density

Mediastinal shift to right
Left diaphragmatic and left heart silhouettes lost
Left hemithorax larger

408
Pleural masses become evident after the fluid is removed and with some air.

Pleural masses are not clearly evident except for the apical pleural mass.

Massive Pleural Effusion

Unilateral homogenous density

409
 Loss of diaphragmatic and right sided cardiac silhouettes
No mediastinal shift

Other findings include:

Blunting of left cardiophrenic angle

LUL gloved finger density. Sorry I do not remember the etiology for this
case.

Pleural Mass / Cystadenoma

Carcinoma

Post tap film with pneumothorax

on right
Parietal pleural masses

Subpulmonic Effusion
410
 Blunting of costophrenic angle
Medial displacement of costophrenic angle
"Elevated diaphragm"
The peak of the dome of diaphragm more medial

P) Pneumothorax is air in the pleural space.

Radiological criteria:

Air (black) in pleural space. No lung markings in pleural space.

Recognition of atelectatic lung (lung margin). The lung recoils to a resting
state as the negative pressure in the pleura is lost (relaxation
atelectasis).
Shift of mediastinum to the opposite side. The mediastinum is held in
the middle by balance between pleural pressures. When the negative
pressure on the side of the pneumothorax is lost, the mediastinum gets
pulled by the normal negative pressure from the opposite side.
Progressive shift subsequently could result from a push secondary to
tension pneumothorax.
Larger hemithorax. When negative pressure in the pleura is lost, the
chest wall reaches the TLC position. Note the following chest tube the
hemithorax returns to FRC position.
Opposite lung gets the entire cardiac output and the vascular markings
become prominent.

Tension: Make a decision about tension by evaluating the clinical

situation, BP and pulse. Radiologic signs are not reliable. The size of
pneumothorax or shift of mediastinum do not suggest tension. Mediastinum
will be shifted to the opposite side even without tension, as the negative
pressure is relatively more compared to the side with pneumothorax. A very
small pneumothorax in a patient with pre-existing lung disease can cause more
symptomatic findings.

Pneumothorax

No vascular markings on right

No shift of mediastinum to left

Deep sulcus

Atelectatic right lung

Increased haziness on left:

Diversion of entire cardiac output

411
 Small fluid level near costophrenic angle: Hydro Pneumothorax

Pneumothorax

No vascular markings on right

Shift of mediastinum to left
Deep sulcus
Atelectatic right lung
Increased haziness on left: Diversion
of entire cardiac output

Tension Pneumothorax

No vascular markings on right

Shift of mediastinum to left
Deep sulcus
Atelectatic right lung
Increased haziness on left: Diversion
of entire cardiac output

412
Pneumothorax

Atelectatic lung is dense implying that it is abnormal ("normal lung" will

not be dense)
Bleb is easily recognized in the close-up.
Bleb is easily recognizable.
Look for blebs along the margin of the atelectatic lung in pneumothorax.
If present, you can detect blebs easily.

413
Pneumothorax

Air in pleural cavity: no vascular markings

Lung margin: adherent to chest wall at one site
Increased density of atelectatic lung: abnormal lung
Larger right hemithorax

Other findings include:

Calcified diaphragmatic pleural plaque

Q) Thoracoplasty

414
R) Empyema

Nature of fluid indistinguishable radiologically

Findings suggestive of empyema
o Loculation
o Spontaneous air fluid level in pleural space
o Chest wall edema

415
Amoebic Empyema

Amoebic liver abscess ruptured into pleural space

S) Pancoast Tumor

Apical shadow
Apical cap
Destruction of posterior first two ribs
Shoulder droop: Brachial plexus involvement

416
Pancoast Tumor

Right apical mass

Cavitating mass
Para tracheal nodes
2nd rib destruction
Calcified nodes (silicosis)

Pancoast Tumor
417
 Apical density
Rib destruction not evident
Right paratracheal nodes

Pancoast Tumor

Apical density
2nd rib destruction

Left para tracheal nodes

Old rib fractures on left

Close up showing rib destruction

418
Pancoast Tumor

Apical density
2nd rib destruction

close up showing rib destruction.

Pancoast Tumor

419
 Right apical mass
Destruction of upper two ribs
Progressive breakdown into cavity

Note the start of break down

Mass protruding into cavity

T) Pulmonary Metastasis

How often is the lung the site of metastases?

What are the means by which the tumor cells reach the lung?
Is it common to see the lung as the only site of metastasis?
What are the different metastatic patterns?
Can one predict the probable primary source from a given roentgen
pattern?
What are the modes of presentation?
What is the best way to make a diagnosis?
What is the best way to care for it?

Multiple Lesions

420
 Multiple discrete lung lesions occur due to widely disseminated
hematogenous metastasis.
The pattern can vary from:
o diffuse micronodular shadows resembling miliary disease, or
o to multiple large well defined masses cannon balls.
Occasionally, cavitation or calcification can be noted.
Symptoms:
o Due to the interstitial location, these lesions are often
asymptomatic.
o Cough and hemoptysis are the usual symptoms.
Needle aspiration or transbronchial biopsy would be the procedure of
choice for confirmation of the nature of the lesion.
Treatment:
o Chemotherapy is the choice when the tumor is responsive.
o Occasional surgical resection of multiple lesions were attempted
with some reported success.
o In refractory hemoptysis, selective occlusion of bronchial arteries
by Teflon is a consideration.

Cannon Balls:

Neoplasms with rich vascular supply draining directly into the systemic
venous system often present in this fashion.

Miliary Pattern: This presentation is seen in patients with the following:

Thyroid carcinoma
Renal cell carcinoma
Sarcoma of the bone
Trophoblastic disease

Cavitating Lesions:

Cavitation is identified in 4% of metastatic deposits and, as with primary

bronchial carcinoma, is more likely in squamous cell lesions.
Colon, anus, cervix, breast and larynx account for 69% of such
occurrences.
Generally, small thin walled metastases usually indicate a primary site
in the head or neck, where as most large, thick walled secondaries arise
from the gastrointestinal tract.
Avascular necrosis of the lesion secondary to vascular occlusion, is the
presumed mechanism for cavitation.

Calcification:

421
 Calcification or ossification is rarely visible in metastasis to the thorax.
o Calcification of metastasis from ovarian, thyroid, breast and
mucin producing gastrointestinal neoplasms.
o Calcification in lymphomatous nodes has most often occurred
following therapy.
o Lung metastasis may also calcify following therapy.
o Almost all calcified or ossified lung metastasis occurring prior to
therapy are due to osteosarcoma or chondrosarcoma.
o Isolated cases of such metastasis have also been reported
with synovial sarcoma and giant cell tumor of the bone.

Solitary Pulmonary Nodule

Pulmonary metastases clinically present as a solitary pulmonary

nodule.
Similar to other solitary pulmonary nodular lesions, these are detected
by routine chest x-rays.
Of the solitary pulmonary nodular lesions, solitary metastases accounts
for less than 3% of cases.
Colon, chest, sarcoma, melanoma and genitourinary
malignancies account for 79% of such instances.
Solitary metastatic lesion can precede, follow or appear concomitantly
with the malignancy.

Diagnostic Strategy:

When it appears concomitantly or following definitive therapy of the

primary, thin needle aspiration of the lesion is probably the best
procedure to establish the nature of the lesion.
CT scans are superior to whole lung tomograms in evaluating the
presence of other occult metastatic lesions.
When the solitary pulmonary metastasis precedes clinical recognition of
the primary, standard management of the solitary pulmonary nodular
lesion should follow.
o This clinical presentation accounts for less than 1% and routine
search for primary is not recommended.

Treatment:

Surgical resection of single metastasis should be considered:

o when the primary tumor is resectable
o no other organ metastasis is evident
o and no effective alternate therapy is available

422
 Surgical resection of solitary lung lesions occurring a few years following
curative resection of primary have a better prognosis than the lesions
that manifest concomitantly with the primary tumor.

Endobronchial Lesion

Endobronchial metastases are rare in comparison with parenchymal

deposits and account for 2% of patients who died from solid neoplasms.
Diagnostic challenge:
o They simulate primary bronchogenic carcinoma in clinical
presentation and are often difficult to distinguish, even
pathologically.
o Simultaneous occurrence of two primaries is a difficult differential
to settle on many occasions.
o The usual roentgen findings are bronchial obstruction and
obstructive atelectasis or pneumonia.
o The endobronchial lesion may have characteristic pigment on
bronchoscopy in metastatic melanoma.
Patients may complain of persistent cough, hemoptysis, wheezing and
may have normal chest x-rays.
Kidney, colon, breast sarcoma and melanoma account for 67% of
the cases.
The metastases is located subepithelially and is due to hematogenous
metastases through the bronchial arteries.
It is unlikely to be secondary to endobronchial drop metastasis as tumor
cells often require fibrin thrombin to impact. The cough and mucociliary
reflex may efficiently clear aspirated cells.
Palliative radiation or resection becomes necessary if the patient has
hemoptysis or refractory obstructive pneumonitis.

Tracheal Metastasis

When the lesion is located in the trachea, patients will present with severe
wheezing and have normal chest x-ray findings.

Lymphadenopathy

The incidence of lymph node metastasis is high with extrathoracic

primaries, as well as bronchogenic carcinoma.
Autopsy incidence related to various primaries range from 20-60%.
However, the reported incidence and radiographically visible
lymphadenopathy vary greatly.
Radiographically visible enlargement is probably found in less than 5% of
all patients with extrathoracic primary neoplasms.

423
 Head and neck and genitourinary tract neoplasms most often cause
visible intrathoracic enlargement followed by malignant melanoma and
breast carcinoma.
Diagnostic challenge
o Lymphadenopathy may be hilar, mediastinal or both.
o This opposed to sarcoidosis, which rarely causes mediastinal
nodular enlargement without hilar enlargement.
o Lymph node metastasis is not always associated with lung
metastasis.
o The radiographic appearance may, therefore, be indistinguishable
from sarcoid, non-infectious granulomatous disease, lymphoma,
leukemia or a primary mediastinal tumor.
o Diagnostic problems arise in the minority of patients who do not
have known primary neoplasms.
o Asymptomatic patients with symmetric hilar enlargement usually
have sarcoidosis.
o Metastatic disease may cause bilateral hilar enlargement. However,
these patients are usually symptomatic.
o Anterior mediastinal node masses are common in lymphoma but
rare in sarcoid, as seen on chest radiographs.

Pleural Effusion

Pleural effusion is one of the common metastatic patterns.

The effusions often tend to be massive, recurrent and associated with
shortness of breath.
This pattern is associated with extensive underlying lung and systemic
metastases.
Most patients expire within three months.
Malignant effusions account for more than 50% of exudative pleural
effusions.
Lung, breast, stomach and ovary account for 81% of cases.
Pleural biopsy and fluid cytology establish the malignant nature of the
process.
Pleural sclerosis with tetracycline instillation is the palliative procedure
of choice in problem effusions.

Pleural Masses

Significant pleural masses can exist without recognition (as in the

adjoining CXR), even in the absence of pleural effusion.
Iatrogenic pneumothorax facilitates visualization of pleural masses.

424
 CT scan can reveal pleural masses that are not seen on routine x-rays.
Thymoma, multiple myeloma and cystadenocarcinoma lung are
reported to give such a metastatic pattern.

Spontaneous pneumothorax
Pneumothorax occurring secondary
to pulmonary metastasis is rare.
This mode of presentation occurs
secondary to necrosis of
subpleurally located metastases
with the resultant bronchopleural
fistula.
Cavitating sarcoma is reported to
present in this manner.
In some instances, the subpleural
metastases are not sufficiently large
enough to be recognized in x-rays
and pneumothorax is the presenting
manifestation.

Chest Wall Lesion

Metastatic lesions to ribs are common.

Occasionally, these lesions expand and encroach on the lung,
masquerading as a lung lesion.
The characteristic extrapleural signs, namely the peripheral location,
indistinct outer margin with a sharp inner margin and biconcave edges
help point towards the true location of the lesion.
Recognition of such lesions focuses ones attention to the ribs and
facilitates easy biopsy by percutaneous techniques.

Alveolar Pattern

Alveolar form of metastases is relatively rare and is often an

unrecognized form of metastatic pattern.
Histologically, they are indistinguishable from primary alveolar cell lung
carcinoma.

425
 Pancreatic carcinoma is the most common primary to present in such a
fashion.
Metastatic liposarcoma and laryngeal carcinoma have occasionally
been reported to give a similar pattern.
The metastatic lesions from choriocarcinoma also have features of
alveolar pattern.
o However, this is secondary to bleeding into the lesions rather then
due to tumor, per se.

Interstitial Pattern

Less than 10% of lung metastases have a lymphangitic pattern.

Pathogenesis:
o Lymphangitic metastatic disease in the lung is generally believed to
be the result of tumor spread along the perivascular lymphatic
after initial deposition of tumor embolus in a pulmonary capillary
by hematogenous route.
o There is evidence that gastric carcinoma is an exception to this
with direct lymphatic extension occurring from the abdomen to
chest, across the diaphragm.
The stomach, lung and breast account for 80% of cases.
The large majority of patients with unilateral diseases have bronchogenic
carcinoma.
Most patients have dyspnea with or without cough. Initially, symptoms
can be mild.
Diagnostic challenge:
o There is evidence of lung tissue disease on chest radiographs:
small linear and nodular densities, reticular nodular pattern,
septal lines.
o The appearance is similar to interstitial changes seen in
pulmonary edema, pneumoconiosis, usual interstitial pneumonitis
or sarcoid.
o There is frequent pleural effusion on hilar lymphadenopathy.
o Some symptomatic patients have normal radiographs.
Transbronchial lung biopsy or needle aspiration can provide tissue for
diagnosis.
In the absence of suitable chemotherapy, only symptomatic therapy can
be provided.
Most patients become severely dyspneic and expire within a few months.

426
Subacute Cor Pulmonale

This form of presentation occurs

when small subliminal tumor
deposits obstruct a sufficient cross
section of the pulmonary vascular
bed.
The spectrum of pulmonary
symptoms is identically to
thromboembolism.
Patients are in prolonged respiratory
distress with normal chest x-ray, and
with or without signs of pulmonary
hypertension.
Choriocarcinoma, hepatoma, breast
and stomach tumors account for
most of the primaries with such
presentation.
This entity should be considered in a
female with severe respiratory
distress with a history of recent
abortion or delivery chorionic
gonadotropin levels are high.
When recognized, chemotherapy
offers a favorable prognosis in
patients with choriocarcinoma.
Prognosis is poor with other primary
malignancies.

Conclusion

Lung metastases occur in approximately 30% of malignant disease cases.

Frequently, it is the presenting manifestation and search for the primary
is lengthy and cumbersome.
The roentgen patterns of thoracic metastases vary. Awareness of the
common primaries presenting with a metastatic pattern facilitates the
search for the source.
The venous and lymphatic drainage of the organ and the cell type are
some variables that seem to determine the metastatic pattern.
Each metastatic pattern has a unique clinical presentation because of its
locale and extent.
Each pattern raises a distinct differential diagnosis, differs in the best
diagnostic procedure and the choice of therapeutic modality.
427
Bilateral Diffuse Alveolar Disease

Cancer Pancreas

Lung Metastasis

Soft fluffy lesions

Coalescing
Air bronchogram

Cannon Balls - Lung Metastasis - Rectosigmoid Cancer

428
 Multiple
Bilateral
Round mass densities
Sharp margins

Cannon Balls / Lung Metastasis

Multiple
Bilateral
Round mass densities
Sharp margins

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Cavitating Metastasis

Multiple Thin Walled Cavities

Cancer Cervix

Lung Cancer

RUL primary lesion

Para tracheal nodes
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 Contralateral lung metastasis in second film

Lung Metastasis

Cancer Colon

Multiple cavitating lesions

Thick walled cavities

Right pleural effusion

DIAGNOSIS OF PATHOLOGY OTHER THAN HEART & LUNG FROM THE

CHEST RADIOGRAPH

A) Strictures

In the table on the left common and uncommon causes of esophageal

strictures.

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On the far left a stricture (arrow) with irregular mucosal folds at stricture site
on air-contrast view.
This patient had Barrett's esophagus.
Mid esophageal strictures and ulcers are suspicious for Barrett's esophagus.

The two images on the right show a Barrett's esophagus with an irregular
stricture due to adenocarcinoma.

On the left a long, symmetric tapered benign stricture months after

radiotherapy.

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On the left images of a patient with a benign stricture high in the esophagus
(arrow).
There is bilateral lower lobe lung consolidation due to repeated aspiration.

Approximately 5,000-15,000 cases of caustic congestion occur in the US every

year.
About 50%-80% occur in the pediatric population.
On the left a high stricture (arrow) following caustic ingestion

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Osteophytes (arrow) can impinge on the esophagus and hypopharynx.
However they rarely cause symptoms.

Multiple structures are uncommon.

On the left a table with diseases that may present with multiple esophageal
strictures.

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On the left a patient with benign pemphigoid.
Mucosal bullae have led to multiple strictures (arrows).

On the left a patient with benign epidermolysis bullosa.

Multiple strictures (arrows) are a residual of mucosal bullous disease.
Extensive bullous skin disease has led to webbed fingers and contractions.

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Corrosive ingestion can result in multiple strictures.

B) Acute esophageal syndromes

In the table on the left are etiologies of an acute esophageal syndrome.

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Boerhaave syndrome

Boerhaave syndrome is rupture of the esophageal wall.

It is most often caused by excessive vomiting in eating disorders such as
bulimia although it may rarely occur in extremely forceful coughing or other
situations, such as obstruction by food.
Boerhaave syndrome is a transmural or full-thickness perforation of the
esophagus, distinct from Mallory-Weiss syndrome, a nontransmural
esophageal tear also associated with vomiting.
These syndromes are distinct from iatrogenic perforation, which accounts for
85-90% of cases of esophageal rupture, typically as a complication of an
endoscopic procedure, feeding tube, or unrelated surgery.

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On the left a patient with Boerhaave syndrome.
Chest radiographs show pneumomediastinum (arrows).
Esophagram with extravasated water soluble contrast material in left
hemithorax (asterisk)

Perforation is almost always on left side of distal esophagus.

Radiographs show mediastinal gas, effusion, and later pneumothorax.
Esophagram is used to confirm leak, first with water-soluble contrast, then
barium if no leak demonstrated.

On the left a patient with Boerhaave syndrome.

The barium study shows extraluminal gas (arrow) without contrast
extravasation.
CT shows extraluminal gas (arrows).
Rent of distal left esophagus confirmed at surgery.
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 CT can show small amounts of extraluminal gas or extravasation not visible on
radiographs or esophagram.

Mallory-Weiss tear

A Mallory-Weiss tear results from prolonged and forceful vomiting, coughing or

convulsions.
Typically the mucous membrane at the junction of the esophagus and the
stomach develops lacerations which bleed, evident by bright red blood in
vomitus, or bloody stools.
It may occur as a result of excessive alcohol ingestion.
This is an acute condition which usually resolves within 10 days without
special treatment.

On the left a patient with a Mallory-Weiss tear.

Spot films show barium (arrows) in linear mucosal tear near gastroesophageal
junction.
Tears may be in distal esophagus, gastric fundus, or extend across the GE
junction.

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Esophageal hematoma

These unusual lesions have been associated with increased esophageal

intraluminal pressure, most often vomiting, instrumentation, and
anticoagulation or bleeding disorders.
Some are spontaneous.
Blunt trauma is a rare cause.
Hematomas are self-limited and almost never progress to perforation.
Most esophageal hematomas resolve in 1-2 weeks with conservative treatment.

On the left a patient with an esophagus hematoma.

He presented with chest pain and dysphagia after vomiting.
Aside from tortuous aorta chest radiograph is normal.
The barium study shows a narrowed lumen (arrows) on AP view and flattened
lumen on lateral view (arrowheads) suggestive of a intramural hematoma.
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On CT the diagnosis of an intramural hematoma was confirmed.
A high density mural hematoma (arrowhead) is seen next to NG tube (arrow).
Following conservative treatment, six months later the barium study was
normal.

On the left a patient who had a complicated endoscopy.

Instrumentation caused a mucosal tear and dissecting intramural hematoma
resulting in double lumen with separating stripe of mucosa (arrows).

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On the far left an intramural extravasation (arrow) after distal dilation for
achalasia.
In the middle an intramural extravasation (arrow) after complicated
endoscopy.
On the right a perforation after biopsy with extravasation of contrast material
(arrow).

C) Benign neoplasms

On the left a list of benign esophageal masses.

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Leiomyomas

Leiomyomas are the most common benign esophageal neoplasm and are often
large yet nonobstructive. Gastrointestinal stromal tumors (GIST) are least
common in the esophagus.

On the left an asymptomatic patient with a leiomyoma.

On the chest film an abnormal opacity is seen behind the heart (arrow).
The barium study demonstrates a lobulated mass (arrow) that does not
obstruct despite its large size.

Mucosal lesions are indicated by mucosal irregularities.

Submucosal intramural lesions produce smooth filling defects, and in profile,
the margins often form close to a right angle with the esophageal wall.
Extrinsic lesions tend to form longer obtuse angles if not fixed to the
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esophageal wall, and their epicenter may be outside the esophagus. In practice,
the location of a lesion may be difficult to determine.

On radiograph, tumor (arrows) protrudes into azygoesophageal recess.

On esophagram, the inferior margin of this intramural lesion forms close to a
right angle (arrow) with esophageal wall.

A calcified esophageal mass is almost always a leiomyoma.

On the left a patient with a calcified esophageal lesion (arrows) protrudes into
azygoesophageal recess on radiograph.
Lesion (arrow) on CT and surgical specimen radiograph showing calcification.

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On the left a patient with granular cell myoblastomas, an uncommon benign
tumor.
These two lesions (arrows) are nonspecific in appearance, but the proximal
lesion does demonstrate overhanging and right angle margins indicating mural
location.

Fibrovascular polyp

Pedunculated fibrovascular polyps are rare lesions, that are difficult to

diagnose on esophagrams.
Their movement during the examination producing an inconstant position and
shape may be suggestive as in this patient.
The stalk is often difficult to identify.

Duplication
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On the left a patient with an esophageal duplication.
The findings on the barium study are non-specific.
Lesion (arrows) is visible behind the heart on radiograph.
Esophageal narrowing (arrows) is caused by duplication.

A foregut duplication cyst is a congenital cyst.

In the case on the left it displaces hypopharynx and opacified esophagus
(arrow) posteriorly and trachea and larynx (asterisk) anteriorly.

D) Malignant neoplasms

On the left a list of malignant esophageal masses.

Early and small esophageal carcinoma are not synonymous.

Early esophageal carcinoma is limited to the mucosa, submucosa with no
lymph node metastases.
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Most are small ( Small esophageal carcinoma is defined by the size of the
lesion, a diameter So an early carcinoma may be small, but a small carcinoma
may be invasive or metastatic and thus not an early carcinoma.

On the left a patient with an early esophageal carcinoma.

Lesion is not visible on single contrast esophagram.
Air-contrast esophagram shows surface irregularity (arrows) indicating a
mucosal lesion.
This was both a small lesion and a pathologically early squamous carcinoma.

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Advanced carcinoma has many gross appearances:

Polypoid
Varicoid
Infiltrative
Ulcerative
Superficial spreading
Stricture
Pseudoachalasia

On the left two cases of polypoid carcinoma.

On the left a patient with an infiltrative ulcerated carcinoma.

This lesion has an abrupt transition forming an acute angle and overhanging
edge.
This indicates mural involvement and is different than obtuse angles usually
produced by extrinsic lesions that are not fixed to the esophagus.

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On the left a patient with a varicoid carcinoma.
Unchanging appearance of filling defects indicate tumor rather than varices.
Note sharp upper margin of lesion and ulceration (arrows)

On the far left a patient with a varicoid carcinoma.

Long lobulations simulate varices but did not vary during fluoroscopy.
Note large irregular folds and soft tissue mass (arrow) of gastric fundus

Next to it a patient with a superficial spreading carcinoma.

Extensive superficial spread involves distal esophagus.
This appearance can be seen with both early and advanced lesions.

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On the far left a patient with a carcinoma with stricture.
An irregular, asymmetric stricture is highly suggestive of carcinoma.
Smoothly tapered, symmetric strictures are characteristic of a benign etiology,
but malignant strictures can have similar characteristics and mimic benign
lesions.

Next to it a patient with a carcinoma with stricture resembling achalasia.

Distal esophageal malignancy may closely resemble achalasia.
If esophageal motility is normal, achalasia can be excluded.
If abnormal, however, subtle imaging features; asymmetric, irregular, abrupt,
or high narrowing, mucosal abnormality, or fixed abnormality suggest
diagnosis.

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On the left another case of pseudoachalasia.
Distal narrowing simulates achalasia, but narrowing is eccentric, shoulders
(arrows) asymmetric, mucosa irregular at tip of narrowing.
CT shows gastric fundus thickening (arrows) due to adenocarcinoma.

Tracheoesophageal stripe
Width of the juxtaposed posterior tracheal and anterior esophageal walls > 5
mm on a lateral chest radiograph is suspicious for pathology, most often
esophageal carcinoma or achalasia.

On the left a patient with a widened 1 cm stripe (arrows).

Esophagram shows widened stripe (arrows) and irregular margins of
midesophageal carcinoma.
CT shows abnormal soft tissue dorsal to trachea.
The tumor invades mediastinum adjacent to aortic arch (arrow)

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Barrett's esophagus and Adenocarcinoma

Barrett's esophagus is a proven risk factor for the development of an

adenocarcinoma.
The incidence of cancer in Barrett's however is controversial.
Who, how, and when individuals should be screened is unresolved.

Adenocarcinoma was 10% of esophageal malignancies in 1960s.

Since 1960s, incidence increasing in USA greater than any other carcinoma.
Incidence now approaching or exceeding squamous carcinoma in Caucasian
men in the USA and Europe.

On the left a patient with an ulcerated (arrow) plaque like adenocarcinoma in a

Barrett's esophagus.

Primary gastric fundus adenocarcinoma can invade the esophagus, but means
of differentiating invasion from a primary esophageal tumor are a subject of
debate.
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On the left a patient with a gastric fundus adenocarcinoma.
The barium study demonstrates marked irregular thickening of distal
esophagus and folds at gastroesophageal junction.
CT shows thickened irregular lesser curvature wall (arrows) near
gastroesophageal junction.

Spindle cell carcinomas are rare neoplasms, also called carcinosarcomas.

They are often bulky but nonobstructive as in the case on the left.
Leiomyosarcomas and rare primary melanomas of the esophagus also tend to
be bulky but not cause significant obstruction.

On the left a patient with a leiomyosarcoma of the esophagus.

Margin (arrows) of bulky lesion visible on chest radiograph.

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Lateral view of esophagram shows marked irregularity and esophageal
narrowing (arrows).

On the left another patient with a leiomyosarcoma of the esophagus.

Large lesion distorts esophageal lumen.
CT shows lesion distorting but not obstructing esophageal lumen (arrow).

On the left three patients with esophageal narrowing as a result of metastatic

mediastinal lymphnodes.
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On the far left a bronchogenic carcinoma.
Extrinsic mediastinal lymph nodes produce long obtuse angles at the interface
with esophagus.
In the middle another bronchogenic carcinoma.
Irregular distal esophageal wall due to invasion of esophagus.
In the right a patient with a breast carcinoma.
There is mediastinal lymphadenopathy with esophageal invasion and
obstruction.

Due not confuse normal esophageal irregularities for impressions by

lymphnodes.
On the left a normal esophagus.
The esophagus (arrow) protrudes under aortic arch into right side of AP
window.
Next to it mediastinal nodes (arrows) that displace the esophagus to right in a
patient with bronchogenic carcinoma.

E) Vascular impressions

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On the left a list of vascular structures that may cause impressions on the
esophagus.

Uphill varices

With portal hypertension, elevated portal venous pressure leads to reversed

(hepatofugal) flow bypassing the liver through the left gastric vein to dilated
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esophageal and periesophageal veins that anastamose with the azygos and
hemiazygos veins which drain uphill into the superior vena cava.
Filling defects due to varices are characterized by change in appearance during
the examination related to breath holding and thoracic pressure.

On the left are CT images of a patient with large Uphill varices secondary to
cirrhosis with portal hypertension.

On the left CT images of a patient with uphill varices.

Uphill varices can be mass-like as seen in the case on the left.

Continue with next image.

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The CT shows mass-like mediastinal and esophageal varices (arrows).

Varices have to be differentiated from varicoid carcinoma.

On the left the fixed appearance of filling defects indicates tumor rather than
varices.
Note sharp upper margin of lesion (arrows)

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Downhill Varices
With superior vena caval obstruction, upper body venous blood flows
caudally downhill through esophageal veins to the azygos vein which empties
into the superior vena cava caudal to the obstruction.
If the obstruction is at or below the azygos, the blood flow extends further
caudally to the portal system and then the hepatic veins to the inferior vena
cava and the right atrium.

On the left downhill varices in a patient with a superior vena cava obstruction
due to histoplasmosis.
On the barium study inconstant filling defects (arrows) represent downhill
varices in upper esophagus.
The angiogram demonstrates collateral vessels including a dilated left superior
intercostal vein (arrow).

The barium study demonstrates inconstant filling defects (blue arrows) due to
downhill varices in upper esophagus.

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CT demonstrates esophageal (red arrow) and mediastinal varices.
Continue with venogram.

Upper arm venograms show SVC obstruction.

Aberrant right subclavian artery

This is the most common thoracic arterial anomaly and rarely causes
symptoms.
The artery extends up and to the right producing a dorsal diagonal impression
on the esophagus (arrows).
The CT demonstrates that the aberrant artery (arrow) is last vessel from arch
and extends dorsal to trachea and esophagus.

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Right aortic arch with aberrant left subclavian artery

A right aortic arch with an aberrant left subclavian artery is most often an
incidental finding.
A right aortic arch with mirror-image branching however is almost always
associated with congenital heart disease.

CT shows right arch (R) and aberrant left subclavian artery (arrow) arising low
off arch and extending to left dorsal to esophagus and trachea.
On the left the esophagram of a patient with a right arch that produces a
dorsal indentation on this lateral view (blue arrow).
The diagram shows the aberrant left subclavian artery (L SCA) dorsal to the
trachea and esophagus.

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Double Arch

Double arch most often presents with airway obstruction, dysphagia,

aspiration in children.
The arches indent esophagus at different levels.

On the left another double arch.

Chest radiograph with right lung consolidation due to aspiration in 6-year-old.
Right and left arch indent esophagus (arrows) at different levels

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Aberrant left pulmonary artery

The aberrant left pulmonary artery indents the trachea dorsally and esophagus
ventrally as it extends between them.
Narrowing of right bronchus can cause air trapping or atelectasis.

Tortuous aorta
A tortous descending aorta is a common cause of extrinsic impression on the
esophagus.
The image on the far left shows a narrowed distal esophagus.

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Oblique view shows esophageal indentation by aorta with obtuse margins
(arrows) characteristic of extrinsic compression.

Aortic pathology

On the far left the normal aortic arch impression on the esophagus.
This impression can be enlarged if there is dilatation of the aorta as seen in
this patient with a mycotic aortic arch aneurysm (arrows).

Coarctation

On the left 3 images of a patient with a coarctation.

On the chest film the 'Figure 3' shape of aortic knob due pre and post stenotic
dilatation (arrows).
The barium study demonstrates the 'Reverse 3 figure' indention of esophagus
by pre and post stenotic aortic dilatation (arrows).
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An angiogram demonstrates a coarctation with pre and post stenotic dilatation
in another patient.

Vascular Radiology

A) Overview of Arch Anomalies

1. Aberrant Right subclavian artery

Most common arch anomaly.
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 Not a true ring.
Usually asymptomatic.
Sometimes dysphagia lusoria when dilated suvclavian artery compresses
esophagus posteriorly.
2. Innominate artery compression syndrome
In children the brachiocephalic (innominate) artery is located more to the left
and may compresses the trachea anteriorly.
3. Right Arch Mirror Image
Mirror-image variety of the left arch.
Asymptomatic.
Associated congenital heart disease in 98%, mostly tetralogy of Fallot.
4. Right Arch with Aberrant left subclavian
Left subclavian artery is the last branch.
Obstructing anomaly.
5. Double Aortic Arch
Complete ring encircles esophagus and trachea.
Four vessel sign.
6. Double Arch with Atretic Segment
Left arch is very small and has atretic posterior segment.
Still a four vessel sign.

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Embryology

Double Arch:

In the embryo a double arch with two brachiocephalic vessels on each side is
present.
If double aortic arch persists, it forms a vascular ring around trachea and
esophagus.

Double Arch with Atretic Segment:

Posterior part of the left arch becomes atretic.
This nonpatent remnant persists as a fibrous cord tethering the anterior left
arch to the descending aorta.

Normal Left Arch:

The posterior part of the right arch involutes.

The two brachiocephalic vessels on the right form the right innominate artery.

Right Arch with mirror branching:

Mirror image of normal left arch.

Posterior part of the left arch involutes.
The two brachiocephalic vessels on the left form the left innominate artery.

Left Arch with aberrant right subclavian artery:

Right arch between the right subclavian and right common carotid artery
involutes.
First branch is the right common carotid, followed by the left carotid and the
left subclavian artery. The last branch is the right aberrant subclavian artery.

Right Arch with aberrant left subclavian artery:

Mirror image of the left arch with aberrant right subclavian artery.
Left arch between the left subclavian and left common carotid artery involutes.
First branch is left common carotid, followed by right carotid and right
subclavian artery. The last branch is the left aberrant subclavian artery.

When you look at these illustrations, you have to realize, that these are views
from above, while CT-images have a 'view from feet'.
On a CT-image the ascending aorta will be on the upper part of the image and
the descending aorta will be on the lower part.

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Aortic Arch Anomalies

Axial image and volume rendering posterior view

Right Arch Mirror Image

This is the mirror-image variety of the left arch.

On the left a 2 year old girl with wheezing and coughing.

Study the images and then continue.
You have to realize, that axial CT-images are viewed from the feet, while the
illustrations above are viewed from above

On the axial image there is a right arch

On the volume rendered image there is mirror image branching of the
brachiocephalic arteries, no aberrant subclavian artery, so this is a right arch
mirror image.

Mirror image aortic arch (yellow arrow) and a VSD (red arrow)

This anomaly is asymptomatic, because there is no obstructing ring.

Almost all of these patients however come to our attention because they have
associated congenital heart disease in 98% of cases.
This patient had a mirror image aortic arch and a VSD.
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Mirror image aortic arch in patient operated for tetralogy of Fallot.

On the left an adult who was operated in his childhood for a Tetralogy of Fallot
(pulmonary stenosis, right ventricular hypertrophy, VSD, overriding aorta).
At surgery the VSD was patched and the pulmonary outflow tract was
enlarged.
Notice that there is also a right arch.

In the United States there are now more than one million adults who have
survived their congenital heart disease.
In the ER you will see these patients because they age and get chest pain like
many adults do and so you will see these anomalies more frequently.

View from anterior

Right Arch with Aberrant left subclavian

The Right Aortic Arch with an aberrant left subclavian is an obstructing arch
anomaly.
The first branch of the aorta is the left common carotid, followed by the right
subclavian artery and the left common carotid.
This also is a true ring.
The ligamentum ductus arteriosus between the arch at the level of the left
subclavian artery and the left pumonary artery completes the ring.
If this ligament is very short, there will be a lot of compression.

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Right Arch with Aberrant left subclavian

On the left a patient with a right arch with an aberrant left subclavian
(indicated by the yellow arrow).
Scroll through the images on the left.
Again you have to realize that the axial CT-images have a 'view from feet'.

Which vessels are indicated by the yellow and green arrow?

There is a right arch and the left subclavian artery is the last branch of the
aortic arch, indicating that this is an aberrant left subclavian.
Medially to the left subclavian artery we see the left common carotid, that
originates from the right side and has an oblique course to the left.
The yellow arrow indicates the azygos vein.
The green arrow indicates the left superior intercostal vein, a normal variant,
that we will discuss later.

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Posterior oblique view: Right Arch with Aberrant left subclavian (yellow arrow)

Same patient.
Posterior oblique view of volume rendered image to show the aberrant left
subclavian artery.
In a mirror type right arch, the left subclavian is the first brach and forms the
left innominate together with the left common carotid.

Right Arch with Aberrant left subclavian

On the left images of a symptomatic child.

On the axial image there is a right arch with the left subclavian artery that
comes off on the posterior side and runs behind the trachea and the
esophagus.
The compression of the trachea is demonstrated on the volume rendered view.

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Double Aortic Arch

On the left a chest film of a 6-month old boy with stridor and cough.
The trachea is deviated to the left, otherwise the chest film is normal.
So there is some mass effect on the right side.

On the left the reconstructions demonstrating a double aortic arch.

There are branches coming off the right arch and branches coming off the left
arch.

Double Aortic Arch

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The right arch is typically larger and higher than the left.
There is a complete ring that encircles the esophagus and the trachea and
usually there is stridor or dysphagia.
Two brachiocephalic arteries arise on each side separately (four vessel sign).

On the left a chest film of a young adult with a cough.

There is a right paratracheal mass.
The differential diagnosis is tumor, adenopathy or vessel (right arch, dilated
azygos vein, dilated aberrant right subclavian artery).

On the left axial images and posterior view of volume rendered reconstruction.
Describe the findings and then continue.

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The findings are:

four vessel sign

double arch
right arch higher and larger
esophagus and trachea are completely encircled

The narrowing of the trachea is seen on the axial images, but better
appreciated on the MPR and Volume Rendered image.

Pre-
of Dr.and
W. post-operative
Chu (4) reconstructions of a double aortic archImage courtesy

On the left preoperative and postoperative MDCT studies of a 2-month-old

female infant with double aortic arch presenting with stridor and repeated
apnea.
The smaller left arch is partially resected.

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Double Arch with Atretic Segment
Occasionally the double arch can have an atretic segment.
You should not confuse it for a right arch.
The left arch is just very small and there is still a four vessel sign.

Double Arch with Atretic Segment

On the left a dominant right arch and a small left arch.

The atretic segment is marked by the arrow.
Notice the four vessel sign.

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On a posterior view the interruption is nicely demonstrated.
Remember that there is still a ring, so there is still obstruction.

Another case on the left.

Do not call this a right arch.
It still is a double arch and there is a atretic fibrotic segment on the posterior
side of the left arch, that completes the ring.
Notice the four vessel sign.

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Same patient.
Always look at the airways.
On the recoonstruction the impression on the trachea is better appreciated.

Aberrant Right SCA, no compression of the trachea

Left Arch Aberrant Right SCA

Also known as arteria lusoria.

Most common arch anomaly.
Not a true ring
Usually asymptomatic.

On the left a young patient, who has a CT for another reason.

Study the images and then continue.
Notice that there is a left arch, but the right subclavian artery is the last
brachiocephalic artery to branch off the arch.

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Dysphagia lusoria in patient with dilated aberrant right subclavian artery.

Only rarely these patients become dysphagic (dysphagia lusoria) , when the
origin of the right subclavian artery becomes dilated.
On a barium study of the esophagus you will see a posterior impression with
an oblique course directed towards the right shoulder.

On the left a 78 year old woman with dysphagia.

There is consolidation in the right upper lobe, maybe due to aspiration.
There is a dilated vessel that compresses the esophagus and it originates from
the left-sided aorta, i.e. an aberrant right subclavian artery.

On the left the same patient with dilated aberrant right subclavian artery.
Coronal reconstruction.

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Left Arch-Aberrant Right subclavian artery. Scroll through the images.

On the left another patient with an aberrant right subclavian.

Scroll through the images.
When you follow the artery from inferior to superior, it starts on the left side of
the arch and travels obliquely behind the esophagus to go to the right.

Innominate artery compression syndrome with compression of the trachea

Innominate artery compression syndrome

On the left a sagittal scanogram, axial image and sagittal reconstruction of a 5

year old girl with noisy breathing and occasional episodes of cyanosis.
First look at the images then continue.

The findings are:

anterior compression of the trachea

brachiocephalic (innominate) artery is located more to the left and compresses
the trachea

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The diagnosis is the innominate artery compression syndrome.
In infants the innominate artery arises more to the left than in adults, so it's
got to go in front of the trachea. It may compress the trachea, leading to
stridor, cough and dyspnea. This compression decreases with age and these
patients will outgrow it.

The compression in the innominate artery compression syndrome is located on

the right anterior side and at the level of the thoracic inlet.
This is much higher than in the double arch or Right Aortic Arch with Aberrant
left subclavian

On the left another case with mild compression on the trachea.

Aortic Coarctation

Narrowing at level of distal arch / descending aorta.

Chest film: 'figure 3' sign, inferior rib notching.
Intervention when gradient > 20 mm Hg.

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 Associated with bicuspid aortic valve (75%), cerebral aneurysms (5-10%) and
Turner syndrome (20% have coarctation)

On the left a 2 month old boy with heart failure.

First study the image, then continue

The findings are:

Large thymus which is normal for a 2 month old.

Striking discrepancy between diameter of ascending and descending aorta.

The diagnosis is coarctation, which is nicely demonstrated on the posterior

view of the reconstruction.

There are two types of coarctation.

The type we usually see is the post-ductal type, which is distal to the left
subclavian artery.
The uncommon pre-ductal type is seen in neonates.
They present with severe heart failure, mostly within the first week of life,
usually on the first day.
The occlusion is in front of the left subclavian.

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First study the axial image followed by the sagittal reconstruction, then
continue.

The findings are:

Big internal mammarian arteries on the axial image due to a high grade
stenosis as a result of a coarctation. Probably could not make the diagnosis
based on the axial images alone.
Post-ductal coartation only seen on sagittal reconstruction.
Intercostal collaterals.

Intercostal collaterals in aortic coarctation

The intercostal collaterals typically occur between the 3rd and the 8th rib.

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Pre-ductal type of coarctation

On the left two neonates with the pre-ductal type of coarctation.

The stenosis is in front of the left subclavia and there is arch hypoplasia.
Collaterals do not occur, probably because they don't have time to develop.

Coarctation treated with angioplasty (left) and stent placement (right)

Coarctation is treated with angioplasty, stent placement or patch aortoplasty.

The image on the far left is the result after angioplasty.
Next to it a patient who was treated with a stent.
Notice that the stent is obstructing the orfice of the left subclavian artery.

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Pseudo-aneurysm in coarctation treated with stent-placement

On the far left a patient who was treated with a stent.

The stent ruptured causing restenosis.
Next to it two patients with pseudo-aneurysm.
One after angioplasty and another who developed a pseudo-aneurysm after
stent placement.
They have to be repaired because they will rupture.

Pseudo-aneurysms are seen in

10% after angioplasty.

30% after patch aortoplasty.

B) Pulmonary arterial anomalies

They most common anomalies of the pulmonary arteries are listed in the table
on the left.

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Pulmonary agenesis on the right side
Pulmonary agenesis

Also called congenital interruption of the pulmonary artery.

Unilateral absence of the pulmonary artery.
Small lung and hilum.
Compensatory hyperinflation of contralateral lung with herniation.

On the left a young adult, who had cyanotic spells as a child.

She is now in good health and comes in for another reason.
On the chest film the differential is atelectasis, pneumonia or maybe a tumor.
The CT shows, that he right lung is not developed and the space around the
atresic pulmonary artery is filled with fibrofatty tissue with collaterals.
So this is pulmonary agenesis.
If many collaterals develop there will also be some development of the lung.

Pulmonary agenesis on the left side

On the left another case of absent pulmonary artery with absence of lung
development.

485
On the CT the left lung is absent.
These patients may be totally asymptomatic.

Pulmonary Sling
Pulmonary Sling

On the left a 4 month old girl with abnormal echo, benign heart murmur and
no respiratory or feeding difficulties.
The sagittal reconstruction shows an anomalous vessel on the posterior side of
the trachea.
There is a little mass effect on the trachea.

Pulmonary Sling

In pulmonary sling the left PA originates from the right PA and courses
between the esophagus and the trachea, where it compresses the right main
bronchus.
Pulmonary sling is seen more frequent in children as it is more symptomatic
than in adults, because the chest is smaller, but you can also encounter it in
adults.
486
Pulmonary Sling with long segment stenosis of the trachea. (Courtesy J.
Schoef)

On the left images of a child with wheezing and dyspnea.

The left PA comes off the right PA and runs between the esophagus (with
nasogastric tube) and the trachea.
Some of these patients also have long segment stenosis in the trachea because
of cartilagenous rings.

Patent Ductus Arteriosus

Patent Ductus Arteriosus

On the left an adolescent with a murmur.

On axial image and reconstruction the patent ductus arteriosus is seen.

487
The ductus arteriosus is the communication between the pulmonary artery and
the proximal descending aorta.
It shunts blood in utero from the right ventricle to the aorta to bypass the non-
functioning lungs.
On the first day of life there is a functional closure and an anatomic closure
with fibrosis in the first two weeks.
If it does not close these patients come to attention either with a murmur or
later with pulmonary hypertension.

488
On the left a young adult with a murmur.
The cardiologists are not interested in the flow direction, but just want to
confirm the diagnosis.

Notice the connection between the pulmonary artery and the descending aorta.

When the duct closes it may also calcify.

This a normal variant.

C) Pulmonary venous anomalies

489
 Partial Anomalous Venous Return

The most common features of Partial Anomalous Venous Return are listed in
the table on the left.

The anomalous veins drain into the following structures:

RUL: SVC association with sinus venosus-type ASD.

RLL: IVC (usually), sometimes Portal or Hepatic vein.
Can be isolated finding or combined with pulmonary hypoplasia (Scimitar
syndrome).
LUL: Brachiocephalic vein (isolated finding).
LLL: rare.

490
Right upper lobe anomalous vein drains into the superior vena cava.

Right upper lobe anomalous venous return

On the left a 2 month old, who is asymptomatic but has a murmur on physical
examination.
There is a connection between the SVC and a pulmonary vein, so this is an
anomalous venous return.

Pulmonary
venous return.
hypertension in a patient with partially anomalous pulmonary

All these partially anomalous pulmonary venous returns are left to right
shunts, but when small, they are clinically insignificant.
When there is a significant shunt, they may cause (late) pulmonary
hypertension as seen in the case on the left.

491
The chest film in this adult shows large pulmonary arteries and a large right
atrium and ventricle as a result of pulmonary hypertension.

Right upper lobe anomalous return (2)

On the left a patient with a murmur.

Study the images and then continue.

There is an anomalous return of the right upper lobe to the SVC.

At a slightly inferior level there is also an ASD.
Contrast is seen going almost immediately into the left atrium.
This type of ASD is called the sinus venosus-type ASD.

On the left a similar case.

Notice the anomalous return of the right upper lobe vein into the VCS and the
additional ASD at a lower level.

492
Right lower lobe anomalous return

On the left a right lower lobe anomalous return.

The vein drains into the IVC.
The anomalous vein gently curves to the right cardiophrenic angle and is
shaped like a Turkish sword ('Scimitar')

Right lower lobe anomalous venous return into the azygos vein.

On the left another right lower lobe anomalous return.

The vein drains into the azygos vein.
Upper lobe veins may also drain into the azygos vein.

493
On the left a 10 year old girl suspected of having pneumonia.
Study the images carefully, because there are three findings and then continue
reading.

The findings are:

Small right lung due to hypoplasia

Anomalous venous return
Right aortic arch

This patient has a scimitar syndrome and also a right arch.

So the lesson is, that when you see one anomaly, look for another one.

494
Scimitar syndrome

The features in scimitar syndrome are listed in the table on the left.

Scimitar syndrome with a hypoplastic right lung.

On the left another patient with a scimitar syndrome.

There is a hypoplastic right lung with mediastinal shift and there is anomalous
venous return.
Notice that on the coronal MIP you can nicely see the difference in
vascularization of the lungs with hypovascularity on the right.

495
Left upper lobe anomalous venous return into brachiocephalic vein.

Scroll through the images on the left.

Notice how the left upper lobe vein runs from the hilum cranially into the
brachiocephalic vein.

The differential diagnosis of a left upper lobe anomalous venous return into
brachiocephalic veins is a left Superior Vena Cava (SVC).
A left SVC however drains into the coronary sinus.

D) Systemic veins

Left Superior Vena Cava

Represents persistent left common cardinal vein

Passes anterior to left main bronchus and drains into dilated coronary sinus
0.5% of general population and 5% of patients with congenital heart disease
Small Right SVC in 90% of cases

496
Describe the images on the left and then continue reading.

On the left side there is a vascular structure, that runs inferiorly below the
level of the left hilum and enters into a dilated coronary sinus.
The diagnosis is left or double superior vena cava.

Left Superior Intercostal Vein

Left Superior Intercostal Vein.

This is an anastomosis between the accessory hemiazygos vein and the left
brachiocephalic vein.
It courses along the lateral margin of the aortic arch ('aortic nipple').
It is a normal variant and if you look for this structure you will frequently
notice it.
497
Catheters or pacemaker leads may course along left side of mediastinum.

On the left a patient with a left superior intercostal vein.

Notice the 'aortic nipple sign'.

Left Superior Intercostal Vein

On the left another example of a left superior intercostal vein.

It courses along the lateral margin of the aortic arch from the the accessory
hemiazygos vein to the left brachiocephalic vein.

Summary of left paramediastinal structures

Left VCS: from subclavian vein to coronary sinus

Anomalous LUL pulmonary vein: from left pulmonary hilum to brachiocephalic

vein.
498
Left superior intercostal vein: from accessory hemiazygos vein to left
brachiocephalic vein.

Azygos Continuation of IVC

Abcense of hepatic segment of IVC with azygos continuation.

IVC interrupted above level of renal veins.
Association with congenital heart disease and polysplenia.

Technique and Protocol

Ideally a 64 slice scanner is used, but even a 4-slice scanner will suffice for
studying vascular anomalies.
The technique for these anomalies in the chest is the same as we use for
pulmonary embolus detection.
Thin collimation is used in combination with a fast table speed in order to get
the highest resolution with the lowest radiation exposure.
Usually a pitch of 1.5 is used.
499
In children we preferably do not use thin collimation, because of the higher
radiation exposure, but these anomalies can be very small (voorbeeld dia 18),
so thin collimation is necessary.

mAs and kVp

In a child with a weight of less than 10Kg 40mAs will work in the chest.
In children with a weight more than 45 Kg adult protocols are used with 100
mAs or more.
In small children under 50 kg you can decrease the kVp to 80 and that works
very well in the chest.
Remember in the chest there is inherent contrast from the lungs and by
dropping the kVp you enhance this contrast.

500
On the left a 3-year old.

Non-breath hold images with 50mAs and 80 kVp on a 16 row detector.

Although the axial images are a little bit grainy, the reconstructions are just
fine.

Do these patients need sedation? Well most of the time they don't.
If you can get the patient on the table and they are relatively still, even if they
are breathing, you will get good studies.
If you can't get the patient on the table, because they prefer the floor, you've
got to sedate.
In about 20-25% of pediatric studies we use sedation.

501
If the catheter is not in the antecubital vein, hand injection is preferred.

502
Scan Initiation Time
Bolus tracking is used and the trigger is set at 120 HU.
This may not always work, because in small children the amount of contast
may be too small to trigger or due to breathing the cursor may fall to the
lungs.
If bolus tracking does not trigger, start the scan at 15 seconds.

503
Positioning the ROI

Ascending aorta for aorta and superior vena cava

Main PA for pulmonary arteries
Left Atrium for pulmonary veins

Coronal MPR (left), external volume rendering (middle) and internal volume
rendering.
504
Post-processing
Multiplanar reconstructions (MPR), volume rendered techniques (VRT) and
maximum intensity (MIP) are very helpful.
There is no role for shaded surface or mini-IP's.
On the left an external and internal rendering which provides in contrast to
MPR real 3D information.
In volume rendering the posterior view is preferred to get a good look at the
arch and descending aorta.

Thick slab maximal intensity projection to study the pulmonary vasculature.

If you want to study peripheral vessels you will need thick slab maximal
intensity projections.
For instance if you study arteriovenous malformations or discrepancy in lung
flow.

Thick slab coronal maximal intensity projection image in patient with scimitar
syndrome.

Notice that on the coronal MIP you can nicely see the difference in
vascularization of the lungs with hypovascularity on the right in a patient with
scimitar syndrome.

505
High
on sagittal
grade MPR.
coarctation of aorta not seen on axial images but clearly visualized

3D reconstructions are helpful when there are short focal lesions like
coarctation or when vessels course obliquely (figure).
Adding 3D reconstructions to axial images will increase the sensitivity from
90% to 100%.
On the left a 17-day old boy with minimal cyanosis, mild heart failure and
upper extremity hypertension.
On axial images you will have trouble diagnosis coarctation, because it is focal
and in the same plane as the axial image.

506
 Echocardiography

Introduction:
Echocardiography is the technique of examining the heart by the use of
ultrasound.
Sound is form of energy created by mechanical vibrations. It is
transmitted through different media in the same format of sound waves.
The units used when examining these sound waves are:
The hertz (Hz)- this is used to express the number of cycles per second
1Hz = 1 cycles/s;
The kilohertz (kHz) 1kHz = 1000 Hz;
The megahertz (MHz) 1 MHz = 1000000 Hz.
The range of sound frequency audible to human ear is 20 Hz to 20 kHz.
Ultrasound is a term used to describe sound waves whose frequency is
above the normal audible range, i.e. over 20khz.
When ultrasound transmission travel through human tissue, the part of
waves is absorbed, some passes through the tissues and others reflected
i.e. echoed back.
An echographic examination of the heart is based on the detection and
examination of this reflected echo.
The frequency of ultrasound wave for echo is between 2.5 and 3.5 MHz.
The reflected ultrasound is displayed as
o Amplitude modulation (A-mode)
o Brightness modulation (B-mode)
o Motion modulation (M-mode)
Transducers and scanners: The transducer contain piezoelectric element.
M-Mode imaging-single beam of ultrasound transmits and receives.
2-D imaging-Multiple ultrasound beam is required. They can be
Mechanical or electronic phased array transducers.
507
 Doppler effect-Measures mean blood velocity. It also distinguishes
Laminar from turbulent flow.
Echo techniques
Three echo methods are in common clinical usage:
Two-dimensional (2D) or cross-sectional
Motion or M-mode
Doppler-continuous wave, pulsed wave and colour flow
Motion or M Mode echo-is produce by transmission and reception of
ultrasound beam along only one line. It produces a graph of depth and
strength of reflection with time.
o Changes in movement,
o valve opening and closing,
o ventricular wall movement can be displayed.
o Size of chambers and thickness of wall can be measured.
To create a 2-D image, the ultrasound beam must be swept across the area of
interest. The transducer rotates the beam it produces through a certain angle,
either mechanically or electronically.
2D echo gives a snapshot in time of a cross-section of tissue. If these sections
are produced in quick succession and displayed on a TV screen, they can
show: real-time imaging of the heart chambers, valves and blood vessels.
Doppler echo uses the reflection of ultrasound by moving red blood cells.
The Doppler principle is used to derive velocity information .The reflected
ultrasound has a frequency shift relative to the transmitted ultrasound,
determined by the velocity and direction of blood flow. This gives
haemodynamic information regarding the heart and blood vessels.
It can be used to measure
o the severity of valvular narrowing (stenosis),
o to detect valvular leakage (regurgitation) and
o can show intracardiac shunts such as ventricular septal defects (VSDs)
and atrial defects (ASDs)
508
The 3 commonly used Doppler echo techniques are:
1. Continuous wave Doppler:
Two crystals are used-one transmitting continuously and one receiving
continuously.
This technique is useful for measuring high velocities but its ability to localize
precisely a flow signal is limited since the signal can originate at any point
along the length or width of the ultrasound beam
2. Pulsed wave Doppler:
This allows a flow disturbance to be localized or blood velocity from a small
region to be measured. A single crystal is used to transmit an ultrasound
signal and then to receive after a pre-set time delay. Reflected signals are only
recorded from a depth corresponding to half the product of the time delay and
the speed of sound in tissues (1540m/s). By combining this technique with 2-D
imaging, a small sample volume can be identified on the screen showing the
region where velocities are being measured. The operator can move the sample
volume. Because the time delay limits the rate at which sampling can occur,
there is a limit to the maximum velocity that can be accurately detected, before
a phenomenon known as aliasing occurs, usually at velocities in excess of
2m/s.
Continuous wave and pulsed wave Doppler allow a graphical representation of
velocity against time and are also referred to as spectral Doppler
3. Colour flow Mapping:
This is an automated 2-D version of pulsed wave Doppler. It calculates and
directions at points along a number of scan lines superimposed on a 2-D echo
image. The velocities and directions of blood flow are colour-encoded. Velocities
away from the transducer are in blue, those towards it in red. This is known as
the BART convention (Blue Away, Red Towards). Higher velocities are shown in
progressively lighter shades of colour. Above a threshold velocity, colour
reversal occurs (explained again by the phenomenon of aliasing). Areas of high
turbulence or regions of high flow acceleration are often indicated in green.
509
Echo windows and obtaining standard views.
Parsternal view-
o PLA- (Base of the heart to apex) 2nd to 4th intercostals space, left
sternal edge and
o PSA Same space and rotating the transducer to 90-degree heart is
seen cut in transverse section at level of MV, AV, LV papillary
muscle and LV apex.
Apical view-Over the apex four views
o 4-chamber heart shape view
o 5-chamber (including aortic outflow)
o 2 chamber long axis
Sub coastal view-under the xiphisternum
Suprasternal view for imaging aorta in coarctation
Rt parasternal view-for AV or ascending aorta
Sequences of an echocardiography examination-
Routine examination follows-
Parasternal window
Apical window
Subcoastal window
suprasternal window
Rt Parasternal window
A) Parsternal view-
PLA (Base of the heart to apex) 2nd to 4th intercostals space, left sternal edge
and
PSA Same space and rotating the transducer to 90 degree heart is seen cut in
transverse
section at level of MV,AV,LV papillary muscle and LV apex.
Long Axis View

510
Two dimensional
The structures and examined in this view are:
_ The mitral valve (MV)
_ The left ventricular outflow tract
_ The basal and the mid part of the interventricular septum (IVS)
_ The left ventricle (LV)
_ The right ventricle (RV)
_ The left atrium (LA)
The pericardium
_ A cross-section of the descending aorta.

511
Parasternal short axis views
A group of different views are obtained in the short axis configuaration by
manipulating the transducer to transect the heart at different levels. The
standard levels for echocardiographic examination in these planes are:
_ The mitral valve
_ The aortic valve
_ The papillary muscle
_ The apex.
Two dimensional
The structures that can be examined at this level are:
1) The mitral valve
_ Regions of the left ventricular wall at the MV level
_ The right ventricular cavity.
Mitral valve
_ Normal both leaflets can be seen in this view with:

512
_ The anterior leaflet (above) and the posterior (below);
_ The anterior leaflet is larger than the posterior;
_ The two leaflets separate in diastole giving the classic fish mouth appearance
and coapt in systole;
_ Planimetry of the MV area can be made from a frozen diastolic frame to
measure the MV orifice.

2) PSA: Aortic Valve Level at the Base of the Heart

This is a cross-sectional cut at the base of the heart. Different modes are used
for examination.
Two dimensional
Three valves (aortic, pulmonary and tricuspid) can be visualized in this view.
The left and right atria, interatrial septum and pulmonary artery can also be
visualized.

513
514
Aortic valve leaflets
The size, shape and number of the aortic valve leaflets can be seen in this
particular view.
_ Normal the valve normally consists of three leaflets which can be visualized
in diastole when they come together giving a shape that resembles the
Mercedes- Benz symbol. In normal conditions the leaflets will separate in
systole to a dimension similar to that of the actual aortic root.
RV Outflow Tract, Pulmonary Valve And Pulmonary Artery.
The RV outflow tract, pulmonary valve and pulmonary artery can be seen to
the right of the aorta in this view.
_ Normal the RV outflow tract appears superiorly and to the right in this view
where it tracks down to the pulmonary valve (PV) location. In most cases the
PV can be visualized but it may be difficult on occasions. One or two of the
three leaflets can be seen to the left of the aortic valve in this view.
The main pulmonary artery is seen distal to the pulmonary valve and
bifurcates into two branches (the right and left pulmonary arteries) giving what
is called the pair of trousers sign.
3) PSA: Papillary Muscle Level
This is a cross-sectional cut of LV at the papillary muscle level.
Two dimensional
_Normal
_ Morphology
oLV wall circular, cross-sectional representation of the LV cavity at the
PML is seen. This cut demonstrates the regional wall motion of the LV at
this level.
oPapillary muscles muscles are seen attached to the LV walls inside the
cavity.
_ Contractility and motion
oIn systole the LV walls become thicker and they move towards each
other, resulting in a smaller cavity.
515
oThe associated papillary muscles become thicker and move in a similar
way to the LV motion.
In diastole thinning of the LV walls is a feature of diastole caused by the
movements of LV walls in different directions.
oRegional wall motion abnormalities at the level of the papillary muscles
can be easily seen in this view and used to help evaluate overall
ventricular function.

4) PSA: Apical Level

Two dimensional
This can be used in LV regional wall motion assessment.
It can also help in estimating the extent of:
_ LV hypertrophy
_ LV dilatation
_ LV wall scars
_ The presence of thrombus

516
_ Apical aneurysm.

B) APICAL VIEWS
APICAL 4 CHAMBERS
The structures visualized are
LV
RV
IVS
LA
RA
IAS
MV
TV
Doppler blood flow is seen across MV & TV and abnormal intracardiac
communication.
LV Cavity
The LV cavity can be seen with the apex at the top of the screen and,
depending on preferred technique the cavity may be seen either to the left of
the screen or to the right.
Right ventricle Cavity
The RV cavity appears in the same orientation as the LV cavity and is the
smaller of the two. The RV can be also identified by the presence of the
moderator band near the apex.
IVS
Thickness
Motion (real time)
Continuity with anterior aortic wall
LA atrium
RA atrium
Interatrial septum is seen as the structure separating the two atria.
517
Mital Valve/ Tricuspid valve
Normal
_ In systole the MV is closed with the leaflets coapted at the same level of the
MV annulus
_ In diastole opening of the MV can be seen as the leaflets move freely into the
LV cavity

518
APICAL 5 CHAMBERS
The structures visualized by angulation of transducer is aortic valve and
ascending aorta. This is a good view for aortic stenosis and AR.

519
APICAL 2 CHAMBERS
The structures visualized by rotating the transducer on the cardiac apex are
2 chamber view can show different segment of the LV.

520
 C) SUBCOSTAL WINDOW
The subcostal window is an additional window in the echocardiographic
examination and it is particularly useful in the following situations.
_ When it is difficult to use other windows, for example, in patients with
emphysema or barrel chest.
_ In the detection of congenital abnormalities in newborn and young infants.
_ In visualizing the IAS; it is the best window to examine this structure. (The
ultrasound beam is perpendicular to the IAS in this view.).
There are two main groups of views in this window:
_ The four chamber view

521
_ The short axis views.

522
 D) SUPRASTERNAL WINDOW
With the transducer placed in the suprasternal notch and titled superiorly.
A longitudinal and a transverse cross sectional can be obtained.
_ Aorta (ascending, arch and descending)
_ Aortic pulmonary artery relationship
_ Left atrial appendage.
The views obtained in this window are:
_ Longitudinal cross section (Parallel to the aortic arch);
_ Transverse cross section (Perpendicular to the aortic arch.).

523
524
525
 VALVULAR HEART DISEASE ( Echo& cath)
MITRAL STENOSIS
Echocardiography:-
Indications
1. Diagnosis of MS.
2. Haemodynamic for severity mTMGr, MVA, PAP.
3. Assessment of RV size & function.
4. Assessment of valve morphology to determine suitability for
PBMV.
5. Diagnosis & assessment of concomitant valvular lesions.
6. Reevaluation of pt. with known MS with changing symptoms
/signs.
7. Assess for presence /absence of LA thrombus for PBMV /
cardioversion.
A) M-Mode Echo-
1957 Gustafson & Edler.
# Closure rate of AML Reduces in MS.
# Increases after commissurotomy.
# Reflection of rate of diastolic filling of LV.
# Any condition that reduces rate of diastolic filling reduces EF
Slope.
# Normal EF Slope 150 mm/sec.
# In MS 0-35 mm/sec.

526
2. Initial diastolic movement of PML.
# Normal Posterior leaflet moves away from anterior leaflet

527
 In diastole.
# MS PML moves anterior during early diastole, because
of commissural fusion.
3. Calcification of MV-
Thick, conglomerated, fuzzy or shaggy echoes duplicating MV
motion.
4. MT/ST Ratio-
# Nicoloi et al. - Best echo evidence of a calcified MV is obtained by
comparing the Maximum thickness of the MV echo (MT) with the
Maximum thickness of ventricular septum (ST).
A MT/ST Ratio 1.5/> predictive accuracy 87%.
CXR /Fluoroscopy 91%.
2D Echo most sensitive.
5. Maintenance of a fixed relation ship of the two leaflets of each other
throughout diastole.
6. Loss of A wave (In NSR).
7. Enlarged LA.
B) 2D ECHO-
1. Density-
Increased echo density of the leaflets due to thickening. Initially
involves margins of valve orifice along the leaflet commissure-
expand towards annulus.

528
2. Leaflet excursion-
Reduced diastolic excursion of the mitral leaflets.
Motion
Restricted motion of the leaflet tips due to commissural fusion.
3. Diastolic doming of AML in LV.
4. Immobility of PML.
5. MV orifice reduced Parasternal short axis view-Planimetry.
6. Parasternal long axis view-
AML classically has a Hockey stick deformity in diastole.

529
7. Parasternal short axis view
A Fish Mouth appearance of the opening of the MV.

8. Spontaneous echo contrast in LA (Smoke/SEC)-

530
C) Doppler Study-
1. Trans mitral pressure gradient
The velocity of the flow across the MV can be used to calculate the
pressure gradient,
Measured from continuous wave Doppler integration of diastolic
flow across the MV.
Instantaneous gradient between LA & LV measured by Bernoullis
equation-
Pressure Gradient = 4 x Velocity 2

The Mean gradient through out diastole can be accurately

calculated.
#MS Vs TMGr.
Normal 0 mmHg
Mild < 5 mmHg
Moderate 5 15 mmHg
Severe > 15 mmHg

531
 Fallacies:-
Highly dependant on R-R interval (Heart Rate).
6mmHg at HR 50/min MS+++.
6mmHg at HR 100/min MS+.
In AF avg 10 beats must be obtained for measurement of
Mean gradient.
Affected by CO, MR, Valve area.
The mean diastolic gradient by itself provides only a crude estimate
of valve area.
2. Mitral Valve Area-
Various methods,
@ Planimetry 2D Echo.
@ Diastolic time Method.
@ Continuity equation Method.
@ Proximal acceleration Method.
@ PISA Proximal Isovelocity Surface Area.
@ Gorlins Formula. Cath.

Diastolic pressure Time Method :-

# This is the time required for the instantaneous gradient

across the valve to fall from peak value to half of peak.
# As MS progressively more severe, the rate of fall of LAP during
diastole slows so that > time is required for the peak pressure to
be reduced to half.
# Simple measurement made by a computer installed in echo
eqp.
$ Diastolic pressure time measurement & MVA-

532
 I---------DT----------I
Derived from Trans mitral flow velocity curve obtained from
Doppler echo using the Deceleration Time (DT).
DT measured by extrapolating the deceleration of early diastolic
flow to the base line & measuring the time from peak mitral
inflow velocity to the point of intersection of the deceleration of
flow at the baseline.
Diastolic Pressure time = DT x 0.29.
MVA = 220/ Pressure time (in MS).
- Adv.-
! Sufficiently accurate for clinical use.
! Independent of
. Preceding cycling.
. Arrhythmias.
. CO.
. MR.

- Fallacies-
Affected by other factors that alters the gradient between the
LA & LV,
! Non compliant LV-
. Rate of increase of ventricular diastolic pressure will
increase P time.
. Shortens the deceleration time (DT).
. Over estimate MVA.
533
 ! AR
. Increases the rate of diastolic filling of LV.
. Shortening of the Pressure time.
! Post valvotomy/Repair/PBMV (Abnormal LA Compliance)-
. Not valid for several days.
. Because reduction in LAP without a commensurate
improvement in LA compliance.
. Pressure > 300 msec MS+++.
Continuity Equation Method
. In the absence of valve regurgitation & intracardiac shunt
the amount of blood flow across the MV equals the amount
of blood flow across the Aortic valve Continuity principle.
Amount of blood flow
Across valve = Valve area X Time velocity integral
(TVI)

MVA = AVA X AoTVI / MiTVI

. Inaccurate in presence of MR.

PISA Proximal Isovelocity Surface Area.

Based on calculation of volumetric flow through MV from colour
flow images of the convergence of flow proximal to the stenotic
valve.

# MS Vs MVA

Grade MVA Symptoms

Normal 4 6 cm2 None
Trivial > 2.5 cm2 None
Mild 1.5 -2.5 cm2 DOE
534
 Moderate 1 1.5 cm2 PND & Pulmoric Edema
Severe < 1 cm2 Orthopnoea
Critical < 0.5 cm2

D) TEE
1. MV, LA, LAA thrombus -100% accuracy.
2. May detect spontaneous echographic contrast in LA/LAA appears
as a multitude of tiny echoes with a swirling motion often
described as smoke This phenomena is probably due to low
blood flow velocity with red blood cell rouleux formation.
- MS with AF. - Reduced LAA contractility
- Large LA. - Smaller MVA.
- LAA thrombus. - Absence of Mod-Sev MR.
3. Doubt about presence /severity of MR.
4. As a guide to placement of catheter for the atrial Trans septal
puncture.
Wilkins et. al.s Echo Score for Modality of treatment.

1 2 3 4

Leaflet Rigidity Mobile Valve - - Immobile Valve

Leaflet Thickening Thin - - Sev. Thickening

Valvular Calcification No bright echoes - - Multiple Bright

Subvalvar Disease Sparse echoes - - Multiple Thick

Score =/< 8 BMV/CMV Excellent immediate & long term results.

Score >8 Less impressive results of BMV/CMV- MV Repair /MV Replacement.
535
Schematic presentation of Wilkins Scoring system
1. Leaflet Mobility

I Highly mobile valve with restriction at the tip of the leaflet.

II Mid portion & base of the leaflets have reduced mobility.
III Valve leaflet move forward in diastole mainly at base.
IV No / minimal forward movement of leaflets in diastole.
2. Leaflet thickening
I Normal 4- 5 mm thick.
II Mild leaflet thickening.
III Diffuse thickening 5- 8 mm.
IV Marked thickening of all leaflet tissue - .8 10 mm thick.
3. Valvar calcification
I Single area of increased echo brightness.
II Scattered areas of brightness confined to leaflet margins.
III Brightness extending into mid portion of the leaflets.
536
 IV Extensive brightness through most of the leaflet tissue.
4. Subvalvar thickening
I Minimal thickening of chordal structure below the valve.
II Thickening of chordae extending upto 1/3rd of chordal length.
III Thickening extending to the distal 3rd of the chordae.
IV Extensive thickening & shortening of all chordae extending to the
PML.
Limitations of Wilkins Scoring system
Assessment of commissural involvement is not included
Limited in ability to differentiate nodular fibrosis from calcification.
Doesnt account for uneven distribution of pathologic abnormalities.
Frequent underestimation of subvalvular disease.
Doesnt use results from TEE or 3D echo.
Cormiers method

Cardiac Cath.
Indications
Clinical & Echo diagnosis not confirmative.
CAG required.
537
 Associated congenital lesions.
To perform PBMV in properly selected pt.
Data acquired
Confirmation & quantification of MV obstruction.
Detection & quantification of MV regurgitation.
Detection of complications of MS (PVD, RVF, TR).
Status of Aortic Valve.
Assessment of LV/RV function.
Coronary circulation.
MVA
Normal MVA is 4 cm2, No gradient across valve.
Richard Gorlin & father S.G. Gorlin 1951,
Hydraulic formulas of Flow across the mitral valve &
simultaneous pressure gradient across MV (LA & LV Mean
Pressures).
MV flow (ml/sec of diastole) = CO (ml/min) / HR x DFP
Normal mitral flow is 150 ml/sec of diastole.
CO increases MV flow increases.
HR increases MV flow reduces.
LV diastolic mean 5mmHg.
LA diastolic mean measured by trans-septal catheter / PCWP.

MVA (cm2) = CO (ml / min) / 38 LAdm LVdm x HR x DFP.

MVA = MV Flow (ml/sec of diastole) / 38 LAdm LVdm.

Pitfalls
. Associated MR under estimate MVA (Because of Regurgitant flow).
. For MVA measurement CO/HR/DFP/Pressure gradient should

538
 be simultaneous.
. PCWP is used as LAP- can be confirmed by withdrawing blood
that is fully saturated.
Other parameter by Cath.
If exercise Doppler capabilities not available.
1. Increased Trans-Mitral Gradient - > 15 20 mmHg.
2. Increased PA Pressure - > 60 mmHg.
3. Increase in PA Wedge Pressure - > 30 mmHg.
MITRAL REGURGITATION
Echocardiography : -

Indications : -

1. Severity of MR & LV function.

2. Mechanism & Etiology of MR.
3. Annual surveillance of LV function.
4. Post surgery MVR/MV Repair Evaluation.
5. TEE
. Intra op. to establish the anatomic basis for MR & to guide
repair.
. Evaluation of MR Severity, Mechanism, LV function.
Major tool in assessment of MR.
1. Morphologic lesions of MV.
2. Degree of MR.
3. Ventricular & Atrial function.
A) Morphology of MV :-
a) Rheumatic MR
@ Thickening of leaflets at tips & chordae.
@ Reduced mobility of PML.
@ AML mov. Normal /Doming if asso. Comm. fusion.
539
 @ Valvar prolapse rare except Ruptured chordae / Active Rh.
Carditis.
b) Degenerative MR
@ Valvar prolapse defined by the passage of valvar tissue
beyond the plane of the annulus. Long axis view.
Involves one / both leaflets, PML >.
. Initial jet
Central equal bileaflet prolapse.
Inferior & External AML involvement.
Superior & Medially PML involvement.
. Flail leaflet diagnosed on basis of leaflet co aptation in the
regurgitant area. TEE > useful.
. Ruptured chordae TEE > useful.
@ Diffuse myxomatous changes Diagnosed by diffusely thickened
leaflets & excessive valvar tissue.
@ Mitral annular calcification Limit the possibility of conservative
surgery.
c) Endocarditis MR
@ Flail leaflets TEE.
@ Perforation of leaflet, > difficult to diagnose.
@ Mitral annular abscess rare, TEE.
@ Vegetations seen on the leaflets & on the ruptured chordae
TEE >.
d) Mitral annular dilatation
@ Ischemic / functional MR.
@ Regional / Global LV dysfunction.
@ Normal / mildly sclerotic leaflets.
@ Apical displacement of AML with tenting is due to abnormal
tension on the principal chordae & results in combination with

540
 the annular enlargement, incomplete leaflet coaptation with a
central jet of MR.
e) Others
1. Obstructive Cardiomyopathy-
@ Systolic anterior motion of mitral valve is asso. with a
loss of coaptation & the jet of MR is directed inferiorly &
externally.
@ If jet is directed medially & superiorly, suspect asso.
Ruptured chordae of PML.
2. Eosinophilic heart disease
Characteristic infiltration of region below the PML by
thrombus can be demonstrated with immobilization of
the PML & resultant MR.
B) Severity of MR
a) Clinical
@ Systolic thrill.
@ Intensity of Murmur.
@ S3.
@ Diastolic rumble.
b) Laboratory
1. Qualitative :
@ Jet Area
Up to 4 cm2 Mild.
4 7 cm2 Moderate.
= /> 8 cm2 Severe.

@ Systolic pulmonary vein flow reversal

541
 01+ 2+ 3+

@ Dense contrast in LA.

2. Quantitative :

MR severity Regurgitant Fraction (%) RF Orifice Area Colour

Doppler

Mild < 30 = /< 0.1 < 20% of LAA.

Modearte 30 50 > 0.1 -0.3 20 -40% of LAA.

Severe > 50 > 0.3 > 40% of LAA.

Vena Contracta
Smallest jet width immediately below the regurgitant orifice - > 0.5 cm MR
+++.

542
MR severity Apical 4 chamber view.

RV LV

1 + Trivial

2 + Mild
RA

3 + Moderate

4 + Severe
C) LV & LA Function
Guided M- mode diameter is used for the assessment of
1. LV size LVSD & LVDD.
2. LV mass.
3. Wall Stress.
4. LA size.
5. EF.
LV Volume
Ellipsoid formula Req. measuring length of
ventricle & its diameter at base.
Simpson formula Req. measuring length of
ventricle from apical view.Predetermined disc like
# sectional segment from base to apex.
LV function ( Systolic )

543
 Wall motion & degree of wall thickening during
systole.
Hyperkinetic, Hypokinetic, Akinetic, Dyskinetic.
EF
EF = LVDD2 LVSD2 / LVDD2 X 100
ESD - < 45 mm Normal
45-50 mm Mild
50-55 mm Moderate
>55 mm Severe
EF - > 60% Normal
50-60% Mild
30-50% Moderate
< 30% Severe
$ Predictors of poor post operative out come in chronic MR
# EF 60%
# ESV Index 60 ml/m2
# ESD 45mm
# ESP / ESVI 3.4 mmHg/ml/m2
# ESSI (wall stress index) 195 mmHg
# ESS /ESVI 1.72.4 (kdynes/cm2)/ml/m2
# dp /dt 900 mmHg /sec.
Cardiac Cath : -
Indications
Non invasive tests are inconclusive regarding severity of MR, LV
function or the need for surgery.
When there is a discrepancy between clinical & non invasive
finding regarding severity of MR.
CAG required in
1. Angina or previous MI.
2. > / = 1 risk factor for CAD +.
544
 3. Ischemia is suspected as etiologic factor.
Parameters on Cath
Hemodynamic status
Low CO, Increased LAP, Large V wave.
Severity of MR
@ I Mild Opacification of only of the LA adjacent to the MV.
@ II Moderate Opacification of the entire LA, Usually clearing on
the succeeding beat.
@ III- moderate-Severe Dense opacification of the LA for 2-3 beats
before clearing begins.
@ IV Severe LA opacification > dense than the LV, going into the
PVeins & taking several beats to clear.
LV function
LV volume, Duration of MR, Etiology, LVSV, EF, RWMA.
Coronary anatomy RWMA.

AORTIC STENOSIS

Echocardiography : -

Indications : -

1. Diagnosis & assessment of severity of AS.

2. Assessment of LV size, function, & hemodynamics.
3. Re evaluation of pt. with changing symptoms & signs.
4. Assessment of changes in hemodynamic severity & ventricular function
in pregnancy.
5. Reevaluation of asymptomatic pt. with AS+++.

A) M Mode Echo Shows

545
1. Post stenotic dilatation.
2. LV Mural thickening.
3. Dilatation of LV cavity in pt. with myocardial failure.
4. Abnormal valve leaflets.

@ Normal Aortic valve : -

. Two aortic leaflets are seen to separate & move towards the aortic
wall in systole & to come together in diastole.
. The systolic echoes are two thin parallel lines & the diastolic echo
is a single line roughly midway between the aortic walls.
. Fine oscillations esp. evident in the anterior leaflets.

AoAW

AV

AoPW

Normal Parallelogram

@ Aortic sclerosis : -
Thickening, sometimes calcification of the aortic cusps but without
systolic obstruction.

546
 The echoes of two aortic leaflets are seen in apposition with the
aortic walls in systole producing a fully open Box demonstrating
the absence of stenosis.
In diastole, the single thin line of normal leaflet closure is replaced
by multiple heavy echoes, corresponding to the thickened leaflets.
@ Bicuspid Aortic valve : -
Diastole The eccentric echo of aortic valve closure that lies much
closure to the anterior wall of the aorta than to the posterior wall of
aorta.
The Eccentricity Index (The Ratio of aorta radius to the distance
between aortic valve closure & the closest aortic wall) is 3.5 or about 3 times
the upper limit of normal.
Normal Index 1.0 1.2
of BAV - > 1.3
Range 1.5 - 4.5
Systole Because the posterior leaflet does not come closure to the
Aortic post. wall the valve opening is also eccentric & smaller than
normal.
The multiple diastolic echoes demonstrate leaflet thickening.

@ Valvar Aortic stenosis : -

. Thickened echoes of Av through out systole & diastole.

. The small Box produced by movement of leaflets towards
the Aortic anterior wall during systole.
. Multiple echoes during diastole.
B) 2 D Echo : -
@ Views
Long axis
. Outflow tract.
547
. Valve maximum separation of aortic cusps.
. Ascending aorta.

548
Short axis
. Valve orifice Direct measurement of area.

549
550
 @ Valve Anatomy
1. Rheumatic AS
. Presence of mitral valve involvement.
. Commissural fusion of leaflets.
2. Calcific aortic valve disease
. Increased echogenicity.
. Reduced systolic motion.
3. Mild disease ( Aortic sclerosis )
. Calcification in base of leaflets.
. NCC involves > often initially.
C) Doppler study : -
@ Severity of stenosis
a) Jet velocity
. Apical & Rt. Parasternal view.

551
 . Velocity increases in proportion to stenosis.
. Severity Velocity (meter / sec)
Normal valve 1
Mild AS > 2.5
Moderate AS 34
Severe AS >4
b) Maximal & Mean Trans aortic pressure gradient
. Calculated based on Bernoullis relationship between Flow Velocity (V) &
Pressure Gradient (P) across an orifice,

P = 4 V2
. Maximal gradients are calculated using the maximum velocity.
. Mean gradients are calculated by averaging the instantaneous gradient
over the systolic ejection periods.
. Valve Status Mean gradient (mmHg)
Normal 0
Mild AS < 30
Moderate AS 30 -50
Severe AS > 50
c) Aortic valve area
. Calculated from Doppler data using Continuity Equation,
Stroke Volume just proximal to & in the narrowed orifice must be equal,
SV prox. = SV orifice
Stroke volume is the product of the cross sectional area (CSA) & the Velocity
Time Integral (VTI) of flow at that site,
Using LVOT for proximal SV & AV for stenotic orifice.

. AVA (CSA AV) = CSA LVOT x VTI LVOT / VTI AV

. Parasternal Long axis & Apical view

552
 LVOT diameter Parasternal long axis view.
Velocity Apical view.

d) Other Potential measures of severity of stenosis

. Ventricular stroke work loss.

. Valve Resistance.
. Simplified indices of severity of stenosis.

@ Co existing valve diseases

. AR Pulsed / Cont. wave Doppler AR jet velocity, Holodiastolic flow

reversal in descending aorta.
. MR.

@ LV response to pressure overload.

@ LVOT obstruction Site of obstruction with pulsed Doppler.

Cardiac Cath. : -

Indications : -

1. Coronary angiography before AVR, pt. at risk for CAD.

2. Assessment of severity of AS in symptomatic pt. before AVR.
3. Non invasive tests are inconclusive / discrepancy with clinical findings.

Parameters : -

1. To confirm diagnosis of LVOTO.

553
 2. Localization obstructing lesion.
3. Estimation of severity of lesions.
4. Determination of the + / - of other valve lesions.
5. Assessment LV functional status.
6. Evaluation of coronary circulation.

AORTIC REGURGITATION
Echocardiography : -
Indications : -
1. Confirm presence & severity of acute AR.
2. Diagnosis of chronic AR with equivocal physical findings.
3. Assessment of etiology of AR (Valve & Ao root size morphology).
4. Assessment of LV hypertrophy, Dimension (Volume), & systolic function.
5. Semi quantitative estimate of severity of AR.
6. Reevaluation of pt. with changing symp.
7. Reevaluation of LV size & function in asymp pt. with severe AR.
8. Reevaluation of asymp pt. with AR & Enlarged aortic root.
Morphology : -
1. Abnormality of AV, MV & LV.
2. In absence of MV disease AR demonstrates,
$ A broad band (3- 4 mm wide) of diastolic flutter or,
$ Vibration (20 70 Hz) of the AML.
Increasing severity increases diastolic fluttering.
3. Other abnormality of mitral valve echo in AR are,
$ Rapid diastolic closure rate.
$ MV closure prior to the onset of QRS complex.
4. Fluttering of AML asso. with PML & IVSeptum.
5. Aortic root dilated.
6. Coarse diastolic oscillations of AV leaflets.
7. LVEDD increases in AR. LVVO pattern.
554
 8. LV hyperdynamic wall motion. LVVO pattern.
9. Reduced myocardial performance.

Severity of AR : -
Parameters Mild Moderate Mod. Sev. Severe
1. Jet height in LVOT 24% 25-45% 46-64% > / = 65%
2. Pressure Time (m/s) > 500 350 500 200 350 < 200
3. Regurgitant Fraction < 20% 20 35% 35 50% > 50%
4. Vena contracta I--------< 5 mm----------------I > / = 6 mm
5. ERO > / = 30mm
6. Regurgitant volume > / = 60 ml.

Trivial

Mild

Moderate
Severity of AR by Echo.

Severe

555
LV Function : - LV dysfunction.

Parameters Normal Mild Moderate Severe

1. EF (%) 50 -60 40 -50 25 40 < 25

2. LVSD (mm) < 45 45 -50 50 -55 > 55
3. LVDD (mm) < 60 60 -70 70 -75 > 75

Indications for Exercise Testing of Chronic AR : -

556
 1. Assessment of functional capacity & symptomatic responses in pt.
H/O equivocal symp.
2. Evaluation of symp.before participating in athletic activities.
3. Prognostic assessment before AVR in pt. with LV dysfunc.
Indications for Radionuclide Angiography : -
1. Initial & serial assessment of LV volume & function at rest with
suboptimal /equivocal echo data.
2. Assessment of LV volume & function in asymp pt. with mod-sev AR when
echo evidence of reduced LV function is suggestive but not definitive.
3. Confirmation of subnormal LVEF before recommending surgery in asymp
pt. with borderline echo evidence of LV dysfunction.
4. Assessment of LV volume & function in mod-sev AR when clinical & echo
data are discordant.
Cardiac Cath : -
Indications
1. Coronary angiography before AVR with risk of CAD.
2. Assessing severity of AR when non invasive tests are inconclusive.
3. Assessing LV function when non invasive tests are inconclusive or
discordant with clinical findings.
Parameters
1. Hemodynamic measurement
$ LV dysfunction Increased LV filling pressures
. LV diastolic mean.
. LAP.
. PCWP.
. PA diastolic pressure.
$ Low CO.

2. LV gram in AR

557
 $ Increased ED volume.
$ Abnormal roundedness (increased eccentricity).
$ Reduced regional & global systolic contractile function with resultant
decrease in EF & abnormal apex base shortening.
$ Abnormally elevated ESVolume & abnormal ESPressure Volume
relationship.
3. Severity of AR
Grade Findings

I Trace Slight regurgitation with opacification only of the

ventricle adjacent to the aortic & MV.

II Mild Moderate opacification of entire LV, clearing on

successive beat.
III Moderate Dense opacification of LV for 2 3 beats before
clearing.
IV Severe LV opacification denser than Aorta & lasting
several beats after the end of the injection.

Echocardiography for Congenital Heart Disease

Introduction
According to anatomy and surgical repair, congenital anomalies are classified
as simple anomalies and complex anomalies.
Using segmental analysis to describe abnormal cardiovascular connections
Most congenital heart malformations occur with normal connections of the
cardiac chambers, but the chambers should be analysed sequentially before
the specific lesions are highlighted. Sequential segmental analysis of the heart
enables complex congenital heart malformations to be described in a simple
fashion.

558
First, the apex of the heart should be determined from standard subcostal
view.
From this view the diagnosis of dextrocardia (apex is pointing to the right),
levocardia (apex is pointing to the left) or mesocardia (apex is pointing to the
middle) can be established.
All hearts, normal or abnormal, are formed of three segments the atria, the
ventricular mass, and the arterial trunks.
The sequential approach begins by determining the position of the atrial
chambers. Thereafter, the atrioventricular (AV) connection and the
ventriculoarterial (VA) connection and relations are analysed.
a) Atrial arrangement:
There are four possible atrial arrangements:
Usual atrial arrangement (also known as situs solitus, when the
morphological right atrium is on the right and the morphological
left atrium is on the left),
Mirror-image arrangement (also known as situs inversus, when
the morphological right atrium is on the left and the morphological
left atrium is on the right),
Left or right atrial isomerism (also known as situs ambiguous,
where there are bilateral right or left atrial morphologies) .
The right or left atrial morphology is decided by the appendages.
The right atrium has a triangular appendage and left atrium has a
narrow tube-like appendage. However appendages are difficult to
visualize by transthoracic echocardiography especially in adult
patients.
Indirect methods need to be used. The locations of the abdominal
aorta and the inferior caval vein (IVC) relative to the spine can
provide clues to the atrial arrangement.
Atrial situs follows abdominal situs in about 70-80% of cases.
From a standard subcostal view, with the probe pointing at a
559
 right angle to the spine, the abdominal aorta (pulsatile, red colour
Doppler) and IVC (nonpulsatile, blue colour Doppler) can be
visualized.
o When aorta is to the left and IVC is to the right of the spine,
there is abdominal situs solitus and corresponding atrial
situs solitus (normal arrangement).
o When the aorta is to the right and the IVC is to the left of
the spine, this arrangement corresponds to situs inversus.
o In isomerism, the great vessels lie on the same side of the
spine.
In left isomerism, the inferior vena cava lies posterior
to the aorta and is interrupted and continued via a
hemiazygos vein in the majority of cases.
In right isomerism, the IVC is anterior to the aorta.
b) Atrioventricular connection: AV connections can either be
biventricular or univentricular.
Biventricular connections can either be concordant, when the
morphologic right atrium empties into the morphologic right
ventricle and the morphological left atrium empties into the
morphologic left ventricle, or
Discordant, when the morphological right atrium empties to the
morphological left ventricle and the morphological left atrium
empties to the morphological right ventricle.
In contrast, univentricular atrioventricular connection describes
hearts where only one ventricle is connected to the atrial chamber.
Depending on the morphology of the ventricle, it can be described
as a double inlet right, left, or indeterminate ventricle.
The morphological right ventricle has following features that distinguish it from
the morphological left ventricle:
Coarse trabeculations at apex
560
 Moderator band
The septal leaflet attachment of the tricuspid valve is more apically
positioned when compared to the mitral valve
Tethering of the tricuspid valve septal leaflet to the septum
The characteristics of a morphologic left ventricle are:
Smooth trabeculations at apex
No moderator band
No septal attachment of the mitral valve
Higher (more basal) insertion of the mitral valve compared to the
tricuspid valve
The feature of a solitary and indeterminate ventricle are:
More coarse trabeculation than the morphological right ventricle
There is no other chamber in the ventricular mass
(c) The ventriculoarterial connection:
There are four possibilities:
o Concordant (connection to an appropriate ventricle),
o Discordant (connection to an inappropriate ventricle),
o Double-outlet (one arterial trunk and more than 50% of the other
arterial trunk are connected to the same ventricle, be it of right
ventricle, left ventricle or indeterminate morphology) and
o Single outlet (common or solitary arterial trunk).
The aorta and pulmonary trunk are distinguished by their branching patterns
and origins of the coronary arteries.
The pulmonary artery branches into left and right pulmonary arteries.
The aorta has coronary arteries arising from its root and head and neck vessels
from aortic arch. A common arterial trunk has a single arterial valve and
always gives rise to at least one coronary artery, at least one pulmonary artery
and some of the systemic arteries.
Simple Anomalies
Atrial septal defects (ASD)
561
Fig 1 Assessing ASD

562
 Fig 3

Secundum ASD

3D image of secundum ASD and image during transcatheter occlusion

Fig 4

TOE secundum ASD

LA

RA

Transesophageal longitudinal view of the atria Colour flow image from the same view demonstrating
demonstrating an ostium secundum defect. left-to-right shunting across the ASD

563
Fig 5
Primum ASD

LV

RV

RA LA

Apical four chamber view demonstrating Colour Doppler flow image from same view
a primum atrial septal defect illustrating left-to-right shunt across the primum
atrial septal defect

Fig 6

Parasternal short axis view demonstrating

tri-leaflet left atrioventricular valve in a patient
with a primum atrium septal defect

564
Fig 7

Primum ASD

LA Subcostal four chamber view

demonstrate an large primum atrial
septal defect which is located at the low
RA LV part of normal atrial septum and the
junction with atrioventricular valve.

RV

Fig 8

Primum ASD repaired

LV

LA

Apical four chamber view of patient with a Colour Doppler flow mapping of the same
primum ASD repair. Note the thickened patient demonstrating severe left AV valve
left AV valve leaflet and markedly dilated regurgitation.
left atrium

565
Fig 9

SVC type ASD

Apical four chamber view
showing a sinus venous defect
of the superior vena caval type

Fig 10

SVC type ASD (TOE)

LA

RA

Transesophageal longitudinal view of the atria Colour flow image from the same view
demonstrating a sinus venousus defect of the demonstrating left-to-right shunting across the ASD
superior vena caval type.

566
Fig 11
Sinus venousis ASD (SVC type)

Transesophageal longitudinal view of the atria demonstrating a sinus venosus defect of

the superior vena caval type.

This is one of the most common defects in the Congenital Heart Disease . When
assessing patients with ASDs, the following features should be considered:
a) Type and location of the ASD
Secundum ASD (most common, 60%): The majority of ASDs are of this type. The
defect is localized centrally in the intra-atrial septum. There can be multiple
defects and the defect may be fenestrated. This is best viewed in a modified
para-apical 4chamber view and the subcostal view.
Primum ASD (20%): This defect is less common and forms part of the spectrum
of atrioventricular septal defects. It is often associated with an abnormal left
atrioventricular valve (trileaflet left-sided AV valve). Significant AV valve
regurgitation is often seen in adult patients. This is best viewed in a modified
para-apical 4chamber view and the subcostal view.
Sinus venosus defect (SVC 15%, IVC 2-3%): These defects are positioned outside
the limbus of the fossa ovalis, on the right septal surface next to the drainage
site of either the superior or inferior vena cava. Partial anomalous venous
567
return of the right upper pulmonary vein is a common association. This is best
viewed in a modified para-apical 4chamber view and the subcostal view.
Coronary sinus defect (unroofed coronary sinus, 1-2%): This defect is located in
the wall which separates the coronary sinus from the left atrium (LA). It may be
fenestrated or completely absent. An enlarged coronary sinus with drop out
between the LA and the coronary sinus is seen. The best imaging view is the
4 chamber view with slight posterior angulation.
While transthoracic echocardiography confirms the diagnosis of ASD
particularly from the parasternal short axis, apical four chamber and
subcostal views, it may not always be conclusive.
A transoesophageal echo utilises different angles and echocardiographic
windows and usually demonstrates clear images of the location, size and
relations of each of these different defects.
Colour flow Doppler demonstrates left to right shunts at atrial level, and right
heart contrast studies using agitated saline help to assess for any shunt
reversal.
b) Haemodynamic effects
Significant left-to-right shunting may result in right heart dilatation. Some
patients may even develop pulmonary hypertension. The following anomalies
are features of significant shunting:
Right atrial and ventricular dilatation
Abnormal 'paradoxical' septal motion due to volume overload
Elevated right ventricular pressure
The left to right shunt can be expressed as Qp:Qs and calculated using
the continuity equation:

RVOT-right ventricular outflow tract, LVOT- left ventricular outflow tract, VTI -
Velocity time integral
568
c) Interventional closure of ASD
At present, only secundum ASDs can be closed percutaneously by occluder
device. Transoesophageal or intracardiac echocardiographic guidance is used
during interventional closure of secundum ASDs. Before device closure, the
adequacy of the ASD rim needs to be defined. 3D TOE is increasingly used for
this purpose.
d) ASD post closure
After surgical or interventional closure, the following features need to be
assessed:
Presence of residual shunt
Position of the device relative to other cardiac structures (figure 5)
RV size
Presence of pulmonary hypertension
AV-valve regurgitation (especially after repair of an ostium primum ASD)
Ventricular septal defect (VSD)
a) Classification of VSD
A VSD is a defect in the septum that separates the left and right ventricles.
VSDs can simply be classified into three anatomic groups: perimembranous
defects, muscular defects, and doubly committed or juxta-arterial defects.
i. Perimembranous VSD: This is the most common type. The defect is located in
the area of the membranous septum, or on its border. A defect may extend so
that it opens from the subaortic area mostly into the inlet, outlet or trabecular
portion of the right ventricle, or it can be large and confluent. The parasternal
short axis and apical four chamber views demonstrate the proximity of
the VSD to the tricuspid valve, while parasternal and apical long axis views
show its relation to the aortic valve. Perimembranous defects extending to
the inlet portions are best shown in the apical four chamber view.
ii.Muscular VSD: This type of defect is characterised by its muscular border and
can be located at either the inlet, outlet or trabecular area of the ventricular
septum. They can be singular or multiple. The entire length of the septum
569
should be carefully scanned before excluding the presence of a muscular septal
defect. Best shown in the apical four chamber view.

iii. Doubly-committed and juxta-arterial VSD: This rare type of VSD is

characterised by the fibrous continuity between the adjacent leaflets of aortic
and pulmonary valves. Superiorly, these defects are roofed by the arterial
valves while postero-inferiorly the margin may be muscular or
perimembranous. The defect can be partially or completely closed by the
herniation of the aortic sinus. This commonly creates various degrees of aortic
regurgitation. A doubly-committed VSD is best seen from the parasternal
position with the transducer slightly rotated counterclockwise from the
long axis view. Due to the location of this type VSD, left to right shunt flow
directly enters into pulmonary artery. If left untreated, patients develop
pulmonary hypertension very early in life.
b) Defect size and hemodynamic significance
The VSD should be measured in at least two dimensions. The defect can
be described as small (<5 mm), moderate (5-10mm) or large (>10mm).
Large left-to-right shunting results in left atrial and ventricular
dilatation. LA size, volume and LV dimensions should therefore be
measured.
A restrictive VSD has a significant peak instantaneous gradient (> 75
mmHg) and is not associated with LA, LV dilation or pulmonary
hypertension. A non-restrictive VSD will have a small peak
instantaneous gradient (<25 mmHg) and have significant LA / LV
dilation with pulmonary hypertension
A VSD can be associated with pulmonary arterial hypertension (PHT). RV
pressures can be estimated with continuous Doppler interrogation of the
gradient across the VSD:

570
 Significant pulmonary vascular disease may result in bidirectional or
predominantly right-to-left shunting across the VSD (Eisenmenger's
syndrome)
c) Associated anomalies
Important associated lesions include
Prolapse of the aortic cusp with progressive aortic insufficiency and
Development of a double-chambered right ventricle from hypertrophy of
RV muscle bands.
Muscular defects and some form of perimembranous defects can now be closed
by percutaneous means. Most defects are closed surgically if indicated.
Following interventional or surgical closure, the following features need to be
assessed:
Residual VSDs
Pulmonary artery pressure
Aortic insufficiency

Fig 12

Ventricular septal defects

PA Doubly committed subarterial defect

Muscular defect

RA

Perimembranous defect

RV

Diagram of the ventricular septum seen from right ventricular aspect, showing the
positions of various types of ventricular septal defects.

571
Fig 13
Small perimembranous VSD

Echocardiogram demonstrating
shunting through a perimembranous
ventricular septal defect. Parasternal
RV long-axis view with the transducer
tilted toward the right ventricular
inflow.

LV

LA

Fig 14

Large perimembranous VSD with PH

LV
MPA
RV
AO

LA
RA

Apical four chamber view demonstrating a large Parasternal short axis view from same patient
perimembranous inlet ventricular septal defect showing significantly dilated main pulmonary
artery, indicating the presence of pulmonary
hypertension

572
Fig 15
Muscular VSD

Apical five chamber view

demonstrating a small muscular
outlet ventricular septal defect
(arrow)

LV
RV

AO

Fig 16

Doubly committed VSD

RV PA
vsd

Ao

RA
LA

LA
Modified Parasternal short axis view demonstrating the presence of doubly committed
subarterial ventricular defect (arrow). Note there is no septal tissue between aortic and
pulmonary valve.

573
Fig 17

Residual VSD
Parasternal long-axis view
showing a residual VSD. The
RV echogenic patch on the septum
suggests a previous repair.

LV
AO

LA

Atrioventricular Septal Defect (AVSD)

The hallmark of this defect is the common atrioventricular junction guarded by
a common valve. The abnormal junctional anatomy is associated with an
elongated and anteriorly positioned aortic outflow tract. The atrioventricular
valve is abnormal, having a five leaflet configuration, two of which bridge the
ventricular septum anteriorly and posteriorly, and two other leaflets are
exclusive to the right ventricle. The bridging leaflets together with the
remaining leaflet guard the left ventricular inlet in a trileaflet configuration.
a) Classifcation:
ASD represents a spectrum of lesions and is usually divided into following
the types:
Partial AVSD: is similar to a primum ASD.
IntermediateAVSD: is characterised by a primum ASD, a small restrictive
VSD, separate right and left AV valves and a trileaflet left AV valve.
Complete AVSD: has a primum ASD, a non-restrictive VSD and a
common AV valve The echocardiographic landmark is the lack of normal

574
 offset arrangement of valvular leaflets at the septum which is best
demonstrated in the apical four chamber view.
Most AVSDs seen in adulthood would have been treated surgically in infancy.
Unoperated AVSDs with large ventricular components are commonly
associated with irreversible pulmonary vascular disease.
b) Hemodynamic significance
The atrial and ventricular shunt can result in atrial and ventricular
dilatation
Presence of pulmonary hypertension
c) Post surgical assessment
Detection of residual shunts
Assessment of left and right AV valve function. AV-valve regurgitation is
common and valvular stenosis may also be present
Assess left ventricular outflow obstruction
Assess the presence of pulmonary arterial hypertension

Fig 18
Complete atrioventricular septal defect

Apical four chamber view from a patient with complete AV septal defect. Note the large atrial
and ventricular septal defects with a common atrioventricular valve.

575
Fig 19 Atrioventricular septal defect

LA
RA LV

LV
RV
RV

Apical four chamber view showing a complete Subcostal coronal position with slight obliquity.
atrioventricular septal defect Image taken during diastole; the common
atrioventricular valve in the open position.

Patent ductus arteriosus (PDA)

The arterial duct connects the bifurcation of the pulmonary trunk to the aortic
arch opposite to the origin of the left subclavian artery.
a) Identifying the PDA
Infraclavicular or high parasternal views are the best to study the ducts
where both the pulmonary artery and aorta can be seen and with a slight
rotation of the transducer the duct is clearly defined. Other views can also help
in confirming the diagnosis: suprasternal, subcostal, sagittal and
parasternal short axis.
b) Hemodynamic effects
A small PDA will show left-to-right shunting with high velocity
continuous flow pattern on Doppler
A large PDA with pulmonary vascular disease will show low velocity left
to right or bidirectional shunting
Significant left-to-right shunting results in left atrial and left ventricular
volume overload and may progress to pulmonary arterial hypertension
and Eisenmenger syndrome.
576
c) PDA post surgical or interventional closure
A PDA or duct can be closed surgically or by transcatheter techniques using a
coil or a duct occluder. Following closure, these should be assessed:
Residual shunt through the duct
Residual pulmonary hypertension
Residual LV dilatation and mitral regurgitation
Obstruction of the left pulmonary artery after coil/device placement
Fig 20

Patent Ductus Arteriosus

PDA

Ao
PA

577
Fig 21
PDA b
b

RVOT
a PDA

Ao

MPA
Ao

cc
PDA

a: Parasternal short axis view,Dshowing

Ao the
position of a patent ductus.
b:Colour flow mapping showing a left to
right shunt through the duct.
C:Continuous wave Doppler recording from
the duct flow showing continuous flow
with a peak velocity of 4.2 m/s.

Right ventricular outflow tract obstruction (RVOTO)

The right ventricular outflow tract is best visualized in the parasternal short
axis and parasternal long axis pulmonary outflow view (leftward and slight
superior tilt from the usual parasternal long axis) and apical 5 chamber
view with further anterior tilt.
a) Level of stenosis: RVOT obstruction can be classified into valvular,
subvalvular or supravalvar stenosis.
Valvular stenosis: makes up the majority (80%) cases. Normally the valve
opens fully so that the leaflets are adjacent to the pulmonary arterial
wall. Pulmonary stenosis is due to disease of one leaflet or dysplasia of
both leaflets and shows a characteristic doming picture of the thickened
leaflets in systole. Colour flow Doppler helps in localising the site of
maximum velocity and may also confirm the presence of pulmonary
regurgitation. Continuous wave Doppler quantifies the severity of
pulmonary stenosis and regurgitation.
Subvalvular stenosis: This includes infundibular stenosis or double-
chambered right ventricle (DCRV).
578
i. DCRV is characterized by muscle bundles dividing the RV into a proximal
pre-stenosis (high pressure) chamber and a distal post-stenosis (low pressure)
chamber. DCRV is differentiated from infundibular stenosis in that the
obstruction is located lower within the body of the RV. A concomitant
perimembranous VSD may be identified. This is best seen in the parasternal
short axis or the apical five chamber view with anterior tilt.
ii. Infundibular stenosis is located at the inferior region of the right ventricular
outflow tract where the infundibulum unites with the trabecular portion of the
RV (usually a ring or diaphragm with a central orifice).
Supra-valvular pulmonary stenosis: The stenosis is distal and superior to
the pulmonary valve, located in the main pulmonary artery but can also
be at branch pulmonary arteries.
b) Haemodynamic significance
Degree of severity. Stenosis is severe if the peak gradient (using CW
Doppler) measures > 80mmHg.
Right ventricular hypertrophy with restrictive physiology is often seen.
Dilatation of the pulmonary arteries. Often seen in valvular pulmonary
stenosis.

579
Fig 22

Pulmonary valve stenosis

RVOT

MPA

Parasternal short axis view of a thickened
and stenotic pulmonary valve (arrow). Note
that poststenotic dilatation of main pulmonary
artery, and significant right ventricular
hypertrophy
Continuous wave Doppler trace demonstrating
very high systolic velocity and the small a
wave during atrial systole. The later is the sign
for restrictive right ventricular physiology.

Fig 23

Pulmonary Regurgitation
A B

Continuous wave Doppler recording obtained from the parasternal position directed through pulmonary
valve.
A: From a patient with mild PR, note the regurgitation signal persist till the end of diastole.
B: Patient with severe pulmonary regurgitation; the regurgitation signal ends at the middle of diastole.

Left ventricular outflow tract obstruction (LVOTO)

a) Level of obstruction: Left ventricular outflow tract obstruction may be at
valular, subvalvular or supravalvular level.

580
i. Valvular obstruction: Common valvular lesions include a bicuspid aortic
valve, unicuspid aortic valve with central perforation, or tricuspid aortic valve
with dysplastic leaflets. Although bicuspid aortic valve is the most common
congenital aortic valve malformation, its function can remain normal for many
years. Development of valve calcification or the onset of endocarditis are
usually the cause of valve deterioration.
ii. Subaortic stenosis: This can be due to a membrane, a fibromuscular ridge
or tunnel-like narrowing that narrows the subaortic area and creates a
significant obstruction. Subaortic stenosis may also be caused by hypertrophy
of the proximal septum which bulges into the left ventricular outflow tract
causing significantly elevated blood flow velocities and a pressure gradient
across the outflow tract.
iii. Supra-aortic stenosis is a rare condition and is commonly above the level of
the sinus of Valsalva. The narrowing can be focal or diffuse involving a
considerable length of the ascending aorta. Supra-aortic stenosis is commonly
seen with Williams syndrome.
A high parasternal long axis view is ideal for identifying the exact site
of the stenosis.
Short axis views are useful for the determination of leaflet anatomy
and morphology in patients with valvular stenosis.
The supra-sternal window may also help in visualising the ascending
aorta and the site of supravalvular stenosis.
Parasternal views obtained from the right sternal edge are also
useful in delineating the ascending aorta.
Colour flow Doppler is useful for localising the exact site of narrowing and the
degree of aortic regurgitation, commonly seen in this condition. The degree of
stenosis can be quantified with continuous wave Doppler by obtaining the peak
velocity, the maximum instantaneous pressure gradient and the mean
pressure gradient. The modified Bernoulli equation (4V2) is the conventional
means for assessing valvular stenosis.
581
b) Echocardiographic assessment should include:
Valve morphology
Aortic root dimensions including the ascending aorta
Severity of obstruction
Impact on the left ventricle
Associated abnormalities
Fig 24
Bicuspid AV

Parasternal long axis view demonstrating

Parasternal short axis view of aortic root;
eccentric valve closure in a patient with a
a bicuspid aortic valve can be identified
bicuspid aortic valve; note the aortic root
within the aortic root.
is dilated as well.

582
Fig 25

Bicuspid aortic valve causing aortic stenosis

Parasternal long axis view in a patient with a Doppler colour flow demonstrating the proximal
bicuspid aortic valve, demonstrating thickened acceleration and distal flow disturbance.
valve leaflets.

Fig 26
Bicuspid aortic valve with AR

RV

Ao
LV LV Ao

LA
LA

Parasternal long axis view in a patient with a Doppler colour flow demonstrating the
bicuspid aortic valve, demonstrating thin but aortic valve regurgitation during diastole.
doming aortic valve leaflets.

583
Fig 27

Congenital AS

RV
Ao
Ao
LV

Parasternal longaxis and short axis view showing a congenital aortic stenosis causing
by a possible unileaflet aortic valve. The valve leaflet itself looks dysplastic.

Fig 28
Sub AS
b

a
LV

LV RV

RV vsd

Ao LA

c
a:Apical five chamber view demonstrating a
sub-aortic ridge.
b:Colour flow Doppler showing turbulent
flow start from sub-aortic area and a shunt
through a VSD.
c: Continuous Doppler trace from the LVOT
showing a peak velocity of 4.2 m/s

584
Fig 29
Sub aortic stenosis

LV Ao

3D imagines demonstrating a sub-aortic fibrio-muscular ring

Fig 30
Small Aortic Root

Parasternal long-axis view of a fibromuscular Colour Doppler demonstrate mild aortic

subaortic tunnel. The aortic root itself is also regurgitation
small

585
Coarctation of the aorta (COA)
a) Assessing native coarctation
Coarctation is a narrowing of the aortic arch or descending thoracic aorta. The
most common form is a discrete (localised) coarctation in the form of a fibrous
ridge that commonly occurs distal to the origin of the left subclavian artery. In
contrast, the lesion may also be diffuse in the form of a tubular hypoplasia of
the artery. Aortic coarctation is best imaged from the high parasternal,
supraclavicular or suprasternal windows.
Colour flow Doppler defines the exact site of the narrowing and continuous
wave Doppler quantifies the degree of stenosis. The characteristic continuous
wave Doppler spectrum is a high velocity flow profile during systole from which
the peak pressure drop can be estimated and a continuous "tail" during
diastole. The coarctation is significant if high velocities (>30mmHg peak
gradient with CW across the descending aorta) are present with anterograde
diastolic flow seen (also known as 'diastolic runoff'). But in extreme cases, the
Doppler peak gradient may be absent, especially when ductal or collateral flow
exists.
b) Repaired coarctation of aorta (Figure 48)
Residual coarctation or development of re-coarctation is seen long after the
initial repair. The chance of developing re-coarctation is related to the age of
repair and surgical technique. Factors related to higher risk of recurrence are
early repair and an end-to-end anastamosis.
Aneurysm formation or dilatation at the site of repaired coarctation is another
late complication. This may not be visualized by echocardiogram and MRI or
CT scan are the imaging modalities of choice for full anatomical assessment of
the descending aorta.
The presence of any associated defects should also be assessed. The most
commonly associated lesions are bicuspid aortic valve, ventricular septal
defect, and mitral valve stenosis or regurgitation. Also, systemic hypertension
is a life long risk for these patients, which is increased with later repairs.
586
Although hypertension cannot be directly assessed echocardiographically, its
sequelae, presence of left ventricular hypertrophy can be noted.
Fig 31
COA

Suprasternal long-axis view of the aorta. There Colour Doppler flow map through the
is shelf at the site of the ductal junction causing descending aorta shows aliasing at the
narrowing site of narrowing.

Fig 32
Spectral Doppler recording through
the descending aorta demonstrating
high velocity during systole, and
continued flow during diastole.

Continuous flow detected in

abdominal aorta.

587
Fig 33
Re-coarctation

Supra-sternal view of the aortic arch in a Continuous wave Doppler trace across the
patient with previous repaired coarctation of the coarctation area showing a long diastolic tail.
aorta. Note the narrowing at the previous repaired
area. The bright echo from the aortic wall suggests
previous surgery.

Mitral stenosis/regurgitation (MS/MR)

Congenital mitral valve stenosis is rare. It either takes the form of a hypoplastic
valve or a parachute mitral abnormality. A hypoplastic valve is where the
papillary muscle inserts directly into the mitral leaflet tips and the chordae are
completely absent.. In parachute mitral valve lesions, chordae from both
leaflets are inserted into a single papillary muscle. Both of these lesions can
easily be detected from both the parasternal long axis view and the apical
four chamber view. Congenital mitral regurgitation is mainly caused by either
a cleft of the anterior leaflet of the mitral valve or mitral valve prolapse which
commonly affects the posterior leaflet. Colour flow Doppler and continuous
wave Doppler are excellent methods for assessing the degree of valve stenosis
and regurgitation.

588
Fig 34
Congenital mitral valve stenosis

Ao
LV

LA

Parasternal long axis view showing congenital mitral stenosis. Note the thickened valve
leaflets with a small opening orifice. The left atrium is dilated due to the mitral stenosis.

Fig 35
A B

LV
LA

A. Parasternal short axis view demonstrating a

parachute type abnormality of the mitral valve.
Note the small valve orifice (arrow) due to all chordae
attached to the single anteriolateral paplliary muscle.
B. Colour flow mapping showing flow acceleration
through the valve during diastole.
C. Continuous wave Doppler trace showing increased
flow velocity

589
Fig 36
MVL prolapse

Ao
LV

LA

Parasternal long-axis view demonstrating Colour Doppler flow mapping showing

mitral valve prolapse. anteriorly directed mitral regurgitation jet.

Tricuspid valve disease: Ebstein's malformation

In this condition, the septal leaflet of tricuspid is abnormally displaced towards
the right ventricular apex more than 20 mm or 8 mm/m2 in adults. The valve
itself is dysplastic and the posterior-inferior tricuspid valve leaflet may also be
displaced. The anterior leaflet has 'sail-like' appearance with distal tethering.
Typically, the tricuspid valve orifice is rotated superiorly towards the right
ventricular outflow tract. Leaflet displacement results in significant
atrialisation of the basal part of the right ventricle and varying degrees of
tricuspid regurgitation. The apical four chamber view is ideal for assessing
the degree of valve dysfunction and severity of tricuspid regurgitation. Colour
flow Doppler demonstrates the extent of any tricuspid regurgitation.
Continuous wave Doppler quantifies the peak pressure drop across tricuspid
valve in systole. The commonest anomaly associated with this condition is an
atrial septal defect.
After surgical repair or replacement of the tricuspid valve, the following should
be assessed:
The presence of tricuspid valve stenosis or regurgitation
590
 Left and right ventricular function
Residual shunt lesions

Fig 38
Ebsteins anomaly

RA RA

Apical four chamber view in Ebsteins Colour Doppler flow map demonstrating tricuspid
malformation of tricuspid valve showing regurgitation in the same patient.
the degree of displacement of the septal
leaflet

Complex Anomalies
Tetralogy of Fallot (TOF)
Tetralogy of Fallot is the most common cyanotic congenital heart disease seen
in infancy. Most adults will have had surgery - either palliative or, more
commonly reparative. Rarely, adults present without previous operation.
a) Un-repaired Fallot:
The four features of this anomaly are:
Right ventricular outflow tract obstruction
Right ventricular hypertrophy
Ventricular septal defect
Overriding of the aorta (an aorta which overrides the ventricular septum
and so receives blood from both ventricles due to the VSD).

591
The basic anatomical malformation is the anterior deviation of the outlet
septum which causes the subpulmonary stenosis and over-riding aorta. Right
aortic arch is common in this condition.
The parasternal long axis view is ideal for studying the detailed anatomy of
this anomaly. From this view, the overriding aorta and sub-aortic VSD are
clearly shown.
Lateral angulation of the transducer displays the right ventricular outflow
tract, pulmonary valve area and pulmonary artery. Right ventricular out flow
tract obstruction can be confirmed by Doppler.
The parasternal short axis view demonstrates clearly the anatomy of the
outflow tract of the right ventricle and the proximal arterial tree as well as the
ventricular septal defect.
Similar information can be obtained from conventional apical four chamber
view and also subcostal view. The suprasternal view can assess any
additional anomalies of the great arteries and their branches.
b) Tetralogy of Fallot Palliation Techniques (Figure 49)
1. Type of palliation
Blalock-Taussig shunt (BT). Communication which redirects flow from
the left subclavian artery to the left pulmonary artery. This shunt is best
visualized from the suprasternal or supraclavicular views. Colour flow
imaging allows detection of turbulence. Continuous wave Doppler shows
a high peak velocity during early systole and gradually declines before
the next systole.
Waterston shunt - Communication between ascending aorta and right
pulmonary artery. Best visualised from high left or right parasternal
views or suprasternal views. Distortion of the anatomy of the
pulmonary artery may be seen.
Potts shunt - communication between the left pulmonary artery and the
descending aorta. Best visualised from parasternal or suprasternal
views.
592
 More rare surgeries include interposition grafts between the PA and
Aorta and the Brock procedure (resection of the infundibular stenosis
without closure of VSD).
2. The following should be assessed:
Residual RVOT obstruction
Residual VSD
Right and left ventricular dilatation and function, presence of restrictive
RV physiology
Peripheral pulmonary artery stenosis
Aortic insufficiency
For late repair, important factors to consider are:
Ventricular function,
Pulmonary pressures and pulmonary artery anatomy after shunt
surgery. Coronary angiogram is the preferred imaging technique to rule
out an anomalous course or coronary artery disease.
Estimate pulmonary pressures. (rarely, pulmonary vascular disease may
occur if the shunts were too large).

4Vshunt2 = peak velocity across the shunt)

Note: It is important to exclude peripheral pulmonary arterial stenosis before
using this technique.
c) Echocardiographic assessment of repaired TOF:
The following should be assessed:
The degree of pulmonary regurgitation (qualitative assessment)
Right ventricular dilatation and function
Residual RVOT obstruction
Residual VSD
Peripheral pulmonary artery stenosis
Aortic dilatation and aortic valve regurgitation

593
 Left ventricular function
a) Pulmonary regurgitation
One of the most common problems after Tetralogy of Fallot repair is pulmonary
regurgitation (especially after transannular patch) which can result in
progressive RV dilatation and dysfunction. Replacement of the pulmonary valve
can prevent irreversible damage to the right ventricle and arrhythmic
complications. The following are echocardiographic features of severe PR:
Early termination of the PW spectral Doppler signal (PR index <0.77)
Broad laminar retrograde colour Doppler diastolic jet seen at or beyond
the pulmonary valve. (PR jet width > 0.98)
Dense spectral CW Doppler signal
Paradoxical septal motion
b) Right ventricular dimension and function
Significant RV dilatation: RV inlet diameter > 4.2 cm and RV outflow >
2.7cm.
Two-dimensional Fractional Area Change (FAC): RV systolic function is
impaired if FAC < 35%
M-mode of the lateral tricuspid annular plane systolic excursion (TAPSE)
>1.5 cm = good ventricular function
RV myocardial performance index (normal = 0.280.04)
Peak systolic tissue Doppler velocity (normal >11.5cm/s)
IVA (isovolumic acceleration) (normal =1.40.5m/s2)
Calculating the dP/dt (normal = 100-250mmHg/s)
RV Strain and strain rate
RV diastolic dysfunction, especially restrictive RV physiology presented
as 'a' wave on pulmonary Doppler throughout respiratory cycle is
common. Pulse wave Doppler interrogation of the IVC Doppler would
show retrograde flow during atrial systole.
It is important to know that aneurysm of right ventricular outflow tract with
akinetic patch is very common in adult with repaired Fallot. The aneurysmal
594
dilatation of RVOT will contribute significantly to increased RV volume and the
akinetic patch will of course affect global right ventricular function. This should
be carefully assessed from parasternal long and short axis view.
c) Residual RVOT obstruction
This is classified into mild (peak gradient < 40mmHg), moderate (40-70mmHg)
and severe (>70mmHg). Patients with surgical or percutaneous valve
replacement (figure 20) should also be assessed periodically for
stenosis/regurgitation.
d) Aortopathy
Progressive aortic root dilatation can occur years after TOF repair. Therefore
the aortic dimensions and presence of aortic regurgitation should be closely
monitored.
e) Left ventricular dysfunction
This is increasingly recognized as a marker of increased disease severity. LV
diastolic dysfunction is commonly seen in later in the life of repaired Fallot
patients.
Complete transposition of the great arteries-TGA (Ventricular
arterial discordance)
In complete transposition of the great arteries, the morphological atrial and
ventricular connections are concordant but the connection of ventricles and
great arteries are discordant, i.e. the left ventricle is connected to the
pulmonary artery and the right ventricle to the aorta.
In the absence of additional anomalies it is described as simple transposition of
great arteries. The commonly co-existing lesions are patent ductus arteriosus,
ventricular septal defect, pulmonary stenosis, or aortic coarctation. The
majority of adult patients have had a surgical repair in early life. Few patients
present in adulthood without repair and do so only if there is 'balanced
circulation'.
a) Echo features of transposed great arteries

595
 Two great vessels are parallel with each other with aorta anterior to the
pulmonary artery and arising from anterior morphological RV. This is
best seen from parasternal long axis view.
From the short axis parasternal view the aortic and pulmonary roots
and the semilunar valves can be seen with a so-called "double circle"
appearance.
Additional anomalies such as VSD and left ventricular outflow tract
obstruction (sub-pulmonary stenosis) can be assessed from different
conventional views, in particular the subcostal and parasternal long
axis views.
Variable coronary artery anatomy should also be assessed from the
parasternal short axis view. The most common coronary variant is the
circumflex originating from the right coronary artery.
Fig 39
Tetralogy of Fallot

596
Fig 40

Tetralogy of Fallot

RVOT

RV VSD

Ao

LV
Ao

Parasternal long axis view showing aortic

overriding and large sub-aortic VSD (arrow)
in a patient with Tetrology of Fallot.
Parasternal short axis view demonstrating
The right ventricular outflow tract is
narrowed by the outlet septum.

Fig 41

Tetralogy of Fallot

RVOT

Ao

Continuous wave Doppler trace taken from the

RVOT showing the peak velocity of more than
Colour Doppler showing a narrowed right 4 m/s.
ventricular outflow tract (RVOT) with
turbulent flow.

597
Fig 42

Repaired Fallot

LV
RVOT
RV

LA
Ao

RA RA

Parasternal short axis view showing a Apical four chamber view demonstrating a
residual right ventricular outflow tract severely dilated RA from long standing high
obstruction in an adult patient with repaired right ventricular pressure and tricuspid
Tetralogy of Fallot regurgitation.

Fig 43

Transposition of Great Arteries

Parasternal long axis view from a patient with

transposition of the great arteries. Note the two
great arteries are parallel and the pulmonary
artery is positioned posterior to the aorta.

598
Fig 44

RV
LV

Apical four chamber view in a patient with

transposition of the great arteries after a Mustard
repair. Note the intra-atrial baffle (arrow)
directing the pulmonary venous flow into the
Mustard Procedure right side atrium. The right atrium and right
ventricle are dilated.

Fig 45

TGA post Mustard

LV
RV

RA

PV

Apical four chamber view in a patient with Colour Doppler mapping demonstrate mild
transposition of great arteries after a Mustard tricuspid regurgitation
repair. Note the intra-atrial baffle (arrow)
directing the pulmonary venous flow into the
right side atrium. The right atrium and right
ventricle are dilated.

599
Fig 46 TGA post Mustard repair

A B

mRV

mLV

A. Subcostal four chamber view demonstrating

pulmonary venous pathway obstruction.
B.Colour Doppler flow mapping showing
velocity aliasing at the site of stenosis.
C. Pulsed wave Doppler trace detecting high
flow velocity.

Fig 47

TGA post Mustard repair

mLV

mRV

Apical four chamber view showing severe pulmonary venous pathway obstruction. Note
The continuous flow detected at the site of stenosis.

600
Fig 48
Mustard TR

MRV
MRV

PV atrium

Apical four chamber view from a patient with

a Mustard repair demonstrating a severely
dilated pulmonary venous atrtium which may
be the result of severe tricuspid regurgitation Colour flow map showing the tricuspid
and/or impaired right ventricular function. regurgitation.

b) Repaired transposition of great arteries

The long-term complications associated with repaired transposition of the great
arteries depend on the type of repair.
There are essentially three types of repair:
i. Intra-atrial repair (Mustard or Senning). This is the earliest type repair seen in
relatively older patients. In atrial switch, an intra-atrial baffle utilizing the
atrial wall or pericardium is placed in order to direct blood from the superior
and inferior vena cavae towards the mitral valve, and from the pulmonary veins
towards the tricuspid valve.
ii. Arterial switch operation. This operation is performed by switching the great
arteries with re-implantation of the coronary arteries. It is currently the
preferred surgical procedure.
iii. Rastelli type repair. In patients with concomitant VSD and LVOT
obstruction, Rastelli operation is performed. A conduit runs from the LV
through the VSD to the aorta. A RV-PA conduit is also implanted. This was
recently replaced by the Nikaidoh procedure (aortic translocation) in selected
cases.
601
Echocardiographic evaluation after the atrial switch procedure (Senning
or Mustard operations)
The following should be addressed:
Ventricular function (especially the systemic right ventricle)
Tricuspid valve regurgitation
Establish the presence of baffles leak or obstruction in all 3 pathways
Assessment of pulmonary arterial pressures
Assess for LVOT obstruction
o Progressive tricuspid regurgitation and systemic RV dysfunction
are common problems following the atrial switch operation.
o It is also important to identify the venous pathways to rule out
baffle obstruction or baffle leaks.
o All venous connections should be assessed.
o The best view of the atrial baffles are the apical views with non
standard probe angles to display the connection of the SVC and
IVC to the left atrium and the pulmonary venous connection to the
right atrium.
Doppler interrogation with pulsed wave Doppler in the SVC/IVC will
demonstrate increased velocities if there is significant stenosis. Peak
velocities > 1.6 m/s usually suggesting significant stenosis. Baffle leaks
result in an interatrial shunt. This is best appreciated on colour flow
imaging in the modified apical 4 chamber view. In those with poor
windows transoesophageal echocardiography may be helpful. Contrast
echocardiography with injection of agitated saline through a peripheral
intravenous cannula is also helpful to detect baffle leak.
Echocardiographic evaluation after the arterial switch
Imaging involves:
Assessment of neo-aortic root dilatation and presence of any associated
AR

602
 Assessment of pulmonary stenosis (usually supra-valvar, is best
assessed in the parasternal short axis view) at anastomosis sites
Assessing the coronaries, ventricular size and function
RV outflow tract obstruction is the most common cause for late reoperation
after arterial switch. The obstruction can occur at any level but is most
commonly seen at the site of anastomosis. During arterial switch surgery, the
Lecompte manoeuvre is undertaken, which alters the position of the pulmonary
bifurcation so that it lies anterior to the aorta. In the parasternal short axis
view, the left pulmonary artery is to the left of the aorta and the right
pulmonary artery is to the right of the aorta. This makes imaging the
pulmonary valve and arteries challenging. Peak velocities =2 m/s across the
distal main pulmonary artery and branch pulmonary arteries are within
normal limits after surgery.
Screening for myocardial ischemia should be performed routinely. Apart from
assessment of regional wall motion abnormalities, stress echocardiography can
be used to identify ischemia.
Echocardiographic evaluation after the Rastelli procedure
In the Rastelli procedure, the VSD is closed creating a tunnel between the left
ventricle and the aorta and the right ventricle is connected with a conduit to
the pulmonary arteries. Imaging the patients after the Rastelli procedure
involves:
Evaluation of the conduit and branch pulmonary arteries
Evaluation of the LV-to-aortic valve pathway for obstruction and aortic
regurgitation
Evaluation of left ventricular function. LV dysfunction is a potential late
complication after the Rastelli operation
Exclude residual VSDs
In the late follow-up, the most common sequelae are calcification of the
pulmonary valved conduit with various degrees of stenosis and/or
regurgitation.
603
The conduit is almost always difficult to visualize on 2D. Colour and
continuous wave Doppler are very helpful in detecting conduit stenosis.
Tricuspid regurgitation continuous wave Doppler can assess right ventricular
systolic pressure (RVSP); this indirectly reflects conduit status however it
should be remembered that in cases where RV outflow obstruction is present,
the RVSP does not equal the pulmonary artery systolic pressure. Left
ventricular outflow tract obstruction and residual ventricular septal defect can
also be coexisting complications.
Congenitally corrected transposition (cc-TGA or Discordant
atrioventricular and ventriculoarterial connections, double
discordance)
In this lesion, the morphological right atrium is connected to the left ventricle
which is connected to the pulmonary artery and supports the pulmonary
circulation, while the morphological left atrium is connected to the right
ventricle which is connected to the aorta and supports the systemic circulation.
Therefore, both atrioventricular and ventriculo-arterial connections are
discordant.
From the apical four chamber view the morphologic left ventricle lies to the
right and the right ventricle to the left. Diagnosing this condition depends on
the correct identification of the ventricles by their morphology from known
features and thorough assessment of the cardiac crux.
Echo assessment should included the following aspects:
Atrioventricular and ventriculoarterial connections
Ventricular function for both morphologic right and left ventricle.
presence of valvular regurgitation and quantify its severity
Associated anomalies
Determination if further intervention is required.
Assessment of post repair patients.

604
a) Verifying the diagnosis
In usual situs, the tricuspid valve (more apically displaced AV valve) and
morphological RV are on the left. The ventricles, septum and great vessels are
often vertically oriented and requires vertical angulation of transducer in
parasternal planes to optimize imaging. The sub-pulmonary morphologic left
ventricle may appear compressed. From the parasternal short axis view aorta
is to the left of pulmonary artery and usually anterior.
b) Ventricular function
In this condition, the morphologic right ventricle supports the aorta and
systemic circulation. With time, ventricular dysfunction and heart failure
ensues. Echocardiography may be able to identify ventricular dysfunction
before overt clinical symptoms.
c) Tricuspid regurgitation (systemic AV valve)
Tricuspid valve regurgitation (TR) is common. Some patients may have
associated Ebstein's anomaly of the tricuspid valve. In the presence of
significant tricuspid regurgitation, right ventricular dysfunction can easily be
underestimated. Besides TR, mitral, pulmonary and aortic regurgitation should
also be assessed.
d) Associated anomalies
Commonly associated anomalies are ventricular septal defect, LVOT
obstruction (sub-pulmonary stenosis) and abnormal tricuspid valve (such as
Ebstein's anomaly or a straddling valve).

Role of echocardiography in guiding further intervention and assessment

after surgery
Assess the timing and suitability of repair or replacement of the tricuspid
valve.
Evaluate systemic right ventricular function.
Assess the feasibility of biventricular repair or need for pulmonary artery
banding.
605
 After pulmonary artery banding, assess left ventricular function,
hypertrophy and tricuspid regurgitation.
Assess for worsening ventricular function and atrioventricular valve
regurgitation.

Fig 49
Congenitally Corrected Transposition of Great
Arteries (CC-TGA)
Apical four chamber view of patient with
congenitally corrected transposition of the
great arteries. Note the presence of a
moderator band (arrow) and the apical
MRV displacement of the left sided
atrioventricular valve, distinguishing the
MLV left sided ventricle is a morphological
right ventricle.

LA
RA

606
Fig 50
Congenitally Corrected Transposition of Great
Arteries (CC-TGA)

MRV
MLV MRV MLV

PA

RA LA

Apical four chamber view showing a left sided Apical five chamber view showing a
morphological right ventricle with moderater pulmonary artery which bifurcates and arises
band and an apically displaced tricuspid valve. from right sided morphological left ventricle

Double outlet right ventricle (DORV)

A double outlet right ventricle is diagnosed when more than half the
circumference of both great arteries are connected to the morphological right
ventricle.
A double outlet right ventricle is usually considered within the spectrum of
other conditions, e.g. transposition of great arteries or Tetralogy of Fallot.
In this condition, detailed assessment of the position of the ventricular septal
defect is crucial.
The parasternal long axis view is ideal for differentiating between the double-
outlet right ventricle and Tetralogy of Fallot, with an aortic override of more
than 50% in the former. When the VSD is subpulmonary, a double outlet right
ventricle has to be differentiated from transposition of great arteries.

607
Fig 51
Double outlet of right ventricle (DORV)

RV
Ao

LV

LA

Parasternal long axis view of a patient with a double outlet right ventricle and a sub-aortic
VSD, demonstrating the aorta is mainly arising from RV, and the separation between the
mitral valve apparatus and the base of the aortic root (arrow)

Fig 52
Double Outlet Right Ventricle

LV

RV vsd

PA
Ao

Apical five chamber view in patient with double-out right ventricle. Note both aorta
and pulmonary artery are arising from right ventricle with the aorta more anterior and
on the right side of the pulmonary artery.

Common arterial trunk (Truncus arteriosus)

The majority of patients presenting in adulthood have usually undergone
surgical repair with VSD closure and a right ventricle-pulmonary artery (valved)

608
conduit. Those patients who have not undergone surgery and survived have
often developed Eisenmenger's syndrome.
Echo features of common arterial trunk
Single and large arterial trunk originating from the heart supplying the
coronary, pulmonary and systemic circulation.
Typically associated with a large VSD (figure 21).
The truncal valve has variable anatomy with varying degrees of stenosis
and regurgitation.
Evaluation of patients who have had surgery for common arterial trunk
includes assessment of:
residual VSDs
truncal valve function for stenosis or regurgitation. The truncal valve
may be tricuspid, quadricuspid or bicuspid. Occasionally, the valve may
have been replaced with a prosthetic valve
neoaorta dilatation
right ventricular conduit for obstruction and/or regurgitation
pulmonary branch stenosis
ventricular function
Eisenmenger's syndrome
Eisenmenger syndrome is characterized by irreversible pulmonary vascular
disease due to systemic-to-pulmonary communication (eg. ASD, non-restrictive
VSD, non-restrictive PDA, atrioventricular septal defect, aortopulmonary
window, surgical systemic-to-pulmonary shunt). Whilst initially the shunt may
have been left to right, the shunt reverses direction following an increase in
pulmonary vascular resistance and arterial pressures.
The following should be assessed:
Severity of pulmonary hypertension
Direction of shunting across an intra-cardiac communication
Underlying lesion
Associated lesions
609
 Biventricular function
Determining the degree of pulmonary hypertension
Right ventricular hypertrophy with flattening and bowing of the interventricular
septum in systole ('D' shaped septum ) is seen in the parasternal short axis.
Systolic flattening occurs with disease progression.
With tricuspid regurgitation and the absence of RV outflow obstruction, the
PASP can be estimated using the modified Bernoulli equation,

VTR = maximal velocity of the tricuspid regurgitation by CW Doppler

RAP= right atrial pressure (estimated by the IVC dimensions and its respiratory
variation).
Mean PA pressure can be estimated from early diastolic pulmonary
regurgitation velocity:

The end diastolic pulmonary artery pressure can also be estimated from the
end diastolic pulmonary regurgitation velocity: End-diastolic PA pressure =
4XV2 (end-diastolic PR) +RA pressure.

Univentricular heart (univentricular atrio-ventricular

connections or single ventricle)
In most univentricular hearts, there are actually two ventricular chambers but
one is dominant and the other is rudimentary. A small superior and rightward
subarterial outlet chamber is typically a morphologic RV. A small inferior-
posterior rudimentary chamber is typically a morphologic LV.
After the diagnosis of atrial situs has been established, the mode of
atrioventricular connection needs to be determined.

610
Atrioventicular connection: There are three specific patterns in the
atrioventricular junction:
i. Double inlet ventricle
ii. An absent right (tricuspid atresia) atrioventricular connection
iii. An absent left (mitral atresia) atrioventricular connection
These three atrioventricular junction types can be connected to one of the three
possible morphologies in the ventricular chamber. The first is a dominant left
ventricle with a rudimentary right ventricle. The second is a dominant right
ventricle with a rudimentary left ventricle. Finally, there may be a solitary
ventricle of indeterminate morphology.
Ventriculo-arterial junctions: There are also possibly three types:
i. Concordant
ii. Discordant connection
iii. Double-outlet connection
The most characteristic ventriculo-arterial connection is discordant in which
the pulmonary artery arises from the main chamber posteriorly while the aorta
arises from the rudimentary chamber.
A functionally single ventricle (left or right morphology) supports the systemic
circulation. As expected, there can be many anatomical diagnoses.
Occasionally, two adequately sized ventricles are present, but their anatomy
prevents septation (eg straddling atrioventricular valves or very large VSDs).
The following associated lesions should be assessed:
The size and location of the accompanying VSD
The atrioventricular valve is assessed for straddling (tricuspid valve more
common) across the ventricular septal defect (usually muscular) as well
as stenosis or regurgitation
Restriction at the atrial septum may be important for specific lesions eg
absent right/ left connection
Presence of pulmonary stenosis or pulmonary hypertension need to be
established
611
 Finally, ventricular function should be assessed
Fig 53

Double inlet Left Ventricle

LV
MLV Apical four chamber view showing
RV double inlet left ventricle. Note the
presence of two atrioventricular valves
connecting to a single morphology left
ventricle.

RA LA
LA LA
RA

Fig 54
Tricuspid atresia

LV

RV
vsd

LA
RA

Apical four chamber view from a patient with an absent right atrioventricular connection
(tricuspid atresia). The position of the tricuspid valve is replaced by strand of tissue (arrow).
The right ventricular cavity is very small. A perimembranous VSD is also present.

612
Fig 55
CLASSICAL GLENN BIDIRECTIONAL GLENN FONTAN

SVC
SVC

RPA LPA PA PA

RA RA
RA

IVC
IVC

TOTAL CAVOPULMONARY CONNECTION

SVC

PA

RA

IVC

Fig 56

Tricuspid atresia
Apical four chamber view of a univentricular
atrioventricular connection with atresia of the
MLV
right sided atriovenricular valve (tricuspid
atresia).The patient had a Fontan type repair
(right atrium to pulmonary artery connection).
The valve between the IVC and right atrium can
just be seen in the right atrium (arrow).
LA
RA

613
Fig 57

TCPC

Apical four chamber view of a patient with a

univentricular atriovenricular connection
and a common atrium, post TCPC. Note the
V TCPC pathway (arrow) at the back of the atrium.

Common atrium

Fig 58
Tricuspid atresia post Fontan operation

Apical view of a univentricular

atrioventricular connection resulting
from atresia of the right-sided
atrioventricular valve (tricuspid
LV atresia). The patient had a Fontan type
operation. Note that the right atrium is
LA severely dilated with thrombus inside.

RA

614
Fig 59
Fontan: The giant RA and large clot

RA RA

TOE image taken from a patient with a double inlet left ventricle post Fontan (atria-pulmonary
connection) repair. Note the severely dilated right atrium with giant thrombus and
spontaneous contrast inside the atrial chamber (arrow).

Univentricular heart (single ventricle) after surgical palliation

Treatment of patients with a single ventricle varies according to anatomy:
Palliative procedures: systemic-pulmonary artery shunt (Blalock-Taussig
shunt, central shunt etc.) to increase pulmonary blood flow and
pulmonary artery banding to limit pulmonary blood flow
Fontan type operation or total cavopulmonary anastomosis (TCPC). In
the modern era, these right-heart bypass operations are the most
definitive procedures in this situation
Originally, the Fontan operation consisted of performing a Glenn type of
anastomosis between the superior vena cava and right pulmonary artery,
placing a valve at the inferior vena cava-right atrial junction, closing the atrial
communication, transecting the pulmonary trunk with oversewing of the
proximal end and placing a valved conduit between the right atrium and distal
pulmonary artery. Over the years, there has been many modifications based on
this type repair.
TCPC is a modification of Fontan which includes a bidirectional Glenn and
placement of intra-atrial conduit or baffle to connect the inferior vena cava to
615
pulmonary artery. Bi-directional Glenn consists of an end-to-side anastomosis
of superior vena cava, transected just above its junction to the right atrium,
into the superior surface of the right pulmonary artery. The anatomic integrity
of the pulmonary branches is maintained, hence the term 'bidirectional' as
blood from the SVC fills both the left and right pulmonary arteries.
It is important to establish the exact surgery performed before commencement
of echocardiography.
Echocardiographic assessment includes:
Integrity of the Fontan connection (left and right parasternal views)
Integrity of the Glenn connection (right supraclavicular view)
Exclusion of pulmonary venous obstruction (apical and suprasternal
views)
Assessment of AV valve pathology and ventricular function
Establishing the presence of collaterals

616
 Coronary Angiography
Catheter Selection
Selecting the right catheter is important and is dependent
upon the following:
Access site: Choice of catheters depends to certain
degree on the access site - femoral vs. radial vs.
brachial
Aortic width: Normal aortic width - 3.5 to 4.0 mm;
Narrow- <3.5 mm, Dilated >4.0 mm
Coronary ostial location: high vs. low; anterior vs.
posterior
Coronary ostial orientation: Superior, inferior,
horizontal or shepherds crook (for RCA only)
Standard workhorse catheters for routine coronary
angiography are Judkins right size 4 (JR4) and Judkins left
size 4(JL4) and the ostia are engaged in the LAO projection
Always ensure co-axial alignment of the catheter
Catheters generally have two curves: Primary (distal) curve
and a secondary (proximal) curve. The distance between the
two curves is the length of the catheter
Shorter curve more ideal for superior take-offs
Longer curve more ideal for inferior take-offs
Flow Rate and Volume
If using a power injector for contrast opacification, the
following settings may be considered:
RCA- 2 to 3ml/sec for 2 to 3 seconds, i.e., 3 for 6
represents a flow rate of 3ml/sec for a total volume of
6ml

617
 LCA- 3 to 4ml/sec for 2 to 3 seconds, i.e., 4 for 8
which represents a flow rate of 4ml/sec for a total of
8ml
Ventriculography - 10 to 16ml/sec for 30 to 55ml, i.e.,
13 for 39 which represents a flow rate of 13ml/sec for
a total of 39ml
Common carotid artery - 8ml/sec for 10 cc
Internal carotid artery - 8ml/sec for 8cc
Vertebral artery - 7ml/sec for 7cc
Renal artery - 5ml/sec for 5 to 10cc
Iliofemoral - 7 to 9ml/sec for 70 to 120 cc
Standard Angiographic Views
Left Coronary Artery
LAO-Caudal view: 400 to 600 LAO and 100 to 300 caudal
Best for visualizing left main, proximal LAD and
proximal LCx
RAO-Caudal view: 100 to 200 RAO and 150 to 200 caudal
Best for visualizing left main bifurcation, proximal LAD
and the proximal to mid LCx
Shallow RAO-Cranial view: 00 to 100 RAO and 250 to 400
cranial
Best for visualizing mid and distal LAD and the distal
LCx (LPDA and LPL)
Separates out the septals from the diagonals
LAO-Cranial view: 300 to 600 LAO and 150 to 300 cranial
Best for visualizing mid and distal LAD, and the distal
LCx in a left dominant system
Separates out the septals from the diagonals
Left Coronary Artery (other views)
PA projection: 00 lateral and 00 cranio-caudal
618
 Best for visualizing ostium of the left main
PA-Caudal view: 00 lateral and 200 to 300 caudal
Best for visualizing distal left main bifurcation as well
as the proximal LAD and the proximal to mid LCx
PA-Cranial view: 00 lateral and 300 cranial
Best for visualizing proximal and mid LAD
Left lateral view:
Best for visualizing proximal LCx, proximal and distal
LAD
Also good for visualizing LIMA to LAD anastomotic site
Right Coronary Artery
LAO 30: 300 LAO
Best for visualizing ostial and proximal RCA
RAO 30: 300 RAO
Best for visualizing mid RCA and PDA
PA Cranial: PA and 300 cranial
Best for visualizing distal RCA bifurcation and the PDA
An easy way to identify the tomographic views is to use the anatomic
landmarks - catheter in the descending aorta, spine and the diaphragm.
The rough rules are:
RAO vs. LAO- If the spine and the catheter are to the
right of the image, it is LAO and vice versa. If central,
it is likely a PA view
Cranial vs. caudal - If diaphragm shadow can be seen
on the image, it is likely cranial view, if not, it is
caudal

619
Left Coronary Artery

RAO 20 Caudal 20

620
RAO 20 Caudal 20

PA 0 Cranial 30

621
LAO 50 Cranial 30

LAO 50 Caudal 30
Spider view

622
PA0 Caudal 30

Right Coronary Artery

LAO 30

623
RAO 30

PA 0 Cranial 30

Angiogram-Interpretation
A systematic interpretation of a coronary angiogram would
involve:
Evaluation of the extent and severity of coronary
calcification just prior to or soon after contrast
opacification
Lesion quantification in at least 2 orthogonal views:
624
 Severity
Calcification
Presence of ulceration/thrombus
Degree of tortuosity
ACC/AHA lesion classification
Reference vessel size
Grading TIMI flow
Grading TIMI myocardial perfusion blush grade
Identifying and quantifying coronary collaterals
ACC/AHA Lesion Classification
Type A Lesion: Minimally complex, discrete (length <10 mm), concentric,
readily accessible, non-angulated segment (<45), smooth contour, little
or no calcification, less than totally occlusive, not ostial in location, no
major side branch involvement, and absence of thrombus
Type B Lesion:Moderately complex, tubular (length 10 to 20 mm),
eccentric, moderate tortuosity of proximal segment, moderately
angulated segment (>45, <90), irregular contour, moderate or heavy
calcification, total occlusions <3 months old, ostial in location,
bifurcation lesions requiring double guidewires, and some thrombus
present
Type C Lesion: Severely complex, diffuse (length >2 cm), excessive
tortuosity of proximal segment, extremely angulated segments >90, total
occlusions >3 months old and/or bridging collaterals, inability to protect
major side branches, and degenerated vein grafts with friable lesions.
Other Definitions
Lesion length: Measured shoulder-to-shoulder in an unforeshortened
view
Discrete Lesion length < 10 mm
Tubular Lesion length 1020 mm
Diffuse Lesion length 20 mm
625
 Lesion angulation: Vessel angle formed by the centerline through the
lumen proximal to the stenosis and extending beyond it and a second
centerline in the straight portion of the artery distal to the stenosis
Moderate: Lesion angulation 45 degrees
Severe: Lesion angulation 90 degrees
Calcification: Readily apparent densities noted within the apparent
vascular wall at the site of the stenosis
Moderate: Densities noted only with cardiac motion prior to
contrast injection
Severe: Radiopacities noted without cardiac motion prior to
contrast injection
TIMI Flow Grades
TIMI 0 flow: absence of any antegrade flow beyond a coronary occlusion
TIMI 1 flow:(penetration without perfusion) faint antegrade coronary flow
beyond the occlusion, with incomplete filling of the distal coronary bed
TIMI 2 flow: (partial reperfusion) delayed or sluggish antegrade flow with
complete filling of the distal territory
TIMI 3 flow: (complete perfusion) is normal flow which fills the distal
coronary bed completely
TIMI Myocardial Perfusion Grades
Grade 0: Either minimal or no ground glass appearance (blush) of the
myocardium in the distribution of the culprit artery
Grade 1:Dye slowly enters but fails to exit the microvasculature. Ground
glass appearance (blush) of the myocardium in the distribution of the
culprit lesion that fails to clear from the microvasculature, and dye
staining is present on the next injection (approximately 30 seconds
between injections)
Grade 2: Delayed entry and exit of dye from the microvasculature. There
is the ground glass appearance (blush) of the myocardium that is
strongly persistent at the end of the washout phase (i.e. dye is strongly
626
 persistent after 3 cardiac cycles of the washout phase and either does
not or only minimally diminishes in intensity during washout).
Grade 3: Normal entry and exit of dye from the microvasculature. There
is the ground glass appearance (blush) of the myocardium that clears
normally, and is either gone or only mildly/moderately persistent at the
end of the washout phase (i.e. dye is gone or is mildly/moderately
persistent after 3 cardiac cycles of the washout phase and noticeably
diminishes in intensity during the washout phase), similar to that in an
uninvolved artery.
Coronary Aneursym

Coronary Aneurysm: Vessel diameter > 1.5x neighboring segment

Incidence: 0.15%-4.9%; very rare in LMCA
Etiology: mainly atherosclerosis; other causes include Kawasakis, PCI,
inflammatory disease, trauma, connective tissue disease
Treatments: include observation, surgery, occlusive coiling, covered
stents, therapeutic coiling

627
 Cardiac Catheterisation

Hemodynamic Principles the Fundamentals

Shunt Determinations
Normally, pulmonary blood flow and systemic blood flow are equal
most commonly used method for shunt determination in the cardiac
catheterization laboratory is the Oxymetric method
unexplained PAO2 saturation exceeding 80% should raise suspicion of L-
R shunt
unexplained arterial desaturation (<93%) may indicate R-L shunt
Arterial desaturation commonly results from
1. alveolar hypoventilation
2. oversedation from premedication,
3. pulmonary disease,
4. pulmonary venous congestion,
5. pulmonary edema, and
6. cardiogenic shock.
If arterial desaturation persists after the patient takes several deep
breaths or after administration of 100% oxygen, a right-to-left shunt is
likely.
Oxymetric Method
Oxymetric method is based on blood sampling from various cardiac
chambers for the determination of oxygen saturation.
L-R shunt is detected when a significant increase in blood oxygen
saturation is found between two right-sided vessels or chambers.
screening oxygen saturation measurement for L-R shunt is performed by
sampling of blood in SVC and PA
If the difference in oxygen sat between these samples is 8% or more, a L-
R shunt may be present, and an oximetry run should be performed.

628
 obtains blood samples from SVC, IVC, RA , RV, and PA
In cases of interatrial or interventricular shunts, it is recommended to
obtain multiple samples from the high, middle, and low RA or the RV
inflow tract, apex, and outflow tract to localize the level of the shunt
Another method of Oxymetric determination of intracardiac shunts uses
a balloon-tipped fiberoptic catheter that allows continuous registration of
oxygen saturation as it is withdrawn from the pulmonary artery through
the right-heart chambers into the SVC and IVC.
Shunt Detection & Measurement
Indications
Arterial desaturation (<95%)
Alveolar hypoventilation (Physiologic Shunt) corrects with deep
inspiration and/or O2
Sedation from medication
COPD / Pulmonary parenchymal disease
Pulmonary congestion
Anatomic shunt (RtLt) does not correct with O2
Unexpectedly high PA saturation (>80%) due to LtRt shunt
Shunt Detection & Measurement
Methods
Shunt Detection
Indocyanine green method
Oxymetric method
Shunt Measurement
Left-to-Right Shunt
Right-to-Left Shunt
Bidirectional Shunt
Shunt Detection & Measurement
Indocyanine Green

629
 Indocyanine green (1 cc) injected as a bolus into right side of circulation
(pulmonary artery)
Concentration
measured from
peripheral artery
Appearance and
washout of dye
produces initial 1st
pass curve followed
by recirculation in
normal adults

Shunt Detection & Measurement

Left-to-Right Shunt

630
Shunt Detection & Measurement
Right-to-Left Shunt

Shunt Detection & Measurement

Indocyanine Green Method

631
Shunt Detection & Measurement
Oxymetric Methods
Obtain O2 saturations in
sequential chambers,
identifying both step-up
and drop-off in O2 sat
Insensitive for small
shunts (< 1.3:1)

Shunt Detection & Measurement

Oximetry Run

MVO2 is the average oxygen content of the blood in the chamber

proximal to the shunt.

632
 Shunt Detection & Measurement
Oximetric Methods

RA receives blood from several sources

SVC: Saturation most closely approximates true
systemic venous saturation
IVC: Highly saturated because kidneys receive 25% of
CO and extract minimal oxygen
Coronary sinus: Markedly desaturated because heart
maximes O2 extraction
flamm Equation: Mixed venous saturation used to
normalize for differences in blood saturations that
enter RA
3 (SVC) + IVC
Mixed venous saturation =
4

Measurement of Shunt

Shunt Detection & Measurement

Detection of Left-to-Right Shunt
Mean
Level of Differential
O2
shunt diagnosis
% Sat

Atrial ASD, PAPVR, VSD with TR,

(SVC/IVC RA) 7 Ruptured sinus of Valsalva,
Coronary fistula to RA
Ventricular
(RA RV) 5 VSD, PDA with PR,
Coronary fistula to RV

Great vessel Aorto-pulmonary window,

(RV PA) 5 Aberrant coronary origin,
PDA
ANY LEVEL
(SVC PA) 7 All of the above

633
Shunt Detection & Measurement
Oximetric Methods
Lungs
Fick Principle: The total uptake or
release of any substance by an organ is RA (MV) LA (PV)
the product of blood flow to the organ
and the arteriovenous concentration
difference of the substance.

RV LV
Pulmonary circulation (Qp) utilizes
PA and PV saturations
PA Ao
O2 content = 1.36 x Hgb x O2 saturation

O2 consumption
PBF =
(PvO2 PaO2) x 10

Shunt Detection & Measurement

Oximetric Methods
Fick Principle: The total uptake or
release of any substance by an organ is RA (MV) LA (PV)
the product of blood flow to the organ
and the arteriovenous concentration
difference of the substance.

Systemic circulation (Qs) utilizes MV RV LV

and Ao saturations

PA Ao
O2 content = 1.36 x Hgb x O2 saturation
Body
O2 consumption
SBF =
(AoO2 MVO2) x 10

634
 Shunt Detection & Measurement
Oximetric Methods
Fick Principle: The total uptake or
release of any substance by an organ is RA (MV) LA (PV)
the product of blood flow to the organ
and the arteriovenous concentration
difference of the substance.
Pulmonary circulation (Qp) utilizes PA
and PV saturations
RV LV
Systemic circulation (Qs) utilizes MV and
Ao saturations

PA Ao
O2 content = 1.36 x Hgb x O2 saturation

O2 consumption O2 consumption
PBF = SBF =
(PvO2 PaO2) x 10 (AoO2 MVO2) x 10

Detection Effective Pulmonary Blood Flow

Shunt Detection & Measurement

Effective Pulmonary Blood Flow

Effective Pulmonary Blood

Flow: flow that would be
present if no shunt were
present
Requires
MV = PA saturation
PV PA = PV - MV PBF

Effective Pulmonary O2 consumption O2 consumption

= =
Blood Flow
(Pv MV O2) x 10 (Pv Pa O2) x 10

635
Left -Right Shunt

Shunt Detection & Measurement

Left-to-Right Shunt
Left to right shunt results in step-
up in O2 between MV and PA
Shunt is the difference between
pulmonary flow measured and
what it would be in the absence of
shunt (EPBF)
Systemic Blood Flow = EPBF
Left-Right Shunt = Pulmonary Blood Flow Effective Blood Flow
O2 consumption O2 consumption
=
(PvO2 Pa O2) x 10 (PvO2 MVO2) x 10
(AoO2 MVO2)
Qp / Qs Ratio = PBF / SBF =
(PvO2 PaO2)

ASD
VSD
Coronary Cameral Fistula
Ruptured Sinus of Valsalva
Partial Anomalous Pulmonary Venous Return
Aorto Pulmonary Window
PDA
Aberrant Coronary Origin

636
 Shunt Detection & Measurement
Effective Pulmonary Blood Flow

Effective Pulmonary Blood

Flow: flow that would be
present if no shunt were
present
Requires
PV = Ao saturation
PV MV = Ao - MV SBF

Effective O2 consumption O2 consumption

= =
Pulmonary Flow
(Pv MV O2) x 10 (Ao MV O2) x 10

Right- Left Shunt

Shunt Detection & Measurement

Right-to-Left Shunt
Rt to lt shunt results in step-down
in O2 between PV and Ao
Shunt is the difference between
systemic flow measured and what
it would be in the absence of
shunt (EPBF)
Pulmonary Blood Flow = EPBF
Right-Left Shunt = Systemic Blood Flow Effective Blood Flow
O2 consumption O2 consumption
=
(AoO2 MVO2) x 10 (PvO2 MVO2) x 10
(AoO2 MVO2)
Qp / Qs Ratio = PBF / SBF =
(PvO2 PaO2)

Tetralogy of Fallot
Eisenmenger Syndrome
Pulmonary arteriovenous malformation
637
 Total anomalous pulmonary venous return (mixed)
If a PV is not sampled, systemic arterial oxygen content may be
substituted, assuming systemic arterial saturation is 95% or more.
if systemic arterial saturation is less than 93%, a R-L SHUNT may be
present.
If arterial desaturation is present but not secondary to a right-to-left
shunt, systemic arterial oxygen content is used.
If a R-L shunt is present, PV oxygen content is calculated as 98% of the
oxygen capacity
flow ratio PBF/SBF (or Qp/Qs) is used clinically to determine the
significance of the shunt.
A ratio of less than 1.5 indicates a small left-to-right shunt, and a ratio of
1.5 to 2.0, a moderate-sized shunt.
A ratio of 2.0 or more indicates a large left-to-right shunt and generally
requires percutaneous or surgical repair to prevent future pulmonary or
RV complications.
A flow ratio of less than 1.0 indicates a net R-L shunt.
If oxygen consumption is not measured, the pulmonic-to-systemic blood
flow ratio may be calculated as follows:

where SAO2, MVO2, PVO2, and PAO2 are systemic arterial, mixed venous, PV
, and PA blood oxygen saturations
Estimation of Vascular Resistance

638
 Vascular resistance calculations are based on hydraulic principles of
fluid flow, in which resistance is defined as the ratio of the decrease in
pressure between two points in a vascular segment and the blood flow
through the segment.

Vascular Resistance
Definitions
Normal reference values
Woods Units x 80 = Metric Units
Systemic vascular resistance

Ao - RA 10 20
SVR = 770 1500
Qs
Pulmonary vascular resistance

PA - LA 0.25 1.5 20 120

PVR =
Qp

Baim DS and Grossman W. Cardiac Catheterization, Angiography, and Intervention. 5th Edition. Baltimore:
Williams and Wilkins, 1996.

Vascular Resistance
Systemic Vascular Resistance
Increased
Systemic HTN
Cardiogenic shock with compensatory arteriolar constriction
Decreased
Inappropriately high cardiac output
Arteriovenous fistula
Severe anemia
High fever
Sepsis
Thyrotoxicosis

639
Vascular Resistance
Pulmonary Vascular Resistance
Increased
Primary lung disease
Eisenmenger syndrome
Elevated pulmonary venous pressure
Left-sided myocardial dysfunction
Mitral / Aortic valve disease
Volume flows are expressed in liters per minute,
Pressures are expressed in (mm Hg).
Resistance in - resistance units (R units) expressed in mm Hg per liter per
minute, also called hybrid resistance units (HRUs).
These HRUs are sometimes referred to as Wood units
They may be converted to metric resistance units expressed in dynes-
sec-cm-5 by use of the conversion factor 80.
In pediatric practice, it is conventional to normalize vascular resistances
for body surface area (BSA), thus giving a resistance index.
SVRI equals SVR multiplied by BSA
PVRI equals PVR multiplied by BSA

640
Hemodynamic Parameters
Reference Values

Hemodynamic Parameters
Reference Values
Average Range Average Range

Right atrium PCWP

a wave 6 2-7 mean 9 4 - 12
v wave 5 2-7 Left atrium
mean 3 1-5 a wave 10 4 - 16
Right ventricle v wave 12 6 - 21
peak systolic 25 15 - 30 mean 8 2 - 12
end diastolic 4 1-7 Left ventricle
Pulmonary artery peak systolic 130 90 - 140
peak systolic 25 15-30 end diastolic 8 5 - 12
end diastolic 9 4-12 Central aorta
mean 15 9-19 peak systolic 130 90 - 140
end diastolic 70 60 - 90
mean 85 70 -105
Davidson CJ, et al. Cardiac Catheterization. In: Heart Disease: A Textbook of Cardiovascular Medicine,
Edited by E. Braunwald, 5th ed. Philadelphia: WB Saunders Company, 1997

Fick Oxygen Method: O2 Consumption

Polarographic O2 Method
Metabolic rate meter
Device contains a polarographic oxygen sensor cell, a hood, and a
blower of variable speed connected to a servocontrol loop with an
oxygen sensor.
The MRM adjusts the variable-speed blower to maintain a unidirectional
flow of air from the room through the hood and via a connecting hose to the
polarographic oxygen-sensing cell.

641
 Fick Oxygen Method: O2 Consumption

Polarographic O2 Method
VM = VR + VE - VI VE
VM = Blower Discharge Rate VI
VR = Room Air Entry Rate
VI = Patient Inhalation Rate VR VM
VE = Patient Exhalation Rate

VO2 = (FRO2 x VR) - (FMO2 x VM)

FRO2 = Fractional room air O2 content = 0.209
FMO2 = Fractional content of O2 flowing past polarographic cell

Fick Oxygen Method: O2 ConsumptionDouglas Bag Method

Volumetric technique for measuring O2
Analyzes the collection of expired air
Utilizes a special mouthpiece and nose clip so that patient
breathes only through mouth
A 2-way valve permits entry of room air while causing all expired
air to be collected in the Douglas bag
Volume of air expired in a timed sample (3 min) is measured with a
Tissot spirometer

642
 Fick Oxygen Method: O2 Consumption

Douglas Bag Method

Barometric pressure = _________ mm Hg
Barometric temperature = _________ C
Corrected barometric pressure = _________ mm Hg
pO2 room air = _________ mm Hg
pO2 expired air = _________ mm Hg
Tissot: initial = _________ cm
Tissot: final = _________ cm
Sample volume (oxygen analysis) _________ L
Correction factor _________ (standard tables)
Collection time _________ min

Fick Oxygen Method: O2 Consumption

Fick Oxygen Method: O2 Consumption

Douglas Bag Method

Step 1: Calculate oxygen difference
pO2 room air x 100
O2 content room air =
Corrected barometric pressure

pO2 expired air x 100

O2 content expired air =
Corrected barometric pressure

Oxygen difference =
O2 room air - O2 expired air = ______ mL O2 consumed / L air

643
Fick Oxygen Method: O2 Consumption

Douglas Bag Method

Step 2: Calculate minute ventilation
Tissot difference = Tissot initial Tissot final = _____ cm
Tissot volume = Tissot difference x correction factor = _____ L

Total volume = Tissot volume + sample volume = _____ L

Ventilation volume (corrected to STP) =

Total volume expired air x correction factor = _____ L
Ventilation volume
Minute ventilation =
Collection time

Fick Oxygen Method: O2 Consumption

Douglas Bag Method

Step 3: Calculate oxygen consumption
O2 consumption = O2 difference x minute ventilation

O2 consumption
O2 consumption index =
Body surface area

644
Commonly used Formulas

645
Calculation with Example

646
 TYPICAL ANGIOGRAPHIC PROJECTIONS AND LESIONS BEST IMAGED
Projection Degrees Vessel/Chamber Lesion(s)
Imaged
Long axial oblique 70 LAO, LV Membranous VSD,
30 cranial conotruncal VSD, LVOT
obstruction
Hepatoclavicular 45 LAO, LV AV canal defect, midmuscular
45 cranial VSD
Four chambers LV-RA connections
PS/PPS/TGA/DORV
Coarctation/PDA
Lateral 90 RV/branch PAs Coarctation/aortic valve
Descending aorta disease
LAO 6070 Aorta TOF/PA stenoses
LAO
LAO-cranial 15 LAO, MPA-branch origins ASD, PFO
30 cranial
Steep LAO-cranial 60 LAO, Atrial septum TOF/PS/DORV
15 cranial
AP-cranial 0 LAO, RV/conduits TGA/DORV/ anomalous CA
30 cranial origins
AP-caudal 0 LAO, Ascending TGA/DORV/peripheral PS
45 caudal aorta/coronary artery
origins
AP 0 RV, peripheral PAs Pulmonary vein
Pulmonary veins stenoses/anomalies of
origin/connection
RAO 30 RAO LV Anterior VSD, mitral valve
disease
Ao, aorta; ASD, atrial septal defect; AV, atrioventricular; CA, coronary artery; DORV,

647
double-outlet right ventricle; LAO, left anterior oblique; LV, left ventricle; LVOT, left
ventricular outflow tract; PA, pulmonary artery; PDA, patent ductus arteriosus; PFO, patent
foramen ovale; (P) PS, (peripheral) pulmonary stenosis; RAO, right anterior oblique; RV, right
ventricle; TGA, transposition of the great arteries (L, left; D, right); TOF, tetralogy of Fallot;
VSD, ventricular septal defect.

Common Operations
ASD OS closure
Under GA & Supine position. Parts are painted &Draped. Chest opened
through Median sternotomy. Hemostasis achieved. Thymus removed.
Pericardium opened towards the rt. Side & stays put. Anatomy assessed.
Looked for LSVC & Rt. PAPVC.Systemic heparinisation done with 3-5mg/Kg
Heparin.Aortic & caval purstrings taken.Cardioplegia purstrings
taken.Cannulated with Aortic & two caval cannulae. Once ACT crossed 480
seconds went on CPB. Cardioplegia cannula put. Cavae looped & SVC snugged.
Aorta was cross clamped. Patient was cooled to 28 degree centigrade. Cold
blood antegrade cardioplegia used (20ml/kg). IVC snugged & RA opened
obliquely. Stays put on RA. Anatomy assessed. Mitral & tricuspid valve
checked for regurgitation. Pericardium was harvested as per the size of ASD. 4-
0/5-0 Polypropylene suture taken & 1st suture passed through the septum at
the 50 clock position & suturing was done towards the surgeon till upper edge
of the ASD. Reawarming started. Now the other end of the suture is used &
closure of the remaining part of the ASD done. Deairing of the left heart done
by asking anaesthetist to ventilate & hold the breath. Root vent connected,
trendlenberg position put. Cross clamped released. RA closed with 5-0
polypropylene suture. Right heart deaired after clamping the IVC cannulae&
releasing the snugger. Heart started beating into SR spontaneously. Came off
CPB gradually.Decannulated.Protamine given. Hemostasis achieved.

648
Pericardium closed over the heart. Pacing wire put. Pericardial & mediastinal
chest drains put. Sternum & chest closed in layers.
ASD OP Repair
Kirklins Technique
After median sternotomy, the pericardium was cut on rt. side & stayed. After
heparinising the patient, the purse string sutures were taken around the aorta;
proposed site for ante plegia cannula, SVC & IVC.The SVC was looped around.
The aorta was cannulated. The SVC & IVC were cannulated with angled
cannulae. Established standard CPB. Went around the IVC after dissecting
around & looped it. Ante plegia cannula put. Patient cooled. SVC snared. Cross
clamped & gave antegrade blood cardioplegia. Snared the IVC & opened the
RA. The ASD was visualized. After satisfactory arrest the RA margins were fixed
with silk stays. The ASD margin was retracted & the Mitral valve was
visualized. It was found to be as described. The cleft in the Mitral valve was
sutured with four separate interrupted 5-0 prolene sutures. There was trivial
MR after repair. The OPASD was closed with untreated autologous pericardial
patch keeping the Coronary sinus on the LA side. The patient was rewarmed.
The left heart was deaired through PFO. With head end down with root vent
connected & on, declamped & defibrillated into SR. RA closed on beating heart.
Came off CPB without support.Decannulated in stages. Mediastinal
&pericardial tubes put. After verifying the counts chest was closed after
satisfactory hemostasis. Shifted to ICU with stable hemodynamics & connected
to the ventilator.
McGoons Technique
After median sternotomy, the pericardium was cut on rt. side & stayed. After
heparinising the patient, the purse string sutures were taken around the aorta;
proposed site for ante plegia cannula, SVC & IVC.The SVC was looped around.
The aorta was cannulated. The SVC & IVC were cannulated with angled
cannulae. Established standard CPB. Went around the IVC after dissecting
around & looped it. Ante plegia cannula put. Patient cooled. SVC snared. Cross
649
clamped & gave antegrade blood cardioplegia. Snared the IVC & opened the
RA. The ASD was visualized. After satisfactory arrest the RA margins were fixed
with silk stays. The ASD margin was retracted & the Mitral valve was
visualized. It was found to be as described. The cleft in the Mitral valve was
sutured with four separate interrupted 5-0 prolene sutures. There was trivial
MR after repair. The OPASD was closed with untreated autologous pericardial
patch keeping the Coronary sinus on the RA side. The patient was rewarmed.
The left heart was deaired through PFO. With head end down with root vent
connected & on, declamped & defibrillated into SR. RA closed on beating heart.
Came off CPB without support.Decannulated in stages. Mediastinal &
pericardial tubes put. After verifying the counts chest was closed after
satisfactory hemostasis. Shifted to ICU with stable hemodynamics & connected
to the ventilator.
ASD SV Repair
Double patch technique
Under GA,chest painted and draped, median sternotomy was done,
pericardium was opened to the right after dissecting the thymus, Stays taken,
patient was heparinised,went on to CPB aortic, SVC & IVC cannulae.Cooled to
28 deg celicius,aorta was cross clamped, cold antegrade cardioplegia was used
to arrest the heart with surface ice slush to cool the myocardium. With good
arrest the cavae snugged, RA was opened through posterior vertical incision
and stays taken. SV type of ASD was enlarged towards the septum secundum
& margins endothelialized.ASD SV closed with rerouting of RSPV & RMPV into
LA using autologous untreated pericardial patch using 5-0 prolene sutures.
Patient was rewarmed, left heart was deaired with head end steep down with
aortic root vent on and cross clamp released. RA was closed & SVC was
enlarged with autologous untreated pericardial patch. Came off CPB. Heparin
was reversed, decannulated, after obtaining satisfactory haemostasis the
sternotomy was closed in layers with chest tubes & pacing wires .Shifted to
ICU with stable haemodynamics.
650
Single patch Technique
Under GA,chest painted and draped, median sternotomy was
done, pericardium was opened to the right after dissecting the thymus, Stays
taken, patient was heparinised, went on to CPB with aortic, RAA straight &
IVC angled venous cannulae. Cooled to 30 deg Celsius, aorta was cross
clamped; cold antegrade cardioplegia was used to arrest the heart with surface
ice slush to cool the myocardium. With good arrest the cavae snugged, SVC-RA
junction was opened through vertical incision. ASD SV closed with rerouting of
RSPV & RMPV into LA using autologous untreated pericardial patch using 5-0
prolene sutures by single patch technique. Patient was rewarmed, left heart
was deaired with head end steep down with aortic root vent on and cross clamp
released. Came off CPB. Heparin was reversed, decannulated, after obtaining
satisfactory haemostasis the sternotomy was closed in layers with chest tubes.
Shifted to ICU with stable haemodynamics.
Closed Mitral Valvotomy
Under GA patient was positioned in the right lateral, part painted and draped,
chest entered through left anterolateral throacotomy through 5th ICS.
Pericardial was opened anterior to the phrenic nerve & stays taken. LV apical
purstring suture taken using 2-0 silk & controlled ventriculotomy was done,
purse string sutures were taken on the LAA. LAA was calmped using satinsky
clamp & opened the LAA. Opening extended using potts scissor. Index finger of
the rt. Hand inserted in the opening of LAA. Ask assistant to remove the clamp.
The MV felt at both commissures & MR assessed. Tubbs dilator inserted
through ventriculotomy. The tip of the Tubbs dilator passed across the MV
opening. If opening is small finger fracture technique to be used to widen the
mitral valve opening. Tubbs dilator placed across the maitral valve & opened
against the leaflet/ perpendicular to commissures. Dilatation to be done
gradually. Tubbs dilator removed & Silk suture with snugger tightened. Assess
MV for opening, Subvalvar pathology & MR. Finger is removed from the LAA
with the remaining 3 fingers pressing against the LAA. The purstring suture
651
tied. Reinforcing suture over LAA put. LV opening closed with 4-0 prolene
suture & silk purstring tied. Pericardium washed with plenty of normal saline
& Pericardium was approximated. After obtaining satisfactory haemostasis, the
thoracotomy was closed in layers with ICD tube and shifted to ICU with stable
haemodynamics in NSR.
Mitral Valve Replacement
Under GA chest was opened by median sternotomy incision. Pericardium
opened & stayed. Purse string sutures were taken over the aorta, RAA /SVC
and inferior venacavae. After heparinisation the vessels were cannulated.
Went on CPB. Patient was cooled up to 28 Deg cels. Cross clamped the aorta &
started cold antegrade plegia . The Waterston groove was dissected & LA was
stabbed. After satisfactory arrest, the LA was opened. MV was assessed. The
AML was caught with Vulsalum/ Allis forcep/ Silk stay suture. Incision made
on AML at 12 Oclock position. Incision was extended on both the side. Valve
was excised & replaced with 29M St. Jude bileaflet prosthetic valve using 2-0
Ethibond interrupted pledgetted sutures. Valve was checked for opening &
closing. A Foley catheter put across the valve. All sutures cut. Saline wash
given.LA closed directly after deairing & Foley catheter removed.
Rewarmed.Declamped & defibrillated .Came off CPB. After satisfactory
hemostasis, chest tubes were put. Pericardium was closed .Chest closed in
layers after verifying the counts. Shifted to ICU.
Aortic Valve Replacement
Under GA, part painted and draped, median sternotomy done, thymus divided
in the midline, pericardium opened in the midline and marsupialised, Aortic
and RAA purse string sutures were taken,heparinised and went onto CPB with
aortic & two stage venous cannulae,LV vented through RSPV,Core cooled to 28
degree C, aorta was cross clamped, retrograde cold blood cardioplegia was
started and aorta was opened with reverse hockey stick incision about 1.5-1.75
cms above the RCA origin and stays taken, direct ostial antegrade cold blood
cardioplegia was delivered to both the coronaries, Topical ice slush was applied
652
to further cool the myocardium ,After obtaining satisfactory arrest, the aortic
valve was excised . The root & cavity were thoroughly washed. Aortic annulus
sized. The valve was taken & ,2-0 Polyester interrupted pledgetted sutures were
passed along the annulus and passed through the valve ring, parachuted and
tied, Valve checked for opening & closing.Aortotomy was closed using no.4`0
prolene suture, Rewarmed,aortic cross clamp was released with head end steep
down with aortic root and LV vent on, defibrillated, Gradually came off CPB in
SR,Heparin was reversed,decannulated in stages, After obtaining satisfactory
hemostasis, chest drains were placed, one ventricular pacing wire put,
Pericardium approximated loosely throughout, Chest closed in layers, Shifted
to ICU with stable hemodynamics and electively ventilated.
MVR & AVR (DVR)
Under GA & supine position, Parts painted & draped. Median sternotomy done,
Pericardium opened, Purstring sutures taken over Aorta, SVC /RAA & IVC.
After systemic heparinisation, went into CPB after cannulating the aorta, SVC
& IVC. Core cooled, cross clamped & stabbed the LA. Opened the aorta & gave
direct coronary osteal plegia. After satisfactory arrest, the aortic valve was
assessed & excised. The sutures were taken & driven through the prosthetic
valve but the valve was not lowered.
Next, the LA was opened fully, mitral valve assessed. It was excised & replaced
with prosthetic mitral valve using interrupted pledgetted sutures. Next, the
aortic valve was lowered & the sutures tightened & tied so as to fix the aortic
valve. The aorta was next closed in two layers of continuous Prolene.
Rewarmed. Foley's catheter put through the mitral valve while LA was closed
with continuous Prolene. The heart was declamped with root vent on.
Defibrillated. LA vented. Later Foleys catheter removed & suture line tightened
& tied. Came off CPB.Decannulated in stages. Chest tubes put. Counts verified.
Chest closed in layers. Shifted to ICU with stable hemodynamics & connected
to ventilator.

653
VSD Closure
Under GA, patient positioned, part painted and draped, median sternotomy
done, thymus divided in the midline, right lobe of the thymus excised,
pericardium opened in the midline and marsupialised, Aortic, SVC and IVC
purse string sutures were taken, heparinised and went on to CPB with aortic ,
SVC and No IVC straight venous cannulae, Core cooled to 28 degree C, aorta
cross clamped, root cold blood cardioplegia was delivered ,SVC and IVC were
snugged and RA opened and stays taken, LA/LV vented through PFO, After
obtaining satisfactory arrest, VSD was closed with Dacron patch using
interrupted pledgetted prolene ,
Suturing for various types of VSDs
1) PM/SA VSDs- Start from the base of tricuspid valve. Transition from
valve to ventricular septum about 0.5-1.0 cm below the VSD margin.
2) SP/DC VSD- Approach through MPA. Start from Centre of VSD at septal
level. Come on both side up till you reach pulmonary valve. Pass part of
the sutures through pulmonary annulus.
3) MM/Inlet Muscular VSD- Start from the base of tricuspid valve,
Transition 0.5cm below the VSD margin. Care to be taken at upper
margin of VSD as conduction runs there.
PFO was closed directly, Rewarmed, left heart was deaired through aortic root
vent on with head end steep down and aortic cross clamp was released,
Defibrillated. RA was closed using no. 5`0 prolene suture, Came off CPB,
Heparin was reversed and decannulated in stages, pacing wires placed, chest
drains were placed, pericardium was loosely approximated throughout, After
obtaining satisfactory haemostasis, chest was closed in layers, Shifted to ICU
with stable haemodynamics and electively ventilated.

654
TOF Correction

Trans RA without TAP:

Under GA & Supine position, parts painted & drapped.After median
sternotomy, the pericardium was opened towards right & stays put
.Cannulated the aorta, SVC, & IVC. MPA was dissected from the aorta. SVC &
IVC looped. Antegrade plegia cannula put. After heparinisation went on CPB.
Core cooled to 28 Deg C .Cross clamped the aorta. Gave antegrade cold blood
cardioplegia with topical ice-slush to cool the heart. After satisfactory arrest,
cavae snugged & RA opened. LV vented through PFO. Anatomy assessed. The
RVOT was cored out from RA. Bands & bundles cut, starting at 1 Oclock
position. Avoid cutting TSM. The RVOT was sized with Hegars. The VSD was
closed through the RA using a Dacron patch with interrupted pledgetted
Prolene. Surgically created PFO closed directly after deairing the left heart.
Rewarmed.Declamped with root vent on with head end down. Heart started
beating. RA closed directly on beating heart. Came off CPB on
inotropes.Decannulated in stages. Chest tubes & pacing wire put. Chest closed
after verifying counts after satisfactory hemostasis. Shifted to ICU with stable
hemodynamics & connected to ventilator.
Trans RA & PA with TAP:
Under GA & Supine position, parts painted & drapped.After median
sternotomy, the pericardium was opened towards right & stays put
.Cannulated the aorta, SVC, & IVC. MPA was dissected from the aorta. SVC &
IVC looped. Antegrade plegia cannula put. After heparinisation went on
CPB.Core cooled to 28 Deg C .Cross clamped the aorta. Gave antegrade cold
blood cardioplegia with topical ice-slush to cool the heart. After satisfactory
arrest, cavae snugged & RA opened. LV vented through PFO. Anatomy
assessed. MPA opened vertically. The RVOT was cored out from RA& PA.
Bands & bundles cut, starting at 1 Oclock position from RA. Avoid cutting
TSM. Pulmonary valvotomy/valvectomy done. The RVOT was sized with
655
Hegars. The VSD was closed through the RA using a Dacron patch with
interrupted pledgetted Prolene. RVOT & MPA augmented with autologous
pericardial transannular patch. Surgically created PFO closed directly after
deairing the left heart. Rewarmed.Declamped with root vent on with head end
down. Heart started beating. RA closed directly on beating heart. Came off CPB
on inotropes.Decannulated in stages. Chest tubes & pacing wire put. Chest
closed after verifying counts after satisfactory hemostasis. Shifted to ICU with
stable hemodynamics & connected to ventilator.
TAPVC Correction
Supracardiac TAPVC
Under GA, chest was painted and draped. Pericardium was opened to the right
after excising the thymus. Vertical vein dissected & looped doubly outside the
pericardium. Patient was heparinised. Went on to CPB with aortic, angled SVC
& IVC cannulae. LAA tip was ligated & suture kept on clamp to determine the
LAA base. Cooled to 28 degree celicius, aorta was cross clamped, cold
antegrade blood cardioplegia was used to arrest the heart with surface ice
slush used to cool the myocardium. Common Chamber stabbed near RA-CC
junction. The RA was opened by vertical incision. The incision extended across
the ASD into LA posterior wall till the base of LAA. Common chamber incision
was extended towards the left till the opening of left pulmonary veins. Anatomy
of all pulmonary veins assessed. Common chamber draining LPV& RPV
anastomosed with LA using prolene suture, The opening should be at least the
size of Mitral valve. ASD closed with autologous pericardium. Left heart
deaired at the end of ASD closure. VV ligated near its junction with innominate
vein. Declamped with root vent on & head end down. Defibrillated the heart.RA
closed on beating heart. Came off CPB. Pacing wire & chest tubes put. Chest
closed. Counts verified. After satisfactory hemostasis shifted to ICU with stable
haemodynamics.

656
Pericardiectomy
Under GA & supine position, part painted and draped, median sternotomy,
thymus divided in the mid-line, Pericardium opened over the ascending aorta
and extended over RVOT, LV was released first over the inferior wall and lateral
wall, Dopamine started electively at 3 mics/Kg/mins .Densely adherent
pericardium over the RA, RVOT and over the inferior wall of the LV was slowly
and gradually debrided, SVC and IVC were fully released. Pericardium was
excised from right to left phrenic nerves& innominate vein to diaphragm. Both
pleura opened widely. After obtaining satisfactory haemostasis, chest drains
were placed, Chest closed in layers and shifted to ICU with stable
haemodynamics and electively ventilated.
PDA Ligation
Under GA & left lateral position. Chest opened by left posterolateral
thoracotomy. Mediastinal pleura over the aorta opened, Left superior
intercostals vein ligated & cut. Stays put on mediastinal pleura. PDA dissected
& looped around with silk. Under hypotensive anaesthesia, the PDA was ligated
doubly with no. 2 silk/Floss silk .After satisfactory hemostasis, the overlying
mediastinal pleura was closed. Chest tube was put. The chest was closed in
layers. Shifted to ICU with stable hemodynamics in SR.
PDA D/S
Under GA & left lateral position. Chest opened by left posterolateral
thoracotomy. Mediastinal pleura over the aorta dissected & stays taken. PDA
dissected & looped around with silk. PDA was clamped & divided & both ends
of the PDA sutured with 5-0 prolene suture. After satisfactory hemostasis, the
overlying mediastinal pleura were closed. Chest tube was put. The chest was
closed in layers. Shifted to ICU with stable hemodynamics in SR.
Coarctation Repair
Under GA & left lateral position. Chest opened by Left posterolateral
thoracotomy through the fourth space. The aorta was exposed after cutting &

657
staying the overlying mediastinal pleura. The coarcted segment & the great
vessels identified, dissected around & looped. The intercostals were divided &
looped respectively. The aorta above & below the coarct was looped. After
systemic Heparinisation, the aortic arch proximal to the Coarctation was
clamped with a curved clamp proximal to LSCA, & the left subclavian was also
clamped with straight clamp. The aortic arch distal to the coarctated portion
was also clamped with a straight clamp. The PDA dissected looped & divided,
the end was sutured with 5-0 prolene suture. The Coarctation segment was
next excised leaving wide lumen of the aorta on either side. Both end s were
anastomosed with continuous prolene. The distal mean arterial pressure [as
measured by the Lt FA pressure-line always maintained around 35-40 mmHg
throughout the anastomoses]. After the anastomoses, the aortic clamps were
released one by one & satisfactory hemostasis ensured. Mediastinal pleura
were closed. Chest closed after verifying the counts & putting the chest tube.
Shifted to ICU in stable condition.

Cardiovascular Medications

Terminologies
1. Adrenergic: Norepinephrine as a neurotransmitter, Effect on cells of
Autonomic nervous system (ANS).
2. Cholinergic: Acetylcholine as a neurotransmitter, Effect on cells of
Autonomic nervous system (ANS).
3. Sympathomimetic: Sympathetic nervous system stimulant.
4. Sympatholytic: Sympathetic nervous system blocker.
5. Chronotropic: Affecting the Heart rate.
6. Inotropic: Affecting the force of myocardial contraction.
7. Dromotropic: Affecting the velocity of conduction.
Adrenergic receptors

658
Types Receptor sites Stimulation
Response
Alpha () Peripheral arteries Vasoconstriction
Beta1 (1) Myocardium & Increase contractility &
(remember 1 heart, conduction system Heart rate
two lungs)

Beta2 (2) Vascular smooth Coronary & peripheral

muscle vasodilatation
Bronchodilatation
Bronchi(Lungs)
Dopaminergic Renal & Mesenteric Vasodilatation
Vasculature
Cardio active Drips
Drugs to Improve Cardiac output
Dobutamine
Action :Almost exclusively a Beta-1 agonist with no alpha effect, and
minimal beta-2 effect
Effect : Inotropic and chronotropic effects on the heart,
Decrease in peripheral vascular resistance (Decreases afterload)
and
Improvement of AV node conduction
Use: To improve cardiac output and blood pressure, can be administered
peripherally.
Dose: 5-20 Micgm /Kg/Min.
May cause tachyarrhythmia, fluctuations in BP.
Cardiac & hemodynamic monitoring is recommended.
Risk: Increases myocardial oxygen demand may increase heart rate
excessively.

659
Dopamine
Action : precursor of norepinephrine, stimulates dopaminergic, alpha
and beta adrenergic receptors (little or no beta-2 effect)
Effect :
Low doses (2-5mcg/kg/min) minimal alpha effects, causes more
splanchnic dilatation, improving renal blood flow (a dopaminergic
response).
Medium doses (5-10mcg/kg/min) beta effects start to predominate.
High doses (10-20mcg/kg/min) alpha effects more prevalent
Use : Good first line to improve cardiac output when used in mid-range,
Hypotension with signs & symptoms of shock
Risk: High doses may cause vasoconstriction. Adverse effects on
immune function.
Use only after volume replacement in hypovolemic patient.
May cause tachyarrhythmia, excessive vasoconstriction.
Avoid extravasation administer phentolamine SQ in area of extravasation
to minimize tissue necrosis.
Epinephrine (0.01 to 1 mcg/kg/min, or higher in very critical situations, usual
dose range in cardiac patients is 0.03-0.3, in septic patients doses may be
higher)
Action : Potent non-selective beta agonist also an alpha agonist
(Beta>alpha)
Effect : Increases inotropic and chronotropic cardiac activity also causes
peripheral vasoconstriction, decreasing peripheral perfusion
Use :
To increase cardiac output and blood pressure, at lowest doses
(<0.1mcg/kg/min has primarily beta-1 effects).
Ventricular fibrillation, pulseless ventricular tachycardia, asystole,
pulseless electrical activity
Severe allergic reactions, anaphylaxis
660
 Cardiac arrest - 1.0 mg IVP; may repeat q 3-5 minutes
Endotracheal administration - 2.0-2.5 mg diluted in 10 ml. NS
Profound bradycardia - 2-10 mcg/minute
Risk: Can cause profound peripheral vasoconstriction, compromising
tissue perfusion. Long term use down regulates catecholamine
receptors, decreasing effect, also increases myocardial oxygen demand
If administration causes rapid, marked rise in BP, can see aortic rupture,
cerebral hemorrhage, or angina pectoris.
ADMINISTRATION OF SC PREPARATION BY IV ROUTE MAY CAUSE
SEVERE OR FATAL HYPERTENSION OR CEREBROVASCULAR
HEMORRHAGE
Drugs to Improve Cardiac Output and cause Vasodilatation
Milrinone, Amrinone
Action : Phosphodiesterase inhibitor,
Prolonging the effect of cAMP allowing increasing ionized calcium
entry into cardiac cells increasing myocardial contractility, and cAMP
dependent vascular relaxation
Effect: Peripheral vasodilator and positive inotropic effect on heart,
improved diastolic relaxation. May cause reflex tachycardia due to
vasodilatation
Use: Afterload reduction, additional inotropic support when
catecholamines already in use. Severe CHF unresponsive to diuretics,
vasodilators, and conventional inotropic therapy
Dose: 0.75 mg/kg loading dose over 2-3 minutes; may repeat after 30
minutes if necessary. Maintenance infusion of 5-10 mcg/kg/minute.
Risk: As with other inotropes, can also potentially cause too much
vasodilatation leading to hypotension, use caution in severely
hypovolemic patients
May cause tachycardia, hypotension, or thrombocytopenia.

661
 Incompatible with dextrose solutions & other IV drugs.
Isoproterenol (Isoprenaline)
Action: Potent Beta 1 & 2 stimulant.
Effect : Inotropic (beta), chronotropic effects
Use : Symptomatic bradycardia unresponsive to other therapy
Dose: 0.05- 1 micg/Kg/min.
Quickly elevates the heart rate.
Increases myocardial oxygen requirements; may increase myocardial
ischemia.
Contraindicated in tachyarrhythmia & digitalis toxicity.
Do not give with epinephrine - may cause VF/VT.
Drugs to cause vasodilatation
Nitroprusside (Nipride)
Action : It has direct activity on vascular smooth muscle (donates an NO
group to be specific)
Effect: Peripheral vasodilator by relaxation of smooth muscles in vessels-
Arteriolar dilator.
Use: Used as an afterload reducer, primarily an arteriolar vasodilator
can increase tissue perfusion in patients receiving vasoconstrictors, can
be given peripherally.
Hypertensive crisis
To reduce afterload in heart failure, acute pulmonary edema, or acute
mitral or aortic valve regurgitation
Begin at 0.10 mcg/kg/minute and titrate upward every 3-5 minutes to
desired effect (up to 5.0 mcg/kg/minute)
Dose : 0.5-10mcg/kg/min
Risk: Cyanide and Thiocyanate toxicity from prolonged usage of high
doses: blurred vision, tinnitis, confusion, hyperreflexia, seizures. (Using
Na thiosulfate decreases risk 10mg/mg nitroprusside).

662
 Risk of severe hypotension in patient who is intravascularly dry.
Drug is light-sensitive; therefore, wrap drug reservoir in aluminum foil.
Use with an infusion pump; closely monitor blood pressure during
therapy.
Nitroglycerin
Action : Relaxes peripheral vascular smooth muscle by donating an NO
group
Effect : Causes peripheral vasodilatation, decreasing pre-load and
decreasing blood pressure, helps prevent vasospasm (General
venodilatation)
Use: Most commonly used in post-operative, arterial switches to help
prevent coronary vasospasm, sometime used as a preload reducer, can
be given peripherally.
Low doses - venous; high doses - arterial
Preload reduction and coronary vasodilatation
Useful in management of ischemia
Decrease LVEDP and pulmonary vascular congestion
Chest pain of suspected cardiac origin
Unstable angina
Dose : 0.5-5mcg/kg/min
Risk: Can cause severe hypotension in patient who is intravascularly
dry, risk of methemoglobinemia, otherwise similar to nitroprusside.
Complications of acute myocardial infarction, including CHF & LV
failure
Monitor VS & EKG during therapy
Drugs to increase systemic vascular resistance (increase afterload)
Norepinephrine (Levophed)
Action : Potent alpha adrenergic agonist and beta agonist (alpha>beta)

663
 Effect : Vasoconstriction and inotropic and chronotropic effects,
increasing blood pressure, both by increasing SVR and by increasing CO
Use : In patients already on vasopressors requiring more support to
maintain blood pressures, Septic shock, Cardiogenic shock
,Hemodynamically significant hypotension
Dose : Initial dose 0.05-0.1mcg/kg/min, titrate to effect
Risk : Decreases blood flow to all organs and tissues, can cause
worsening metabolic acidosis due to ischemia
Increases myocardial oxygen requirements and may induce arrhythmias,
therefore use cautiously in patient with cardiac ischemia.
Extravasation causes tissue necrosis
Phenylephrine (Neo-Synephrine)
Action : Alpha adrenergic agonist
Effect : Constricts both arterial and venous blood vessels, increasing
systemic vascular resistance without changing cardiac dynamics
Use: In patients who need blood pressure support, where muscular
outflow obstruction may be worsened by the use of Beta agonists, such
as unrepaired TOF or hypertrophic cardiomyopathy.
Treatment of hypotension in shock and shock-like states
Dose : 0.1-0.5mcg/kg/min as drip, 5-20mcg/kg as bolus
Risk: Decreases flow of blood to all organs, reducing oxygen supply and
potentiating ischemia at very high doses can have some beta effect.
Continuous monitoring of cardiac rhythm & BP is required during
infusion.
Avoid extravasation; if it occurs, administer phentolamine locally to
prevent tissue necrosis.
Also Epinephrine and Dopamine to some extent
Cautions for vasopressors
- Adversely affect Stroke volume, myocardial oxygen demand & Blood flow
to non vital organs.
664
 - Ineffective & contraindicated in volume depleted patients.
- Local tissue ischemia & necrosis can occur with extravasation of infusion
in peripheral site.(should be given through central line)
- Induce cardiac arrhythmias.
Drugs to cause pulmonary vasodilatation
Nitric Oxide (0-80ppm inhalation)
MOA: Activates cGMP pathway causing direct smooth muscle
relaxation in local vascular bed
Effect: Since given as inhalational agent, causes relaxation of
pulmonary vascular bed only, with no systemic effect
Use: Used to decrease pulmonary vascular resistance in patients in
whom pulmonary hypertension is a problem, either from a cardiac
output standpoint or from a oxygenation standpoint
Risk: Can combine with Hgb to form methemoglobin, needs closed
ventilatory circuit and constant monitoring.
Blockers
Mechanism of stimulation :
receptor stimulation
1 stimulation Increase Calcium in cells HR, Conduction,
Contraction
2 stimulation Smooth muscle relaxation
Types
1. Cardioselective- Blocks only 1 receptors ATENOLOL, METOPROLOL
2. Non selective agents Blocks both receptors(1+ 2)- PROPRANOLOL
3. + Blocking effect- LABETOLOL
4. Ultrashort acting blockers ESMOLOL
Effects
1. Heart Negetive Chronotropic-SA node
Negetive Dromotropic AV node
Negative Inotropic Myocardium
665
 Anti ischemic
Anti arrhythmic
2. Coronaries & Myocardial perfusion
Coronary vasospasm
Better diastolic myocardial perfusion
3. Systemic circulation
Norepinephrine release
adrenergic outflow
Circulatory rennin
Uses
1. CVS- IHD,HTN,Arrhythmia,Cardiomyopathies
2. Other CVS- Aortic dissection, Marfans syndrome, TOF
3. Non cardiac Anxiety, Tremor,Migraine,Glaucoma,Oesophageal varieces
Contraindications-
1. Cardiac Severe bradycardia, Heart blocks, LVF.
2. Pulmonary Asthma, bronchospasm.
3. CNS- Severe depression.
4. Vascular Active PVD with rest ischemia.
Side effects Bronchospasm, Cold extremities, Bradycardia, Heart block,
Insomnia, Depression.
No blocker is completely safe in presence of Asthma, low dose of
cardioselective agents can be used with care in patients with
bronchospasm/chronic lung disease/chronic smoking.
Dose
1. PROPRANOLOL-
IV 0.1mg/kg x 10minutes then 0.1-0.3mg/kg/dose 3hourly.
Oral 0.2-0.5 mg/kg/dose 6-12 hourly
2. ATENOLOL
1-2mg/kg/dose 12-24 hourly
3. METOPROLOL
666
 IV 0.1mg/kg
Oral 2mg/kg/dose 6-12 hourly.
4. LABETOLOL
1-2mg/kg/dose 12 hourly
Less bronchospasm & vasoconstriction, Reduce BP very fast.
S/E- Postural hypotension.
5. ESMOLOL
t1/2- 9 minutes.
Used for perioperative SVT & HTN.
Dose- 500 micgm/kg/min over 1 minute
50 micgm/kg/min x 4minute infusion.
100 -300 micgm/kg/min if previous fails.
Extravasation leads to skin necrosis.

Nitrates
Mechanism Exogenous source of Nitric oxide (NO).
Nitroglycerine- SL tabs- effect in a minute, last for 1 hour,
0.3-0.6mg-> 1.5mg
Spray 0.4mg/metered dose
Oral capsule 2.5-13mg 1-2 tabs
Ointment 2%- 6x6 inch or 15x15 cm or 7.5-40mg.
Patch 0.2-0.8mg/hr patch on for 12 hours & off for 12 hours.
Isosorbid dinitrate- Sorbitrate 2.5-15mg.
Mononitrates Monotrate 20mg 12 hourly.
S/E Hypotension, Headache, Tachycardia.
C/I HOCM.
Indication- Angina, MI, CHF.

Calcium Channel Blockers

Most commonly agents used for angina & HTN.
667
Mechanisms
Interference of Ca2+ - mediated smooth muscle contraction - coronary and
peripheral smooth muscle relaxation
Selective Ca2+ channel inhibition
Use: Treatment of angina pectoris / supraventricular tachycardia /
hypertension

Types DHPs- Nifedipine Non DHPs Non DHPs- Dilzem

Verapamil
Effects Vascular Myocardial selectivity Myocardial
selectivity selectivity
Site Peripheral AV node SA node
Dose 0.25-1mg/kg 6- IV 0.1-0.2mg/kgx 1-3 mg/kg/dose
12 hrly 10minutes then 8hrly
5micgm/kg/min
Oral 1-3mg/kg/dose
8-12 hrly
Indications HTN,Coronary Angina, Coronary Angina, Coronary
spasm spasm, HTN, SVT spasm, HTN, SVT
C/I AS/HOCM/Severe Sick sinus Sick sinus
Myocardial failure syndrome,Digoxin syndrome,Digoxin
toxicity blockers, toxicity, blockers,
Systolic LV failure Systolic LV failure
Others Amlodipine- Long Less constipation
duration of action
0.05-0.2mg/kg/d

Angiotensin Converting Enzyme Inhibitors

Mechanism
668
Angiotensin system Kinin system
Angiotensinogen Kininogen

Angiotensin I Stops Breakdown of Bradykinin
ACE ACE Inhibitors blocks
Angiotensin II Prostaglandin &
NO

1. Aldosteron release Vasodilatation
2. Sympathetic activity
3. Vasoconstriction
Indications HTN, CHF
C/I Bilateral renal artery stenosis
Hypotension
AS, HOCM
Pregnancy
S/E Cough, Hypotension, Renal failure, Hyperkalemia.
Caution Can not be used with Potassium sparing Diuretics.
Dose should be reduced in case of hepatic or renal dysfunction.
Class Drugs Dose Special
I Captopril 0.1mg/kg/dose 8hrly
II Enalapril 0.1mg/kg /d Less cough
Ramipril 0.05mg/kg/d
III Lisinopril 0.1mg/kg/d Water soluble

Angiotensin II receptor Antagonist

Inhibit formation of Angiotensin II.
Used in HTN & heart failure.
Adv- No cough, reduced cholesterol level.
Disadv Absence of renal vasodilatation & endothelial protection by NO.
669
 LOSARTAN 0.5-2mg/kg/d
TELMISARTAN 1mg/kg-2mg/kg/d.

Diuretics
Drug of 1st choice in treatment of symptomatic Heart failure.
Mechanism
1. Heart Failure
Reduce pulmonary & peripheral symptoms & signs of congestion.
Sodium & Water retension.
2. HTN
Natriuresis (Sodium removal) - Shrink the fluid volume.
May work as a Vasodilator.
Types

Type Mechani Drug Dose S/E Special

sm
Loop Removes Furosemide 0.5- Hypokalemia C/I in
Na,K,Cl (Lasix) 1mg/kg/do Dehydrati
from loop se 6-24hrly on &
of Henley Hypokale
mia
Thiazide Inhibit Hydrochlorthi Hypokalemia Longer
reabsorpt azide Hypomagnes action
ion of Na emia Low dose
& Cl in Gout maximu
distal m
part of response
nephron

670
K sparing Inhibit Triameterene 2mg/kg/do Hyperkalemi Independ
Na- se 8-24hrly a ent of
Proton Amiloride 0.2mg/kg/ Aldestero
exchange dose 12- n effect
r 24hrly
Loss of
Na
without
loss of K
K sparing Inhibit Spironolacton Kg Drug of
Spironolact Na-K e dose choice in
one exchange 0-10- NIDDM &
at the 6.25mg bd Gout
site of 11-20-
Aldestero 12.5mgbd
n action 21-40-
25mg bd
Carbonic Acitazolamide 5- Used in
anhydrase 10mg/kg/d Glaucom
inhibitor ose 6-8hrly a

Digitalis (Digoxin)
Inotropic bradycardic action.
Action & Effect:
Inhibit Na-K-ATPase calcium transport into myocardium- positive
inotropic effect
Parasympathomimetic and anti-adrenergic mechanisms-Anti arrhythmic
effect
Mechanism
1. Sodium pump inhibition- Ca++ in cell- Contraction.
671
 2. Parasympathetic activation- Sinus slowing & AV nodal inhibition.
3. Sympathetic inhibition- sympathetic nerve discharge.
4. Renin release- vasodilatation.
Drug interaction - Quinidine, Verapamil, Amiodarone
Indications-

1. CHF with AF/SR.

2. AF.
3. Valvular Heart disease.
4. LVF.
C/I-
1. HOCM.
2. WPW Syndrome.
3. AV nodal heart block.
4. Diastolic dysfunction.
S/E Coloured vision & arrhythmias
Caution IV Digoxin should not be given if K+ is < 4mmol.
Antidote = digibind
Always remember
- Consult a senior member of the staff before starting Digoxin.
- You can give always more, so always start with small doses.
- Always make sure that serum potassium level is > 4.0 mmol/L.
- Be very cautious with digoxin in presence of ventricular
arrhythmias.
Anti Arrhythmic

Class Action Agents

IA Inhibit Na+ transport Quinidine

Reduced dV/dT of action potential Procainamide

672
 IB Slow dV/dT of phase 0 Disoprymadine

Moderate prolongation of repolarization Lidocaine

Prolongs PR, QRS, and QT intervals Phenytoin

IB Limited effect on dV/dT of phase O Mexiletine

Shortens repolarization Tocainide

Shortens QT in clinical doses

Elevates fibrillation threshold

IC Markedly slows dV/dT Flecainide

Little effect on repolarization Ecainide

Markedly prolongs PR and QRS

II Beta-adrenergic blockers Metoprolol

Decrease nodal conduction Atenolol

Propanolol

III Prolongs repolarization Amiodarone

Alters membrane response Beryllium

IV Calcium channel blockers Verapamil

Decrease nodal conduction Nifedipine

Diltiazem

Lidocaine (Xylocard)

Mechanism-
1. Inhibit fast sodium current.
2. Shortens the action potential duration in normal tissue.
Uses SVT with AMI / Post cardiac surgery.

673
Hypokalemia must be corrected for maximum effect.
Dose 1mg/kg IV then 15-50 micgm/kg/min infusion.
S/E Drowsiness/Numbness.

Amiodarone (Cordorone)
Mechanism
1. ERP by prolonging action potential duration.
2. Inhibit inactivated sodium channel.
3. Blocks (Noncompetitively) & receptors.
4. Calcium antagonist action at SA node.
5. Coronary & peripheral vasodilatation.
Widespectrum of action.
Class I/II& III action.
Slow onset of action.
Universal antiarrhythmic drug.
C/I Severe SA node dysfunction.
S/E pulmonary infiltrate.
Dose 5mg/kg loading dose x 30-60 minutes (Hypotension)
5-15 micgm/kg/min.

Adenosine
Adenosine receptors.
3 types
A1- on myocytes: decrease the rate of depolarization
A2a- in CNS: induce sleep
A2b- on vascular endothelium: decrease platelet adherence & cause coronary
vasodilatation
A3- on mast cells: stabilize the cell membrane
Mechanism-
1. K+ channel opener.
674
 2. Inhibit SA & AV nodes.
t 10-30 seconds.
Indication- narrow complex SVT.
C/I- Asthma, Av Blocks, Sick sinus syndrome.
S/E Head ache, Chest pain, Flushing, dyspnoea.
Dose 6mg with saline flush after 10 min
12mg with saline flush.
Should be given rapidly in central line (preferably)
Watch monitor there will be flat line for a second & heart starts beating.
Uses.
1) In CPB- immediately after cross clamping & during reperfusion
2) Correction of arrhythmias
3) Induce sleep (term fatigue factor)
4) For refractory PH

Action is potentiated by dipyridamole

Action inhibited by caffeine & aminophylline
Side effects.
1) Headache & flushing
2) Arrhythmias
Contraindication for adenosine.
Heart block & bradyarrhytmias
Antidote for adenosine.
Aminophylline
Anti thrombotic

Intact Endothelium Anti Aggregatory Prostacycline

Vasodilatory NO
Fibrinolytic tPA
Anti thrombotic Thrombomodulin
675
Vascular Injury Platelet aggregate Coagulation system activated
Antiplatelets
Aspirin,Dipyridamole,Ticlopidine,Clopidogrel
Inhibit platelet aggregation.
Uses- Atrificial heart valves, CAD, PVD, Arteriovenous shunts.
Aspirin- Gastritis
C/I Haemorrahge, Intolerence, GI Bleed.
Dose 3-5mg/kg/d
Dipyridamole ( Persantin)-
Coronary vasodilatation effect.
Dose 1-2mg/kg/dose 6-8 hrly.
Ticlopidine/Clopidogrel GP IIb/IIIa receptor antagonist
Thrombocytopenia & Neutropenia.
Ticlopidine 5mg/kg/dose 12 hrly
Clopidogrel 1.5mg/kg/d.

Anticoagulant
Heparin-
Mechanism- On Coagulation mechanism-Anti thrombin III & Thrombin.
Antiplatelet effect.
Uses- AMI, Acute venous thrombosis, Acute pulmonary embolism,
Coronary angioplasty, Cardiac surgery.
Dose - 1 mg=100 Units
Low dose 75 U/kg then 15U/kg/hr
Full dose 200 U/kg then 15-30 U/kg/hr
S/E Haemorrahge, Thrombocytopenia.
Check APTT Should be 1.5- 2.5 times normal.
ACT - >400 sec.

676
LMWH-
Low-molecular-weight heparin is a relatively recent addition to the list of
therapies for prophylaxis and treatment of deep venous thrombosis (DVT). As a
prophylactic, low-molecular-weight heparin is as effective as standard heparin
or warffarin and does not require monitoring of the activated partial
thromboplastin time or the International Normalized Ratio.
Advantages of low-molecular-weight heparin over standard heparin include
predictable blood levels, lower likelihood of bleeding and no reports of
thrombocytopenia or osteoporosis.

Dalteparin 16 mg per 0.2 mL; 2,500 IU SC 1 to 2 hours before surgery,

(Fragmin) 32 mg per 0.2 mL then 2,500 IU every day for 5 to 10 days

#Heparin was discovered by McLean in 1916.

#It requires the presence of antithrombin III for its action.
Heparin binds to AT III brining about a conformational change converting AT III
from a slow progressive thrombin inhibitor to a very rapid inhibitor.

#Only 1/3rd of the administered dosed of heparin binds to AT & this fraction is
responsible for most of its anticoagulant effects.

#Mechanism of action is:

1) The heparin- AT III complex inactivates a number of coagulation enzymes;
including Thrombin factor IIa, Xa, Ixa, XIa & XIIa. The major effects are due to
inhibition of IIa & Xa.
2) Binds to heparin cofactor II & catalyses inactivation of IIa.
3) Binds to platelets- contributing to the hemorrhagic effects of heparin.
XIIa AT III- heparin complex

XIa AT III- heparin complex

677
IXa AT III- heparin complex

Xa AT III- heparin complex

IIa AT III- heparin complex

Fibrinogen Fibrin

molecular size= 3.000 to 30,000 daltons (approx.=15,000 daltons)

(- Mol wt. of LMWH= 5000 daltons_

#Clearance- High molecular weight moieties are cleared more rapidly than the
low molecular weight moieties.
Heparin is cleared by 2 mechanisms:
Rapid- binding to the endothelial cell receptors and macrophages, where it is
depolymerised
This makes the anticoagulant response to heparin non linear at therapeutic
doses, with both the duration and intensity of the effect rising
disproportionately with increasing doses.
Thus the biological life increases from
30 minutes with IV bolus of 25 IU/ Kg
to
60 minutes with IV bolus of 100 IU/ Kg &
to
150 minutes with a bolus of 400 IU/Kg.

#Action is potentiated in cirrhosis & action is depressed in pulmonary

embolism.

#What is 1 IU heparin?
678
1U of heparin is the amount of heparin that is required to maintain the fluidity
of 1 ml of citrated sheep blood for 1 hour, at 37 C, with calcification.
#Side effects:
Decreases the SVR by decreasing the amount of ionized calcium.
DIC
Osteopenia
Heparin induced thrombocytopenia & heparin resistance

#Protocol for management of a patient with post CPB non-surgical bleeding.

A) Check for & correct
Heparin- residual/ rebound
Platelet number & function
Coagulation factors
Activation of fibrinolytic system
Hypothermia &
Hypocalcemia.

#Criteria for heparin induced thrombocytopenia

If in a patient receiving heparin treatment;
the platelet count drops by 50% of the pretreatment levels, or
the platelet count drops to < 1 lac/ mm3

#Advantage of LMWH over unfractionated heparin?

Due to low molecular weight, higher bioavailability by s.c. route, hence OD
dosage suffices
bioavailability of LMWH (s.c. route)= 100%
bioavailability of unfractionated heparin (s.c. route)= 30%
Due to increased bioavailability, clinical effect is predictable & hence no need
for repeated APTT monitoring
Lesser rate of thrombocytopenia, osteopenia & hemorrhagic side effects
679
#Disadvantage of LMWH
Lower antithrombotic properties
No drug to reverse its effect

#Heparin related drugs

LMWH
Medium MWH
High MWH
Dermatans (Danaparoid)
Heparans
Heparinoids (Lomoparon)
Murine polysaccharides

#Heparin resistance is seen in:

AT III deficiency- congenital/ acquired
Prolonged administration- in unstable angina/ IABP
Septicemia
Pregnancy
NTG treatment

#Management of heparin resistance.

Administering higher dose of heparin (up to 1000 IU/ Kg)
Accepting a lower ACT (up to 420 sec)
Administering 2-3 unit FFP or AT III concentrate
Using hirudin/ danapariod
Oral anticoagulants-
Warfarrin & Acitrom (Nicumalone)
Inactivate Vit K in hepatic microsomes-Interfere with Vit K dependent clotting
factors.
680
Uses AF, Clot in LA/LAA, Prosthetic valves, AMI & Pulmonary embolism.
To check Prothrombin time.
Warfarin
#What does warfarin stand for?
Wisconsin Alumini Research Foundation coumaRIN
It is a 4-hydroxy coumarin derivative & was introduced as a rodenticide.

#It is metabolized in the liver (by enzyme cytochrome P 450) & excreted in bile
life= 25- 60 hours (action lasting for 2 5 days)
#Drug interaction with warfarin.
Drugs that potentiate action of warfarin (increasing INR) are:
1) Inhibiting metabolism (Cytochrome P 450 inhibitors)
- cimetidine
- metronidazole
- omeprazole
- amiodarone
2) Prevent active form of Vit K formation
- 3rd generation cephalosporins
- ciprofloxacin
3) decreased availability of Vit K
- diet
4) direct anticoagulation
- aspirin
- dipyridamole
Drugs that decrease action of warfarin (decrease INR) are:
1) decreased absorption of warfarin
- sucralfate
- cholestyramine
2) increased metabolism
- gardinal
681
 - eptoin
- alcohol
- rifampicin
3) Increased GI uptake of warfarin
- dairy products
- fruits
- tea/ coffee
- raddish/ onion/ potato

Thrombolytic Agents
Streptokinase - Indirectly activate plasminogen to plasmin => fibrin into FDP's
(non-specific)
Urokinase - Indirectly - thrombolysis (non-specific)
tPA (Alteplase) - Clot specific thrombolytic - binds directly to clot via fibrin
Uses- AMI, Pulmonary embolism, Thrombosed Av shunt,Thrombosed
mechanical valve.
C/I Haemorrahge, CVA, Coagulation defects.
S/E hemorrhage stroke.
Dose tPA 0.2-0.5 mg/kg/hr 6-12 hrly.
STK MI 30000 U/kg over 1 hour
DVT/Pulmonary embolism 5000 U/kg for hr then 2000
U/kg/Hr
PTT > 5.
Lipid Lowering Drugs
Required when dietary management fails/CV drugs are not at fault/No other
ppt. disease present (Hypothyroidism, DM)
1) Bile acid sequestrant Cholestyramine
Moderate LDL elevation, Young men, and Premenopousal women.

682
 Binds bile acids Increase Liver LDL receptors level Blood LDL
attaches to receptors Removes LD from blood.
S/E Constipation, Gastritis.
2) Nicotinic acid Inhibit secretion of lipoproteins from liver
Reduce LDL.
S/E - Flushing, Palpitation.
C/I - Peptic ulcer, Pregnancy.
3) Statins HMG CoA inhibitor
Less S/E, Reduces LDL.
Lovastatin, Atorvastatin.
Used as a single dose at night because cholesterol synthesis occurs
at night.
S/E Myopathy & renal failure.
4) Fibrates used for high triglyceride levels.
Lopid (Gemfibrozil)
C/I with statins- cause myopathy.
5) Probucol Lowers HDL & LDL cholesterol.
Increase excretion of cholesterol in bile.
Analgesics
Morphine sulfate (MSO4) (0.05 - 0.2 mg/kg initial dose)
Class: Opiate Analgesic
Half-life: 2-4 hours (4.5-13.3 hours in neonates)
Duration of action: 3-4 hours
Metabolism: by liver, excreted in urine and bile
Dosing Frequency: Q1-4 hours or as a continuous drip
Precautions: respiratory suppression with increasing doses, histamine
release, has caused seizures in neonates
Uses: post-operative pain control, sedation, tet spells, can also increase
cardiac output
Fentanyl (1-2mcg/kg per dose initially)
683
 Class: opioid analgesic
Half-life: 2-4 hours
Duration of action: 1-2 hours
Metabolism: by liver, excreted by kidney (<10%)
Dosing Frequency: Q30min-1hour, continuous drip
Precautions: may cause chest wall rigidity in neonates at high doses.
Uses: Post-operative pain management, rapid tolerance develops,
may need to increase drip rate daily to maintain equianalgesic dose.

Sedatives
Midazolam (Versed) (0.05-0.1mg/kg initial dose)
Class: benzodiazepine
Half-life: 1-4 hours
Metabolism: extensively by liver (microsomally), excreted in urine, some
in feces
Dosing Frequency: Q1-2 hours, to continuous drip
Precautions: respiratory depression, when used alone in some patients
can produce paradoxical effect. Cimetidine can prolong half life when
used concomitantly
Uses: as anxiolytic/sedative in association with analgesic agents for
patients with severe pain, or in whom sedation is desired for various
reasons.
Lorazepam (Ativan) (0.03-0.09mg/kg/dose)
Class: benzodiazepine
Half-life: 10-12 hours (40 hours in neonates)
Metabolism: liver, excreted in urine
Dosing Frequency: Q4-8 hours
Precautions: as with Versed, longer acting so prolonged effect of
respiratory suppression

684
 Uses: Sedative for patients who will need prolonged sedation. Can also be
used to help wean patients from Versed drips
Propofol (Diprivan) (25-50 mcg/kg/min drip, 0.5-1mg/kg bolus)
Class: sedative hypnotic
Half-life: minutes, increases with increasing duration of therapy
Metabolism: by liver excreted in urine
Dosing Frequency: Only used as continuous drip or short acting bolus
Precautions: severe myocardial depressant proportionate to dose. No
preservatives in solution so at high risk for infection unless aseptic
technique is adhered to, particularly for prolonged drips.
Uses: Insoluble in water so supplied in solution of 10% Intralipid. Used
for short term sedation when extra sedation is needed. Also used
overnight prior to extubation on patients who have had prolonged
sedation to allow decreasing other sedatives, rapid wean prior to
extubation. FDA does not approve use in pediatric patients for sedation
in the PICU
Paralytic Agents
Vecuronium (Norcuron) (0.1mg/kg, 0.2mg/kg for rapid sequence intubation)
Class: non-depolarizing neuromuscular blocker
Duration of action: 30-40 minutes
Metabolism: excreted primarily in bile, partially in urine
Dosing Frequency: Q1-2 hours prn to continuous drip
Precautions: must be prepared to manage airway or intubated prior to
use. Does not use without adequate sedation/pain control. Prolonged
administration can produce prolonged muscle weakness after stoppage
Uses: as a paralytic in patients who need prolonged mechanical
ventilation with significant lung disease, those with significant
pulmonary hypertension,
Pancuronium (Pavulon) (0.04-0.1mg/kg initially then 0.01mg/kg per dose as
needed)
685
 Class: non-depolarizing neuromuscular blocker
Duration of action: 35-45 minutes
Metabolism: excreted mostly unchanged in urine, some metabolism by
liver and elimination in bile
Dosing Frequency: Q25-60minutes
Precautions: must be prepared to manage airway or intubated prior to
use. Do not use without adequate sedation/pain control.
Uses: as a paralytic in patients
Cisatracurium (Nimbex) (0.1mg/kg)
Class: non-depolarizing neuromuscular blocker
Duration of Action: 20-35 minutes, up to 45 minutes
Metabolism: rapid non-enzymatic degradation (Hofman elimination) in
bloodstream
Dosing Frequency: usually a continuous drip or prn
Precautions: Cis form minimizes Histamine release caused by
Atracurium
Uses: ideal as neuromuscular blocker in patient with compromised renal
and/or hepatic function
Calcium Chloride
Hyperkalemia, Hypocalcemia
Antidote for overdose of calcium channel blocker
8-16 mg/kg IV slowly
Not routinely used for cardiac arrest
Do not mix with sodium bicarbonate.
Magnesium sulfate
Cardiac arrest related to torsades de pointes or low serum magnesium
VF refractory to lidocaine & beryllium
Ventricular arrhythmias associated with digitalis toxicity or tricyclic overdose
Cardiac arrest -1-2 Gm IVP

686
Acute myocardial infarction -1-2 Gm. diluted in 50-100 ml 5% dextrose in
water IV over 5-60 minutes; follow with 0.5-1.0 Gm/hour IV for up to 24 hours
Rapid IV administration may cause hypotension.
Use with caution in patient with renal disease.
May cause respiratory failure. Do not administer if patient has absent patellar
reflexes, respiratory depression, or oliguria.
Sodium Bicarbonate
Known preexisting hyperkalemia
Known preexisting bicarbonate-responsive acidosis
Over dosage of tricyclic antidepressants or aspirin
May be used in prolonged resuscitation with effective ventilation or upon
return of spontaneous circulation after long arrest
Initial dose: 1 mEq/kg IV bolus
Repeat half of initial dose every 10 minutes thereafter
ABG analysis of pH, pCO2, and base deficit is helpful in guiding bicarbonate
therapy.
Harmful in hypoxic lactic acidosis, i.e. cardiac arrest & CPR without
intubation/adequate ventilation.

Atropine
First-line therapy for symptomatic bradycardia
Second-line therapy for asystole or bradycardic pulseless electrical activity
(after epinepherine)
For asystole - 1 mg IVP; may repeat every 3 - 5 minutes to maximum dose of
0.03 - 0.04 mg/kg
For bradycardia - 0.05 - 1 mg IVP; may repeat every 3 - 5 minutes to maximum
dose of 0.03 - 0.04 mg/kg
Endotracheal administration - 2 - 3 mg diluted in 10 ml NS
Use cautiously in patients with myocardial ischemia and/or hypoxia; increases
myocardial oxygen demand.
687
Avoid in hypothermic patients

INSTRUMENTS

SURGICAL Instruments:
Principles of Handling Instruments:
Economy of movements
Relaxed handling.
Avoidance of awkward movements.
Safety (patient and staff)

Basic Surgical Instruments are:

Retracting and Exposing Instruments
Cutting and Dissecting Instruments
Clamping and Occluding Instruments
Grasping and Holding Instruments

Retracting & Exposing Instruments:

Used to hold back or retract organs or tissue to gain exposure to the
operative site.
They are either "self-retaining" (stay open on their own) or "manual" (held
by hand).
When identifying retractors, look at the blade, not the handle.
Retracting & Exposing Instruments:
1) A Richardson retractor (manual) is used to retract deep abdominal or
chest incisions

688
2) An Army-Navy retractor (manual) is used to retract shallow or
superficial incisions. Other names: USA, US Army.

3) A goulet (manual) is used to retract shallow or superficial incisions.

4) A malleable or ribbon retractor (manual) is used to retract deep

wounds. May be bent to various shapes.
Uses: Retraction of Lung in
1. PDA
2. CoA/IAA
3. Thoracic Descending aortic surgery
4. Oesophageal surgery

689
5) A Weitlaner or Mastoid retractor (self-retaining) is used to retract
shallow incisions.

Uses in Cardiac Surgery

1. SVG harvest from Thigh
2. Radial artery harvest
3. Exposure of femoral vessels for cannulation/embolectomy
4. Peripheral vascular surgery
5. Carotid surgery
6) Single/double hook retractor

Uses
To retract skin edges
690
 To retract tough fascia
7) Cats paw/volkmans retractor

Uses
a. Retraction of skin and tough fascia
b. Redo sternotomy-retraction of rectus & lower part of sternum

8) Langenbecks retractor
Used for
1) Retracting lower & upper edges of incision prior to sternotomy
2) Retracting inferior angle of RVOT incision for VSD closure
3) 2 for retracting LA during MV procedures
4) Retracting anterior lip of aorta during VAR
5) Retract RA
6) Retract sternum to check for wire bleeders/ internal mammary artery
bed post harvesting

*Techniques for retraction of right atrium.

1) Stay sutures
2) Right angled retractors
3) Kirklin retractors.

691
 Uses
In operation involving a lot of dissection in superficial muscle pane which
requires retraction

9) Czernys retractor

Uses
Superficial retraction of skin incisions during laparotomy
Retraction of skin & Sc tissue in Suprasternal notch
Retraction of sternal blades for hemostasis
Retraction of skin & inguinal ligament during embolectomy

692
10) Finochiettos self retaining chest wall retractor

Uses
1. Retracting two ribs apart during thoracotomy operations
2. To separate two halves of sternum

11) IMA retractor

- Favalaro retractor
- Keep long blade at the upper end of the sternum.
- Keep short blade at the lower end of the sternum.

12) Mayo retractor:

Uses in Cardiac Surgery

1. To retract Tricuspid valve in VSD closure.

693
2. To retract RA wall during Tricuspid valve surgery.
3. To retract PA.
4. To retract aorta.

13) VSD pole retractor

It is used for
1) Retracting the anterior tricuspid leaflet to expose anterior & superior
margin of VSD (RA approach)
2) Retracting the RV wall (RV approach) to visualize the posteroinferior
margin
3) To retract pulmonary leaflets for VSD closure (SP/Outlet VSD),RVOT
procedure (TOF/DCRV)
4) Aortic valve surgery
5) MV surgery- to lift the AML to see underneath the valve

694
14) Loop retractor

Uses;
Retracting LA wall in Mitral valve surgery in small LA.
Retraction of LA wall in mitral procedures in pediatric patients.
Retraction of inter atrial septal wall for the surgery on the LA through
RA-trans septal approach.

15) Cooleys LA retractor

For retraction of LA in
1. Mitral valve surgery
2. LA myxoma
16) Ross retractor

695
 This instrument is specially designed for use in aortic retraction.
The unique angled head, crest-shaped beak design and long neck
allow for optimal maneuverability while allowing as much
unobstructed access to the surgical field as necessary.
Uses in Cardiac Surgery:
o Aortic Surgery
o RVOT surgery
17) Allisons lung retractor

Uses
Thoracic surgery to retract lung special blades protect the lungs from
damage
18) Duvals lung holding forceps

For holding lung parenchyma during various lung procedures

D/D with Freidrichs lung holding forcep.

696
Cutting & Dissecting Instruments:

Are sharp and are used to cut body tissue or surgical supplies.
1) Blade & handle
7 handle with 15 blade (deep knife) - Used to cut deep, delicate tissue.
3 handle with 10 blade (inside knife) Used to cut superficial tissue.
4 handle with 20 blade (skin knife) - Used to cut skin.

697
2) Straight Mayo scissors

Used to cut suture and supplies. Also known as: Suture scissors.
EX: Straight Mayo scissors being used to cut suture.
Curved Mayo scissors - Used to cut heavy tissue (fascia, muscle, uterus,
breast). Available in regular and long sizes.

Uses in Cardiac Surgery:

1. To cut patch/Grafts & sutures
2. To cut rectus fascia before redo sternotomy
3. To cut sternum in neonates/Pediatric patients

3) Metzenbaum scissors

Used to cut delicate tissue. Available in regular and long sizes.

698
 Uses:
To cut pericardium
To release adhesions in redo cases
Suture cutting
Sharp dissections
Cut Valves
Dissection of Radial artery/SVG

4) Toureq Valve cutting Scissor

Uses:
To cut the PML of mitral valve

5) Potts Scissor

699
 Uses:
To open the aorta.
To cut MPA.
During pulmonary valvotomy.
To open the LA & Common chamber in Schumacher kings operation.

6) Coronary Potts Scissor/ Iris scissor

Uses:
Coronary arteriotomy
Venotomy
Arteriotomy for embolectomy/peripheral cannulation

700
 Tube cutting Scissor

Use: To cut the CPB tubing.

7) Lister Bandage cutting Scissor

Used to remove bandages and dressings
Probe tip is blunt; inserted under bandages with relative safety

8) Wire Cutter

701
Use: To cut the sternal wire

Clamping & Occluding Instruments:

Are used to compress blood vessels or hollow organs for hemostasis or to
prevent spillage of contents.

1) A Kelly clamp
Used to clamp larger vessels and tissue.
Available in short and long sizes.
Other names: Rochester Pean.

Uses in Cardiac Surgery:

To catch the structure in depth.
To catch mitral sutures before removal of ring/valve

2) A right angle
Is used to clamp hard-to-reach vessels and to place sutures behind or
around a vessel. A right angle with a suture attached is called a "tie on a
passer." Other names: Mixter.
IVC MIXTER
This an IVC mixter used for going around the IVC for the purpose of looping it.
It is also used for dissection & looping the aorta.

702
Complications of looping IVC are:
1) Damage to RIPV
2) Damage to IVC

Used for
1) Looping vessels like
- SVC
- PDA
- Vertical vein
- Peripheral vascular structures
2) OMC- for hooking the subvalve
3) Clamping the RCA at the initiation of cardioplegia delivery ti prevent air
from entering the RCA
4) Deairing the aorta, from the LV, at the start of the repeat cardioplegia

*How to manage torn SVC, during looping

Insert aortic cannula & be on suction bypass
Or
IVC cannulation & partial CPB (with SVC cannula connected & clamped)
Or
IVC & Innominate vein cannulation & full CPB

703
 3) Cooleys clamp

This is a Cooleys vascular clamp

Instrument is used for
1) Waterston Cooley shunt
2) Proximal anastomosis construction on aorta, during a CABG.
3) Aortic cannulation
4) BT shunt
5) PDA surgery (division & suturing)
6) Peripheral vascular surgery
7) Right atrial appendage cannulation
8) Ligation of left atrial appendage

*Why marks on the inner aspect of the clamp

These marks where constructed at a distance of 4 mm, to indicate the limit of
anastomosis during a Waterston Cooley shunt
4) Debakey Vascular Clamp

704
 Debakey Vascular Clamp angeled

Debakey Vascular Clamp Straight

This is a DeBakey vascular clamp made out of stainless steel.

*Advantage of this clamp

1) Atraumatic
2) Doesnt come in way of surgery

*Used for
1) Peripheral vascular surgery
2) Cross clamping aorta in pediatric patient
3) Clamp PDA (larger size clamp)
4) Clamping aorta in thoracic & abdominal aortic procedure (larger sized
clamps)

*Why crest present beyond the clamp jaws

For accommodating arterial wall, to avoid puckering

705
 5) Satinsky clamp

*Specific uses are

1) Side biting of aorta for proximal anastomoses during CABG
2) Clamping LAA during CMC
3) During Waldhausens repair for coarctation
4) Rest like Cooleys clamp

6) Aortic cross clamp

This is an aortic cross clamp used for cross clamping the aorta during an open-
heart procedure

*Surgeries on CPB that are/ can be performed without cross clamping

1) CABG on fibrillating arrest or CABG on CPB with aid of stabilizer
2) Right sided surgeries (on TV/ PV)

706
*Other ways of cross clamping aorta?
Using endoluminal balloon occlusion for
1) Port access surgery
2) Atherosclerotic aorta

*Which conditions to clamp early

1) AR
2) AP window
3) Truncus arteriosus
4) Myxoma

*Complication of cross clamp?

1) Clamp MPA
2) Dislodgement of plaque
3) Can clamp tip of arterial cannula
4) Clamp may be applied partially

*Disadvantage of cross clamp

1) Can come in way of surgery

*Why on clamp removal is the flow lowered

As the aortic cusps are open & on release of the clamp, the gush will distend
the LV (even before the cusps can close)

Grasping & Holding Instruments:

Are used to hold tissue, drapes or sponges.

1) An Allis is used to grasp tissue. Available in short and long sizes. A

"Judd-Allis" holds intestinal tissue; a "heavy allis" holds breast tissue.

707
 Uses in Cardiac Surgery: Traumtic instrument
To hold the pericardium in pericardiectomy
To hold the skin of the leg incision during SVG harvest
To hold mediastinal tumours

2) A Babcock is used to grasp delicate tissue (intestine, fallopian tube,

ovary). Available in short and long sizes.

Uses in Cardiac Surgery:Non traumatic

To hold the LA wall during removal of LA myxoma through LA approach
3) Valsellum and Tenaculum

Uses
Mainly used in gynecological operations to hold the tip of cervix

708
 This structure is similar to allis forceps except they are very long .
Uses in Cardiac Surgery:
To hold the AML during excision of mitral valve.

4) Artery forceps ( Mosquito)

Uses in Cardiac Surgery

Holding stay sutures on RA, PA & heart.
Creating / Dilating existing PFO
Preparing rubbershods
Catching venous branches during SVG harvest
For dilatation of SVG mouth before cannulation
Rubber Shod

5) A Kocher is used to grasp heavy tissue. May also be used as a clamp.

The jaws may be straight or curved. Other names: Ochsner.

709
 Uses in Cardiac Surgery
To hold the ends of sternal wires
To pull out sternal wires in redo cases

6) A Foerster sponge stick is used to grasp sponges. Other names: sponge

forcep.
Uses in Cardiac Surgery
1) Painting & draping
2) LA clot removal
3) As an aid in internal mammary artery dissection

7) A Backhaus towel clip is used to hold towels and drapes in place. Other
name: towel clip.

710
 Uses in Cardiac Surgery
To secure & Fix the aortic cannula & tubing
Retract & retain the venous cannulae in particular position
To hold cautry cable/Pressure lines/Pacing cable wire/Epicardial Echo
probe in position

8) Pick ups, thumb forceps and tissue forceps are available in various
lengths, with or without teeth, and smooth or serrated jaws.

Russian tissue forceps are used to grasp tissue.

Uses in cardiac surgery

To remove clots from LA.
To remove Myxoma.

Adson pick ups are either smooth: used to grasp delicate tissue; or with
teeth: used to grasp the skin. Other names: Dura forceps.

711
 Uses in cardiac surgery
During closure of skin.

DeBakey forceps are used to grasp delicate tissue, particularly in

cardiovascular surgery.

9) Mayo-Hegar needle holders are used to hold needles when suturing.

They may also be placed in the sewing category.

10) Castro Viejo

712
 Uses in Cardiac surgery
Used in pediatric cardiac surgery for suturing
Used when finer sutures required for suturing
11) Nerve Hook

Uses in Cardiac Surgery

To remove the loop in suture
To remove / adjust the suture fall
To retract the patch/graft when the edges are folding/ working in narrow
space
To retract the mitral & tricuspid chordae
To check the gap between the sutures in VSD patch

12) Mitral Valve Hook

Uses in Cardiac Surgery

To retract the MV leaflet during repair
713
 To retract the TV leaflet during VSD closure
13) Tubbs dilator

This is a transventricular dilator called as the Tubbs dilator, made of stainless

steel & is used during a CMC

*Points to be checked prior to using the dilator

1) It should open against resistance
2) Smooth opening
3) Should close completely
4) Blade should not rotate

*Maintenance of dilator
1) Oiling of the screw
2) Immediately post procedure, flush the proximal portion with saline/
hydrogen peroxide & let the effluent escape from the distal portion

*Techniques of using Tubbs

- Logan: open dilator in any direction
- Cooley: open dilator perpendicular to the commissure

*Modifications of MV dilators over time

714
Original transventricular dilator: Logan & Turner
Modifications introduced by:
- PK Sen
- Cooley
- Beck
- Glenn
- Tubb (Oswald Sydney Tubb)

*Modification by Tubb in dilator.

He introduced a screw to enable a predetermined opening distance of the
dilator

*Complications due to use of dilator.

1) Avulsion of LV pursestring due to dilator getting stuck in it
2) Dilator stuck in open position
3) Tip getting disengaged & remaining in the LA/ LV
4) Tearing of leaflet resulting in an acute MR

*Acceptable MR after CMC.

Grade I MR

*Unacceptable MR post CMC.

1) Grade II or more
2) MR with unrelieved MS
3) MR due to tear in leaflet/ rupture chordae
4) Associated with a high preoperative PH

*Pursestring for a small LAA.

715
 The pursestring should be over the posterior aspect of LA- extending over
the PVs

*Ways of going on CPB during CMC.

Either thru same incision or thru a midsternotomy depending upon the
emergency.
Ways of going on to CPB are thru the same incision are:
1) RVOT & femoral artery
2) RA & femoral artery (cut the pericardium perpendicular to the incision to
expose RA)
Dissect between the PA & aorta for cross clamping & cardioplegia
pursestring & delivery)

*Which pliable MS is difficult to open during CMC?

Eccentric MS

14) Octopus Stabilizer (presently available Octopus IV)

This is an Octopus stabilizer for stabilization of a portion of the ventricle, on a
beating heart, during an off pump CABG.

It has 3 parts
1) Foot plate
2) Stabilizing system
3) Locking system
716
*Amount of suction applied?
300 psi.

*Advantage of the device.

No compression on the heart
*Disadvantages??
1) May cause damage to epicardium & myocardium (suction injury)
2) Produce arrhythmogenic areas
3) Damage to vennules
4) Cost
15) Coronary probes

Uses
During OPCAB/CABG to check doubtful lesions.
During AVR to check doubtful lesion.
During Bentall keep probe in the coronary and dissect the tissue around
the coronary to prevent injury.
To check IMA injury/ Spasm if no/low flow.
16) Endarterectomy Spatula

717
 Uses
Coronary endarterectomy
Carotid endarterectomy

Technique of Off Pump Coronary Endarterectomy

RCA &Cx
Closed technique
- Large arteriotomy
- Plaque dissection
-`Push on distal artery
LAD
Open technique
- Long patch arterioplasty using IMA & SVG

Technical difficulty
Exposure and stabilisation of long segment of coronary arteries
Haemostasis
Non availability of long shunts and occluder

Anticoagulation regimen
All will get antipletelets and anticoagulants.
Aspirin was started 6 hours after surgery and Warfarin & Clopidogrel on
next day.
INR to be maintained around 2.0.
The clopidogrel to be continued for 3 months
Warfarin for 6 months and Aspirin for lifetime.
If the patient on ventilator the above drugs to be given through
nasogastric tube.

718
 Heparin to be continued postoperatively and adjusted as per Activated
clotting time (ACT) if the patient on intra aortic balloon pump (IABP).
Current Indications for Carotid Endarterectomy
Asymptomatic Patients With CAD
For Patients With a Surgical Risk of <3%
1. Proven indications: none1
2. Acceptable but not proven indications: ipsilateral carotid endarterectomy for
stenosis 75% with or without ulceration, irrespective of contralateral artery
status, ranging from no disease to total occlusion1
3. Uncertain indications
Stenosis <50% with a B or C ulcer irrespective of contralateral internal
carotid artery status
Unilateral carotid endarterectomy with CABG, coronary bypass graft required
with bilateral asymptomatic stenosis >70%
Unilateral carotid stenosis >70%, CABG required, unilateral carotid
endarterectomy with CABG
4. Proven inappropriate indications: none defined
For Patients With a Surgical Risk of 3% to 5%
1. Proven indications: none
2. Acceptable but not proven indications: ipsilateral carotid endarterectomy for
stenosis 75% with or without ulceration but in the presence of contralateral
internal carotid artery stenosis ranging from 75% to total occlusion
3. Uncertain indications
Ipsilateral carotid endarterectomy for stenosis 75% with or without
ulceration irrespective of contralateral artery status, ranging from no stenosis
to occlusion
Coronary bypass graft required, with bilateral asymptomatic stenosis >70%,
unilateral carotid endarterectomy with CABG
Unilateral carotid stenosis >70%, CABG required, ipsilateral carotid
endarterectomy with CABG
719
4. Proven inappropriate indications: none defined
For Patients With a Surgical Risk of 5% to 10%
1. Proven indications: none
2. Acceptable but not proven indications: none
3. Uncertain indications
Coronary bypass graft required with bilateral asymptomatic stenosis >70%,
unilateral carotid endarterectomy with CABG
Unilateral carotid stenosis >70%, CABG required, ipsilateral carotid
endarterectomy with CABG
4. Proven inappropriate indications
Ipsilateral carotid endarterectomy for stenosis 75% with or without
ulceration irrespective of contralateral internal carotid artery status
Stenosis 50% with or without ulceration irrespective of contralateral carotid
artery status
Symptomatic Patients With CAD
For Patients With a Surgical Risk of <6%
1. Proven indications
Single or multiple TIAs within a 6-month interval or crescendo TIAs in the
presence of a stenosis 70%, with or without ulceration, with or without
antiplatelet therapy
Mild stroke within a 6-month interval, in the presence of a stenosis 70%,
with or without ulceration, with or without antiplatelet therapy
2. Acceptable but not proven indications
TIA (single, multiple, or recurrent) within a 6- month interval, in the presence
of a stenosis 50%, with or without ulceration, with or without antiplatelet
therapy
Crescendo TIAs in the presence of a stenosis >50%, with or without
ulceration, with or without antiplatelet therapy
Progressive stroke in the presence of a stenosis 70%, with or without
ulceration, with or without antiplatelet therapy
720
 Mild stroke in the presence of a stenosis 50%, with or without ulceration,
with or without antiplatelet therapy
Moderate stroke in the presence of a stenosis 50%, with or without
ulceration, with or without antiplatelet therapy
Ipsilateral carotid endarterectomy combined with CABG in a patient
experiencing TIAs, in the presence of unilateral or bilateral stenoses 70%,
coronary bypass grafting needed
3. Uncertain indications
TIA (single, multiple, or recurrent) with stenosis <50% with or without
ulceration, with or without antiplatelet therapy
Crescendo TIAs, with or without ulceration, and a stenosis <50%
TIAs in a patient who requires coronary bypass grafting and has a stenosis
<70%
Mild stroke with carotid stenosis <50%, with or without ulceration, with or
without antiplatelet therapy
Moderate stroke with carotid stenosis <69%, with or without ulceration, with
or without antiplatelet therapy
Evolving stroke with carotid stenosis <69%, with or without ulceration, with
or without antiplatelet therapy
Global ischemic symptoms with ipsilateral carotid stenosis >75% but
contralateral stenosis <75%, with or without ulceration, with or without
antiplatelet therapy
Acute dissection of internal carotid artery with persistent symptoms while on
heparin
Acute carotid occlusion, diagnosed within 6 hours, producing transient
ischemic events
Acute carotid occlusion, diagnosed within 6 hours, producing a mild stroke
4. Proven inappropriate indications
Moderate stroke with stenosis <50%, not on aspirin
Evolving stroke with stenosis <50%, not on aspirin
721
 Acute internal carotid artery dissection, asymptomatic, on heparin
For Patients With a Surgical Risk of 6% to 10%
1. Proven indications: none
2. Acceptable but not proven indications
Single or multiple TIAs within a 6-month interval, in the presence of a carotid
stenosis 70%, with or without ulceration, with or without antiplatelet therapy
Recurrent TIAs, while on antiplatelet drugs, for a carotid stenosis 50% in the
presence of ulceration, or 70% with or without ulceration
Crescendo TIAs with a stenosis 50%, with or without ulceration, with or
without antiplatelet therapy
Mild stroke in the presence of a stenosis >70%, with or without ulceration,
with or without antiplatelet therapy
Moderate stroke with a stenosis >70%, with or without ulceration, with or
without antiplatelet therapy
Evolving stroke in the presence of a >70% stenosis with large ulceration
3. Uncertain indications
Single TIA with stenosis <70%, with or without ulceration, with or without
antiplatelet therapy
Multiple TIAs within 6 months with stenosis <70%, not on antiplatelet drugs,
with or without ulceration
Recurrent TIAs while on antiplatelet drugs with stenosis <70%, with or
without ulceration
Crescendo TIAs for stenosis <70%, with or without ulceration, with or without
antiplatelet therapy.
Acute carotid occlusion with transient cerebral ischemia
Acute occlusion with mild stroke
Acute carotid artery dissection with continued symptoms while on heparin
Patient with transient cerebral ischemia secondary to a stenosis 70%, in
need of CABG, with or without contralateral stenosis, use of combined
operation
722
 Mild stroke with stenosis <70%, with or without ulceration, with or without
antiplatelet therapy
Moderate stroke with stenosis <70%, with or without ulceration, with or
without antiplatelet therapy
Evolving stroke with stenosis <70%, with or without ulceration, with or
without antiplatelet therapy
Global ischemic symptoms with an ipsilateral stenosis >75%, with or without
symptoms, irrespective of contralateral artery status, with lesions up to and
including contralateral occlusion
4. Proven inappropriate indications
Single TIA, <50% stenosis, with or without ulceration, not on aspirin
Multiple TIAs within 6 months, stenosis <50%, not on aspirin
Mild stroke, stenosis <50%, not on aspirin
Moderate stroke, stenosis <50%, with or without ulceration, not on aspirin
Evolving stroke, stenosis <50%, with or without ulceration, not on aspirin
Global ischemic symptoms with stenosis <50%, with or without ulceration
Acute dissection of internal carotid artery, no symptoms while on heparin
Asymptomatic unilateral carotid stenosis 70% in patient undergoing CABG

17) Intracoronary shunts (anastaflow)

This is an intracoronary shunt & is used during an off pump CABG to maintain
distal perfusion of the coronary, during the procedure.

723
*Advantage:
1) Tapering end- provides easy insertion
2) Bulbous end- prevents slipping out & prevents leak
3) Transparent- allows to see blood flowing
4) Avoids taking of the posterior wall at the angles in small coronaries

*Sizes available are

From 1mm to 3.5 mm

*Disadvantage:
1) Provide inadequate flow if a small shunt is used
2) Plaque dislodgement during insertion
3) Sutures may go thru the shunt
18) Coronary Potts Scissor

Reverse cutting coronary potts scissor

724
 Right angeled coronary potts scissor

Iris scissor

Also called Beall/ DeBakey/Diethrich/Potts coronary scissors

Available with
250 angle
450 angle
600 angle
900 angle
1200 angle
19) Fine coronary forcep

725
20) Ringed coronary forcep

Uses
To hold vein & IMA during anastomosis
21) Coronary Castro Vijo

Uses
To hold finer sutures & needles (6-0,7-0,8-0)

726
 22) Clip applicator

Uses
Clip the branches of IMA/Radial artery/Gastroepiploic
artery/SVG/Small venous or arterial branch
23) Starfish

Uses
To stabilize heart without compromising hemodynamics especially for
OM/RCA in crux.
24) Coronary punch / aortic punch
This is a plastic/ metal aortic punch used for punching holes in the ascending
aorta for the purpose of proximal anastomosis, after having sideclamped &
stabbed the artery.
*Sizes available are
4, 4.5,4.7 & 5mm

727
*Uses
1) Proximal anastomosis in a CABG
2) ASD/ VSD patch septostomy
3) Bentalls procedure- to punch holes in the graft

*Size used for proximal anastomosis over the aorta

Generally for radial artery- 4 or 4.5 mm
For reversed Saphenous vein graft- 4.5 or 5 mm.

25) Snuggers

728
 Uses
To snug Cave /Aortic cannula/Cardioplegia cannulae
26) Wall Suckers/External Suckers:

Uses
To suck blood & fluid from pericardial cavity
While testing valves after repair
To remove clots/Calcium debris (without tip)
For blunt dissection
27) Hegar Dilators

Uses in Cardiac Surgery

To Size RVOT
To Size Valves after repair
To size Mitral & Tricuspid valve in AV canal repair

729
 28) Pump Suckers

To keep surgical field dry

29) Sternotomy saw

*Various instruments available for sternotomy?

1) Oscillating saw
2) Labsche
3) Gigli saw
4) Saurebrochs sternal cutter
5) Stout scissors (in neonates & infants)

730
 30) Fogarty catheter

*Historical techniques of embolectomy?

1) Milk the artery to the arteriotomy (Laheys technique)
2) Pass a catheter & flush the artery
3) Pass a catheter, apply suction to it & withdraw

*General specifications of Fogarty

Balloon capacity is 2 ml.
Length is 80 cm
3 markings at 70, 60 & 50 cm.

*Sheileys embolectomy catheter.

Has 2 balloons. One is at the regular place while the other is near the site of
inflation, to gauge the extent of inflation of the inner balloon.

*Use of stylus in Fogarty.

If a firm clot, it will not permit the Fogarty to pass thru without a stylus
(beyond the clot)

*Modifications of Fogarty?
1) Fogarty with side holes
731
 2) Fogarty with ribbed balloon (for increased strength)

*Other uses of Fogarty?

1) Lung occlusion technique
2) PDA occlusion for closure on CPB
3) Pulmonary embolectomy

*Overdistension of the balloon leads to:

1) Intimal tear
2) Plaque disruption

*When to stop passing the Fogarty.

Till no more clots retrieved.

*Non-balloon embolectomy catheter.

1) Adherent clot catheter
2) Graft thrombectomy catheter

31) Line clamp

732
Used for
1) Clamping the aortic cannula post insertion for
- Deairing
- Checking pulsatile flow
- Color of blood
2) Clamping the venous cannula just prior to going on bypass & also when
on bypass with single cannula in situ.

32) Baileys rib approximator

Used for approximation of ribs post thoracotomy.

33) Mist blower

This is a mist blower & is used to aid visualization during OPCAB.

It has an added advantage of opening up the angles for increased ease of
suturing.

733
*Gas used
1) O2- cheap & easily available
2) Co2- preferred as less chances of embolism

34) Doyen rib raspatory

This raspatory has a bulb shaped handle from which a slightly spiraled
hook shape extends.
This blade like portion can be used to scrape away at an individual rib.
This instrument comes in either left or right handed as well as in adult
or pediatric sizes
Uses
To perform periostostomy

734
 How to use rib raspatory?
Make incision along the rib
Elevate the periosteum with periosteal elevator
Pass the rib raspatory beneath the periostium & move from one end to
other end

How to identify the Rib Raspatory is of which side?

When you hold the rib raspatory in hand or put on the table, which ever side
the tip face is the side for which it can be used.
e.g. Tip facing right side- For Rt sided ribs

35) Bronchoscope

Rigid bronchoscope

Rigid bronchoscopy is used for retrieving foreign objects.

Massive hemoptysis, defined as loss of >600 mL of blood in 24 hours.

735
 For therapeutic approaches such as electrocautery to help control the
bleeding.
Retrival of foreign body aspiration because it allows protection of the
airway and controlling the foreign body during recovery.

Flexible Bronchoscope

A flexible bronchoscope is longer and thinner than a rigid bronchoscope.

It contains a fiberoptic system that transmits an image from the tip of
the instrument to an eyepiece or video camera at the opposite end.
Using Bowden cables connected to a lever at the hand piece, the tip of
the instrument can be oriented, allowing the practitioner to navigate the
instrument into individual lobe or segment bronchi. Most flexible
bronchoscopes also include a channel for suctioning or instrumentation,
but these are significantly smaller than those in a rigid bronchoscope.
Flexible bronchoscopy causes less discomfort for the patient than rigid
bronchoscopy and the procedure can be performed easily and safely
under moderate sedation.
It is the technique of choice nowadays for most bronchoscopic
procedures.

736
Indications for Bronchoscopy
1. Broncho-alveolar lavage for C/S, AFB, cytology
2. Biopsy of tracheo-bronchial tumours
3. Investigation of chronic cough, hemoptysis, Lt vocal cord palsy, atelectasis,
obstructive emphysema, mediastinal growths
4. Removal tracheo-bronchial of foreign bodies
5. Removal of retained respiratory secretions
Difference between Rigid & Flexible bronchoscopy

Rigid Bronchoscopy Flexible

Also functions as airway No
Better for removal of foreign body No
Allows use of Laser No
Visualizes up to 3rd bronchial division 5th division
Not done under local anesthesia Done
Not done in cervical spine problems Done
More risky & traumatic Safer
Not done for trans-bronchoscopic biopsy Done

36) Oesophagoscope

Rigid Oesophagoscope

737
Jackson scope Negus scope
Distal illumination Proximal illumination
No markings Marked
Narrow Broad
Constant diameter Tapered
Single bulb Double bulb

Indications for Oesophagoscopy

1. Investigation of dysphagia, haematemesis, GERD, neck node metastasis of
unknown origin
2. Oesophageal foreign body removal
3. Excision biopsy of benign oesophageal lesions
4. Dilatation of oesophageal strictures
5. Sclerotherapy for oesophageal varices
6. Insertion of palliative oesophageal feeding tube

Contraindications of rigid esophagoscopy

1. Severe cervical spine deformity
2. Large thoracic aortic aneurysm
3. Recent MI
738
 4. Struggling, uncooperative & agitated patient

Flexible oesophagoscope

How to differentiate the rigid oesophagus from rigid bronchoscope?

Rigid bronchoscope will have Multiple holes on the shaft & a ventilation port at
the end
Rigid oesophagoscope will have markings on the shaft but will not have holes &
ventilation port.

Difference between rigid & fexible oesophagoscopy

Rigid Oesophagoscopy Flexible

Better for cricopharynx examination No
Better for removal of foreign body No
Allows use of Laser No
Not good for lower oesophageal examn Good
Not done under local anesthesia Done
Not done in cervical spine problems Done
More risky & traumatic Safer

739
Perfusion Instruments

Arterial Cannulae

Plastic peripheral arterial cannula

This is a plastic arterial cannula for peripheral arterial cannulation for the
purpose of CPB.

This cannula (peripheral arterial cannulation) is used for

Unchallenged indications are:
1) Ascending aortic aneurysm surgery
2) TOF ICR with previous Potts shunt
3) AP window
4) Dissection Stanford Type I
Also used for
5) Emergency bypass
6) Right thoracotomy approach open heart surgery
7) Redo surgery
8) Port access surgery
9) CPB for constrictive pericarditis.

Advantages are:
1) Single cast
2) Beveled
740
 3) Only the tip is narrow

Disadvantages are:
1) Resistance to flow due to small inner diameter ratio as compared to outer
diameter.
2) Can get kinked
3) No markings present
4) Can come out

Complete metallic cannula for same purpose

Used by Solomon Victor.
Has the advantage of reusability & optimization of inner diameter: outer
diameter ratio.

*Why iliac cannulation preferred over femoral

because
1) Iliac artery is larger hence larger cannula can be inserted
2) Lesser chances of infection & lymphorrhea

Aortic cannula

Site For Advantage Disadvantage

Cannulation
( Skin incision
site)
Ascending Aorta 1.Performed through surgical 1.Cerebral embolism
( Sternotomy) incision 2.Clean area 3.Size of
cannula is not a limitation
4.complications related to

741
 cannulation can be easily
detected
Femoral Artery ( 1.Used for quick cannulation
Groin) 2.Percutaneous cannulation
possible
3. Can be performed prior to
surgical incision
4.Scar can be concealed
Iliac Artery ( 1.Can be performed prior to
Lumbar- surgical incision
retroperitoneal 2.Size of the cannula could be
incision) larger than in femoral
cannulation
3. Cannulation in a cleaner
area
Axillary Artery ( 1.For cerebral perfusion
Axilla) 2.Used in combination with the
above mentioned sites
742
1.In a potentially infected
area
2.Lymph collection
possible
3.Retroperitoneal
dissection
1.Deeper dissection than
femoral cannulation
required
2. Possibility of injury to
ureter
3.Retroperitoneal
dissection due to
cannulation
743
This is a short/ long tipped curved, 2 cast, vented/non vented, wire/ non wire
reinforced aortic cannula, made of PVC, used for cannulation of the ascending
aorta during an open heart surgery.
It can also be used rarely for
1) Proximal arch cannulation
2) Venous cannula

Sizes available in adults are: 20, 22 & 24 F.

Advantage of metal tipped cannula are

1) maximum optimization of inner diameter/ outer diameter ratio
2) has a hub for retaining it in position
3) has a fixed distance from hob to tip of metal, hence less chances of
branch cannulation.

Disadvantage of the cannula are:

1) Maximum RBC damage
2) Formation of air vaccoules at the sides of the jet emerging from the tip
3) Non wire reinforced, hence can get kinked/ clamped

*Double arterial cannulation

In cases of large descending thoracic aortic aneurysm, 2 cannula, in the
axillary artery & the femoral artery each.

*Chaukar Pandey shunt

Shunt inserted between the subclavian artery & the left CCA for arch surgeries
for cerebral perfusion with the arch clamped

744
*What is Scouring?
A partial thickness incision made over the aorta with a knife (15 no.) for the
purpose of cannulation

*What is the size of the cannula used normally?

It depends on only one factor- the flow required.

*Maximum resistance permissible?

Immediately after insertion of aortic cannula, around 180 mm Hg. 60 mm Hg
of tubing & 120 mm Hg of aorta.

*D/D of no blood in the aortic cannula post insertion?

1) Partial thickness puncture (dissection)
2) Tip abutting aortic wall inside- turn the cannula & pulsatile blood should
flow

*Sign of dissection due to aortic cannulation?

1) No flow in the cannula
2) Non pulsatile flow in cannula
3) Increase in size of hematoma
4) Decrease venous return (if on bypass)

*Management of dissection
Terminate bypass & perform a femoral arterial cannulation & aortic
cannulation.

Assess extent of dissection by TEE & perform corrective procedure

*Disadvantage of small tip cannula

1) May cause partial thickness puncture in the aortic wall
745
 2) Causes increased turbulence & vacoulations

Venous cannulae
A) Cavoaterial cannula

This is a single cast, wire reinforced 2-stage venous drainage cannula, also
called as the cavoatrial cannula, used for the purpose of caval drainage on CPB
& has an obturator inside.

Two stage Venous cannula

Used for
1) Aortic valve surgeries
2) Ascending aortic surgeries
3) CABG
4) LV aneurysm surgery
5) Rarely MVR with a large LA

746
Disadvantages are:
1) Causes early rewarming of the heart
2) The SVC may get tented (& hamper venous drainage) during positioning
for OM grafts
3) Right sided procedures cannot be performed
4) May cause incompetence of the NCC & hinder in delivery of cardioplegia

*Types of tips available

1) Basket tip
2) Bullet tip
3) Swirl tip

Metal tipped venous cannula

This is a long/ short, curved, metal tipped, 2 cast, wire reinforced pacifico
venous drainage cannula for selective caval cannulation

Unchallenged indications for selective SVC cannulation are

1) Sennings
2) Mustard

747
 3) Transplant
4) TCPC

*What does dlp stand for

d- David
l- Linda
p- Philip
they are children of J Davies

*Classical technique of caval cannulation?

The SVC cannula goes from the IVC pursestring & the IVC cannula from the
SVC pursestring (both pursestrings over the RA, & straight venous cannulae
used)

Plastic straight venous cannula

This is a plastic tipped straight; non wire reinforced venous cannula, made of
PVC, for cannulation of iliac/ femoral vein for the purpose of CPB.

748
*Which side is preferred for the cannulation?
Right side is preferred as
1) the left sided common iliac vein is crossed by the iliac artery
2) the left common iliac vein is more angulated

*Indications of iliac vein cannulation

1) Emergency surgery
2) Redo surgery
3) Portaccess surgery
4) Large arch aneurysm (where the caval visualization is impossible)

*Complications of Iliac vein cannulation

1) Lymphorrhea (more common with femoral exposure)
2) Infection

Plastic tip Straight angled Venous cannula

Used for cannulation of SVC through RAA. Having Long curvature goes into
SVC. Better drainage

Cardioplegia Cannulae

A) Retrograde cardioplegia cannula

This is a self-retaining retrograde cardioplegia cannula

749
Which are the operations where retrograde CP cannula required?
1. AVR in Severe AR
2. AVR in AS for uninterrupted surgery
3. AVR in calcific AS to remove debris from coronary artery by giving
hot shot after surgery before removal of clamp
4. MVR for uninterrupted surgery
5. RSOV repair
6. Aortic aneurysm surgery with AR
7. VSD with aortic valve repair
8. CABG
9. Not able to give antegrade root plegia

*Why self retaining

As there is not separate port for balloon inflation

*How to know that the balloon is in the coronary sinus.

1) Balloon is felt in the coronary sinus
2) Dark blood in the cannula as compared to SVC & IVC
3) If a pressure line is connected, it will show ventricular tracings

*Who described insertion techniques?

750
Direct coronary sinus: Menasche
Trans RA: Buckberg

*Site of insertion, over RA, of cannula

A point at the junction of cepahlad 2/3rd & caudad 1/3rd on a line joining the
RAA to the lateral aspect of IVS

*What should be the relation of the retrograde cardioplegia cannula to the 2

stage cannula?
It should be anterior to the 2 stage cannula.

*Technique of insertion
Classically cannula in left hand & guided by right hand.
Generally practiced is the opposite.
# How will you put retrocannula?
- Purstring on the RA -1 cm away from the AV groove & at the
junction of upper 1/3rd & Lower 2/3rd of AV groove.
- Keep volume in the heart
- Stab & hold the cannula with left hand
- Right hand over the CS near IVC
- Put cannula through RA anterior to two stage venous cannula
- Direct posteriorly
- Once it enters the CS opening direct it towards the left shoulder
- Withdraw the stylate & see for pulsatile black blood coming out
- Connect it to pressure line
- Confirm the trace of it with pressure of 4-5mmHg
*If the retrograde cardioplegia cannula is not entering the coronary sinus, with
the patient on CPB with a cavoatrial cannula
The options available are

751
 1) Go off bypass, insert two caval cannulae, snug the cavae, on bypass,
open the RA & then undervision insert the cannula in the coronary
sinus.
2) Push the 2 stage cannula completely into the IVC, loop the IVC, occluded
the SVC, open RA & insert the cardioplegia cannula into the coronary
sinus, close RA, and release caval snares & withdraw the 2 stage
cannula back into the RA.
*Disadvantage of retrograde cardioplegia.
1) It may not perfuse the RV (if the anterior cardiac veins are draining
directly into the RA) or also if the retrograde cardioplegia cannula is inserted
to much inside
2) Impaired perfusion of the IVS
3) Complications due to insertion, viz.
- hematoma at the site of coronary sinus
- coronary sinus rupture
- RV rupture

*Disadvantage of combined antegrade & retrograde cardioplegia.

Myocardial edema

*Advantage of retrograde cardioplegia during CABG

1) Subendocardial perfusion
2) Even distribution in case of diffuse coronary artery disease
3) Washes out air & debris
4) By avoiding direct osteal cannulation, late osteal stenosis may be avoided

*Monitoring retrograde cardioplegia delivery

1) Maximum pressure of delivery is 30 mm Hg
2) Blood will be seen emerging from the coronary ostia
3) TOPS (fine needle probes to monitor PO2 in tissues)
752
*Manual inflatable cannula
Is the Gundrys silicone retrograde cardioplegia cannula

*Rate of delivery
Is 100- 500 ml/min/m2 at 25 mm Hg

Antegrade aortic root cardioplegia cannula

This is an antegrade aortic root cardioplegia cannula with a flange (for fixing it
in position) & with/ without a vent line.

It is used for
1) Delivery of cardioplegia
2) Deairing
3) Venting the LV, transaorta, during

753
 - CPB
- Retrograde cardioplegia delivery
Also rarely used for
4) Pulmonary artery perfusion for
- pulmonoplegia (transplant)
- in patients with systemic PH for PA perfusion during CPB

*Technique of removal of air prior to second cardioplegia

- Clamp RCA
- Make aortic valve incompetent transiently, if possible
- Clamp the vent arm of cannula after air flows out

*Steps of deairing the heart

De-air LA (if LA open) followed by LV apex from aortic vent (+/- aspirate the
apex)

Patient is give a Head low position & patient shaken side to side over the table

a suction is attached to the aortic vent & de airing confirmed on TEE (ideal)

CPB flows are dropped & clamp is partially removed followed by normal flows

Transiently reapply clamp & massage to de-air & then remove clamp, bring the
able to normal position

*Removal of air from coronary arteries

1) Administration of higher pressure cardioplegia
2) Administration of retrograde cardioplegia
3) Milking of the arteries
4) Stab the coronary with fine needle
754
Ostial Cardioplegia cannula

Direct ostial plegia ,which one 1st Left/right?

- Left 1st
- Because
In front of the eye
LV perfusion is more important for its function
755
# How will you give left & right plegia?
- Left Coronary plegia-
Angeled cannula
Directed towards Assitants leg
- Right coronary plegia-
Ask assistant to retract anterior lip with two forceps
Push RCA from outside using back of the forceps inside
Put the cannula in the ostia
Direction facing towards the sky

# How will you say cardioplegia is going?

- Coronary artery distends Left LAD, Right RCA
- Metal part of the cannula cold
- Heart stops beating
- Blood starts coming out from other coronary
- Perfusionists Plegia volume level falls without resistance

# Cardioplegia is not going what are the possibilities?

- Kink in cardioplegia line
- Clamp on cardioplegia line
- Cannula tip is not in ostium
- Cannula tip is touching the wall
- Atherosclerotic ,small artery

756
Left ventricular vent

# How will you put LV vent?

- After going on CPB
- Do not cool keep heart ejecting
- Take purstring on the RSPV-LA junction
- Keep volume in the heart
- Stab the RSPV & Hold the vent in left hand
- Right hand in the Left Av groove
- Direct the vent towards the left hip
- Guide with right hand across the Mitral valve
- Remove the stylate & see for bright red blood ejecting from vent
- Connect to the vent line

757
Which operations requires LV vent through RSPV
1. AVR
2. RSOV repair
3. SAM Excision
4. VSD AR
5. Bentall operation
6. TOF with MAPCAS
What are the various methods to vent left heart?
1. LV vent through RSPV
2. LA venting through PFO
3. PA vent
4. LV apical vent

Left Heart Venting operationwise

LH Operation Vent type

Venting
Site
RSPV AVR, Ascending aortic operation Sump, curved
corrections through RA/RV multiperforated
LA body MV surgery , MV+ other valve Sump
surgery

758
VSD Corrections through RA/RV Long stiff
IAS Only TV surgery, corrections Sump
through RA/RV
PA TOF correction through RV, LA Sump
myxoma excision
LA Only TV surgery, corrections Sump
appendage through RA/RV
LV apex AVR, any operation on aorta Curved multi-
perforated
ASD Any operation involving ASD Long stiff, sump
closure
Aortic Root CABG Root cardioplegia
cannula

Oxygenator & reservoir

*Steps to prevent reservoir overflow are

1) Increase flow
2) Decrease venous return
3) Vasodilators
4) Diuretics
5) Ultrafilteration
6) Use a 2nd reservoir
Prevention is by using minimum prime

Prime Blood flow Minimum Reservoir

rates (litres/ operating capacity
min) level
Affinity NT 270 ml 1- 7 200 ml 4 litres

759
 Minimax plus 150 ml 0.5- 2.3 150 ml 2 litres
Capiox SX 10 135 ml 0.5- 4 100 ml 3 litres
Safe Micro 52 ml 0- 800 ml 25 ml 400 ml

Arterial filter
Filter size: 25- 40 um
Produces a gradient of 30 mm Hg with a flow of 7 litres/ min & requires a
priming of 200 ml.

Advantage
Easy debubbling
High visibility
Safe against macro air
Effective micro air removal
760
Which are the operations where arterial line filter is must?
Excision of myxoma
MVR with clot in LA
Valve replacement in calcific valvular lesion
CABG with aneurysm +/- LV clot
Redo Cardiac surgery
Aortic aneurysms & dissecting aneurysm

761
 SURGEONS & THEIR ACHIEVEMENTS
1) Alexis Carrel (French Born) - Born in Lyons, France, 28 June 1873; Died in
Paris, France, 5 November 1944.

- He was the eldest child of Billiard

and AnneMarie Ricard.
- Carrel became interested in surgery
of the blood vessels about 1894, inspired, it
is said, by the death of President Carnot
from an assassins bullet, which cut a
major artery.
- Such wounds could not at that time
be successfully repaired.
- He developed extraordinary skill in
using the finest needles and devised a
method of turning back the ends of cut
vessels like cuffs, so that he could unite them endtoend without exposing the
circulating blood to any other tissue than the smooth lining of the vessel.
- By this device and by coating his instruments, needles, and thread with
paraffin jelly, he avoided blood clotting that might obstruct flow through the
sutured artery or vein.
- He avoided bacterial infection by a most exacting aseptic technique. His first
successes in suturing blood vessels were announced in 1902.
- Carrels pioneer successes with organ transplants led him to dream of
cultivating human tissues and even whole organs as substitutes for diseased or
damaged parts.
- Carrel succeeded in cultivating the cells of warmblooded animals outside the
body. To prove his results in the face of skepticism, he began his famous
undertaking to keep such a culture alive and growing indefinitely, using a bit of
tissue from the heart of an embryo chick. He kept this strain of connective
tissue cells alive for many years; in the care of one of his assistants it outlived

762
 Carrel himself. In 1912 he received the Nobel Prize for his surgical and cell
culture experiments.
- Vascular suturing techniques
- Sutured homologous free carotid artery between the aorta & coronary (canine)
- Interposed vein bypass of arterial tree
- With the aid of a chemist, Henry B. Dakin, he developed a method of treating
severely infected wounds, which although often effective was too complicated for
general use and has been supplanted by the use of antibiotics.
- About 1930 Carrel undertook another farreaching experimental program,
aimed at the cultivation of whole organs. In this work he was aided by the
celebrated aviator Charles A. Lindbergh, who devised a sterilizable glass pump
for circulating culture fluid through an excised organ. Carrel was thus enabled
to keep such organs as the thyroid gland and kidney alive and, to a certain
extent, functioning for days or weeks. This was a pioneer step in the
development of apparatus now used in surgery of the heart and great vessels.
- Dispute & left Rockefeller university, returned to France
- In France was accused of being Nazi collaborator in 1943.

2) Aldo Casteneda (1930- till date)

- Chief of children hospital Boston

- > 400 scientific articles & books
- Concept of correcting cardiac anomalies at an early age for
TOF, AV canal, TGA
- Norwood worked under him & described the Norwood
operation for HLHS
- Developed needle holder & vascular clamps
- Studied effect of CPB on blood elements & heart lung transplantation in
primates

3) Alfred Blalock (1899- 1964) Baltimore

763
- In 1944 Blalock, with Thomas by his side, performed the first "blue baby"
operation on Eileen Saxon, a 15-month-old baby. Assisted by Longmire
- Blalock continued his research on the heart and vascular surgery.
- With Edwards Park, he developed a bypass operation in 1944, and in 1948,
- with Rollins Hanlon, a cardiac surgeon, he created a technique for overcoming
the transposition of the great blood vessels of the heart- Blalock Hanlon atrial
septectomy
- Blalock loop
- 1st thymectomy
- First PDA ligation
- In personal life was plaqued by illnesses: septicemia with osteomyelitis of
sternum, nephrectomy with permanent ulnar nerve palsy, pulmonary TB

4) Ake Senning (1915- 2000)

- Born in 1915, in Rttvik, Sweden, ke Senning attended medical school at the

University of Uppsala and Stockholm.
- In 1948, he joined the innovative cardiovascular
surgeon Clarence Crafoord, at Sabbatsberg Hospital in
Stockholm.
- Developed one of the first pump oxygenators & used on
patient with LA myxoma
- Described the Atrial switch procedure
- 1st use of elective fibrillation of heart during surgery
- Implanted the first implantable pacemaker in a 43 year old man of Stoke Adams
syndrome (the man now 84 is still alive after changing 26 pacemakers)
- Introduced fascia lata for trileaflet valve & also implanted the 1st mitral
homograft in mitral position
- Worked with Gruntezig towards the 1st transluminal coronary angioplasty
- > 350 publications

5) Alain Carpentier (1933- till date)

- Born August 11, 1933 in Toulouse, France

764
 - The concept and development of valvular
bioprosthesis (Biological valve of animal origin
chemically treated to avoid immunological rejection):
Discovery that Gluteraldehyde reduces
xenograft tissue antigenicity and enhances tissue
stability by crosslinkages.
Development of the "concept of bioprothesis" and application to the
development and manufacturing process of valvular bioprostheses. First
implantation in human (1968).
Today, more than 50% of valve replacements are carried out using a
bioprosthesis.
- The concept and development of dynamic cardiomyoplasty (Physiological
and biological transformation of a skeletal muscle by sequential electrical
stimulation prior to its use as a myocardial substitute in the human) (1982-
1985) :
Original protocol of progressive sequential stimulation of a skeletal
muscle for the transformation of fatigable glycolytic myosine into non
fatigable oxydative isoform (personal contribution).
Development of the technique of cardiomyoplasty (with Pierre Grandjean
and Juan-Carlos Chachques). Over 1000 clinical applications in humans
worldwide.
This technique led to the recent development of "cellular cardiomyoplasty", a
technique which uses muscular cells instead of muscular tissue.
- Concept of annular remodeling. Mitral and tricuspid valves reconstructive
techniques
Concept of annular remodeling using prosthetic rings in valve surgery (1969)
Development of mitral and tricuspid valve reconstruction techniques.
These techniques widely used today worldwide allow to repair rather than to
replace 70% of the diseased mitral valves and 90% of the diseased tricuspid
valves.

765
- Functional classification of heart valve diseases
First description of the various types of cardiac valve dysfunction using the
concepts of Functional analysis and Segmental analysis. This approach
of valve analysis is now widely used in echocardiography and cardiac
surgery (1980).
Recognition and first description of the clinical and pathological
characteristics of a new entity of degenerative mitral valve disease, the
Fibroelastic deficiency.
- Other original contributions
New techniques for the surgical treatment of complex cardiac
malformations: atrioventricular canal (1977), Ebstein's disease (1989),
hypertrophied obstructive myocardiopathy.
First total biventricular support by extracorporeal artificial ventricles (1986)
First use of the radial artery as a conduit to bypass coronary artery lesions
(1972)
First world case of cardiomyoplasty (1985)
First case of complex open heart surgery with video assistance (1996)
First case of computer assisted open heart operation (1998)
- Research in progress
Cardiac xenotransplantation.
Induced tissue transformation.
- In Short:
o Discovered Gluteraldehyde,
o Coined the term bioprosthesis (Phd thesis in 1975)
o Describe dynamic cardiomyoplasty
o 1st bioprosthetic valve implantation
o Reconstruction surgeries of valves
o Technique for complete AV canal correction
o Surgical technique for Ebsteins
o Introduced radial artery as conduit for CABG
o 1st cardiomyoplasty
o 1st videoassisted open heart

766
 o 1st computer assisted open heart
o Developed various instruments

6) Clarence Walton Lillehei: Born in Minneapolis in 1918

- Because Dr Lillehei pioneered a direct, safe approach to open heart operations
in the 1950s, he was known as the father of open heart surgery. Indeed,
hardly any other cardiac surgeon has introduced a greater number of
innovative techniques and concepts.

- Father of modern cardiac surgery

- From University of Minnesota, Medical Center, Variety
Heart Hospital, Minneapolis
- Described hypothermia with inflow occlusion (with
Lewis)
- Azygous flow principle
- Cross circulation (maternal)
- Autologous oxygenation
- Infusion of oxygenated blood only during CPB (but the reservoir would empty &
gas emboli)
- Biological oxygenation (using Baboon lung)
- Bubble oxygenator (along with DeWall)
- 1st open heart surgery & also 1st to perform OMC, AVR, TOF ICR, TAPVC, TGA
- Proposed PML preservation
- Developed 3 valves:
-Lillehei Kaster valve- pivoting disc valve
-Lillehei Kalke valve- bileaflet valve with a 60 opening angle (only one
human implantation done & patient died within 24 hours)
-Lillehei Naqib valve- Toroidal disc valve (disc with central hole)
- First to describe external cardiac pacing

Indians trained under him are:

767
- Dr. Gopinath
- Dr. Kalke
- Suffered from a left parotid malignancy for which 2 surgeries were performed
(radical resection with radical neck dissection & mediastinal dissection)
- On July 5, 1999, Clarence Walton Lillehei, one of the worlds foremost cardiac
surgeons, researchers, and educators, died at his home in Minneapolis,
Minnesota, of prostate cancer at 80 years of age.

7) Charles Theodor Dotter

- Charles Theodore Dotter is generally credited

with developing a new medical specialty, interventional
radiology.
- He was a leading force in Machlett's development
of an x-ray tube capable of obtaining millisecond
exposures.
- 1st peripheral angioplasty
- Dotter was the 1st to describe flow-directed
balloon catheterization, the double-lumen balloon
catheter, the safety guide wire, percutaneous arterial stenting, and more.
- Percutaneous transluminal angioplasty was his landmark contribution.
- He also introduced the concepts of percutaneous arterial stenting and
stent grafting by placing the 1st percutaneous coilspring graft in the
femoral artery of a dog.
- He pioneered the techniques of low-dose fibrinolysis with injection of
streptokinase directly into an occluding thrombus. Dotter (along with
Marcia K. Bilbao) invented the loop-snare catheter for retrieving
intravascular foreign bodies.
- He developed tissue adhesives for vascular occlusion and organ ablation.
- Won Nobel prize

768
8) Charles Dubost

- Developed the vertical RA-LA incision for MV exposure

- transatrial MV dilators
- Endocardial resection with atrioventricular valve
replacement for endomyocardial fibrosis
- 1st abdominal aortic aneurysm resection
-

9) Clarence Crafoord

- Clarence Crafoord (1899 1984) was a Swedish

cardiovascular surgeon
- 1st surgery for Coarctation aorta- resection with end
to end anastomosis
- Developed ventilators
- Co-developer of heart lung machine (along with
Bjork, Senning)
- Crafoord also introduced heparin as thrombosis prophylaxis in the 1930s and
- He pioneered mechanical positive-pressure ventilation during thoracic
operations in the 1940s.

10) Donald Nixon Ross

- Donald Nixon Ross was born to Scottish

parents on October 4 1922 in Kimberley,
South Africa, and trained in Medicine at the
University of Cape Town, winning the
University Gold Medal for the most
distinguished graduate in Medicine in 1946.
- As well as his surgical firsts, in the
early years of heart surgery Ross developed the

769
 Guys-Ross hypothermic bypass machine.
- Carried out Britains first heart transplant in 1968.
- His greater achievement was the development of the pulmonary autograft (also
known the Ross procedure).
- 1st aortic homograft

- Described the various types of sinus venosus defects

11) Denton Cooley

- On August 20, 1920, a self-described shy and

insecure boy was born to Ralph and Mary Cooley of
Houston, less than two miles from the site of what is today
the Texas Medical Center.
- Founded Texas Heart Institute
- Cooleys clamp
- Cooleys retractor for LA
- Concept of stone heart
- Waterston Cooley shunt
- Cooleys vascular graft
- 1st heart transplant in US
- 1st artificial heart
- 1st aortic aneurysm surgery
- 1st LV aneurysm surgery on arrested heart
- LV apicoaortic conduit
- Developed Cooley Cutter valve

12) Gerard Brom

- 3 patch technique for supravalvar AS

- Trouser patch for mustard operation
- Broms incision- Rt. Thoracotomy for ASD

770
13) John Heysham Gibbon, Jr., 1960

- Born: September 29, 1903, Philadelphia,

Pennsylvania, United States
- In 1931, after witnessing the death of a
patient from pulmonary embolectomy, Dr. John
Gibbon had an idea for a machine that could take
deoxygenated blood, oxygenate it, and pump it
back into the arterial system.
- Collaborating with his wife Mary, Dr.
Gibbon worked from 1934 to 1942 to develop an
extracorporeal circulatory device.
- By 1942, he was able to keep cats alive on his experimental devices, with
continued survival after bypass.
- In 1950, he received support from IBM to build a heart-lung machine on a more
sophisticated scale.
- Dr Gibbon did his first human operation in February 1952, using his machine
on a 15-month-old girl with an alleged atrial septal defect. At this time, cardiac
catheterization was a major event, especially in children, and the patient was
too small to have a catheterization before surgery. Unfortunately, this patient
died on the operating table because the patient did not have an atrial septal
defect but rather a left-to-right shunt through a large patent ductus arteriosis.
- On May 6, 1953 at Jefferson Medical College Hospital, Dr. John Heysham
Gibbon, Jr. and his staff, with the help of his latest-designed heart-lung
machine Model II, closed a very serious septal defect between the upper
chambers of the heart of eighteen-year-old Cecelia Bavolek.

771
- This was the first successful intercardiac surgery of its kind performed
on a human patient.
- Ms. Bavolek was connected to the device for three-quarters of an hour
and for 26 crucial minutes; she totally depended upon the machines
artificial cardiac and respiratory functions.
- Dr Gibbon subsequently operated on 2 additional patients in July 1953, both of
whom were young girls about 5 years of age with atrial septal defects. These two
patients died at surgery with difficulties again of imprecise diagnosis of atrial
septal defect and complications related to bleeding during long time periods on
the heart-lung machine.5 After these two cases, Dr Gibbon, quite upset at these
failures, declared a moratorium on open-heart surgery with his heart-lung
machine.
- The first truly commercial heart-lung machine was the Mayo-Gibbon device,
which was the most widely used heart-lung machine of the 1950s and early
1960s and was developed by Kirklin and coworkers at the Mayo Clinic after the
design of Dr Gibbon.
- After the development of the heart-lung machine, Dr Gibbon returned to the
active practice of general thoracic surgery, leaving cardiac surgery to others,
recalling that his primary interest had always been thoracic surgery and that
his sentinel case of pulmonary embolism was a complication of a general
surgical operation.
- He gave his last talk on the development of the heart-lung machine at Baylor in
late 1972 and shortly thereafter passed away in early 1973 at the age of 69
from a fatal heart attack.

14) Sir Magdi Yacoub

- The son of a surgeon of a Coptic family, Yacoub was

born on 16 November 1935 in Belbis, Ashraqya, Egypt. He
studied at Cairo University and qualified as a doctor in 1957.
- Under Yacoub's leadership, the Harefield Hospital
transplant programme began in 1980 and by the end of the

772
 decade he and his team had performed 1000 of the procedures and Harefield.
- In December 1983 Yacoub performed the UK's first heart and lung transplant
- Extensive work on homografts
- AV repair techniques
- Proposed PA banding to train the LV for arterial switch
- VSD with AR- closure of VSD from aorta while plicating the AV with the
same Sutures
- MVR thru aorta
- He continues to operate on children through his charity, Chain of Hope.
- He is also notable for saving many lives by pioneering a technique for
'switching' the heart vessels of babies born with transposition of the great
arteries

15) Micheal Debakey

- Born: September 7, 1908, Lake

Charles, Louisiana, United States
- Died: July 11, 2008, Houston, Texas,
United States
- Established MASH units
- Invention of roller pump
- Development of double velour Dacron
- 1st carotid endartrectomy
- 1st use of LVAD
- Classification system for aortic dissection
- DeBakey clamp
- Debakey-Surgitool valve
- CTS center at Baylor College named after him.

16) Norman Shumway

773
- Norman Edward Shumway (February 9, 1923 February 10, 2006) was a
pioneer of heart surgery at Stanford University. He is widely regarded as the
father of heart transplantation.
- In collaboration with Randall B. Griepp, he was the first doctor to
successfully carry out a human heart transplant operation in the United
States in 1968, after Barnard's 1967 operation in South Africa, which
was based upon the work of Shumway and Richard Lower.
- The early years of the procedure were difficult, with few patients
surviving for long. Shumway was the only American surgeon to continue
performing the operation after others abandoned it after poor results.
- Norm Shumway's first patient, the first adult human-to-human heart
transplant in the United States, underwent surgery on January 6, 1968,
at Stanford University School of Medicine in Palo Alto, California. The
patient was a 54-year-old man who received the heart of a 43-year-old
man. The recipient died 15 days later of multiple systemic complications.
- In the 1970s he and his team refined the operation, tackling the
problems of rejection and the necessity for potentially dangerous drugs
to suppress the immune system. In particular he pioneered the use
of cyclosporine, instead of traditional drugs, which made the operation
safer.
- Shumway nonetheless persevered in the field amid controversy over legal and
economic issues, particularly the issue of what constitutes brain death among
potential donors.
- He died of cancer on February 10, 2006, in Palo Alto, California.

17) PK Sen (1915- 1982)

- Born Calcutta, MBBS from GSMC (KEM)

- Dept. of CTS at KEM is by his name
- Founder of CTS in India as a speciality

774
- 1st CMC in India
- 1st ASD with inflow occlusion in India
- Work on Transmyocardial accupuncure (forerunner of TMLR)
- Cardiac transplant in canine
- On 20-Feb-1968 - first ever heart transplantion in Asia. The operation was
performed by the Indian surgeons at K.E.M. Hospital, Bombay.
- 1st heart transplant in human in India & 6th in the world (1968)
- Described a technique for arch replacement
- Extensive work on aortoarteritis
- Married Marie Barnes, no children
- Received Padma Bhusan

18) Rene Favalaro (1923- 2000)

- Dr Favaloro was born in La Plata, Argentina.

He grew up in a poor neighborhood of La Plata but
was influenced by his maternal grandmother, who
taught him an enduring love of the land and nature,
and by an uncle, who was a general practitioner
and was often accompanied by the young Favaloro
on his daily rounds in the neighborhood.
- He then developed a lasting friendship with
Dr Mason Sones, the father of coronary cineangiography, who taught him to
read and interpret coronary and ventricular images.
- 1st documented aortocoronary bypass using an autologous saphenous vein on
9th May 1967
- CABG in patient with acute myocardial infarction
- CABG along with AVR
- Wrote book with > 20 1st technical contributions to the field of cardiac surgery
- Developed retractor for harvesting internal mammary artery
- Established Favalaro foundation in Argentina

775
- It has been estimated that more than 400 cardiologists and
cardiovascular surgeons have been mentored and/or trained under his
decisive influence.
- Because Dr Favaloro revolutionized the natural history and quality-of-life
of patients with ischemic heart disease, it is not surprising that Dr
Mason Sones once said that 20th century cardiology can be divided into
the pre-Favaloro and the post-Favaloro eras.
- Dr Favaloro will be remembered as a man with a love for his country, a
passion for work and ethics, and a strong sense of social responsibility.
And, overall, he will be remembered as a great innovator and pioneer in
the field of cardiothoracic surgery.
19) Robert Edward Gross

- Robert Edward Gross (July 2, 1905

October 11, 1988) was an American surgeon
and a medical researcher
- 1st successful PDA surgery
(performed division & suturing)
- Interposed Dacron graft for coarctation
aorta
- Atrial well technique for ASD closure
- 1st pediatric pneumonectomy
- 1st surgery for double aortic arch
- Classification of esophageal atresia
- Described various vascular rings & slings
- 1st congenital diaphragmatic hernia surgery
- 1st AP septal defect surgery (direct ligation)

776
20) Vincent Gott

- VINCENT L. GOTT is a skilled researcher and gifted surgeon and led the
Division of Cardiac Surgery for many years.
- In 1969, with Hopkins surgeon Harvey Bender, Dr. Gott performed the first
heart transplant at the John Hopkins hospital.
- During his more than 35 years with the university, he has helped to train more
than 50 cardiac surgeons and influenced the lives of countless other physicians
and patients.
- Dr. Gott was a primary researcher in
the development of the pacemaker, as well as
the co-inventor of the Gott-Daggett Valve and the
Gott Shunt.
- In conjunction with his clinical interest in
Marfan syndrome, he has conducted a record-
setting 150 aortic and root replacements.
- Dr. Gott co-directed the Broccoli Center for
Aortic Diseases.
- He retired from active cardiac surgery in 1994; in 2008 he was appointed
professor emeritus of surgery.
- Gott shunt (between LV apex & descending thoracic aorta)
- Gott Dagget valve (bileaflet valve)
- Work on biocompatibility studies for valves

21) Willis Potts

- Born in Sheboygan, WI, in 1895, Potts

was raised in the Unitarian faith.
- He was comfortable enough in his
relationship with his God and secure enough in
his technical excellence and genius not to feel

777
 threatened by the ambitious young people he attracted about him.
- His mission was to develop and improve surgical procedures for children, and
in this mission, he was a superb teacher and an excellent role model.
- Stanley Gibson, a gifted pediatric cardiologist. Together, they embarked on a
determined program for the diagnosis and treatment of congenital heart
disease.
- In cooperation with Dr. Joseph Boggs, Head of Pathology, they collected and
preserved more than 200 specimens of congenital heart problems. This valuable
collection was utilized for the basic education of would-be surgical residents.
- Devised Potts-Smith Aortic Exclusion Clamp.

778
 - Pottss malleable two fingered
lung retractor,
- Described Potts shunt
- described the various types of
vascular rings & slings

History of Cardiac Surgery & who has done first

1st heart surgery- Ludwig Rehn, 1896 Frankfurt

Inflow occlusion by- Lewis & Varco
1st open heart- John Gibbon, 2nd Sept 1952
Concept of hypothermia- Bigelow (1950)
Concept of topical hypothermia- Normal Schumway (1959)
Hypothermia & inflow occlusion- Lewis, Tauffic & Varco
Hypothermia & CPB-Sealy
Concept of hemodilution during CPB- Zuhdi, Gott & Lillehei
Concept of cardioplegia- Melrose (1955, used 200 meq/ litre potassium)-
abandoned
Reintroduction of potassium cardioplegia- Gay & Ebert (1973, 30 meq/ litre
potassium)
Cold blood cardioplegia- Follette

779
 First oxygenator- Gibbon (1953, screen oxygenator)
First surgery on oxygenator- Kirklin (1955 on screen oxygenator)
Bubble oxygenator- DeWall & Lillehei (1955)
Hypothermic circulatory arrest- concept- Charles Drew
Deep hypothermic circulatory arrest-clinical application- Randall Grippe
Retrograde cardioplegia- Zuhdi & Gott
TransRA technique of retrograde cardioplegia- Buckberg
Direct coronary sinus cannulation for retrograde cardioplegia- Menache
Retrograde cerebral perfusion- Ueda & Miki
Total body retrograde perfusion- Yasuarra (1994)
1st pericardiectomy- Ludwig Rehn
1st ASD closure- Lewis & Varco (using inflow occlusion)
1st ASD closure on pump- Gibbon (1953)
1st PDA surgery- Streider (1937- but patient died of distension & aspiration)
1st successful PDA closure- Gross (1939)
1st Pneumonectomy- Nissen
1st prosthetic graft- Voorhes (1952- using Viniyon- parachute material)
PTFE- Edwards (1957)
Dacron- DeBakey (1960)
ePTFE- Sayer & El Gore
1st cardiac transplantation- Christian Bernard (3rd December, 1967)
1st pediatric transplantation- Kantrowitz (1967)
1st successful pediatric transplantation- Bailey (1967)
1st heart lung transplant- Reitz (1981)
1st lung transplant- Cooper (1984)
1st reversed saphenous vein graft for peripheral vascular- Kunlin
1st insitu saphenous vein grafting- KV Hall- popularized by Leather
Elective cardiac fibrillation- Ake Senning
DC defibrillator- Berkovits
1st clinical application of internal defibrillator- Harken
Concept of counterpulsation- Moulopolous

780
 The term counterpulsation- Harken
Clinical use of counterpulsation- Kantrowitz
1st surgery of coronary artery to RA fistula- Bjork & Crafoord (ligation in 1947)

Etiology 1st description 1st surgery

ASD Leonardo da Vinci Lewis & Varco by
inflow occlusion
Gibbon on CPB
VSD Roger Lillehei on cross
circulation
Kirklin on CPB
TOF Nicholas Steno Lillehei on cross
Etiene Louis circulation
Arthur Fallot Lillehei on CPB
PDA Galen Gross (division &
Leo Botali suturing)

Coarctation Morgagni Craaford

Angina Heberden various

INDIAN SCENARIO
1st open-heart surgery- Dastoor
1st single vessel bypass- KM Cherian (1975)
1st triple vessel bypass- KR Shetty (1975)
1st VSD closure Gopinath
1st Heart Transplantation in India & Asia P K Sen (1968)

INSTRUMENTS WITH INDIAN CONTRIBUTION

Koles cardioplegia chamber

Pandey Joshi oxygenator (bubble type)

781
 Lillehei- Kalke valve (precursor of St. Jude)

Cardiac Intensive Care Unit Management

Pt. comes from theatre
Monitor set up
Set up limits of HR, BP, CVP, Saturation, and Temprature.
Ventilator set up
Check for setting.
Action list in ICU
Examine pt.
Hemodynamics, Peripheral perfusion
Air entry, Heart sound & murmur.
Check-
ABG, Electrolytes, Hb-Hct
Chest X ray
Position of ET tube-Ideal between medial ends of two clavicles.
Position of NG tube.
Position of CVP line.
Position of chest drains.
Heart size.
Lung field-Collapse/Effusion/Pneumothorax/Congestion.
Order list
IV fluids
1 ml/kg/hr initially
2ml/kg/hr once peripheral temp >30degree
Usually 5% Dextrose / Ringer lactate unless C/I.
Antibiotics
Prophylactic antibiotic is administered for all Cardiac Surgery cases.
o Inj. Cefuroxime 50-100 mg/kg administered just before induction.

782
 o Repeat dose of Inj. Cefuroxime administered after 4 hours if surgery is
prolonged.
o Inj. Cefuroxime 50-100 mg/kg 8th hourly for 48 hours post- operatively (6
Doses).
o Antibiotic is continued for a patient for more than 48 hours if persistent fever
with elevated WBC counts.
o Inj. Amikacin 18mg/kg, once in a day for cases undergoing re-exploration,
along with Inj. Cefuroxime.
o If patient is reported to have a positive ET / Blood Culture, the antibiotic is
started according to the sensitivity report.
Antacid- Inj. Ranitidine
1mg/kg/dose x 12 hrly.
Digoxin 10 micgm/kg/d
Valves cases, PAH, TOF.
HR > 80/min & SR.
Used in fast JR.
Calcium & D 25% - Pt. < 10 kg
Calcium 3ml x 8hrly
D 25% 5ml x 8 hrly
Watch for
Heart rate ( Rhythm )
Blood Pressure.
CVP
Temperature Peripheral / Core.
Urine output.
Drainage.
ABGs & Electrolytes.
Hypokalemia
Ideally serum K to be kept around 4mmol/L.
(4.5 Pts K) x BW/4 = mmol/L/2= ml
0.3 x BW x (4.5-Pts K) = mmol/L/2 = ml
783
 Always under correct.
In renal failure According to Creatinine clearance
Hyperkalemia
K+ > 4.5mmol/L.
Check K+ every hourly.
Stop all K+ containing fluids (RL/FFP/Blood).
Correct metabolic/respiratory acidosis.
Calcium Gluconate 0.2-0.5ml/kg over 5 min.
Insulin 0.1 U/kg with 0.5 gm/kg of glucose.
Use Lasix if it persistently remaining high.
K Oxylate powder 1gm/kg 4th hrly through NG/PR.
Metabolic acidosis
0.3 x base excess x Body weight = ml of sodabicarb.
Quick calculation
o Base excess >5.0 7.5 -Pts wt = ml of sodabicarb
o Base excess > 7.5 1.5 times Pts wt.
Assessment of Cardiac output
Physical examination CO Normal CO

Peripheral perfusion Capillary filling Poor Good

(<3 Sec)

Core peripheral temp. Gr. > 3 degree < 3 degree

Peripheral pulses Impalpable/ weak Normal

Urine output <1 ml/hr >1ml/hr

784
Mental status CNS Disoriented Co-operative

Arterial pressure wave Small area under Large area under curve
curve Dicrotic notch occurs
Dicrotic notch later
soon after peak

Metabolic acidosis Base excess > -5 mmol/L < -5mmmol/L

In ICU setting
Parameters CO Normal CO

Heart Rate Tachycardia Normal HR

Blood pressure Low Normal

CVP High/Low Normal range

785
Peripheral temp Cooling Warm
( > 30 degree)

Urine output < 1ml/kg > 1ml/kg

Low Cardiac output

Rule out
o Cardiac tamponade (CxR , Echo )
o Pneumothorax ( Clinical , CxR)
Volume required
o Use blood if Hct is < 33
o Otherwise Haes 3%
Albumin 20% 100 ml in RL

Low CO

Adequate preload Inadequate preload

Increase/Add Inotropes Give
colloids

Reassess preload
Keep LAP 5-10mmHg or CVP 4-6mmHg.

Inotropes

786
 Infusion rate Mic/kg/min Indication
Starting dose

Dopamine - Mild/mod myocardial dysfunction

5 (5 - 20) st
- Use 1 .
- Renal vasodilatation
- If dose >15mics/kg/min consider adrenaline

Dobutamine -Mild-mod myocardial dysfunction with labile

5 ( 5 20) pulmonary vasculature.
-Vasoconstriction & Tachycardia to be avoided.
-Expensive.

Isoprenaline -Relative bradycardia/AV block.

0.05 ( 0.01 - 0.5) -Isoprin is a potent vasodilator & may be poorly
tolerated in patients with low coronary perfusion
pressures.

Milrinone - Inodilator.
50mic/kg loading dose - Beneficial effect on RV dysfunction.
(0.5-0.75mics/kg/min) - Hypotension & thrombocytopenia.

Dose calculation
ml/hr = Wt (Kg) x Dose (mcg/kg/min) x 60min
------------------------------------------

787
 1000 x Drug conc. (mg/ml)
Digoxin
Inotropic-Bradycardiac.
Uses
- Volume overloaded heart-ASD/VSD/AVCD
- PVH MS/MR
- CHF with tachycardia.
0.03mg/kg/24hrs Digitalizing dose.
0.01mg/kg/24hrs - Maintainace dose.
Care Should not be given if S.K+<4.0mmol.
HR < 100/min, Renal impairment, Digoxin toxicity (Ventricular ectopics,
AV block).

Ventilation & Respiratory support

Factors affecting post- op pulmonary function
Perioperative factors
-CT surgery causes VC, FRC small airway closure during tidal
ventilation-Intrapulmonary shunting-Needs oxygen.
-CPB results in extra vascular lung water- Lung compliance.
-Pain contributes to respiratory dysfunction.

-Drugs-Anaesthesia, Analgesia, Sedatives-Somnolence- Respiratory

depression
Pre-operative factors
-Airway problems.
-Parenchymal lung disease.
-Effect of cardiac lesion Pulmonary oedema.
PEEP
FRC & improves oxygenation.
Applied in most cases 4-5cms.
788
 Higher level of PEEP useful in
o Post perfusion wet lung.
o Pulmonary oedema.
o Lobar collapse.
o Tracheo-bronchomalacia.
o Excessive mediastinal bleeding.
C/I Hypovolemia & Fontan Operation.
After connecting pt. on Ventilator Check
Chest is moving.
Air entry on both sides is equal.
Oxygenation- Colour of lips & skin,SpO2
Check for O2 inlet is properly pushed or not.
Ventilator is achieving the set parameters.
ABGs
- 15 min after shifting & connecting to ventilator
- 1 hour after resetting the parameter
- 6th hrly on operative & 1st po day
Chest X-ray.
When to do Chest X-Ray
When pt. comes to ICU.
1st Po day morning for all open hearts.
Ventilation or oxygenation deteriorates
- To detect
1. Pneumothorax.
2. Pleural collection.
3. Lobar collapse.
4. Pulmonary oedema.
5. Position of ET tube.
Pt. gets reintubated.
Weaning from ventilator

789
 Routine
1. Stable hemodynamics with modest inotropic support.
2. Peripherally warmed up (>30 degree)
3. Good ABGs on FiO2 - 40%.
4. Normal peak inspiratory pressure (<25cm H2O).
5. Wide awake with good respiratory rate.
6. No major bleeding
7. No major neurological deficit or residual pharmacological impairment
of consciousness.
8. Good CxR
No parenchymal pathology.
No fluid (in or out of lung)
Long term Ventilation
1. No signs of chest infection or other major sepsis.
2. Adequate nutritional state.
3. Able to tolerate weaning without resort to excessive sedation.
4. Should tolerate T Piece trial.
RR < 25 ideal, < 30 Acceptable
PCo2 between 30-40
PO2 > 80-85
5. Weaning down to CPAP may take several days if lung compliance is
poor.
6. Never ignore Ventilatory alarms.
ET suction
Immediately after receiving in ICU.
Every 4th hrly.
If Blood tinged secretion
Use normal saline to clear blood.
Use 1:10 / undiluted adrenaline.
Frequent suction to clear the blood.
790
 If thick secretions Nebulize & put normal saline to clear the secretion.
High PCO2
Check ventilatory parameter.
Increase rate & MV.
Remove BVF from inspiratory limb & put on expiratory limb.
Check for thick secretion.
Check for Blood in ET.
Low PO2
Check FiO2.
Check inlet of O2 port.
Hyperinflate lung & see for SpO2 ing/not.
Check for thick secretion.
Check for blood in ET.
Extubation
Ability to breath satisfactorily on CPAP prior to extubation.
Routine cases 30 minutes.
Long term ventilation longer time with rest on pressure support
overnight.
For pediatric cases < 20 Kg give Hydrocortisone (2-4 mg/kg) &
Dexamethasone (0.25mg/kg/dose) 15-30 min before extubation.( To
avoid stridor)
Fast track for pediatric patients.
Post Extubation
Keep O2 on 6 L mask.
Check ABG after 1 hour.
Reduce O2 to 2 L if PO2 is >120.
Keep off O2 after 2-3 hours.
Need of O2 for longer time CABG/TOF.
Post Extubation Stridor
Give Hydrocortisone & Dexamethasone.
791
 Dexamethsone (0.25mg/kg/dose)6hrly with Ranitidine.
Oxygen
Recemic epinephrine Nebulization.
Or
2ml neat 1:1000 adrenaline Nebulization.
If resolution does not occur reintubate.

Fever
First 24 hours
Stress response due to CPB & Surgery
Causes
Stress induced - Common
Sepsis - Unusual in early PO
Low CO - Peripheral Vasoconstriction with central pyrexia
Malignant Hyperpyrexia - Very rare
Up to 37.5-37.9 degree One / two spike
o Use fan / Paracetamol.
Continuous fever & > 38 degree
o Fan / Paracetamol
o Cold saline Lavage in RT
o Tepid sponging
o Cooling blanket if >40 degree
Continuous fever for >4-5 hrs Hemogram
Continuous fever with > 38 degree Blood culture.
Fever after 48 Hours
Must investigate for infection.
Neurological damage can cause Hyperthermia.
Investigations includes
o Hematology, Biochemistry, Urine C/S, Blood C/S, ET secretion C/S.
Antibiotics to be changed

792
Blood Loss
Surgical bleeding.
Bleeding due to coagulation abnormality
-Preexisting coagulopathy.
-Residual Heparin effect.
-Removal /consumption of coagulation factors.
-Platelet defects.
1-2ml/kg/hr for 1-2 hrs - should be alert.
>2ml/kg/hr Significant.
Surgically significant bleeding
Loss in Any
1 hour 10% of blood volume
2 hour 8% of blood volume
3 hour 6% of blood volume
Estimation of blood volume
85ml/kg in <10kg
80ml/kg in 10-20kg
75ml/kg in >20kg

Management of blood loss

Replace blood loss.
Check ACT (80-120).
If ACT >130 Protamine 1mg/kg.
ACT normal Hemostat ( Aminocaproic acid) 100 mg/kg
If only mediastinal tube draining - PEEP
One unit of warm fresh blood.
Hypotension
The following is an approach to managing the hypotensive patient;
1. Look at the recent hemodynamic parameters.
793
2. Assess the cardiac output/index. Is this a "pump" problem? Or is it due
to low SVR?
3. Look at the cardiac rhythm.
4. Look at the CVP to assess preload.
5. Is the afterload high?
6. Is contractility decreased?
7. Is this tamponade? Is this an acute graft occlusion or spasm? Is this an
acute dehiscence of a valve repair?
Look at the recent hemodynamic parameters obtained from the Swan-
Ganz catheter.
Obtain another set as soon as possible if they have not recently been
done or if there has been a sudden change.
Assess the cardiac output/index.
If the cardiac index is in the normal range or high, then the patient does
not have a significant "pump" problem and the cause of the hypotension
is secondary to diminished peripheral arterial tone (low SVR). A
vasopressor agent should be considered.
The differential diagnosis of low SVR includes;
o SIRS - a proportion of patients post CPB will have significant
cytokine increases
o Sepsis
o Anaphylactic or anaphylactoid reactions including protamine
reactions,
o Drug-induced, toxicological - nitrates, antihypertensives, narcotics
and sedatives, etc
o Adrenal insufficiency (Was the patient steroid dependent pre-
operatively?)
o Hyperthyroidism, hypothyroidism,
o Neurogenic (spinal) shock

794
 If the cardiac index is low (< 2.0 to 2.2 L/min/m2) then the cause of the
hypotension is inadequate flow or a "pump" problem.
Look at the cardiac rhythm. Absolute or relative bradycardias or
tachycardias (commonly new atrial fibrillation) can lead to decreased
C.O. and should be corrected.
Look at the CVP to assess preload. A patient with a low C.I. and a CVP
that is "relatively" low should be given a fluid challenge.
Volume required
o Use blood if Hct is < 33
o Otherwise Haes 3%
Albumin 20% 100 ml in RL

Low CO

Adequate preload Inadequate preload

Increase/Add Inotropes Give
colloids

Reassess preload
Keep LAP 5-10mmHg or CVP 4-6mmHg.
High afterload. Secondary to vasoconstriction and hypertension.
Decreased contractility. This should be managed with inotropic agents
while simultaneously looking for the cause.
o Low pre-operative ejection fraction
o Prolonged CPB time or cross-clamp times, difficulty with
myocardial protection intra-op
o Acute bypass graft occlusion (check the ECG)
o Graft spasm (especially LIMA) - check the ECG for ST elevation
Tamponade.
795
 Acute valvular regurgitation. A valve repair or replacement can rarely
have acute dehiscence. Check for a new regurgitant murmur and new 'v'
waves on the PCWP tracing in the case of a MVR.
Management
Head low position.
Inj. calcium to be given 500mg.
Check
- Support lines are Ok.
- Support not changed recently.
- Arterial line position.
- CVP.
If CVP low give volume.
Purge 0.1 ml of support.
Adrenaline 1:10 dilution 1ml.
Add support if required.
Hypertension
Check with NIBP.
Check support line.
Increase NTG.
Add Nitroprusside.
Give Captopril 0.1mg/kg/dose-1mg/kg/dose.
Maintain intravascular volume.
VPCs/ Tachyarrhythmias
Check Electrolytes K+
Give Magnesium 0.5%W/V 0.2ml/kg.
Give Xylocard 1mg/kg then 15-50 micgm/kg/min.
Care during Xylocard
Give Amiodarone 5mg/kg then 5-15micgm/kg/min.
Care during Amiodarone
Bradyarrhythmias
796
 Check
Electrolytes, Rhythm, Pacemaker
Give Atropine
Give Salbutamol Nebulization.
Start Isoprenaline.
Broad QRS complex Hemodynamically unstable Pacing wires are there-
Start pacing.
Tamponade
Cardiac tamponade is compression of the heart that impairs ventricular filling
and leads to a low cardiac output.
The incidence of cardiac tamponade post-cardiac surgery has been reported to
be as high as 3 to 6 %.
The presentation of tamponade can be variable and requires a high index of
suspicion.
No single bedside test or finding is sensitive or specific enough to absolutely
rule in or out tamponade.
A "typical" presentation would be a patient who had initially excellent
hemodynamic parameters, bled from the mediastinal tube moderately, then the
bleeding "stopped" or blood ceased to drain from the tubes. (Always check to
make sure the tubes are not obstructed).
This is followed by hemodynamic deterioration with tachycardia, declining
cardiac output and stroke volume, and decreasing mixed venous oxygen.
The urine output typically decreases and other signs of end-organ
hypoperfusion develop including CNS changes and acidosis.
1. Search for alternate explanations for the low cardiac output (i.e.,
hypovolemia, myocardial ischemia, etc.).
2. Assure patency of the tubes.
3. Look for "equalization" of central pressures. In "classic" cardiac
tamponade, the pericardium is intact and the raised pericardial
pressures are transmitted equally to all four cardiac chambers. This

797
 results in an elevation and equalization of the CVP, PCWP, and PAD
associated with low CO. (CVP=PCWP=PAD).
4. In the post-op cardiac surgery patient, it is possible to have a small, well-
localized clot that impedes filling to only one chamber and thus cause
unequal pressure changes. For example, a right sided clot may raise only
the CVP and impair filling to only the right atrium or ventricle.
5. Low voltages on the ECG or an increase in the width of the superior
mediastinum on serial chest X-rays are generally poorly sensitive or
specific. They are rarely helpful.
6. Echocardiogram. This is the best test to assess for tamponade. Often a
trans-esophageal Echo (TEE) will be required because of poor "windows"
common in the post-operative state with Trans-thoracic echo (TTE).
7. The only treatment for cardiac tamponade
o Return to the OR,
o Re-sternotomy, and
o Evacuation of the clot with hemostasis of any ongoing bleeding.
o Volume resuscitation, inotropes, and vasopressors are temporizing
measures only in this situation.
8. If a patient with suspected tamponade suddenly deteriorates and
develops PEA (pulseless electrical activity)
o Urgent sternotomy should be done in the ICU.

Mechanical assist devices

Intra-aortic balloon pump
History
Kantrowitz described augmentation of coronary
blood flow by retardation of the arterial pressure
pulse in animal models in 1952.
In 1958,Harken suggested the removal of some

798
 of the blood volume via the femoral artery during systole and replacing it
rapidly in diastole as a treatment for left ventricular (LV) failure, so called
diastolic augmentation.
Moulopoulos and colleagues developed an experimental prototype of an
IABP whose inflation and deflation were timed to the cardiac cycle.
Bergman and colleagues described the first percutaneous insertion of
IABP.
The first prefolded IAB was developed in 1986.
Basic principles of counterpulsation
Counterpulsation is a term that describes balloon inflation in diastole and
deflation in early systole.
Balloon inflation causes volume displacement of blood within the aorta,
both proximally and distally.
This leads to a potential increase in coronary blood flow and potential
improvements in systemic perfusion by augmentation of the intrinsic
Windkessel effect, whereby potential energy stored in the aortic root during
systole is converted to kinetic energy with the elastic recoil of the aortic root.
Physiological effects of IABP therapy
Primary goal -> improve the ventricular performance of the failing heart
by facilitating an increase in myocardial oxygen supply and a decrease in
myocardial oxygen demand.
Aorta : Reduces systolic pressure, Increases diastolic pressure
Left ventricle: Reduces systolic pressure, Reduces end-diastolic pressure,
Reduces volume & wall tension
Heart : Reduces afterload, Reduces preload, Increases cardiac output
Blood flow : Increases coronary blood flow
IABP may also have favourable effects on right ventricular (RV) function
by complex mechanisms including accentuation of RV myocardial blood
flow, unloading the left ventricle causing reduction in left atrial and
pulmonary vascular pressures and RV afterload.

799
 IABP inflates at the onset of diastole, thereby increasing diastolic
pressure and deflates just before systole, thus reducing LV afterload. The
magnitude of these effects depends upon:
(i) Balloon volume: the amount of blood displaced is proportional to the
volume of the balloon.
(ii) Heart rate: LV and aortic diastolic filling times are inversely
proportional to heart rate; shorter diastolic time produces lesser balloon
augmentation per unit time.
(iii) Aortic compliance: as aortic compliance increases (or SVR decreases),
the magnitude of diastolic augmentation decreases.
Myocardial oxygen supply and demand
Inflation of IAB during diastole increases the pressure difference between
aorta and left ventricle, the so-called diastolic pressure time index (DPTI).
increase in coronary blood flow and, therefore, myocardial oxygen
supply.
Myocardial oxygen demand is directly related to the area under the LV
systolic pressure curve, termed as tension time index (TTI).
Balloon deflation during systole causes a reduction in the LV afterload,
thereby decreasing TTI.
the ratio of oxygen supply (DPTI) to oxygen demand (TTI), known as the
endocardial viability ratio (EVR), should increase if the IABP is working
optimally.
Coronary perfusion
According to the Hagen Poiseuille principle, flow through a tube is
directly proportional to the pressure difference across it and the fourth
power of the radius while being inversely proportional to the length of the
tube and the viscosity of fluid flowing through it.
Renal function

800
 Renal blood flow can increase up to 25%, secondary to increase in
cardiac output.
Decrease in urine output after insertion of IABP should raise the
suspicion of juxta-renal balloon positioning
Haematological effects
The haemoglobin levels and the haematocrit often decrease by up to 5%
because of haemolysis from mechanical damage to the red blood cells.
Thrombocytopenia can result from mechanical damage to the platelets,
heparin administration, or both.
INDICATIONS
Acute myocardial infarction
Refractory LV failure
Cardiogenic shock
Refractory ventricular arrhythmias
Acute MR and VSD
Cardiomyopathies
Catheterization and angioplasty
Sepsis
Refractory unstable angina
Infants and children with complex cardiac anomalies
Cardiac surgery : Weaning from cardiopulmonary bypass
Acute myocardial infarction
IABP is aimed at achieving haemodynamic stability until a definitive
course of treatment or recovery occurs. By decreasing myocardial work
and SVR, intracardiac shunting, mitral regurgitation, or both (if present)
are reduced while coronary perfusion is enhanced.
Severe mitral regurgitation secondary to papillary muscle dysfunction or
rupture after myocardial infarction can lead to significant haemodynamic

801
 instability. This can initially be managed by IABP, pending definitive
surgery.
Refractory ventricular failure
Can aid the progression to more definitive treatments such as ventricular
assist device or cardiac transplantation.
Cardiogenic shock
Class I indication (ACC/AHA guidelines) for the management of cardiogenic
shock not rapidly reversed by pharmacological therapy.
Unstable angina
Increased risk of developing acute myocardial infarction and death. By
improving the haemodynamic condition of these patients, IABP can facilitate
further percutaneous interventions or bridge the patient to surgery.
Cardiac surgery
Elective placement is considered in high-risk patients such as those with
significant left main stem disease, severe LV dysfunction (ejection
fraction, 30%), congestive heart failure, cardiomyopathy, chronic renal
failure, or cerebrovascular disease.
Weaning from cardiopulmonary bypass may be difficult in cases where
aortic cross-clamping is prolonged, revascularization is only partially
achieved, or pre existing myocardial dysfunction is present. Separation
from cardiopulmonary bypass may be marked by hypotension and a low
cardiac index despite the administration of inotropic drugs. The use of
IABP in this setting decreases LV resistance, increases cardiac output,
and increases coronary and systemic perfusion, facilitating the patients
weaning from cardiopulmonary bypass
CONTRAINDICATIONS
Absolute
Aortic regurgitation
Aortic dissection
Chronic end-stage heart disease with no anticipation of recovery
802
 Aortic stents
Relative
Uncontrolled sepsis
Abdominal aortic aneurysm
Tachyarrhythmias
Severe peripheral vascular disease
Major arterial reconstruction surgery

Technique of insertion and operation

The IABP device has two major components:
A double-lumen 8.09.5 French catheter with a 2550 ml balloon
attached at its distal end
a console with a pump to drive the balloon
Balloon is made of polyethylene and is inflated with gas driven by the
pump.
Helium is often used because its low density facilitates rapid transfer of
gas from console to the balloon. It is also easily absorbed into the blood
stream in case of rupture of the balloon.

803
 Before insertion, the appropriate balloon size is selected on the basis of
the patients height (as supplied by Datascope, for a patient, 152 cm in
height, a balloon volume of 25 cc is appropriate; for height between 152
and 163 cm, balloon volume 34 cc; for height 164183 cm, balloon
volume 40 cc, and for height .183 cm, balloon volume 50 cc). Smaller
balloons are available for paediatric use.
The diameter of the balloon, when fully expanded should not exceed 80
90% of the diameter of the patients descending thoracic aorta.
The IABP catheter is inserted percutaneously into the femoral artery
through an introducer sheath using the modified Seldinger technique.
Alternative routes of access include subclavian, axillary, brachial, or iliac
arteries. The catheter can also be inserted surgically using a
transthoracic or translumbar approach, but this is associated with an
increased periprocedural mortality.
Once vascular access is obtained, the balloon catheter is inserted and
advanced, usually under fluoroscopic guidance, into the descending
thoracic aorta, with its tip 2 to 3 cm distal to the origin of the left
subclavian artery (at the level of the carina)
The console is programmed to identify a trigger for balloon inflation and
deflation. The most commonly used triggers are the ECG waveform and
the systemic arterial pressure waveform.
The balloon inflates with the onset of diastole, which corresponds with
the middle of the T-wave. The balloon deflates at the onset of LV systole
and this corresponds to the peak of the R-wave. Poor ECG quality,
electrical interference, and cardiac arrhythmias can result in erratic
balloon inflation.
The balloon is set to inflate after the aortic valve closure (which
corresponds to the dicrotic notch on the arterial waveform) and deflate
immediately before the opening of the aortic valve (which corresponds to
the point just before the upstroke on the arterial pressure waveform).
804
 IABP timing refers to inflation and deflation of the IAB in relation to the
cardiac cycle. The cardiac cycle is monitored by continuous display of the
arterial pressure waveform. As the balloon inflates at the onset of
diastole, a sharp and deep V is observed at the dicrotic notch.
Balloon inflation causes augmentation of diastolic pressure and a second
peak is observed. This peak is referred to as diastolic augmentation.
Diastolic augmentation is ideally higher than the patients systolic
pressure except when reduced stroke volume causes a relative decrease
in augmentation.
Depending upon the patients haemodynamic status, the balloon is
programmed to assist every beat (1:1) or less often (1:2, 1:4, or 1:8). With
haemodynamic improvement, the device can be weaned to less frequent
cycling before complete removal.
The device should never be left unused in situ to prevent thrombosis
Suboptimal timing of inflation and deflation of the balloon will result in
haemodynamic instability
Early inflation: inflation of the IAB before aortic valve closure
Late inflation: inflation of the IAB markedly after closure of the aortic
valve
Early deflation: premature deflation of the IAB during the diastolic phase
Late deflation: deflation of the IAB after the onset of systole

805
COMPLICATIONS
Transient loss of peripheral pulse
Limb ischaemia
Occlusion of a large aortic branch including renal, SMA, or subclavian
arteries with distal ischemia.
Acute aortic dissection or perforation.
Wound infection
Hemolysis, thrombocytopenia.
Thromboembolism
Compartment syndrome
Local vascular injuryfalse aneurysm, haematoma, bleeding from the
wound
Balloon rupture (can cause gas embolus)
806
 Balloon entrapment
Haematological changes, for example thrombocytopenia, haemolysis
Malpositioning causing cerebral or renal compromise
Cardiac tamponade
Patient care should be carried out with three primary goals in mind
Evaluation in terms of haemodynamic status, systemic perfusion, and
relief of cardiac symptoms;
Observation for early signs of complications including limb ischaemia,
balloon malpositioning, thrombus formation, bleeding, and infection;
Ensuring proper functioning of IABP, including correct timing, consistent
triggering, and troubleshooting of alarms.

807
 Question Bank
Long Questions (25 Marks)
Cardiac
- Describe the anatomy of ventricular septum of man & what
developmental anomaly may require surgical intervention.
- Role of mitral apparatus in LV contraction various replacement
operations preserving mitral apparatus.
- Causes and mechanism of Thrombosis of prosthetic heart valves and
MV of a patient with thrombosed prosthetic valve.
- Anatomy of MV apparatus and congenital malformation of MV.
- Discuss normal aortic root, what are the structures encountered during
aortic root enlargement.
- Discuss morphology of TV, etiopathology of TR and highlight basic
principles of surgical management.
- Discuss management in of acute MI indicating pros and cons of each
therapeutic procedure.
- Discuss the modification of fontan operation and their application.
- Discuss surgical anatomy of tricuspid valve and management of tricuspid
atresia.
- Discuss variation in the pathological anatomy of TGA which make
diagnosis difficult / impossible.
- Describe the method of detection and prevention of rejection of human
heart transplant.
- Classify supraventricular tachy arrythmias and their surgical
management.
- Classify DORV, diagnostic criteria and surgical management.
- Discuss surgical management of TAPVC in < 6months of age.
- Development of interatrial septum, Classify ASD,Describe surgical
management of Sinus Venosus type of ASD.

808
- Discuss the diagnosis & management of Dissecting Aneurysm of thoracic
aorta.
- Discuss the embryology & anatomy of interventricular septum.
- Describe the course & relations of arch of aorta.
- Discuss the pathology & management of Acute aortic incompetence.
- Discuss the current status of saphenous vein as a coronary artery
bypass graft & the results of redo CABG procedures.
- Describe the anatomy of the fibrous skeleton of the Heart.
- Describe the anatomy of the conduction system of the normal heart &
TOF.
- Describe briefly the embryology & pathological anatomy of the
endocardial cushion defects.
- Describe the anatomy, pathophysiology and surgery for ruptured sinus of
valsalva.
- Describe the morphology of tricuspid valve. Discuss the various causes of
regurgitation & highlight the basic principles of its surgical management.
- Describe the morphology of mitral valve. Discuss the various etiological
causes if regurgitation highlight the various basic principles involved in
the repair of the mitral valve.
- Describe the anatomical development of aortic abscess & mention
various surgical anomalies that can result because of congenital
malformation.
- Etiopathogenesis of pulmonary arterial hepertension and its significance
in cardiac surgery.
- Describe the venous drainage of the heart & explain in detail the clinical
relevance.
- Anatomy of aortic root & various procedures for aortic root enlargement.
- Describe the development of pulmonary artery. Describe the
characteristics of pulmonary blood flow in diminutive or absent central
pulmonary arteries.
809
- Anatomy of mitral complex.
- Describe the anatomy of mitral valve annulus.Describe the various
techniques of mitral valve repair.
- Describe the anatomy of aortic root & discuss the surgical management
of aortic root.
- Classification of tricuspid atresia & surgical procedures.
- Complications of coronary artery disease & its management.
- Discuss in details the anatomy, physiological consequences &
management of hypoplastic left heart syndrome.
- Redocardiac surgery Problems & management.
- Pulmonary embolism & its management.
- Pulmonary thromboendarterectomy.
- Discuss the fibrous skeleton of the heart & its surgical implications.
- Describe the venous drainage of the heart & its applied significance.
- Describe in brief the development of interventricular septum. Describe
various classifications of VSDs and discuss the clinical relavence of each
classification.
- Discuss brain protection during aortic surgery.
- Discuss various techniques of myocardial pretction and their cellular &
molecular basis.
- Describe various causes of right ventricular outflow tract obstruction &
their treatment with surgery.
- Classify complete AV canal defects & describe the principles of surgical
corrections.
- Discuss the anatomy of the mitral valve apparatus & applied
significance.
- Describe the collateral circulation in the coarctation of the aorta below
subclavian artery & its clinical significance.
- Describe the conduction system of the heart & its surgical importance.

810
- Describe the development of pulmonary venous system & left atrium.
Describe briefly anomalies due to maldevelopment.
- Compare off pump CABG with onpump CABG with respect to multivessel
coronary artery disease.
- Discuss bioprosthetic heart valves & their utility in clinical practice.
- Discuss the pathophysiology of chronic constrictive pericarditis & its
surgical management.
- Discuss the Fontan circulation & describe various modifications of
fontan procedure.
- Discuss the indications for Rastelli procedures.
- Give a diagrammatic presentation of various coronary artery patterns in
transposition of great arteries. Discuss the management of a 5 month old
child with d-TGA. What is the only criteria for the correction of
transposition of coronary arteries.
- Describe the clinicopathological difference between pulmonary atresia
with VSD and pulmonary atresia with intact ventricular septum, Discuss
the role of surgery in both of them.
- Describe the causes of difficulties in weaning of CPB following open heart
surgery & its management.
- Discuss the ductus dependant circulation and management of one of
them.
- Describe various indications for CABG and discuss the conduits used for
CABG.
- Discuss surgical management of Atrial fibrillation.
- Describe surgical techniques of cardiac transplantation.
- Techniques of total arterial revascularisation, conduits used & long term
results.
- Discuss the Jones criteria for rheumatic heart disease & current status
of rheumatic prophylaxis.

811
 - Defie renovascular hypertension . Describe its pathophysiology &
treatment modalities.
- Discuss the role of transthoracic & transesophageal echocardiography in
cardiac surgery.

Thoracic
- Surgical anatomy of thymus & pathogenesis of myasthenia gravis.
- Classify carcinoma of lung discuss various treatment procedures of small
cell Carcinoma of the lung.
- Describe anatomy of lower end of oesophagus and management of reflux
oesophagitis.
- Discuss various treatment modalities used in post thoracotomy pain
management.
- Describe the etiopathogenesis & diagnosis of bronchopleural
fistula.Discuss the management of bronchopleural fistula.
- Development of diaphragm and surgical treatment of diaphragmatic
hernia.
- Describe the Bronchopulmonary segments & discuss the aetiology &
management of Bronchiactesis.
- Describe the congenital tracheoesophageal fistula & discuss the
management.
- Discuss the pathogenesis, investigations & surgical management of
recurrent hemoptysis.
- Describe the anatomy of the mediastinum & discuss the anterior
mediastinal tumours.
- Describe the anatomy of bronchopulmonary segments & its surgical
significance.
- Describe the pathophysiology of pulmonary sequestration & its surgical
management.
- Describe the pathophysiology & management of Bronchiectesis.
812
 - Describe the pathology of mediastinal tumours.
- Describe the surgical anatomy & management of congenital atresia of the
oesophagus.
- Describe the anatomy of thymus & discuss the pathogenesis and various
modes of management of myasthenia gravis.
- Discuss the pathology of Carcinoma of the lung and the principles in
management.
- Anatomy of Trachea. Indications of tracheal surgery & the procedures of
tracheal resections.
- Discuss the anatomy of diaphragm with special reference to different
diaphragmatic hernias.
- Discuss Pulmonary function parameters in relation to cardiothoracic
surgery.
- Anantomy of oesophagus & its lymphatic drainage.
- Discuss the various types of carcinoma of oesophagus & their
management.
- Describe etiology of stricture oesophagus & its treatment.
- Explain the lung volume & discuss various pulmonary function tests &
their clinical application.
- Discuss the surgical anatomy of the mediastinum with special reference
to mediastinal tumours.
- Discuss various endoscopic diagnostic procedures for the diagnosis of
thoracic diseases of surgical importance.
- Discuss the lymphatic drainage of the lungs with reference to
Bronchogenic carcinoma.
- Describe the various fungal infections of lungs & heart which are of
interest to cardiothoracic surgeon and their treatment.

Vascular

813
 - Embryology of carotid arterial system of brain & discuss management of
ICA stenosis.
- Anatomy of radial artery & the tests performed to evaluate the adequacy
of blood flow through the hand.
- Surgical anatomy of aortic root, Pathology and management of annulo
aortic ectasia.
- Discuss clinical features and management of chronic atherosclerotic
aorta iliac obstruction.
Miscellaneous
- Schematic representation of coagulation cascade, evaluation &
management of bleeding disorders after Open heart surgery.
- Etio-pathology & management of Acute renal failure after open heart
surgery.
- Activated clotting time.
- Factors affecting blood loss during open heart surgery & detailed
methods of management to minimize the same.
- Describe the cardiovascular reserves in health & post op cardiac surgery.
How can you manipulate them in post op period in order to achieve
successful result.
- What is Low cardiac output ,Investigations & management modalities of
Low cardiac output
- Discuss the methods in use for blood conservations in open heart
surgery.
- Describe the physiology of Cardiopulmonary bypass.
- Describe various factors contributing to the pathophysiological changes
associated with cardiopulmonary bypass.
- Describe the pathophysiology of hypothermia with reference to open
heart surgery.
- Discuss the consequences of reduced core temperature below 36 degree
centigrade.
814
 - Describe the factors affecting cardiac output & its pharmacologic
manipulations.
- Discuss the cardiopulmonary bypass setup for infant cardiac surgery.
- Describe the recent advances in myocardial protection for cardiac
surgery.
- Discuss the coagulation cascade & outline the mechanism of action of
various anticoagulant & pro coagulant medications.
- What are the various organisms for nosocomial infections in recovery
rooms & intensive care units? Describe methods of preventing them.
- What perfusion strategies you will adopt for the aneurysm of the arch of
aorta? Discuss the technique.
- A 45 year old person came up for double valve replacement. What would
be your preferred method of myocardial management?
- Discuss in brief stem cell therapy in peripheral & myocardial
angiogenesis with reference to source of stem cells, its route of
administration, advantage & disadvantage.
- Discuss the scope & indications of robotics in cardiac surgery.
- When is myocardial viability is assessed? Discuss current modalities
available to assess myocardial viability.
- Describe the concept of tissue engineered heart valve. Discuss in brief
current status of heart valve banking & heart valve substitute in India.
- Describe principles & various uses of PET in cardiac evaluation.

Short Questions (10 Marks)

Cardiac
- Surgery of PDA with PAH.
- COA of aorta .
- Unroofed CS.
- Double aortic arch.
815
- Classification of aortic arch dissection.
- Complete common AV canal.
- Extra cardiac conduits.
- Scimatar syndrome.
- Discuss blood supply of SA node & its surgical importance.
- Coronary sinus type of TAPVC.
- Classify DORV, diagnostic criteria and surgical management
- Interrupted aortic arch.
- Hypo plastic left heart syndrome.
- Post operative pulmonary hypertensive crisis an its management.
- Heart failure in first month of life.
- Ebstein anomaly.
- Persistent LSVC.
- Cor tritriatum.
- Pulmonary artery banding.
- Discuss surgical management of TAPVC in < 6months of age.
- Development of interatrial septum, Classify ASD,Describe surgical
management of Sinus Venosus type of ASD.
- Double Aortic arch.
- Maze procedure.
- Indications of ascending aorta replacement.
- Management of pulmonary hypertensive crisis.
- Indications & techniques of aortic valve repair.
- Etiology, diagnosis & management of endomyocardial fibrois.
- Surgical management of ectopia cordis.
- Indications & techniques of femoral bypass.
- REV procedure.
- DKS operation.
- Anastomotic devices in CABG.
- Geometric repair of LV aneurysm.
816
- Synthetic patches & graft used in cardiac surgery.
- Endartrectomy in coronary artery disease.
- TMR.
- HOCM.
- Surgically induced CHB.
- Management of carotid artery disease in patients with coronary artery
disease.
- Arterial switch operation.
- Surgical treatment in congestive heart failure.
- Vascular endothelial growth factor.
- Aneurysm of ductus arteriosus.
- Nonpulsatile axial pump.
- Recoarctation of aorta, definition and management.
- Congenital vascular ring.
- Infracardiac TAPVC.
- Cryopreservation.
- Phrenic nerve injury.
- Technique of closure of PDA during CPB.
- Conduit reconstruction of RVOT.
- Prevention and treatment of PR following TOF repair.
- Palliative shunts for TOF .
- Surgical anatomy of TOF.
- Discuss RVOT obstruction .
- Absent PV syndrome in infancy .
- Discuss diagnosis complications and management of post operative
bleeding following total correction of TOF.
- MAPCAS.
- TOF correction which small PA.
- Surgical management of RVOT obstruction .
- Anomalies of coronary arteries in management of TOF.
817
- Trans atrial repair of TOF.
- Outline Surgical treatment of single ventricle .
- Anomalous connection of left CA to PA (ALCAPA).
- Management of hypo plastic left heart syndrome .
- Evolution of fontan surgery .
- Discuss the modification of fontan operation and their application .
- Discuss surgical anatomy of tricuspid valve and management of tricuspid
atresia.
- Compare following Mustard, Senning, Arterial Switch .
- How will you prevent AV conduction injury during closure of VSD
associated with correction of TGA .
- Discuss variation in the pathological anatomy of TGA which make
diagnosis difficult / impossible .
- His bundle mapping.
- Atrial Isomerism.
- Azygos vein.
- Classification of aortopulmonary window.
- Coarctation of aorta.
- Absent pulmonary valve syndrome.
- Cervical aortic arch.
- Sites of aneurysm in coarctation fo aorta.
- Truncus atreriosus.
- Cor triatriatum.
- Supracardiac TAPVC & management.
- Taussig bing anomaly.
- Bronchopulmonary collaterals.
- Pulmonary vascular changes in left to right shunts.
- Pathological anatomy in tricuspid atresia.
- Anatomical variations of truncus arteriosus.
- Pathological anatomy of the transposition complexes of the heart.
818
- Endocardial cushion defects- developmental anatomy.
- Unroofed coronary sinus.
- Classification of left ventricular outflow tract obstruction.
- Atrial isomerism.
- Persistant left SVC.
- Right ductus arteriosus.
- Trabecular septomarginalis.
- Glenn shunt.
- Ross procedure.
- Ebstein anomaly.
- Bulbus cordis.
- Pumonary atresia with intact ventricular septum.
- Current role of pulmonary artery banding.
- Treatment of Interrupted aortic arch.
- Long term results after tetrology of fallot correction.
- Explain unifocalisation & its indications.
- Merits & demerits of right atrial approach in VSD.
- Treatment of hypertensive PDA.
- Management of LSVC during ASD closure.
- Classification of endocardial cushion defect.
- Grading of pulmonary vascular disease.
- Dextrocardia.
- ASD surgery using thoracotomy approach.
- Gastroepiploic artery as a conduit in CABG.
- Intracoronary irradiation .
- CABG on beating heart .
- Radial artery as conduit in CABG .
- Transmyocardial and percutaneous laser revascularization .
- Coronary-coronary bypass surgery .
- Management of single CAD .
819
- Coronary artery bypass conduits .
- Minimal invasive CABG.
- Long term results of myocardial revascularization.
- BIMA .
- Coronary collaterals .
- Post infarction VSD.
- Coronary end arterectomy .
- Angiographic anatomy of Coronary artery.
- Recent concept in surgery of CAD.
- Recent diagnostic aids in CAD.
- Total arterial revascularisation.
- Discuss management in of acute MI indicating pros and cons of each
therapeutic procedure .
- Redo CABG .
- Failed Coronary angioplasty .
- Controversies in the management of IHD.
- Graft anastomosis in calcific ascending aorta in CABG.
- Tandem CAD / Tandem Lesions.
- Discuss problem of Coronary artery spasm during CABG .
- All conduits in CABG.
- Anatomy of the coronary sinus with relevance to the retrograde coronary
perfusion.
- Surgical anatomy of the LAD coronary artery.
- Role of CT angio in evaluating coronary artery disease.
- Assessment of myocardial viability.
- Surgical ventricular restoration.
- Role of mitral apparatus in LV contraction various replacement
operations preserving mitral apparatus .
- Causes and mechanism of Thrombosis of prosthetic heart valves and
MV of a patient with thrombosed prosthetic valve .
820
- Complications of mitral valve surgery.
- Anatomy of MV apparatus and congenital malformation of MV .
- MV repair.
- Options available in prosthetic valve.
- Prosthetic valve endocardtis.
- Echo/Doppler assessment of mitral regurgitation.
- Rationale for MVR for IHSS.
- Changing the trends in management of MS.
- Durablity of prosthetic MV.
- Management of giant left atrium during mitral valve procedure.
- Choice of prosthetic MV.
- Discuss balloon valvulo plasty verses surgery.
- Acute rupture of chordae tendinae of MV .
- Restenosis of MV.
- MV replacement in Small LA.
- Discuss the result and indications of balloon valvotomy.
- MVR in giant LA.
- MVR with chordal preservation.
- Complications of MVR.
- Surgical anatomy of mitral valve apparatus.
- A patient develops massive bleeding following mitral valve replacement.
Possbilities & management.
- A 50 year old male develops lowcardiac output after 6-7 hours of
surgery.How will you assess & manage him?
- A patient with mechanical mitral vave comes with acute dyspnoea. What
are the possibilities & management?
- An ideal heart valve.
- Stuck valve.
- AV repair procedure.
- Role of homograft AV in cardiac surgery.
821
 - Discuss normal aortic root, what are the structures encountered during
aortic root enlargement.
- Valve of echo in preop evaluation of AV surgery.
- Homograft AV.
- Surgical management of subaortic stenosis at various levels below AV.
- Discuss methods of AV construction for mild moderate AR .
- Discuss the results of AVR with cryopreserved AV homografts.
- Discuss morphology of TV, etiopathology of TR and highlight basic
principles of surgical management .
- Classification of tricuspid stenosis.
- Current status and future prospective of cardiac transplantation.
- Immunosuppressants in cardiac surgery .
- Factors influencing increased survival rate following the cardiac
transplantation of man .
- Describe the method of detection and prevention of rejection of human
heart transplant .
- LVAD.
- Implantable cardioverter defibrillator.

Thoracic
- Achalasia cardia, Morphological and Physiological changes.
- Lung volume reduction surgery .
- Flail chest, patho physiology .
- Results of lung transplantation.
- Pneumocystic carinii.
- Alveolocapillary membrane.
- Blood supply of trachea.
- Lower esophageal sphincter.
- Diagnosis of broncho pleural fistula & management .
- Clinical indications & current status of lung transplantation .
822
- Use of VATS in thoracic surgery .
- Manometry of lower oesophagus.
- Pleural mesothelioma.
- Management of acquired benign obstruction of lower end of oesphagus .
- Classify carcinoma of lung discuss various treatment procedures of small
cell Carcinoma of the lung.
- Thymomas.
- Thoracoplasty.
- Liemyoma of esophagus.
- ARDS.
- Anatomy of bronchial tree and management of bronchiecteasis.
- Lobar emphysema .
- Discuss middle lobe syndrome.
- Discuss treatment of recurrent pneumothorax.
- Mediastinoscopy.
- Branchial artery embolisation.
- Vanishing lung.
- Jet ventilation.
- Rib notching.
- Foregut cyst.
- Benign tumours of oesophagus.
- Discuss treatment of post pneumonectomy empyema.
- Silhuoette sign.
- Traumatic diaphragmatic rupture.
- Indications of surgery in pulmonary tuberculosis.
- Neurogenic tumours of mediastinum.
- Extralobar sequestration.
- Pulmonary AV fistula.
- Carinal pneumonectomy.
- Bronchial artery embolisation.
823
- Management of multilocular empyema.
- Esophagomyotomy.
- Techniques of lung isolation.
- Esophageal bougienage.
- Malignant pleural mesothelioma .
- Post mediastinal mass lesion.
- Complications following lung resection and their management .
- Differences in lung function test in restrictive and obstructive airway
disease .
- Histological types of broncogenic carcinoma and staging .
- Diagnosis, prognosis, and management of superior sulcus tumors outline
its results .
- Early oesophageal carcinoma .
- Chylothorax .
- Dysphagia lusoria .
- Bronchogenic cyst.
- Diagnostic techniques in evaluation of oesophageal diseases .
- Classify diaphragmatic hernia and their surgical management .
- Occult lung cancer.
- Vigorous achalasia .
- Discuss the life cycle of Echinococcus Granulosus.
- FNAC in thoracic surgery .
- Cystic lesions of mediastinum .
- Adult respiratory distress syndrome.
- VATS.
- Thoracic manifestation of HIV-I infection.
- Fracture first rib .
- Diffuse spasm of oesophagus.
- Pulmonary contusion.
- Ruptured diaphragm .
824
- Oesophageal manometry in health and disease.
- Relevance of thymectomy in myasthenia gravis .
- Oesophagomyotomy .
- Management of tracheal tumors.
- Benign Oesophageal Strictures .
- Traumatic amputation of left lower lobe of lung.
- Hypotension after pnemonectomy.
- Factors preventing gastro-oesophageal reflux .
- Azygos lobe.
- Congenital traecheo-oesophageal fistula.
- Chronic empyema thoracis.
- Pre-cancerous lesions of oesophagus.
- Management of benign tumors of lung.
- Carcinoid tumour.
- Fungal ball in lung.
- Hernia of bochdalak.
- Empyema and pnemothorax in infancy and childhood.
- Congenital lobar emphysema.
- Oesophageal diverticulae.
- Short course of chemotherapy in pulmonary tuberculosis.
- Coin lesion.
- Swan-ganz catheter.
- Describe anatomy of lower end of oesophagus and management of reflux
oesophagitis.
- Surgical management of gastro-oesophageal reflux.
- Bronchial closure following pnemonectomy.
- Tracheal prosthesis.
- Cervical rib.
- Completion pnemonectomy.
- Management of tracheal stricture.
825
- Oesophageal perforation.
- Management of infected dead space in pleural cavity.
- Describe treatment of recurrent pneumothorax.
- Describe method of surgical treatment of budd-chiari syndrome.
- Describe briefly surgical treatment of pulmonary metastasis.
- Pulmonary sequestration.
- Development of diaphragm and surgical treatment of diaphragmatic
hernia.
- Mediastinal tumours in children.
- Measurement of residual lung volume and its importance.
- Rationale of various surgical procedures for relief of hiatus hernia.
- Pulmonary embolism.
- Recent concept in management of mediastinal infection.
- Pulmonary hamartoma.
- Pathophysiology of open pnemothorax.
- Lung volume reduction surgery.
- PEEP.
- Systemic venous oxygen saturation (SVO2).
- FEV1.
- Parameters used in discontinuing respiratory support of patient
following OHS .
- Complication following long term ventilation .
- IPPV.
- High frequency positive pressure ventilation .
- Intermittent mandatory ventilation.
- Congenital sternal anomalies.
- Peek expiratory flow rate.
- Dysphagia lusoria.
- Chylothorax.
- Use of laser in trachea-bronchial lesions.
826
 - Flail chest injury.
- Name the bronchopulmonary segments and describe the lymphatic
drainage of the lung.
- Mediastinal tumours.
- Pharyngeal diverticulum.
- Staging of bronchogenic carcinoma.
- SVC obstruction.
- Discuss mediastinal cyst.
- Malignant pleural mesothelioma.
- Pectus excavatum.
- Mediastinitis.
- Pathology of Bronchial adenoma.
- Right scalene node.
- Azygos lobe.
- Achalasia cardia.
- Treatment of MDR & XDR TB.
- Oesophageal manometry.
- Oesophageal perforation.
- Empyema necessitallis.
- Drug resistance acid fast bacilli.
- Double lumen endotracheal tubes.
- Anantomy of trachea & techniques of mobilisation.
- Zenkers diverticulum.
- Reccurent laryngeal nerve.
- Thoracic duct.
Vascular
- Diagnosis of Thoracic outlet syndrome.
- Middle aortic syndrome .
- Cervical rib and its management .
- Marfanoid aneurysm of ascending aorta .
827
- Classify aorta dissection and its management .
- Coronary subclavian steal syndrome.
- Endovascular stenting.
- PTFE grafts.
- Compatment syndrome.
- Paraplegia following surgery on descen.ding aorta
- Doppler ultra sound in diagnosis of DVT.
- Factors affecting in blood flow through a stenotic artery .
- List the inflammatory collagen disorder lesions of thoracic aorta and
outline the role of surgery .
- Compare various material available for arterial replacement .
- Discuss clinical features and management of chronic atherosclerotic
aorta iliac obstruction.
- Etio pathology of aorta arteritis .
- Surgical anatomy of aortic root, Pathology and management of annulo
aortic ectasia .
- Pathology of syphilitic aortitis verses athero sclerosis.
- Classification and etiopahology of dissecting aortic aneurysm .
- Pathological anatomy of dissecting aneurysm of the aorta.
- Deep vein thrombosis.
- Subclavian steal.
- Internal thoracic artery.
- Schatzis ring.
- Aschoff nodules.
- Metabolic alkalosis.
- Tracheal strictures.
- A victim of a road traffic accidents comes with massive air leak in the rt.
intrecostal drains. How will you proceed to manage him?
- A healthy 5 year old child is brought to the hospital with breathlessness
& mild stridor. What are the possibilities & line of management?
828
 - How will you manage the chylothorax following CABG?
- Investigation and management of pulmonary embolism.

Miscellaneous
- Surgical management of AF.
- Cardiac contusion .
- Management of LV aneurysm .
- Surgical treatment of cardiac arrhythmias .
- Treatment of air embolism during OHS.
- Natriuretic peptids.
- Cardiac myxomas.
- Haemodynamic changes in constrictive pericarditis.
- Pectus excavatum .
- Management of sternal infection.
- Tricuspid valve endocarditis .
- Effect of nicotin on cardiovascular system.
- Rational of Lattisimus dorsi muscle in cardio myopathy .
- Use and complication of laser therapy in CV and thoracic surgery .
- Classify supraventricular tachy arrythmias and their surgical
management .
- Autotransfusion.
- Electrolyte monitoring in post of cardiac ICU.
- Unstable angina .
- Role of platelets in cardiac surgery.
- Surgery of EMF.
- WPW Syndrome.
- AIDS and cardiac surgery .
- Post operative compilations after pericardectomy for constrictive
pericarditis.
- Delayed sternal closure .
829
- Membrane oxygenator.
- Protamine reaction.
- Post surgical heart block .
- Minimally invasive surgery.
- Air embolism in cardiac surgery.
- ECMO.
- Treatment of Intraoperative problems in redo OHS.
- Factors affecting sternal healing .
- Discuss indications and results of dynamic cardio myoplasty .
- Discuss PA collaterals .
- Management of cardio myopathy .
- Blunt chest injury .
- Dual chambered pacemakers.
- Rota laser.
- Left atrial pressure.
- Membrane oxygenator.
- Atrial pacing.
- LVADS.
- Infected cardiac pacemakers.
- Salient design features & haemodynamics of any prosthetic heart
valve of your Choice.
- Cardiac Pacemakers.
- Modes of pacing.
- Pacemaker complications.
- Pulmonary artery balloon counter pulsation .
- Cardiac pacemakers and their use in the treatment of post operative
cardiac arrhythmias.
- Billable prosthetic valves .
- Advances in Cardiac pacing.
- Kaplan meier model.
830
- Triangle of Koch.
- Frank starling law.
- Ischemic preconditioning.
- Compare the haemodynamics of bileaflet valves and tilting disc aortic
valves.
- Compare and contrast early and late prosthetic valve endocarditis
discuss their treatment.
- Intro operative echo.
- DSA.
- Trans oesophgeal echo .
- 2D echo.
- Angiographic anatomy of coronary artery .
- Ultra sound of myocardium.
- Doppler principle.
- Echo in Valvular heart disease.
- CT scan in cardiac surgery.
- Use of MRI in cardiac surgery.
- Noninvasive modalities for Coronary anatomy.
- IABP.
- Retrograde cardioplegia.
- Physiological basis of warm heart surgery .
- Myocardial stunning.
- ECMO.
- Re-Perfusion injury .
- Various factors causing Myocardial injury during OHS and current
concepts of better Myocardial treatment.
- Principle of pediatric CPB.
- Retrograde cerebral perfusion .
- Fibrillatory arrest of heart .
- Cardioplegia .
831
- Physiological and bio chemical basis for Myocardial preservation.
- Hypothermia in OHS (over view).
- Pyrexia after CPB.
- Warm blood cardioplegia .
- Non pharmacological supports of operated heart.
- Prevention of paraplegia in aortic surgery .
- Strategies for Spinal cord protection.
- Infected cardiac pacemakers.
- Salient design features & haemodynamics of any prosthetic heart
valve of your Choice.
- Cardiac Pacemakers.
- Modes of pacing .
- Pacemaker complications.
- Pulmonary artery balloon counter pulsation .
- Cardiac pacemakers and their use in the treatment of post operative
cardiac arrhythmias.
- Billable prosthetic valves .
- Advances in Cardiac pacing.
- Compare the haemodynamics of bileaflet valves and tilting disc aortic
valves.
- Compare and contrast early and late prosthetic valve endocarditis
discuss their treatment.
- Bilateral submammry incision.
- Embryology of carotid arterial system of brain & discuss management of
ICA stenosis.
- Surgical anatomy of thymus & pathogenesis of myasthenia gravis.
- Subxiphoid incisions for cardiothoracic operations.
- Embryology & anatomy of Aortic arch.
- Anatomy of radial artery & the tests performed to evaluate the adequacy
of blood flow through the hand.
832
- Development of interatrial septum.
- Blood supply of sternum .
- Describe the anatomy of ventricular septum of man & what
developmental anomaly may require surgical intervention.
- Broncho pulmonary segments.
- RVOT.
- Schematic representation of coagulation cascade, evaluation &
management of bleeding disorders after Open heart surgery.
- Etio-pathology & management of Acute renal failure after open heart
surgery.
- Activated clotting time.
- Factors affecting blood loss during open heart surgery & detailed
methods of management to minimize the same.
- Describe the cardiovascular reserve sin health & post op cardiac surgery.
How can you manipulate them in post op period in order to achieve
successful result.
- What is Low cardiac output ,Investigations & management modalities of
Low cardiac output.
- Rheumatic carditis.
- Compare lung biopsy findings in MS,TOF,ASD.
- Lifecycle of echinococcus granulosus.
- Pathophysiology of MR.
- Methods of diagnosis & treatment modalities of infective endocarditis.
- Cyanotic coagulopathy.
- Noncardiac pulmonary odema of all OHS.
- Nosocomial infection in cardiac surgery.
- Physical principles of diffusion of gases.
- Additives in cardioplegia.
- Reperfusion syndrome/ Reperfusion injury after the CPB.
- Biopump.
833
 - Pulmonary embolism.
- Oxygen free radicals in cardiopulmonary bypass.
- Platelets & bleeding.
- Pulsatile perfusion.
- Use of filters in CPB.
- Dual chamber pacing.
- Atrial pacing.
- Elaborate on the additives used in cardioplegia.
- Overdrive pacing.
- Cardiac cycle.
- Cardiac metabolism.
- Diabetic foot.
- Saphenofemoral incompetence.
- Marker cardiac enzymes.
- Particulate emboli on CPB.
- Complement activation during open heart surgery.
- 1st heart sound.
- Diaphragmatic pacing.
- Paradoxical movement of chest.
- Diaphragmatic pacing.

Drugs
- Dobutamine.
- Oxygen free radical scavengers.
- Nitric oxide therapy.
- Pharmacological manipulations of pulmonary hypertensive crisis.
- Inotropic support after OHS.
- Vasodilator drugs in common use/ Vasodilators in cardiac surgery.
- Afterload reduction.

834
 - Anticoagulant therapy after prosthetic valve replacement in man &
women.
- Perioperative use of antibiotics in cardiac surgery.
- Beta blockers.
- Nitropruside.
- Isoprenaline.
- Digxoin.
- Compare vasopressor drugs in common use.
- Diltiazem.
- Anticoagulants in cardiac surgery.
- Dopamine.
- Milrinone.
- Amiodarone.
- Epsilon aminocaproic acid.
- Low molecular weight heparin.
- Protamine.

Recent advances
- Robotic cardiac surgery.
- New design of biological valves .
- Tissue valves in valve replacement .
- Principles involved in fabricating arterial substitutes .
- Tissue engineering in cardiac surgery.
- Role of Stem cell in Cardiac surgery.

History
- John Gibbon.
- Rene Favalaro.
- C Walton Lillehei.
- Alfred Blalock.
835
- Denton Cooley.
- Donald Ross.
- P K Sen.
- Alain carpentier.
- Alexis carrel.
- Micheal De Bakey.
- Alexis carrel .
- Norman Shumway.

836
 Theory answer writing samples

Arterial Switch Operation

Definition: -
It is a technique of the arterial switch operation involves transaction of the
great arteries, transfer of the coronary arterial origins & repositioning of great
vessels.

Historical Aspects: -
1975 Jatene - 1st successful Arterial Switch operation.
1978 Aubbert - APwindow creation & baffle technique.
1972 - 1976 - DKS Technique of ASO in TGA with SAS.
Various modifications of arterial switch came thereafter.

Indications: -
Primary ASO
1. TGA, VSD.
2. Simple TGA.
3. DORV with subpulmonic VSD.
ASO , Repair of other anomalies ,Later on Fontan
1. DILV.
2. TGA, SAS, CoA, Severe Arch hypoplasia, OR Interruption with
Ductus dependent descending aortic flow in neonates.
Two stage ASO
1. Simple TGA late presentation.
2. RV dysfunction & TR after Mustard or Senning operation.
Double Switch
1. CCTGA, VSD.
837
 2. Unrestricted PBF with /without Ebsteins anomaly of morphologic RV &
TV.

Contraindications: -
1. Fixed LVOTO / significant PS.
2. TGA with IVS after > 2 - 3 week LV/RV ratio < 0.6.

Rationale for ASO: -

A. Why ASO?
Anatomically LV is > suitable than RV.

Criteria LV RV

Shape Ellipsoid Coma

Contraction pattern Concentric Bellow like

(Twist) (Peristalsis)

Inlet & outlet orifice Proximity > Separated

(Same line) (Perpendicular
to outflow)

Pump Pressure Pressure

Coronaries Two One

Developmental Stratum compactum Thinner

Of Myocardium thicker
838
Derived LV sinus (Primitive Vent) Bulbous cordis

Papillary muscle Two Small, Numerous

Atrio vent valve Mitral,> suitable Tricuspid, < suitable

Mortality
Atrial switch Simple TGA 0 -15 %.
TGA, VSD - 10 60 %.
Arterial switch - < mortality.

Dysrhythmias 13 -100 % with Atrial switch.

< Arterial switch.

Sudden Death - > with Atrial switch.

RV dysfunction CHF, TR, Hypoxia > with Atrial switch.
Systemic venous obstruction 0 -67 % Atrial switch.
Pulmonary venous obstruction 9 -11 % Atrial switch.

Miscellaneous
1. Intra atrial shunts.
2. Selective perfusion of rt. lung.
3. Atrial volume & function.
4. Persistent LVOTO.

Special Physiological & Anatomical considerations: -

839
 LV Status of LV
@ LV must pump against SVR.
@ Risk es with higher wall stress.
Wall Stress = Intracavitary pressure x Dimension / Wall thickness
@TGA, IVS, No PS
LV wall thickness Normal - es with in PVR.
2 -4 months - LV wall thickness adapted to pulmonary circulation,
No longer sustain systemic workload.
ASO performed in < 2 wks.
@ TGA, VSD
LV wall thickness remains normal during 1st yr of life & operation
can be postponed.
LVOTO Present in 10 %.
@ Sub pulmonic membrane, Anomalous mitral valve attachment to
septum, pulmonary valve abn, Prolapsing TV tissue, Dynamic septal
displacement.
@ Since LVOT will function as outlet for systemic ventricle These
abnormality have obvious importance.
MV Anomalies 10 %.
@ Cleft AML ,Parachute MV, AV canal defect, Abnormal attachment of
chordae to the septum leads to MS/MR Important when valve is
systemic AV valve.
Pulmonary root & semilunar Valve
After ASO becoming a systemic valve. 10 % cases have major
malalignment of sinuses, leads to PR.
Coronary Artery Anatomy -

840
 @ Lei dens Convention: In which sinus 1 is on the right of an imagined
observer standing in the non facing noncoronary sinus of Valsalva &
looking toward the pulmonary trunk. Proceeding in a counterclockwise
fashion, the next sinus is sinus 2.

@ 94% have Dual coronary system.

@ 6 % have Eccentric coronary ostia & intramural coronary artery.
@ High Risk coronaries
# LCA abnormalities LAD & LCx from rt. side.
# Single coronary artery.
# Intramural coronary artery.
Pre-operative Preparation: -
TGA, IVS
BAS to be performed

841

Good Palliation Not a good palliation

ASO within 2 wks. PGE 1 infusion

Ductus opens Ductus not
opened

ASO 1 2 days Emergency ASO.
Pts from other hospitals within 2 months primary ASO.
TGA ,VSD / DORV
Manage pt. with Decongestive therapy

Improves ICU dependent Ward dependent

ASO at 68 wks Emergency ASO Early ASO.
TGA ,VSD / DORV with CoA with well formed Arch -
CoA repair through Lt. thoracotomy 1st followed by ASO as described
earlier.
TGA with Multiple VSD
PA banding followed by ASO.
TGA with Arch hypoplasia / severe CoA / IAA with SAS.
@ Paralysis, IPPV.
@ PGE1 infusion.
@ Dopamine, Vasodilators.
@ Correction Acid Base & Electrolyte imbalance.

Improves Does not improve

ASO in 24 hrs Emergency ASO.

842
 @ ASO, VSD closure, CoA /IAA repair, RVOT resection single stage.
@ Arch hypoplasia for repair
Arch diameter - < wt in kg + 1 (3kg - < 4mm, 2.5kg - < 3.5mm).
Echo criteria for ASO: -
1. Normal LV size.
2. Adequate LV posterior wall thickness.
3. LV geometry & Septal wall thickness.
4. LV inflow & out flow normal (dynamic LVOTO is not a C/I).
5. LVSP 2/3 systemic.
Assessment LV for ASO: -
1. LV/RV volume ratio - > 0.6.
2. Interventricular septum convex in RV /straight.
3. LV pressure > 50 mmHg (2/3rd / 1/2 systemic).
4. LV mass index - > 50 gm / m2.

Operative Technique: -
Position
@ Supine with head extended.
Anesthesia
@ GA, morphine or phentanyl induction with non depolarizing muscle
relaxant.
@ Phenoxybenzamine 1 -2 mg / kg.
@ Albumin 5 % with NS.
Exposure
@ Median sternotomy, harvest pericardium.
@ Dissect Aorta, MPA, LPA, RPA, and Ductus.
Perfusion
@ Priming Fresh (<24 Hrs) heparinised Blood, adjusted with clear
volume expanders to achieve a mixture of the patients & prime Hb of 9
gm/dl.
843
 @ Prime volume 100 ml /kg, Fresh blood, 10 mmol / lit soda bicarb, 30
mg / lit Heparin, 20 mg / kg methyl prednisolone.
@ Cooling & warm with blood nasopharyngeal temp gradient not > 10
degree.
@ Bypass flow maintained at 15-0 -220 ml / kg/min.
@ Temperature TGA with IVS 20 -22 degree, TGA VSD CoA 15 18
degrees.
@ Perfusion pressure
25 35 mmHg for 2 -3 kg.
35 - 45 mmHg for 3 -5 kg.
45 55 mmHg for 5 10 kg.
@ Basic perfusion flow 150 ml / kg / min Hb of 9 gm /dl.
@ Most neonate & infants treated with 1-2 mg / kg of phenoxybenzamine
IV before / just as CPB is begun.
Cardioplegia -
@ 110 ml /min /m2 for 2 4minutes.
@ Repeat plegia 110 ml /min /m2 for 2mins.
@ Temp 5 6 degree.
@ Plegia pressure not > 30 mmHg.
Surgical technique
@ Cannulate High Aorta, Bicaval venous.
@ Dissect, ligate & divide ductus.
@ Cool, Distally clamp, Cardioplegia.
@ RA opened, VSD closure, LA vent through PFO.
@ PA transected few mm proximal to bifurcation.
@ Stay sutures taken.
@ Aorta transected in mid portion, 2-3 mm above the coronary ostia
edge.
@ Coronary buttons removed, sinus 1 first, D shaped with 0.5 -1 mm
cuff.
844
 @ Implanted into Proximal PA (Neo Aorta) without kink.
@ LeCompte maneuver to bring pulmonary bifurcation anterior to
aorta, (not required in Side side aorta & L- TGA).
@ Neo aorta constructed needs pericardial patch to augment distal aorta.
@ Proximal aorta gaps of coronary buttons closed with pericardial patch.
@ Neo PA constructed.
@ Associated CoA, IAA, Arch hypoplasia requires TCA.
@ Rewarm, CPB, Declamp, Off CPB.
@ Dopamine 5 - 10 micgm /kg /min.
@ Heart carefully observed for colour change & LA pressure monitored,
Ischemia of myocardium reflected by poor colour or rise in LA
pressure. Due to coronary kink & needs correction.
@ Bleeding Because multiple suture lines require careful hemostasis.
Chest closure : -
@ Pericardial & mediastinal tubes.
@ Silastic peritoneal dialysis catheter to be put.
Post op care : -
1. Ventilation Sedated & paralyzed until hemodynamically stable.
Initial Po2 will be low.
2. Phenoxybenzamine 0.3 -0.5 mg /kg cont.
3. Dopamine rarely reduced to 5 mics / kg /min.
Results: -
Survival
1. month 84 %
2. 1 One year 82 %.
Risk factors
1. Retropulomonary course LCA/ one of its branches.
2. Early date of operation.
3. Old age.
4. Longer circulatory arrest.
845
 Ventricular function No dysfunction.
Rhythm disturbance low.
RVOTO 5 10 % , Valve, Annulus, higher up.
Neo aortic valve incompetence 32 % mild,
Large pulmonary root before switch TBA, Large VSD, PA band
preswitch.
Atrial Switch Procedures

Introduction: -
It is physiological correction of TGA by transposition of the venous blood into
the ventricles.

Technique: -
1. Mustard procedure Use of large patch of pericardium.
2. Senning procedure Use of native atrial tissue.

Mustard Procedure: -

1951 Mustard partitioned atriums with a large patch of pericardium,

redirecting caval venous blood to LV & pulmonary venous blood to RV.
Simple, safe & reproducible operation.
Indications
# TGA with intramural coronaries.
# TGA with IVS late presentation (>2 - 4 wks).
# TGA, VSD, PVOD.
# TGA, VSD, LVOTO.
# Atrio- ventricular discordance.
# Small LV.
Technique

846
 # Performed at any age but risk / complications > with operation. at, < 6
wks age.
# Balloon atrial septostomy at initial cardiac cath.
# Operation performed between 6 wks to 6- 12 month.
# Median sternotomy, Anterior surface of pericardium cleared.
# A large patch of pericardium excised for use as the atrial baffle.
# Pericardium roughly dumbbell shaped with two bulbous ends & a waist
that is 2.5 to 3.0 cms wide.
# For infant of 10 kg, the long side is 7 cm & the e short side 5cm long.
# The SVC end is 4 cm, & IVC end is 5 cm.
# For a child of 5 kg the margins are all 0.5 cm shorter.
# Both ends are rounded, particularly IVC to provide flexibility in
choosing the most appropriate suture line.
# Broms tech. Use of pericardial baffle shaped like a pair of trousers
where the two limbs are sized according to the diameter of SVC & IVC.
# Cannulation Aorta & Bicaval venous.
# Cool, Clamp & Cardioplegia.
# RA longitudinal incision.
# IAS Initial incision from centre on Fossa ovalis to center of SVC till it
reaches top of the atrial septum, care for preserving artery to SA node,
AS lateral to the incision excised.
# CS cut back into the LA.Raw edges of the incision sutured.
# The pericardial baffle is inserted into the common atrial chamber &
sutured in such away that SVC & IVC blood is diverted to the MV.
# Closure of the associated VSD / PS can be done.
# RA closure directly / If juxta position of LAA or mesocardia, RA will be
small Enlarge RA with pericardial patch.
Post operative course:
# Uncomplicated with inotropes except repair done in 1st 2month of life.
# Extubated with in 24 hrs.
847
 # Post op bleeding req. reoperation.
# Phrenic nerve paralysis req. prolongs ventilation.
Results: -
Early mortality 3.6 %, VSD/PS es risk.
Complications
1. Baffle leaks 23 %.
2. SVC obstruction 17 %, common because of residual ridge of septum
between SVC & tricuspid valve.
3. IVC obstruction 3 %.
4. Pulmonary venous obstruction 1.5 %, usually at the level of the original
atrial septum just anterior to the rt. Pulmonary vein orifices. Results
from a progressive adhesion of the baffle to the raw edge of the excised
septum. Suturing raw edge & keeping upper & lower baffle suture line
wide apart by the rt. Pulmonary veins & lateral wall of RA prevents this.
5. Stenosis of rt. & lt. pulmonary venous channels 1.2 % , > common
narrowing of lt. pulmonary venous channel in the posterior LA near the
orifices of the lt. pulmonary veins ,due to upper & lower baffle sutures
lines on LA too close.
6. Dysrhythmias 73 %, due to SA node dysfunc, because of injury to the
SA node artery. Preservation of a ridge of atrial septum between the SVC
& Tricuspid valve reduces this problem.
7. RV dysfunction & TR
Early 11%, due to RBBB, RVEDP, RVEF.
Care Meticulous perioperative myocardial care.
# Efficient CPB.
# Good myocardial protection.
# Short ischemic time.
# Effective myocardial hypothermia.
# Adequate post op CO.
# Avoid serious dyrhythmias.
848
 Late 76 % Class I, 24 % Class II.
Late mortality
Survival -
10 yr - 85 .8 %
15 yr - 81.5 %.
Senning Procedure: -

1959 Senning described an ingenious technique of complete intra atrial

redirection of the venous return by using native atrial tissue.
Advantage
1. Very small amount of material is required.
2. Growth potential.
Indications
@ TGA, IVS > 2 months old.
Too old for BAS.
@ TGA, IVS, LVOTO.
@ TGA, VSD, PVOD.
@ TGA, VSD, LVOTO.
@ DIV, PVOD.
@ AV dissociation with VA concordance.
@ C TGA.
Contraindications
@ Lt. juxta position of appendages.
@ LSVC not a C/I.
Technique
@ Median sternotomy, pericardial flap.
@ Cannulation Aorta & Bicaval venous.
@ CPB, Clamp, Cardioplegia.
@ Dissect Waterstons groove deeply without entering into LA.

849
@ RA Incision Anterior & parallel to the crista terminalis, anterior to SA
node, The distance between interatrial groove & rt. Atriotomy 2/3rd of the
circumference of SVC.
@ Atrial septal flap
Superiorly incision of limbic tissue, towards & within the SVC orifice,
Risk of entering in the roof of RA & damage to the SA node artery,
Ridge of limbic tissue left will cause SVC obstruction,
Fossa ovalis defect closed with patch.
Atrial flap sutured between lt. pulmonary veins & LAA,
Superiorly within the LA to the junction between the SVC & rt.
upper pulmonary veins,
Inferiorly to the junction between the IVC & rt. inferior pulmonary veins,
This makes the floor of the tunnel connect the caval orifices with the
mitral valve.
@ LA incision
Incise deeply in the interatrial groove,
Extend superiorly to the junction between SVC & rt. upper pulmonary
veins,
Inferiorly to the junction between IVC & rt. lower pulmonary veins,
Openings can be further enlarged by incising one / both rt. pulmonary
veins / tissue between them.
@ Posterior RA flap is sutured to the IAS directing caval blood to the MV.
@ Pulmonary venous pathway is created by suturing the anterior flap
of the RA wall to the rt. edge of the LA incision.
Care to be taken
# Avoid a purstring effect that would narrow the caval pathway.
# Damage to the sinus node.
# Restrict the pulmonary venous flow to the tricuspid valve.
@ Four pacing wires put.

850
 Results
1. Complications Early & late.
@ Venous hypertension
# SVC obstruction.
# Pulmonary venous pathway obstruction.
#Atrial dysfunction.
# Ventricular dysfunction.
# Arrhythmias.
# Pulmonary congestion.
@ Electrophysiological disturbances
# SR with junctional escape.
# JR.
# SVT.
@ RV dysfunction.
@ Tricuspid valve incompetence.
@ LVOTO.
2. Mortality - < 10 % (4.6 %).
Acturial survival -
84 % 5 yrs.
81 % 9 yrs.

Damus Kaye Stensel Procedure

Definition: -

It is an arterial switch operation without coronary translocation in patients

with SA obstruction without PS.

Historical aspect: -
851
Damus, Kaye, Stensel described in 1975.

Indications: -

1. DORV with subpulmonic VSD with SAS (Taussig Bing Anomaly).

2. TGA with Intramural / single coronary artery.
3. Stage I of Norwood procedure.
4. Univentricular hearts with SAS.

Operative Technique: -

Median sternotomy, Pericardium harvested.

Cannulation Aortic & Bicaval venous.
CPB, Cool, Clamp, Cardioplegia.
RA / RV approach.
VSD closed to direct LV blood to pulmonary valve.
MPA transected just proximal (5mm) to bifurcation.
Avoid the distortion of the ascending aorta & proximal MPA, by taking
marking sutures on the lt. medial & rt. medial aspect respectively.
Put incision on aorta just above the commissural post of AV.
Identify coronary artery & avoid distortion.
End to side anastomosis of proximal MPA & ascending aorta.
May need augmentation with pericardial / homograft / Gortex patch.
RV PA continuity achieved by homograft valved graft conduit.
Aortic valve still connected to RV, but aortic pressure remains higher
than RV pressure throughout cardiac cycle, so the AV remains closed.
AR poorly tolerated, in such case AV to be sutured.

852
Complications: -

1. AR Immediate / delayed.
2. PR.
3. Distortion of Great arteries.
4. Hemodynamic instability due to pulmonary circulation by systemic
pulmonary shunts.

Results: -

1. Early Mortality 20 -30 %.

2. Intermediate results - Good.

TGA, VSD, LVOTO Damus Kaye Stensel Operation

853
 FONTAN / BD GLENN / TCPC

Def: - It is a technique for diverting systemic (with / without coronary) venous

return to the pulmonary artery circulation (either directly or by way of the RV)
& leaving to the ventricle (s) only the systemic artery circulation.

Normal Anatomy Fontan Circulation

History & Surgical mile stones: -

1949 Rodbard & Wagner RV could be bypassed .

1951 Carlon proved in experimental laboratory, Systemic venous pressure
is adequate driving force for pulmonary blood flow .
1958 Glenn SVC RPA end end anastomosis .
1960 Haller Bidirectional Glenn Modified Glenn.
1971 (1968) Fontan & Baudet Fontan Operation, RA MPA (valved
/ non valved / direct) anastomosis.
854
1973 Kreutzer Atriopulmonary connection. (MPA with valve RAA).
1976 Maghdi Yacoub Fontan procedure for other univentricular hearts .
1988 DeLeval Lateral tunnel Fontan (TCPC).
1989 Hillel Laks & Billingslay Fenestrated Fontan .
1990 Nancy Bridges 1st transcatheter closure of Fenestration by clamshell
device.
1991 Douville HemiFontan operation.
1988 Humes & Marcelletti Extracardiac Fontan.
1997 Bailey Growing extracardiac Fontan.
Indications: -

A. Fontan operation
1. Tricuspid atresia.
2. Lt. Atrio-ventricular valve atresia.
3. Double inlet lt /rt. ventricle.
4. Pulmonary atresia, intact ventricular septum, Hypoplastic RV.
5. Hypoplastic LV/RV in biventricular heart with VSD with/without
straddling AV valve.

B. BD Glenn
1. Young age < 1-2 yrs.
2. Requires extensive PA reconstruction.
3. SAS with severe systemic ventricular hypertrophy.
4. Border line PVR /Systemic ventricular function.
5. Interrupted IVC & azygos continuation.

Glenn Shunt: -

It is a palliative shunt.
855
 3 Types
1. Classical Glenn shunt
@ Cut SVC & close cardiac end of SVC.
@ Cut RPA & close MPA side end.
@ Anastomose Distal end of RPA & Cranial end of SVC end end.

2. Modified Glenn shunt

@ Cut RPA & close the MPA side end.
@ Anastomose Distal end of RPA to side of SVC.

3. Bidirectional Glenn shunt

@ Cut SVC.
@ Anastomose upper end of SVC to the side of RPA.
@ Suture lower end of SVC.
@ SVC post. wall & RPA ant. Wall anstomose, Ligate RA end
of SVC Azzolina.

4. Bilateral bidirectional Glenn shunt when LSVC present.

@ Cut RSVC & anastomose upper end to the RPA, close lower end.
@ Cut LSVC & anastomose upper end to the LPA, close lower end.
@ Hepatic veins drain to LA.

Requisite for Glenn shunt

1. Lack of obstruction to pulmonary blood flow (normal PVR).
2. Good ventricular function.
3. Lack of associated cardiac defects, CoA/SAS/AV valve regurgitation.
Determinants of Glenn flow
1. Systemic ventricular end diastolic pressure.
2. Trans pulmonary gradient.
3. Atrio ventricular regurgitation.
856
 Ideal candidate
1. PA pressure 15mmHg.
2. PVR < 2 WU.
3. Adequate pulmonary artery size (50% of SVC diameter).
4. Good ventricular function.
5. Age (> 3 months; 9 months).
Benefits
1. Improves PBF Oxygenation.
2. No pulmonary artery hypertension.
3. Volume unloads the heart.
Disadvantage of classical Glenn
Commits the RPA (55% of pulmonary capillary bed) to SVC drainage
only (40% of systemic venous return).
Surgical Technique
@ With CPB.
@ With SVC RA shunt.
@ Without CPB & without shunt.
@ Advantage in case of Bilateral SVC only RA cannula required.
@ Non pulsatile MPA ligation, Humes et al.
MPA transaction, Girod et al.
@ Pulsatile No MPA interruption.
Additional BT shunt, Matsuda et al.
Complications
1. SVC syndrome.
2. Pleuro pericardial effusion.
3. Chylothorax.
4. LVEDP ( ventricular wall thickness diastolic compliance).
5. AV valve regurgitation.
6. SAS.
7. Increasing cyanosis (pulmonary thrombosis, Pop offs ).
857
 8. Pulmonary AV malformation.
9. Branch pulmonary artery stenosis.
Results
1. Operative Mortality 5 %.
2. Mean arterial saturation improved from 69% - 83%.
3. Acturial survival at 9 yrs 100%.
4. Hospitals stay 8 +/- 5 days.
5. 5 -7 yrs of palliation rapid deterioration & progressive cyanosis.

Hemifontan Operation: -

Douville et al 1991.
Anastomosis of both end of the divided SVC to both side of RPA with
placement of a prosthetic patch on the cardiac side of SVC.
Anastomosis of SVC- RA Jn. incision MPA/ RPA & patch in the RA to
exclude IVC / CS / Pulmonary venous blood flow.
One of the procedures while taking down of Fontan due to failure of
Fontan circuit / Part of preparation for staged Fontan.

Fontan Operation: -

Requirement
1. Central unbranched hilar portion of rt. & lt. pulmonary artery, be
enlarged if they are small.
2. CS should drain into the pulmonary venous atrium after Fontan &
not in systemic venous compartment,

Because prudent to protect main ventricular coronary venous
drainage against high pressure that are sometime present in the
systemic system after repair.
858
 IIbawi & coll. Have shown quite convincingly that CS pressure
> 15 mmHg reduces systemic ventricular output.
3. Measure PA, CVP, LAP.
4. Two atrial & ventricular pacing wires to be put.
5. Wide drainage of pericardium & both pleurae.

Ten Commandments, Choussat & Fontan 1971.

1. Age > 4yrs or < 15 yrs.
2. Sinus rhythm.
3. Normal systemic venous drainage.
4. Normal sized RA.
5. Mean PA pressure 15 mmHg.
6. PVR 4 U /m2.
7. Pulmonary artery aortic diameter ratio 0.75.
8. Ventricular EF 60%.
9. No AV valve dysfunction.
10. No impairing effects from previous shunts.
Circuit
Power Source
V

Pulmonary veins Systemic arteries

PVR SVR
Pulmo Fontan System
Arteries conduit veins

Ideal candidate ,Mayer et al. Criteria

859
1. Normal PA pressure (< 18 mmHg).
2. Normal PVR (< 4 U / m2).
3. Adequate pulmonary artery size.
4. Repairable localized PA stenosis.
5. Normal systemic ventricular function.
6. No / Mild AV valve regurgitation.
7. No LVOT obstruction.

Surgical Techniques : -

A. Atrio Pulmonary connection (APC).

# RAA PA anastomosis -
@ Non valved direct RAA PA connection.
@ MPA transected.
@ Trapdoor shaped atrial flap for posterior wall.
@ Pericardial / prosthetic patch anteriorly.
@ Primary closure of ASD.

# RA PA anastomosis
@ Roof of RA was incised.
@ MPA / RPA (to protect Art. to SA node).
@ Anastomosis done conventional / Diamond.

B. Lateral tunnel Fontan (TCPC).

@ De Leval et al, 1988.
@ Both RA & RV are unnecessary for Fontan circulation.
@ Tubular channel - # Less energy loss.
# Less Eddie current.
# Smoother flow.
@ + /- adjustable inter atrial communication.
860
@ MPA transected / ligated.
@ BD Glenn.
@ Caval Offset .
C. Fenestrated Fontan (f TCPC).
@ Laks et al, 1989.
@ Adjustable ASD / single or multiple fenestrations in the baffle.
@ R L shunt decrease RAP LV filling & CO.
@ Ideally takes care of transient ventricular dysfunction in early post op
phase.
@ Optimize CO.
@ Low Fontan pressure Lower incidence of pleuro-pericardial effusions.
@ Subsequent trans catheter closure.
@ Fenestrations
4 mm - < 12 kg.
5 mm - 12 -30 kg.
6 mm - > 30 kg.
@ Price paid
# Systemic desaturation.
# Risk of systemic embolisation.
# Need for additional procedure for closure of fenestration.

D. Unidirectional Fontan
@ Laks et al.
@ SVC flow Lt. lung (end end Glenn anastomosis).
@ IVC return to Rt. Lung (end end).
@ + /- adjustable ASD.
@ Improved pulmonary blood flow due to better streaming.
@ 60 % venous return larger Rt. Lung.
@ 40% of venous return smaller Lt. lung.
@ Improved V / Q matching.
861
@ SVC hypertension better tolerated.
@ So adjustable ASD for IVC return.
@ Disadvantage previous BD Glenn difficult candidate.

E. Extracardiac Fontan Operation

@ Marcelletti et al, 1988.
@ Use of Hemashield / Gortex tube graft from IVC RPA as a conduit.
@ Preservation of ventricular function by avoiding aortic cross clamp.
@ Preservation of ventricular & pulmonary vascular function by
minimizing CPB time & avoiding Hypothermia.
@ Preservation of SR by avoiding atrial incision & suture line in the
vicinity
of SA node.
@ Potential for optimal flow dynamics.
@ No separate patch material required for pulmonary artery
reconstruction.
@ SOS fenestration.

F. Growing Extracardiac Fontan

@ Use of rt.sided live pericardium with its blood supply intact for
making conduit from IVC RPA.
@ Bailey et al, 1997.
@ All benefits of extracardiac Fontan.
@ No need of homograft / prosthetic graft.
@ Autogenous tissue with growth potential.
@ Young age group can be benefited.
@ Nonthrombogenic parietal surface.
@ Viable & pliable.
@ Unique elasticity of the conduit may allow the respiratory bellows.
@ Fenestration in post op period easy in Cath lab.
862
 @ Concern - ? compression of rt. Pulmonary veins.

G. JLS Reeds modification of Fontan

@ LSVC CS in Tricuspid Atresia.
@ Upper end of RSVC RPA, Lower end of RSVC closed.
Upper end of LSVC LPA, Lower end of LSVC LPA.
IVC CS pericardial baffle, CS drains in systemic chamber.
OR
Ligate lower end of LSVC.
Anastomose both end s of RSVC RPA.
Baffle IVC SVC.
CS will drain in pulmonary venous chamber.

H. Mayers Modification of Fontan

Divide RPA & anastomose side of SVC.

Operative Steps: -

Under GA, Supine position.

Median Sternotomy, Opened pericardium to the rt.
Cannulation Aorta, High SVC, IVC.
On CPB, Dissect Ao, MPA & RPA, SVC high up to Azygos vein.
Azygos ligate doubly & divide.
Transect SVC.
Anastomose cranial & cardiac end of SVC to the RPA superior &
inferior surface respectively.
Cross clamp aorta & give cardioplegia, Arrest the heart.
RA opened obliquely slightly anteriorly.

863
 Gortex /Hemashield / RA wall used as a Tunnel from IVC SVC,
keeping the CS & ASD on the LA side.
Fenestration created in the patch ,
4 mm - < 12 kg.
5 mm - 12 30 kg.
6 mm - > 30 kg.
MPA transected & suture close both the ends / ligates the MPA.
Rewarm, Decalmp, Defibrillate.
RA closure.
Off CPB, Decannulate, Reverse Protamine.
Open both pleura widely / make window in the pericardium
connecting to the pleura.
Hemostais, close chest after putting pleural & pericardial tubes &
pacing wires.

Post operative Care: -

Parallel circuit circulation in series, Key factors for CO PBF
TPG.
Maintenance of preload (CVP) for adequate forward flow.
Keep PVR low Avoid pain.
Hypercapnia (pCo2 = 20 mmHg).
Respiratory alkalosis (pH 7.45 -7.5).
Hypoxia.
Pulmonary vasodilators (PGE1, NO).
No /less positive pressure ventilation (No PEEP).
Early Extubation.
Semi fowlers position.

Optimize systemic ventricular function,

864
 @ Systemic arterial dilator (SNP, Amrinone).
@ Inotropes.
@ Low hematocrit (30 35%).
AV sequential pacing.
IABP.
Closure of fenestration in appropriate phase.
Management of 3rd space loss with Albumin.
Keep drainage tubes patent.
Monitor CVP (SVC, IVC pressure), LA pressure x 24 hrs.
Remove catheter as soon as possible.
Anticoagulants 1st po day low dose 6- 12 wks.
Aspirin long term.
If pulmonary embolism STKinase.
F up 3-6 wks for fluid retention.

Complications: -
1. Pleuro pericardial effusions (30 5 %).
2. Ascites.
3. Protein loosing enteropathy.
4. Liver dysfunction.
5. Protein C deficiency.
6. Arrhythmias (SVT).
7. Systemic venous thrombosis.
8. Pulmonary venous thrombosis.
9. Thromboembolism - 2.6%.
10. Fontan Failure
@ Persistent low CO Low mixed venous saturation.

865
 Low urine output.
Poor peripheral perfusion.
Elevated LAP > 12 mmHg.
Continuing high Inotropic requirement.
After univentricular repair with need to maintain CVP higher than 18
mmHg & / or inordinately high fluid requirement to maintain systemic
arterial pressure.

Early Fontan takedown to BD Glenn.
Monitoring: -
RA pressure & significance

Normally maintained up to 16 mmHg.

If > that

See LA pressure
See LA pressure

LA > RA LA < RA

Echo for ventricular dysfunc. See PAPressure

Transplant only treatment Normal /Low PAP >

Obst of pathway PVD/
PAspasm/
Small PAs

866

Echo Hyperventilation.
Pco2 25-30
Take down Po2
SNP 0.5-1migm

PA /RAP

Reduced No

Spasm PVD /small PAs

Take down.
LAPressure LV dysfunction / Valve abnormality.
PAPressure Pulmonary vascular disease / Pulmonary spasm.
RAPressure Conduit block.

Closure of Fenestration: -

When RApressure 15 mmHg & SpO2 85 %.

Closure by Tightening Laks ligature or percutaneous balloon.

SpO2 - 100 %

RAP > 15mmHg RAP 15 mmHg
LAP, 7 -8 mmHg LAP to maintain CO.
CO es.

Reopen Close permanently.

867
Aim To avoid / stop pleural effusion formation.
Best results obtained by keeping aperture open for minimum 2months / open
permanently.

Results: -
Survival
Early Death 5-20%.
Time related survival -
Year %
5 70
10 65
15 50
Perfect Fontan operation 15 yrs 73% - Ideal palliative operation,
Not curative.

Modes of Death
Cardiac Failure 73%
Acute / Chronic
Pulmonary failure - 1%
Fluid retention - 10%
Neurologic dysfunc- 8%
Arrhythmias - 2%
Haemorrhage - 2%

Incremental Risk Factors

Acute ventricular decompression
Rx Staged Fontan / Fenestrated Fontan.
Late Pulmonary & ventricular deterioration

868
 @ Long standing non pulsatile pulmonary flow by systemic venous
pressure.
@ Abnormality of dominant ventricle.
Age at operation Young /Old.
Cardiac morphology Lt. AV valve atresia.
Small PAs Mc Goon ratio - 1.5
Z value - < - 3.5
Nakata Index - < 160 mm2 / m2.
PA Pressure MPA - >15 20 mmHg.
PVR - > 2 4 U / m2.
Advanced main chamber hypertrophy.
Atrial isomerism.
RA PA connection.

Functional Status
NYHA Cl I / II 94 %
90 % at 1 yr.
56 % at 10 yrs.

Haemodynamic Status
Resting / Exercise No difference.
Subnormal performance during exercise due to,
1. RAP Reflux.
2. Biphasic pulmonary flow.
3. Effect of Respiration.
4. Valved conduit from RV RV dilatation.

Cardiac Rhythm
SR Better performance.

869
 Atrial arrhythmias >.
CHB Rare.

Abnormality of Pulmonary circulation

upper lower lobe PBF.
Pulmonary arterio venous fistula.

Protein losing enteropathy 10 %

High RAP.
Site Jejunum / pleura / abdomen.
Other causes of protein losing enteropathy,
(CHF /Constrictive pericarditis / Atrial switch operation).
Rx Insertion of valve in IVC/RA/RV.

Thromboembolism 10 %.

Reoperation
Take down.
Pathway obstruction direct connection RA PA < chance.
Conduit valved / non valved > chance.
Other Reoperation 5 %.
Glenn shunt
Early mortality low.
> 6 month 5 %.
Interruption of RPA disadvantage.
85 % survival > 10 yrs.
Redistribution of pulmonary blood flow & Recurrent symptom
due to collaterals.

870
 Kawashima Operation

Introduction: -
It is an Intraventricular tunnel repair in DORV with subpulmonic VSD with
side by side relationship of great vessels, where intraventricular tunnel is lying
posterior to the pulmonary valve.

Historical Aspect: -
1971 Kawashima & coll described the technique of repair.

Indication: -
DORV, subpulmonic VSD, Side by side relation of great vessels Taussig Bing
Anomaly.

Pre-requisite: -
1. Great vessels should be side by side.
2. Enough distance between tricuspid & pulmonary valve.
3. No tricuspid valve chordae should be attached to malaligned septum.

Contraindications: -
1. Taussig Bing Anomaly with anteroposterior relation of great vessels.
2. Insufficient distance between TV & PV.

Procedure: -
Median sternotomy, Pericardiotomy.
Cannulation Aortic & Bicaval venous.
Cool, clamp, cardioplegia.
RA /RV approach.
RV opened transversely.
871
 Assess for distance between PV & TV, TV chordal attachment, VSD
position.
Enlarge VSD anteriorly.
Appropriate Dacron tube graft cut to make intraventricular tunnel from
LV Aorta, lying posterior to PV taking care of conduction tissue.
Rewarm, RV closure.
Off CPB, pacing wires, chest tubes.
TCPC of Kawashima
It is a Fontan operation in patient with persistent LSVC with Hemiazygos
continuation of IVC.
Usually associated with Atrial isomerism.
Persistent LSVC receives IVC blood through Hemiazygos vein.
Hepatic vein drains separately into RA / common atrium in midline /LA.
Modified TCPC is
1. LSVC disconnected from LA & LA end closed.
2. LSVC anastomosed end side / side side to LPA (if LSVC parallel to
LPA).
3. RSVC cut & both ends anastomosed to RPA.
4. Intratrial tunnel / baffle to drain hepatic venous blood to RPA.
5. If tunnel course is tortuous, Hepatic veins allowed to drain into
pulmonary venous chamber (Kawshimas modification), Resting arterial
saturation will be 87 92 % es with exercise.

872
 MIDCAB

Syn: - Minimally invasive direct coronary artery bypass.

Introduction: -
CABG performed via thoracotomy without the use of CPB, ed during early
months of 1996.

Advantage: -
1. Less invasive.
2. Cost effective.
3. Less morbidity.
4. Avoids morbidity of CPB.

873
Disadvantage: -
1. Technical advantage of anastomosis in motionless heart.

Historical Aspects: -
CABG without CPB 1960.
Largest series by Calfiore Italy.

Indications: - Especially for single vessel disease.

1. Single /Double /Triple vessel disease.
2. Primary / Reoperation.
3. Grafting of isolated lesion.
4. When there is C/I of CPB,
@ Diffuse cerebrovascular disease.
@ Multiple embolic events.
@ Extreme ascending aorta calcification.

Contraindications: - Relative,
1. Severe pulmonary disease.
2. Arrhythmias.
3. Multiple CAD, esp. LCx.
4. Poor ventricular function.
5. LAD disease,
@ Extreme calcification.
@ Intramyocardial LAD.
@ LAD Endarterectomy.
6. Non availability of arterial conduits.

Technique: -
874
 Anaesthesia
1. Single lung ventilation.
2. PA pressure monitoring catheter.
3. Rate lowering drugs B blocker / Magnesium.

Position
1. Rt. lateral Lt. anterolateral thoracotomy.
2. Lt. lateral - Rt. anterolateral thoracotomy
3. Supine Subxiphoid. Approach.

Incision
1. LAD 7 -10 cm incision in lt. 4th ICS from lt. border of sternum.
2. RCA rt. 4th ICS.
3. LCx Lt. lateral / posterior mini thoracotomy.
4. PDA & PLV -Sub xiphod mid way between xiphoid & umbilicus, midline
preffered over rt. subcostal for RGEA.

LIMA / RIMA /Gastroepiploic artery as an arterial conduits.

Stabilizing devices
@ CTS foot retractor, CTS Ultima.
@ Octopus II /III /IV.
Intracoronary shunts Flow through / Flow coil / Anastaflow. Or Use of
snares to occlude the Coronary artery.

Complications: -
1. Acute / late graft failure.
2. Post op. bleeding.
3. Chest wall defects.
4. Lung herniation.
5. > post op pain compared to sternotomy.
875
 6. Damage to coronary artery at the occluder site.

Results: -
1. Post op Hospital stay 53 + /- 28 hrs (2 days).
2. Transfusion 1.3 %.
3. Reoperation 6 % - Graft failure.
4. Early Mortality 0.5 -1 %.
5. Late Mortality 7 %.
6. Uncertainity of long-term results.
7. Late graft failure.
8. Use in multivessel diseases - Thoracab.
9. But in patients with risk of CPB / Median sternotomy MIDCAB is of
choice.

Rastelli Procedure

Introduction: -

Those forms of Transposition of great vessels associated with fixed

obstruction of the left ventricular (pulmonary) outflow tract is not candidates
for Arterial switch correction (Jatene Procedure). For these patients, the
Rastelli operation was introduced by G C Rastelli in 1969.

Indications: -

1. TGA, IVS, LVOTO.

2. TGA, VSD, LVOTO.

Contraindications: -

876
 1. Uncommitted VSD.
2. Straddling AV valve.
3. Hypoplastic ventricle.

Pre- operative Assessment: -

Echo, Cardiac Cath Angio required.

Objectives
1. Assessment of ventricular & valvular function.
2. The position & size of VSD & its spatial relationship to the subaortic
area.
3. The central & peripheral pulmonary arterial morphology.
4. The patency of surgical shunts.
5. The coronary arterial distribution.
6. The pressure & resistance of the pulmonary arterial circulation.
Intervention
1. Control of patent systemic pulmonary shunts.

Operative technique: -

Median sternotomy.
Cannulation Aortic & Bicaval venous.
Cool, Cross clamp aorta, Cardioplegia.
Enlargement of restrictive VSD (45 % cases) - Resection of the
infundibular septum so as to avoid damage to the conduction tissue.
Construction of intracardiac tunnel that results in closure of VSD in
such a way as to direct LV outflow through the VSD towards the Aortic
valve.

877
 Connection between the LV & PA is interrupted by division of MPA with
suture closure of the proximal end of or by patch closure of the
pulmonary valve.
Connecting the RV with the distal MPA/ pulmonary confluence with a
valved extracardiac conduit, such as a pulmonary / aortic cryopreserved
homograft.

Complications: -

Requires reoperation for,

Conduit obstruction.
Recurrent / residual VSD.
Residual LV- PA connection.
Sub aortic obstruction.

Results: -
Survival

1. Hospital Mortality-

Atypical defects 43 %.
- Multiple VSD 36 %.
- Straddling & abnormal choral insertion. 25 %.
Typical defects 15 %.
- Single perimembranous SA VSD.
- Without straddling of either AV valve.
2. Late survival

Acturial survival,
Years Overall Typical Atypical
878
 10 61 % 69 % 50 %
18 58 % 66 % 47 %
3. Risk Factors

# Younger age < 5 yrs.

# PRv Post op.

Mode / Cause of Death

Early Late
# Low CO. # Sudden Death.
# MI. # Pulmonary HTN.
# Pulmonary HTN. # LV Dysfunc.
# ARDS. # MR.
# Residual LV PA shunt. # Bacterial
Endocarditis.
# Rt. Heart failure. # SA obstruction.
# Residual LV RA communication. # MI.
# Temponade. # Noncardiac death.

Re-operation

1. Obstruction of Extracardiac conduit by Anterior compression by chest

wall.
31 % 5 yrs.
70 % 10 yrs.
84 % 18 yrs.
Post replacement survival,
62 % 10 yrs.
80 % 15 yrs.
2. Recurrent / residual VSD.
879
 3. Residual LV PA connection.
4. SA obstruction.
Arrhythmias Requires PPI.
Functional class 90 % - Class I II.
73% - Not on any cardiac drugs.
LV function LV function remained abnormal with persistent LV
dilatation & Hypertrophy.
RV function Abnormal RV function & Hypertrophy,
Because of proclivity of obstruction evidenced by the extracardiac
conduit.

Technical Modifications: -

LeCompte / REV operation

@ Make it applicable to small infants & children.
@ LeCompte & coll. Proposed this method.
@ Proposed avoiding the use of extracardiac conduit by anastomosing
the pulmonary artery to the Rt. Ventriculotomy.
@ Aorta & PA transected & proximal end of PA sutured.
@ Distal end of the PA with confluence brought anteriorly & aorta
sutured
( LeCompte Maneuver).
@ Infundibular resection done widely & the intracardiac tunnel
constructed establishing LV to Aorta continuity.
@ PA confluence anastomosed to the RV & augmented anteriorly
with autologous pericardial patch.
@ Need for reoperation due to conduit complication es.

Pugas Technique
@ Lack of VSD in TGA, IVS, LVOTO require Atrial switch operation.
880
@ To benefit this pt. it was proposed that creation of VSD on the
infundibular septum so that it can be corrected using Rastelli
approach.
@ Advantage
# Used for TGA, IVS with fixed valvar & subvalvar PS, not
amenable to Jatne procedure.
# LVOTO should have resulted in preservation of the LV muscle
mass & capacity of this ventricle to sustain systemic pressure.
# Anatomical (Arterial) correction to be done.
# VSD can be placed in the ideal position for better results.

TGA, VSD, LVOTO

881
 Intracardiac Tunnel - LV - Aorta RV PA Conduit

Rastelli Procedure

Tetralogy of Fallot with Pulmonary Atresia

Introduction: -
TOF - 3.9 % of CHD.
5 10 % PAtresia with VSD.
2/3rd associated with MAPCAS.
M > F, Severe cyanosis & hypoxia during neonatal period.
Life expectancy without surgery 50 % at 1 yr., 8 % at 10 yrs.

Definition: -
Tetralogy of Fallot with pulmonary atresia is a congenital cardiac malformation
characterized by under development of rt. ventricular infundibulum with
anterior & leftward displacement of infundibular (conal / outlet) septum & its

882
parietal extension with no luminal continuity between RV & pulmonary trunk
(or both rt. & lt. pulmonary arteries).
Or
Concordant atrioventricular & ventriculoarterial connection with VSD &
absence of continuity between RV & PA.

Under development of RV infundibulum.

Anterior & Lt. ward displacement of infundibular septum.
No luminal continuity between RV & PA or lt. & rt. PAs.
Usually congenital, may be acquired.

Historical Aspect: -
1973-74 Haworth & McCartney described this anomaly.

Morphology: -
Major difference between TOF with PS & TOF with PA,
No blood passes from the RV to the lungs & consequently all pulmonary
blood flow arises from the ductus arteriosus, collateral vessels or fistula.
Pulmonary arterial anomalies are common.
Large aorto pulmonary collateral arteries are common.
1. RVOT
Atresia, congenital Infundibular / Annular.
# Infundibular 70 %.
@ Infundibular portion absent / conal septum fused with anterior
RV wall.
@ VSD large.
@ RV massively hypertrophied.
# Annulus level
@ Infundibulum patent.
@ Obstruction consist of thick fibrous membrane above
883
 the infundibulum.
2. Pulmonary Trunk
Present & reasonable size.
Hypoplastic.
Fibrous cord.
Completely absent 5%.

3. Branch PAs
# Confluence of rt. & lt. PAs
20 -30 % Nonconfluent PAs.
# Stenosis of origins of PAs
10 % RPA stenosis.
20 % LPA stenosis.
# Distribution of PAs (Arborization)
Confluent PAs 53 % complete distribution to all 20 pulmonary
segments.
3% - < 10 pulmonary segment distribution.
Nonconfluent PAs 80 % incomplete distribution of PAS.
>1/3rd has < 10 pulmonary segment distribution.
# Stenosis of PAs on the side of the ductus 65 %.
# Size of PAs Immediately prebranching portion of the RPA /LPA
is extremely small,
McGoon ratio 0.5.
Nakata index 20.
Z value - -10.
# Abnormality of Hilar branch pattern.

Acquired pulmonary atresia

@ Spontaneously after birth in TOF with PS.
@ Because of palliative operation.
884
 @ Acquired atresia is valvar / subvalvar / os infundibulum.
@ Morphologic characteristic > like TOF with PS.

Pulmonary blood supply:-

Derived from True pulmonary arteries & MAPCA.
True PAs
# Located in the anterior hilum.
# Adequate size / varying degree of hypoplasia.
# Confluent / non confluent.
MAPCAS
Robonovitchs Classification
Type I - Bronchial artery collaterals - Unprotected MAPCAS.
Anastomose with true PAs within the lung parenchyma.
Type II Descending aorta / Abdominal aorta Protected MAPCAS.
Enters hilum posteriorly to anastomose with the true PAs or
intra acinar vessels.
Type III From branches of aorta Protected MAPCAS.
Brachiocephalic, IMA, intercostals.
Smaller vessels that anastomose to the true central PAs or
spread out over the surface of the visceral pleura.
Essential collaterals Those that are the only blood supply to a portion
of
the lung or are so large that they are essential to the size of the
pulmonary vascular bed.
Redundant collaterals Those that are small & overlap with the true
pulmonary artery distribution.

Embryology: -
# Lungs develop from the foregut & their nutrient supply as that of the
oesophagous arises initially from the dorsal aortic plexus.
885
# About 27th day in the antenatal period, the arterial branches of paired 6th
aortic arch forms an anastomosis with the pulmonary vascular plexus.
# As a result the lung receives dual supply.
# With time, the branches from the 6th aortic arch enlarge & those from the
descending aorta become comparatively smaller. Persistence of the branches
from the aorta in postnatal life forms the MAPCAS
# They are variable in their origin, size, number, course & arborisation.

Clinically: -
A. Confluent & normally distributing rt. & lt. pulmonary arteries & PDA
50 % in this category.
PBF CHF.
B. Confluent rt. & lt. pulmonary arteries distributing to the majority, but
not all, of the pulmonary arterial segments.
25% are in this category.
PBF - Cyanosis.
50 % at 3yrs
90 % at 10 yrs die.
C. Confluent or nonconfuent LPA & RPA distributing to the minority of
Pulmonary arterial segments.
25 % cases.
PBF.
Only MAPCAS.

Surgical Treatment: -
Aim
Closure of VSD.
Establish continuity between RV & PA without excessive PBF, Pulmonary
congestion, LVVO.

886
Indication for operation
Surgical treatment can be individualized according to,
Arborization of pulmonary vasculature.
Amount of PBF.
Morphology & sizes of the native PAs & MAPCAS.
The age of the patient.
@ Protected PAs & MAPCAS
# PA size good RV - PA conduit.
# PA small Central shunt.
@ Hypoplastic / Absent PAs
# Unprotected MAPCAS - > 1yr? surgical options.
< 1 yr better option.
# Protected MAPCAS 3 options according to the size of the PAs.

Group A Complete repair with TAP.

Group B Complete repair with RV PA conduit.

Group C Unifocalisation +

PAs & MAPCAS Segments of the lung Surgical Rx

Size expected supplied

75% > 15 VSD closure

RV PA conduit.

50 74 % 10 -14 RV- PA conduit

Keep VSD open

< 50 % < 10 Central shunt.

887
Acquired pulmonary atresia - Complete repair with TAP (90 %).

Palliative operations: -
PBF - # Embolisation of MAPCAS.
# MAPCAS banding pledgetted mattress suture placed in the
aortic wall on the side of the collateral vessels.
PBF BT Shunt.

Unifocalization: -
Refers to those procedures that join the multifocal sources (True PAs & one / >
collaterals) into a single source.
Various procedures described
1. Either direct anastomosis of collaterals to the true PAs.
2. Placement of interposition graft (synthetic / autologous vein or
artery/xenograft / autologous pericardium) between collateral vessel &
pulmonary artery.
3. Staged / Single stage.
4. Thoracotomy / Median sternotomy / Clamshell (sub mammary)
approach.
5. Various material used ,
# Iyer & Roger Mee tech. PTFE / Gortex tube.
# Lacks tech. Autologous pericardial tube.
# Cherians tech. Homograft tube.
6. Unifocalization of all MAPCAS > 2mm size.
Ideal Unifocalization should,
1. Allow incorporation of all nonredundant collaterals & the true PA to each
lung without distortion.
2. Utilize conduit that will either grow or be large enough to supply
adequate blood flow in adulthood without replacement.
888
 3. Minimize the risk of thrombosis.
4. Be easily accessible from the mediastinum at the time of definitive repair.

Technique: -
Incisions
Thoracotomy for multistage unifocalization.
Median sternotomy
Clamshell approach
Previous surgery Hilar scar.
No need for extensive dissection.
Good exposure.

Single stage Unifocalization: -

Harvest the pericardium.
Dissection of native PAs & isolated up to their hilar regions.
Ascending aorta & SVC separated.
Dissection of MAPCAS
@ Dissecting along the aorta & the brachiocephalic arteries as per
angiography up to transverse sinus.
@ Descending aortic MAPCAS in posterior mediastinum after opening the
posterior pericardium.
@ In left arch the descending aortic MAPCAS approached by
dissecting between the area of left side of the ascending aorta & LA &
above or below the lt. main bronchus.
@ presence of LSVC & mediastinal lymph nodes made dissection more
difficult.
@ Care should be taken not to compress LCA.
@ In right arch the descending aortic MAPCAS were reached by
approaching between the ascending aorta, SVC & roof of the LA, usually
above or below the carina & rt. main bronchus.
889
 @ Avoid hemodynamic compromise.
@ Precautions were taken not to injure trachea, bronchi, esophagous &
phrenic, vagus & recurrent laryngeal nerves.
@ All MAPCAS were looped before going on CPB.
On CPB & beating heart, all MAPCAs were disconnected from their origin
& proximal end was closed. They were anstomosed end side or side
side to native PAs if present. Otherwise MAPCAs MAPCAS using 8-0
prolene suture.
Under cardioplegic arrest VSD closed with Dacron patch & RV PA
continuity established by cryopreserved aortic /pulmonary homograft
conduit.
Staged Unifocalisation: -
Pericardial / Gortex tube unifocalization.
Double lumen endotracheal tube, single lung ventilation.
Posterolateral thoracotomy.
Apex of the lung retracted inferiorly & posteriorly for true PA at the
anterior & superior aspect of hilum.
Retraction of lung anteriorly for AP collaterals.
Redundant collaterals ligated & divided.
Large patch of pericardium was harvested anterior / posterior to phrenic
nerve.
Patch draped with serous surface upwards over the posterior & superior
hilum with mid portion lying over the collaterals.
Site of incision marked, Coll. Individually clamped with shallow U
shaped clamp.
After incision on the pericardium & Coll anstomosis done with 6-0 / 7-0
prolene suture.
The remaining coll & true PA s anastomosed to the pericardial tube, Edge
of the pericardium folded & make a tube so it reaches anterior

890
 mediastinum, if it does not adult sized ( 16 / 18 / 20mm ) interposition
graft added to the pericardial tube.
Inflow to the tube provided either by a side to side anastomosis to the
ascending aorta /gortex graft from SCA tube.
Pericardial defect replaced with Gortex membrane.
Shunt size adjusted to achieve an arterial O2 sat 80 % at room air & 88-
90 % with Fio2 100 %.
Definitive Repair Criteria to be seen,
@ Mc Goon Ratio
LPA + RPA diameter at upper lobe branch level /Descending aorta at
diaphragm level.
>1 suitable for definitive repair.
@ Nakatas Index
Cross sectional area LPA + RPA / BSA
150 mm2/m2 suitable for definitive repair.
@ Post op pRV > 2/3 rd systemic High risk factor for definitive repair.
Conduit repair
@ After 4-5 yrs / adulthood.
@ Size Infant 14 18 mm.
>5 yrs 22 25 mm.
@ Tech
1. Orthotropic Same as native valve.
Adv. No compression by sternum.
Disadv. circular geometry lost.
2. Dacron hood Circular geometry maintained.
Compression by sternum.

VSD closure 6 18 months, if

L-R shunt, CHF, Improved resting O2 saturation.
Results: -
891
 Survival
1. Early death 5 -20 %.
2. Time related survival - < TOF with PS.
3. Modes of Death Heart failure, Hypoxia, Haemorrhage,
Arrhythmias.
Incremental risk factor for Death
1. Size of central & proximal extra cardiac RPA & LPA.
2. Congenital nonconfluent RPA & LPA.
3. Number of MAPCAS - > risk.
4. Age Early repair, younger, old late repair.
5. Post op PRv /Lv - > 1 risk.
6. Duration of CPB - > risk.
7. Use of valved conduit - risk.
Heart block rare.
Functional status good.
Reoperation
1. Residual VSD 3 %.
2. AVR 1 %.
3. Valved conduit.
Freedom from conduit obstruction
Years % Now
99 -
5 95 95
10 59 90
15 11 -
20 - 60.
Mitral Valve Repair

Anatomy of Mitral Valve: -

892
 Mitral Veil MV forms a continuous veil attach to the circumference
of mitral annulus.
Commissure identified by tips of the corresponding papillary muscle
& by the commissural chordae.
Mitral valve - The leaflets are covered with endocardium.They present
on atrial side a distinct ridge that follows the rim of the leaflets at a
certain distance from the free edge. the ridge defines the line of leaflet
closure & separates the leaflets into two zones.
# Rough zone Distal to ridge closure area represents the surface of
coaptation.
# Proximal zone Membranous & clear on transillumination.
AML Semicircular / Triangular.
Related to LCC & of NCC.
Aorto mitral continuity +.
2 zones Rough & clear.
PML Quadrangular.
Posterior to both commissures.
Wider attachment than AML.
Two indentations scalloped appearance.
3 zones Rough, clear, basal.
Annulus Zone of junction that serves as the attachment of the
muscular fibers of the atrium & the ventricle & on the attachment of
MV.
Annular tissue pliable, permitting sphincter contraction during lt.
atrial & LV systole.
Attached to two fibrous trigone.
In MR dilatation of the annulus occurs at the posterior level.
Mitral annulus in diameter during systole up to 26% due to
contraction of Basoconstrictor muscles.
Chordae
893
 Commissural Arise as a main stem branches rapidly.
Insert into the free margin of the commissual region.
Two in number.
PML chordae have longer, thicker & widespread than
AML chordae.
AML chordae Attach in distal rough zone.
7 paramedial & Para commissural.
2 Main chorade from 2 papillary muscle attach
to ventricular surface
4 5 o clock on PMC side.
7 8 o clock on ALC side.
PML chordae 3 types
2 basal zones
10 rough zone.
2 Cleft chordae.
LV papillary muscles Two groups.
Anterolateral & Posteromedial.
Each one has one or two bellies.
PM papillary muscle has > 2 bellies.
Types
1. Completely tethered with fully adherent
to ventricular myocardium.
2. free & finger like 1/3rd / > portion in LV.
3. Intermediate type.
Arterial supply
Leaflets branch of Kugel artery, running at the base of the IAS,
br. of 1st segment of RCA /proximal LCx.
PM LAD/Diagonal/ OM AL.
LCx / RCA PM.
Physiology: -
894
 Closure of Normal Mitral valve
Process involves 3 phases
1. Leaflets meet edge to edge.
2. Leaflet bulge upwards, ballooning into the atrial cavity, contraction of
myocardial fibers.
3. Surface of coaptation between the two leaflets becomes more & more
extensive, so that during systole the leaflets are disposed against each
other in almost in vertical position.
Functional Approach
Aim Restoring the function rather than the anatomy of mitral valve
apparatus.

Carpentiers functional classification

Type I Normal leaflet motion
Annular dilatation.
Leaflet perforation.
Type II Leaflet prolapse
Chordal rupture.
Chordal elongation.
Papillary muscle rupture.
Papillary muscle elongation.
Type III Restricted leaflet motion
Restricted opening comm. fusion, leaflet & chordal fusion.
Restricted closure Excess tension on chordae during systole.

895


MV Repair: -
Basis of functional repair
Goal defined as either limiting or increasing the leaflet motion in addition
to remodeling the annulus by a prosthetic ring to obtain an optimal
opening of the valve & a good surface of coaptation.
Indications
1. All cases of non calcified valve disease.
2. Rheumatic valve disease Repair possible 50 % adult & 90 % children.
3. Degenerative valve disease excellent indication.
Most durable.
Rate of reoperation 0.7 % / pt. /yr.
896
 Repair feasible in 95 %.
4. Subacute bacterial endocarditis after 15 days of antibiotics.
5. Congenital malformation Repair feasible in 80 %.
Whatever may be the cause of the disease,
# Operation should be carried out at early stage of disease.
# At the 1st onset of AF.
# Alteration of myocardial function.
Contraindications -
1. Valve calcifications.
2. Rheumatic etiology.
3. AML involvement.
* Advantage -
1. Preserves pts native valve.
2. No prosthesis no complications of prosthesis.
3. No complications of chronic anticoagulation (except pt. in AF).
4. Preservation of mitral apparatus & sub valve leads to better preservation
of post op LV function.
5. Preservation of mitral apparatus leads to maintenance of normal shape /
volume & function of LV.
* Disadvantage -
1. Surgical skill & expertise required.
2. Technically more demanding.
3. Require longer CPB, occ. may fail.
4. Valve calcification, Rheumatic involvement & anterior leaflet involvement
reduces likelihood of repair.
5. Uncalcified posterior leaflet disease is almost always reparable.
* Timing of surgery -
1. Symptomatic pt. with normal LV function (EF > 60 %, ESD < 45mm).
2. Asymp with LV dysfunction (EF 60 %, ESD 45mm).
3. Symp with LV dysfunction (EF 60 %, ESD 45mm).
897
4. EF > 30 %, Symp MR.
5. Asymp with normal LV function to preserve,
LV size, Function, Avoid sequence of chronic MR.
6. Asymp with normal LV function with recent onset of AF.
* Valve Analysis -
Atrium examined 1st for jet lesion (indicate porlapse of opposite leaflet).
Annulus for annular dilatation.
Leaflet tissue pliability / restricted motion / prolapse.
Precise prolapse can be checked by Reference point method.

* Technique of Repair -
A. Prosthetic Ring Annuloplasty
One of the major step of valve reconstruction & is mandatory in most
cases of MR.
Aim Reduce size of dilated annulus.
Restore the shape of orifice.
Dilatation of the annulus occurs at PML & commissures leading to gross
deformation of the annulus with anteroposterior diameter > transverse.
Measure surface area of AML with sized obturators.
Assessment of repair by saline injection into the LV.
The adequacy of repair assessed by considering function rather than
anatomic aspect of the result.
Adequate repair is if the line of leaflet closure is parallel to the mural
part of the ring, this indicate good apposition of the leaflets & a good
surface coaptation.
Various types of rings used,
1. Carpentier Edwards complete rigid ring
2. Cosgroves annuloplasty ring incomplete flexible.
3. Durans complete flexible annuloplasty ring.

898
4. Biflex complete flexible ring.
5. Posterior hard felt incomplete rigid ring (PHFA).

B. Repair of PML
PML prolapse due to ruptured chordae treated by Quadrangular resection
of the prolapsed portion & gap repaired by
# Annular placation.
# Sliding plasty of PML.

PML prolapse causing LVOTO Quadrangular resection of posterior

scallop is completed by two triangular resection at the base of PML
reduces height of PML, avoid systolic anterior motion of leaflet, prosthetic
ring annuloplasty to reinforce repair.

C. Repair of AML
Chordal Rupture
1. Leaflet fixation on secondary chordae

899
 Free edge of prolapsed leaflet sutured to adjacent secondary chordae close
to prolapse area.

2. Chordal transposition
Strong chordae of PML located opposite to prolapsed AML are detached
from PML & reattached to free edge of AML, gap in PML closed by
quadrangular or triangular resection.
Secondary chordae of AML can also be transposed.

3. Chordal replacement
Excessive scarring / degeneration of PML chordae PTFE neo chordae.
Chordal Elongation
Can be corrected by shortening plasty of the chordae.
Two techniques
1. Carpentiers technique At papillary muscle level,

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 Invagination of the excess length of the chordae into a trench
created in the papillary muscle.
2. Sampath kumars technique At leaflet level,
Plicating elongated chordae at leaflet level.
Papillary muscle Elongation
1. Sliding plasty of PM
Portion of papillary muscle to which the prolapsed area is attached is
split longitudinally & resutured at a lower level.

2. Cunieform resection
A large papillary muscle with moderate prolapse (2- 6 mm) can be
shortened by a cuneiform resection of its tip. The height of the
resection equal to the degree of shortening. The horizontal trench
closed by separate suture.

3. Concertina technique

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 A thinner papillary muscle with moderate elongation can be treated by
numerous superficial vertical sutures which can be shortened 3 -5
mm.

Papillary muscle Rupture

Requires papillary muscle reimplantation,
Indication
# When large ventricular wall segment is not infracted.
# When PM tip & trunk is only involved in infarction.
1. A ruptured papillary tip with chordae to PML-
The fibrous part of ruptured papillary tip can be attached to adjacent
noninfarcted PM.
Functional closure of leaflet assured before tying suture.
Site of attachment can be measured by chordal length using Carpentier
hook. Reinforced with ring annuloplasty.

2. When ruptured PM is not adjacent to other PM

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 Disjoined tip can be attached to a noninfarcted part of the adjacent
ventricular wall. Tip must be implanted above the original site of rupture
to ensure enough chordal length to avoid restriction.
The suture passed through tip & ventricular wall through & through over
pledget.

D. Repair of Restricted leaflet motion

1. Results from comm. Fusion, chordal fusion, chordal shortening or
chordal hyprtrophy.
2. Resection of secondary chordae (attached to the ventricular surface of the
leaflet) improves movement of leaflet tissue.
3. Fused marginal chordae attached to free edge of leaflet are treated by
triangular resection
(Fenestration).
4. Calcification of mitral apparatus complicates valvuloplasty.
5. Time consuming.
Intra operative assessment of repair: -
Clinical
1. Saline injection.
2. Leaflet coaptation.
3. Jet of saline.
4. Line of closure is parallel to the mural part of the ring.

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 TEE / Epicardial echo After Off CPB.
Residual MR immediately after CPB is due to,
1. Temporary Ventricular dysfunction.
2. Temporary ventricular dilatation.
3. Temporary systolic anterior motion of leaflets whenever ventricle is too
empty & hyperkinetic.

# Cardiac assistance.
# Proper adjustment of filling pressure.
# Cautious use of inotropes.

Restores ventricular function with no MR.

# A persistent 2 3 + MR.
# Persistent systolic anterior motion of the leaflet.
# Trans valvular gradient of > 40 mmHg .
with above precautions needs valve replacement (2 %).
Results: -
Survival
1. Mortality Early 0 %.
5 yr 74 -94 % survival.
15 yrs 72 %.
Modes of Death
1. Cardiac Failure.
2. Subsystem Failure.
3. Infection.
Risk factors
1. Older age.
2. Black.
3. Ischemic MR.
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4. > LV enlargement.
5. Previous CABG.
6. High LVEDP / NYHA.
7. LV resection for Aneurysm.
Residual MR 13 -14 % (9 -20 %).
Freedom from
1. Thromboembolism - 93.9 %.
2. Endocarditis 96.6 %.
3. Anticoagulant Hemorrhage 95.6 %.
4. Reoperation 87.3 % (81 % at 7 yrs).
LVOTO 5- 10 % (Not seen in suture annuloplasty).
1. MVP.
2. Absent anterior motion with CE ring.
3. Myxomatous degeneration.
4. Redundant MV.
Functional Status Excellent.
NYHA I /II - 74 %.

905
 REFRENCES

Adult cardiac surgery R M Bojar

Congenital malformations of the heart Goor & Lillehei

Cardiac surgery John W. kirklin,Brian G. Barratt-Boyes

Glenns Thoracic & cardiovascular Surgery Arthur E. Baue, Graeme

Hammonds, Alexander Geha, Hillel Laks, Keith Naunheim, William W. L.
Glenn

Surgery of the Chest Sabiston & Spencer

Cardiac surgery in Adults Louis Henry Edmunds

The Chest X-Ray: A Survival Guide by Gerald de Lacey et al.

Introduction to chest radiology

Cardiac Valves: Assessment and Identification on RadDaily.com

A Diagnostic Approach to Mediastinal Abnormalities

by Camilla R. Whitten May 2007 RadioGraphics, 27,657-671.

Chest Radiology Plain Film Patterns and Differential Diagnoses

by James C. Reed

Thoracic Imaging: Pulmonary And Cardiovascular Radiology

by Richard Webb and Charles Higgins

Chest Radiology: Plain Film Patterns and Differential Diagnoses sixth

edition by James C. Reed
The Chest X-Ray: A Survival Guide by Gerald De Lacey, Simon Morley
and Laurence Berman

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