24

Cardiovascular System
DETAILS OF PRESENTING SYMPTOMS
1. Chest pain (chest discomfort)-
Ask for
 Site, duration, character, radiation, aggravating & reliving factors
 Any special type of angina (unstable, second wind, nocturnal, pericardial
pain, aortic dissection)
Type Location Character Disease
Angina Retrosternal Constricting pain CAD –
(myocardial pain radiating Atherosclerosis,
ischemia) to arms, throat, Aggr by exertion & arteritis, congenital
jaw rapid relief by rest CAD, embolism
&drugs
Myocardial Same as Same as angina but Acute myocardial
infarction angina more severe & not infarction
easily relived
Pericarditis Central Sharp / Stabbing/ raw Idiopathic,
(retrosternal) (like sand paper) pain Coxsackie B
chest pain infection,
Aggr by deep complication of
radiate to inspiration, cough, myocardial
shoulder / back postural change infarction
Pain of Retrosternal / Severe tearing pain of Aoric dissection
aortic over back in abrupt onset
dissection interscapular
region

 Grading of Angina (Canada heart dissociation)

I Sever exertion
II Walking uphill / climbing >1 flight of ordinary stairs
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III Walking on level ground, climbing 1 flight of

ordinary stairs
IV At rest

2. Dyspnoea
Def: Abnormal awareness of one’s own breathing at rest / low level of exertion

Ask for
At rest/ after exertion
Time of occurrence- day time/ nocturnal
Onset- acute/ insidious

Acute onset Acute pulmonary edema,

pulmonary embolism,
pneumothorax, pneumonia Duration

Subacute / Chronic CF Grading of

chronic dyspnoea-
NYHA class

I No dyspnoea at rest/ moderate exertion

II Dyspnoea at moderate to severe exertion

III Dyspnoea at mild exertion but minimal at rest

IV Significant dyspnoea at rest- often bed bound /

Severe dyspnoea on minimal exertion

Associated symptoms like cough, palpitation etc,

Aggravating & relieving factors
Number of episodes
Cardiac Causes of Dyspnoea
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1. LVF (Dyspnoea is the major symptom)

2. congenital heart disease
3. acquired valvular heart disease
4. CAD
5. hypertensive heart disease
6. cardiomyopathy

In addition ask for

 PND
 Occurs at night
 Patient awakens with a feeling of suffocation and grasps for breath
 Needs longer time in sitting position for relief
 Mechanism – not exactly known,
slow reabsorption of interstitial fluid from dependent position of the body and
resultant expansion of intrathoracic blood volume
sudden elevation of thoracic blood volume and diaphragm which occurs
immediately after recumbency as in case of orthopnoea
Reduced adrenergic support of left ventricular function during sleep
normal nocturnal depression of the respiratory center
Posterior of thorax does not take part in respiration when patient lies down
 Clinical causes -ischemic heart disease, aortic valve disease, HT,
Cardiomyopathy, Atrial fibrillation (AF)
 Orthopnoea
o Dyspnoea in recumbent position, within minutes of recumbency
o Occurs in awake patient
o Relived by sitting up / elevation of head with pillows
o Mechanism is believed to be due to redistribution of fluid in to the
intravascular compartment on lying down with resultant increased venous
return

o Clinical causes - Acute LVF, extreme degree of CCF

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 Platypnoea
o Dyspnoea only in upright position

o thrombus/ tumors of left atrium, Pulmonary AV fistula

 Trepopnoea
o Dyspnoea only in left / rt lat. Decubitus position

o Pts with heart disease

 Cheyne stokes breathing

3. Palpitation
Ask for –
Mode of onset, frequency, duration, occurring at rest/ exertion, aggravating &
relieving factors persistent/ paroxysmal
Rapid & regular of Atrial, junctional, ventricular
abrupt onset tachyarrhythmia
Rapid, irregular AF

4. Syncope
Ask for – onset, duration, causative factors (drug related, arrhythmia related,
exertion related), associated neurological deficit
Clinical disorders
Aortic stenosis, Atrial myxomas, hypertrophic cardiomyopathy, acute MI,
Primary Pulmonary HT, severe pulmonary stenosis,
Tetrology of fallot
Arrhythmias- sick sinus syndrome, ventricular tachycardia,
Supraventricular tachycardia, complete heart block
Features of certain types of syncope

Disorder Description of stimuli, recovery Cause of cerebral hypoperfusion (CP)

Postural hypotension Syncoupe on standing, pt falls to Inadequate baroreceptor- mediated

ground whereupon condition vasoconstriction causes abnormal fall in
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corrects itself BP & CP resulting in syncoupe

Common in elderly

Vasovagal syncoupe Stimuli – emotional /painful Autonomic overactivity provoked by

stimuli, less commonly cough/ stimuli causes vasodilatation &
If frequent = micturition inappropriate slowing of pulse cause
“malignant vasovagal abnormal fall in BP & CP resulting in
syndrome” Rapid recovery if pt lies down syncoupe

Carotid sinus Stimulation of carotid sinus by Exaggerated vagal discharge due to

syncoupe tight shirt collar, Shaving in external stimuli cause reflex vasodil. &
some elderly pts slowing of pulse resulting in fall in BP &
Sick sinus syndrome CP

Valvular obstruction Exertion Fixed valvular obstruction in AS, Lt atrial

tumor prevents normal rise in C.O during
Similar mechanism in exertion such that physiological Vasodil.
vasodilator (nitrates, Occurring in exercising muscle produce
ACE inhibitor) abnormal fall in CP
therapy

Stokes Adams Self limiting episodes of Due to the abnormal rhythm there is loss
syndrome asystole / rapid tachyarrhythmia of C.O. causing syncoupe & striking
(including ventr. Fibrill) pallor
Rapid recovery after normal
rhythm is restored asso. With
flushing of skin

5. H /o easy fatigability
Important symptom of heart failure
More intense towards end of day
Cause – deconditioning & muscular atrophy, inadequate O2 delivery to muscle due
to reduced C.O

6. Peripheral oedema
Ask for – site, duration, progressive/ variable, diurnal variation, associated
weight gain, Drug history (NSAIDS, Ca channel blockers, Steroids)
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7. H /o cyanosis/ cyanotic spells

Def – bluish discoloration of skin & mucous mem due to increased amt of red. Hb > 4 gm / dl
OR > 30% of total Hb & Pa O2 < 85% OR due to presence of abnormal Hb pigments in
perfused areas
Types Causes
Central Decreased art. O2 saturatn.
1. Decresed atm presr-high altitude
2. Impaired pul. Fntn – alveolar hypoventilation, ventilation
perfusion Mismatch, impaired O2 diffusion
3. Anatomical shunt – congenital cyanotic heart disease*,
Pulmonary AV fistula
4. Hb with low affinity for O2
Hb abnormalities
1. Met Hb > 1.5 g/dl
Hereditary
Acquired – drugs (nitrate, nitrite, sulphonamide)
2. sulph Hb > 0.5 g/dl
3. CO- Hb (smokers)
Peripheral Reduced Cardiac Output, cold exposure, redistribution of blood
flow from extremities, obstruction of artery / vein
Differentia 1. Only in LL – PDA with pulmonary HT with rt to lt shunt
l 2. Only in UL - “ “ & transposition of Grt vsls
3. LL + left UL (rarest) – when PDA opens proximal to origin of Lt
subclavian artery

*Congenital Cyanotic heart diseases:

1. Tetrology of fallot
2. Transposition of great vessels
3. Truncus arteriosus
4. Total anomalous pulmonary venous connection
5. Tricuspid atresia

 Cyanotic congenital heart disease with cyanosis seen on the first day of birth

1. Total anomalous pulmonary venous connection

2. Tricuspid atresia
3. Pulmonary atresia

 In Tetrology of Fallot, cyanosis occurs 3 to 6 months after birth due to following

reasons

 Persistence of PDA
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 Presence of fetal haemoglobin

 With growth of child, severity of pulmonary stenosis increases
 Oxygen demand increases with growth of the child

8. Hemoptysis
1. Mitral stenosis
Rupture of bronchopulmonary collateral
(bronchopulmonary apoplexy)
Pulmonary edema
Pulmonary infarction
Winter bronchitis
2. Acute pulmonary edema
3. Pulmonary embolism & infartion

Also ask history about following

9. H /o squatting episodes
10. H /o convulsions, loss of consciousness
11. Respiratory symptoms - Cough, hemoptysis, epistaxis
12. G. I. symptoms
 nausea and vomiting (digitalis toxicity)

 upper abdominal pain (hepatomegaly due to CCF)

 right hypochondrial pain

 abdominal distension – ascites due to CCF, constrictive pericarditis

 loss of appetite (anorexia) / weight

Anorexia - git congestion in CCF

13. urinary symptoms
Oliguria – poor renal perfusion due to CCF, Renal artery embolism
Nocturia- increased renal perfusion in CCF in recumbent position
Hematuria – a manifestation of infective Endocarditis

14. Fever- duration & pattern

15. Joint pain & swelling
1. Acute/ chronic
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2. Joints involved
3. Fleeting (migrating) / addictive
4. Associated fever, rashes
5. Recovery
6. Any residual deformity
16. Hoarseness of voice / hemiparesis

PAST HISTORY
 Specific enquiry about the past history of conditions that may be associated
with cardiac diseases – DM, CAD, AGN, AF, Amyloidosis, Cardiomyopathy
1. similar complaints before – pedal edema, Dyspnoea, infective endocarditis,
stroke
2. H /o recurrent respiratory tract infections
3. Ante natal history in mother- German measles, drug intake, lupus (congenital
complete heart block)
4. Intranatal history – mode of delivery, cry, congenital cyanosis
5. post natal history – feeding difficulties, failure to thrive, delayed milestones,
retarded growth, recurrent respiratory tract infections, cyanotic & squatting
episodes
6. H /o rheumatic fever (rheumatic age: 5- 15 years) – throat pain, fever, joint
pain( pattern of joint involvement & recovery), involuntary movements &
subcutaneous nodules
7. H /o HT, DM, PT
8. Recurrent dental works / other potential cause of bactremia (for endocarditis)

PERSONAL HISTORY
1. Diet
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2. Alcohol (AF, HT, Cardiomyopathy)

3. Smoking
4. Excessive coffee (palpitation)
5. I.V. drug abuse, Recreational drugs like cocaine (chest pain)

OCCUPATIONAL HISTORY
1. Nature of employment- to know about limitation of activities
2. Medico-legal consequences- pilots, drivers of heavy commercial vehicles

DRUG HISTORY
1. List of drugs used
2. H /o OTC drugs (NSAIDS), Alternative medicines, Herbal remedies (they
may contain ingredients with a cardiovascular action)
Drug history is important as

 Drugs may cause/ aggravate cardiac symptoms

 May give a clue for the presence of chronic diseases (DM, Rheumatoid arthritis,
Skin diseases)

FAMILY HISTORY
1. Consanguineous parents – degree

First degree Brothers and sister

Second degree Fisrt generation relative uncle

Third degree Second generation

2. Mother’s Age at delivery

3. Similar complaints in family - Cardiac diseases with genetic component

 33

4. Premature CAD in 1st degree relative

5. Sudden unexplained death at younger age (cardiomyopathy / inherited
arrhythmia) in 1st degree relative

Physical Examination

General examination

1. Comfortable / Dyspnoic
2. Stature
a. short
Condition Features Cardiac lesion

Down Mental retardation, epicanthic folds, low set Endocardial

syndrome ears, mongoloid face, depressed nasal cushion defect
bridge, Hypotonia, macroglossia

Turner Webbed neck, sexual infantilism wide set Coarctation of

syndrome nipples, low hair line, small chin, wide aorta, bicuspid
carrying angle aortic valve

Noonan Same as above but phenotypically male Pulmonary valve

syndrome stenosis

b. Tall stature

Condition Features Cardiac lesion

Marfan’s Dislocation of lens (upward & outward), Irododonesis, Aortic regurgitation,
syndrome High arch palate, Kyphoscoliosis, Arachnodactyly, Dissection of arota.
Thumb sign, Wrist sign (Murdoch sign) MVP, MR

3. Built & nourishment - thin, obese, normal

4. pyrexia
i. infective endocarditis – low grade/ swinging (if
paravascular abscess develops)
ii. myocardial infarction – first 3 days after MI
iii. Recurrent respiratory tract infection in shint lesions, pulmonary
congestion
iv. Acute pericarditis
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v. Pulmonary embolism
vi. CNS infection in cyanotic heart diseases

5. pallor – shock,
6. lymphadenopathy
7. anemia
 Infective endocarditis
 As a result of hemoptysis
 Nutritional anemia
 Anemia may exacerbate angina & Heart failure
8. polycythemia
Infective endocarditis, Cor pulmonate, Eisenmenger syndrome
9. Eyes
1. proptosis,
2. lid retraction,
3. sub conjunctival hemorrhage,
4. xanthalesma (CAD)
5. corneal arcus (CAD)
6. brush field spots, coloboma,
7. irododonesis (shimmering iris) , dislocation of lens– marfan’s
syndrome,
8. cataract

10. neck
1. venous pulse
2. goiter
3. webbing of neck
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1. with low hair line- turner’s (coartation);

2. with low set ears- Noonan’s (PS, HOCM)
11.Cyanosis – (details given in presenting complaints)
12.clubbing - ask for onset, duration
i. congenital cyanotic disease- absent at birth,
develops during infancy & become marked
ii. infective endocarditis – only other cardiac cause of
clubbing
13.fingers & nails
Signs of infective endocarditis
i. splinter hemorrhages in nail-bed
ii. tender erythematous nodules in pulp of finger
iii. janeway lesions – painless erythematous lesions on
palms
14.warm hands – high output states
15.coldness of extremities
Important sign of reduced C.O. in pts hospitalized with severe heart failure
(Measuring skin temp- useful to monitor C.O in ICU)
16.Pedal edema
 Sub-cutaneous, pitting edema – Cardinal feature of CHF
 Pressure applied over bony prominence – tibia, lat. Malleoli, sacrum
 Cause – retention of salt & water by kidney by following mechanisms
o Reduced Na delivery to Nephron
 Symp activtn + AT II => preglomerular arterioles constricted=>reduced
GFR => reduced Na delivered
o Increased Na reabsorption from Nephron
 In PT during early phase
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 In DT as failure worsens (due to activation of R A A)

17. Jaundice
 Congestive hepatomegaly
 Microanglopathic hemolytic anemia – prosthetic valves
 Pulmonary infarction
 Anticoagulant drug – Warfarin

18. Skin

Dry, coarse Myxoedema

Cold and clammy Peripheral vascular collapse

Warm and sweating Thyrotoxicosis

19. Muscular skeletal system

1. high arch palate, arachnodactyly, pes cavus – marfan’s syndrome
2. absence of radius,
3. absence of thumb – (Holtram syndrome) -ASD
4. syndactyly, polydactyly, Kyphoscoliosis,

Peripheral Signs of Infective Endocarditis

1. Fever, anemia,
2. Clubbing – usually three weeks after onset of endocarditis
3. Sub-conjunctival hemorrhage
4. Petechial rashes
5. Splinter hemorrhage under finger and toe nails
6. Osler’s nodes – tender erythematous patches over pulp of fingers and toes
7. Janeway’s lesions – nontender erythematous patches over palms and soles
8. Absence of any peripheral pulse
9. Splenomegaly – usually three weeks after onset of endocarditis
10. Microscopic hematuria
11. Arthralgia
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Vital data
Examination of pulses
 Definition: wave form transmitted along the arterial tree in a peripheral direction much
Ahead of the actual column of blood as a result of cardiac systole.

 Arteries examined
1. superficial temporal
2. brachial
3. carotids
4. radial
5. femoral
6. popliteal
7. dorsalis pedis
8. posterior tibial

 All pulses have to be compared on both sides simultaneously excepts carotids

 Following points have to be noted

1. rate
Bradycardia < 50 per
minute
Tachycardia > 120 / minute
2. rhythm
 Rhythm may be regular or irregular.

 The irregularity may be regularly irregular or irregularly irregular.

Regularly irregular
 Atrial tachyarrhythmias with fixed block
 Ventricular bigemini, bid gemeni
 Sinus arrhythmia

Irregularly irregular
 Ectppics – atrial/ ventricular
 Atrial fibrillation
 Atrial tachyarrhythmias with varying blocks
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3. volume
i. small volume pulse (Hypokinetic pulse)
 Small weak pulse- small volume and narrow pulse pressure

 Causes
o Cardiac failure
o Shock
o Low cardiac output due to
o Valvular heart disease – Mitral / aortic stenosis
o Myocardial disease
o Pericardial disease

ii. large volume pulse (hyperkinetic pulse)

 A high volume pulse with rapid rise – large volume and wide
pulse pressure

 Causes
o High output states- pregnancy; fever, anemia,
thyrotoxicosis, beri beri, paget’s disease
o Mitral regurgitation
o Ventricular septal defect
o Systolic hypertension
o Aortic regurgitation
o PDA

4. character
a. Collapsing pulse (water hammer pulse, Corrigan’s pulse)
 Large volume pulse with rapid upstroke& a rapid down stroke.

Rapid High systolic pressure and increased

upstroke stroke volume

Rapid down Due to very low diastolic pressure

stroke and rapid run off to periphery.
 Best felt in radial or brachial
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True collapsing pulse Pseudo collapsing pilse

Feature Diastolic BP < Pulse prsr Diastolic BP > Pulse prsr
Condition Aortic regurgitation, PDA, AV Severe MR & large VSD
s fistula, aorto-pulmonary window,
rupture of sinus of valsalva

b. Pulsus bisferians ( bis – 2 ferire – to beat )

 It is double peaking pulse both peaks in systole
 Best felt in carotid
 Causes - pure aortic regurgitation, aortic stenous and regurgitation,
hypertrophic cardio myopathy

 Explanation
 1st peak represent force of left ventricular contraction transmitted via aortic
valve & 2nd peak is due to actual ejection of blood
 1st peak is due to sudden ejection of large volume of blood & 2nd peak due to
elastic recoil of aorta
 At the peak rate of flow there is a Bernoulli Effect on the valves on the
ascending aorta causing a sudden fall in pressure on the inner side of aortic
wall
 In HOCM initially there is no obstruction outflow, obstruction appears late
in systole as mitral valve begins to approximate the hypertrophied septal
area. There is a sharp drop in pressure followed by sudden rise to overcome
the obstruction
c. Dicrotic pulse
 Double peaking pulse but one peak in systole & other peak in diastole.
 Best felt in carotids
 Causes –LVF, typhoid, dilated cardiomyopathy, cardiac tamponade
 Explanation
A combination of very low stroke volume and decrease peripheral assistance
produces this type of pulse
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d. Pulsus alternans
 Def: It is the alteration of the strength of the pulse sensed by palpation in
the absence of arrhythmia or of a significant variation in interval between
beats. Rhythm is regular
 Best felt in radial or femoral artery
 Causes - severe LVF, beat following premature ventricular beat

e. Pulsus bigeminus
 It is an irregular rhythm, a normal beat is followed by a premature beat and a
compensatory pause, resulting in alternation of the strength of the pulse.
 It is the sign of digitalis toxicity

f. Pulsus paradoxus
 Def: It is an exaggeration of normal physiological reduction in strength in
arterial pulse during inspiration

Normal fall in less than 10 mm / hg during

quite inspiration

Pulsus More than 10

paradoxus

 Causes - cardiac tamponade, constrictive pericarditis, acute severe asthma

5. whether all peripheral pulses are felt

6. Radio- Femoral delay- +ve in Coarctation of Aorta

Blood pressure
 BP shd be recorded in right upper limb/ all four limbs if indicated
 if atrial fibrillation is present BP shd be recorded 3 times & average taken
 41

 in aortic regurgitation the phase four (muffling phase) of koratoff sounds

shd be taken as diastolic pressure even though koratoff sounds are heard
till 0
 in aortic regurgitation with significant associated aortic stenosis, there will
be systolic decapitation ie systolic pressure will not be very high
o thus when systolic BP is >170 mmHg in a patient with AR
associated significant AS is unlikely
o similarly Diastolic BP > 40 mmHg rules out significant aortic
stenosis
o eg in pure AR the BP will be 200/30 mm hg and in AR associated
with significant AS the BP will be 150 / 40 mm / hg

Examination of neck veins

 Right internal jugular vein is used to assess pressure & wave forms as it is
in line with right atrium
 Inspect the jugular veins in between the two heads of sternomastoid
 Patient shd b inclined at 45 degree to the ground
 Measure the upper level of jugular pulsation from the sternal angle using 2
scales

Jugular pulse Carotid pulse

Laterally placed Medially placed

Better visible Better felt

Varies with posture & respiration No variation

2 waves in each cardiac cycle 1 wave

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Predominantly inward Predominately outward

movement movement

Made more prominent with No effect

abdominal compression

Obscured by pressure over root No obscure

of neck
Examination of Cardiovascular System

INSPECTION
1. Chest wall symmetry
2. Deformities of chest wall
o Sternum – pectus excavatum, pectus carinatum
o Costal cartilages –costochondritis
o Spine – kyphosis, scoliosis, ankylosing spondylitis, straight back
syndrome
3. Position of trachea & AI
4. Precordial bulge => presence of rt ventricular hypertrophy since childhood
5. Pulsations over precordium-
look for pulsations over
i. mitral area (apical impulse)
ii. suprasternal area - Aortic regurgitation, aortic arch aneurysm,
coarctation of aorta, high output states- pregnancy, fever,
thyrotoxicosis, anemia
iii. aortic - Chronic aortic regurgitation, Ascending aorta aneurysm
iv. pulmonary - Pulmonary artery dilatation, Pulmonary hypertension,
Increased pulmonary blood flow- ASD, VSD, PDA, High output
states
v. left parasternal (parasternal heave)
It can be due to right ventricular hypertrophy/ left atrial enlargement
(Also refer “parasternal heave” under palpitation)
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Ill sustained pulsations Shunt lesions- ASD, VSD

Sustained pulsations Pulmonary HT of any cause, PS

vi. Epigastric- Right ventricular hypertrophy, Aortic aneurysm,

Liver pulsations- tricuspid regurgitation, tricuspid stenosis, aortic
regurgitation
vii. back- inter & infra scapular pulsations – Coarctation of aorta

PALPATION
1. Confirm inspectory findings
2. Apical impulse
o Def: lower most outermost point of definite cardiac impulse with a maximum thrust to
the palpating finger

o Normally felt in 5th left intercostal space ½ ” medial to midclavicular line

o inspection in sitting position
o Character has to be assessed in Left Lateral position
o Causes – dextrocardia (present in right 5th ICS), thick chest wall,
Pericardial effusion behind the ribs,
Emphysematous chest, left sides Pleural effusion

Types of AI description disorders

Tapping Palpable S1 Mitral stenosis

Heaving Increase in amplitude & Pressure overload conditions

duration of the lift like systemic hypertension,
aortic stenosis

Hyperdynamic Duration of lift increased Volume overload of left

amplitude is normal. ventricle- mitral& aortic
Pulsations in >1 ICS regurgitation, VSD, PDA

3. Shocks (palpable eqivalentsof heart sounds)

Palpate for any sound in aortic, Pulmonary, Apical (mitral) area

Site Shock Cause

Aortic area A2 …………… Systemic hypertension
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Aortic ejection click

Congenital valvular AS, aortic
root dilatation
Pulmonary P2 … Pulmonary HT
area Pulmonary ejection click Pulmonary valve stenosis &
pulmonary artery dilatation
Apical area S1…………… MS
Opening snap … MS
S3 …… DCM
S4 ……. HOCM

4. Parasternal heave
o Base of hand is used to feel heaves
o Grading of parasternal impulse (AIIMS grading)

I Visible but not palpable

II Visible ,palpable, obliterated by

pressure

III Visible ,palpable, not obliterated by

pressure

Causes
i. Right ventricular enlargement - due to pressure overload / volume overload

Character Clinical condition

Volume overload Fast, ill - sustained Left to right shunts – ASD, VSD
Pressure overload Slow, sustained PS

ii. Left atrial enlargement

Mitral stenosis
Mitral regurgitation- in sever cases aneurismal dilatation of left atrium is seen

5. Thrills
o Palpate for any thrill over precordium & carotids
o Base of fingers are used to feel thrills
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Mitral area
Diastolic thrill….. Mitral stenosis
Systolic thrill…… Mitral regurgitation

Pulmonary area
Continuous thrill… PDA, Rupture of sinus of Valsalva
Systolic thrill…… Pulmonary stenosis, VSD, PDA

Aortic area
Diastolic thrill….. Acute severe AR due to eversion /
infection / perforation of the valve
Systolic thrill….. Aortic stenosis

Carotid thrill
Systolic thrill (carotid Aortic stenosis

Shrudder)

Left lower parasternal VSD

area (3rd & 4th ICS)

PERCUSSION
 Useful to detect
o dilatation of aorta - aneurysm of aorta
o dilatation of pulmonary artery – idiopathic, pulmonary HT
o position & enlargement of heart - Pericardial effusion, Cardiomyopathy

Percuss for
o Right cardiac border
o Left cardiac border

AUSCULTATION
1. All areas systematically in following order
1. mitral (cardiac apex)
2. then tricuspid (lower Left parasternal area)
 46

3. second aortic/ erb’s area (3rd left ICS close to sternum)

4. pulmonary (2nd Left ICS close to sternum)
5. aortic area (2nd Right ICS close to sternum)
2. Concentrate
1. First on heart sounds esp to loudness
Much attention to S2 – loudness, split (physiological / pathological) in
pulmonary & aortic area
2. then on added sounds like opening snaps
3. lastly for murmurs

3. auscultate for murmurs over peripheral arteries –esp femoral & carotids

Better heard with S3, S4, Mid- diastolic murmur, venous hum
bell

Better heard with S1, S2, Clicks, Opening snap, Systolic murmur,
diaphragm early diastolic murmur, pericardial rub

1. Heart sounds
In diseased state following abnormalities can occur
a. Differing intensity- increased / decreased
b. Abnormal split is heard
c. Low frequency sound in diastole- S3, S4 may be heard
d. Additional high pitched sounds may be heard

Features of heart sounds

S1 S2 S3 S4

Cause Closure of Closure of Initial passive filling of Rapid emptying of

mitral and semilunar valve ventricles blood into
tricuspid Physiological- healthy noncompliant
valve young adults, atheletes, ventricle - ischemic
pregnancy heart disease,
Pathological- LVF, systemic HT
MR, ASD, VSD, PDA

Heard best at Apex Base Mitral area in left in left lateral position
lateral position with with bell of steth
 47

bell of steth

Position in Immediately Follows AI Coincide with onset of When bolus of blood

cardiac cycle precedes AI period of rapid is delivered to
Immediately Follows carotid ventricular filling ventricle by
precedes pulse wave contraction of the
carotid pulse atrium (atrial systole)
wave

Other “lub” in “lub- “dub” in lub-dup” Low pitched sound Low pitched sound
characteristic dup” normally split- Heard only in
features A2 P2 (30 ms) presence of sinus
rhythm

Third heart sound

▐ │ ▐
S1 S2 S3 S1
Fourth heart sound
▐ │ ▐
S1 S2 S4 S1

Alterations in heart sounds

First heart sound
Intensity of S1
Loud S1 Exercise, hyperdynamic circulation, sinus tachycardia, MS, ASD
Soft S1 Acute MI, myocarditis, Sinus bradycardia, MR

S1in mitral stenosis

Causes of loud S1 In MS Soft S1 in MS
o Open mitral valve till end of o Calcified MV
diastole o Severe sub valvalular
o Delayed mitral valve closure fusion
o Mitral valve closure at higher o Asso. MR
pressure of the atrium o Asso.AR
o Thickened but mobile mitral valve

In mitral stenosis with AF, S1’s intensity may be varying

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Second heart sound

Concentrate on split & intensity of the 2 components

 S2 in aortic valve disease

Aortic stenosis
Increased intensity Non calcified congenital AS

Normal intensity Hypertrophic cardiomyopathy, sub valvular stenosis

Decreased intensity Calcified bicuspid aortic valve disease, rheumatic

stenosis, aortic valve sclerosis in old age

2. Aortic regurgitation - varies depending on etiology, LV function, asso. Lesions,

LOUD Syphilis, marfan’s , rheumatoid arthritis,annuloaortic ectasia,
(conditions producing aortic root dilatation)

SOFT Rheumatic etiology, asso. Aortic stenosis,infective endocarditis

 Abnormalities of split

Physiology of split S2
 Normally S2 is split into 2 components during inspiration & is single in expiration

Expiration Inspiration

▐ │ ▐ ║
S1 S2 S1 A2 P2

 Postponing of P2: During inspiration, due to –ve intrathoracic pressure the venous return
to heart increases which increases rt ventricular stroke volume prolonging RV ejection. This
postpones P2 of S2
 Preponing of A: At same time venous return to LV is reduced. The reduced LV stroke
volume shortens LV ejection. This prepones A2

Abnormalities
Single S2
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tetrology of fallot, tricuspid atresia, tricuspid arteriosus,

transposition of great arteries
severe calcified AS
severe PS
elsenmenger VSD
wide & fixed S2
ASD
Partial anomalous pulmonary venous connection,
right ventricular diseases,
massive acute pulmonary embolism

Basis for wide & fixed split in ASD

 The increase in RV stroke volume (due to Left to Right shunt at Atrial level) causes
wide split S2.
 The right & left ventricular stroke volumes vary in the same way during the respiratory
cycle (because the right and left atria are in free communication) resulting in fixed split

Expiration Inspiration
▐ │ ▐ │
S1 A2 P2 S1 A2 P2

reversed split S2
hypertrophic obstructive cardiomyopathy,
left bundle branch block,
severe systemic HT,
large PDA,
severe AR

Expiration Inspiration
▐ │ ▐ │
S1 P2 A2 S1 S1

Added sounds
i. S3
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 Combination of tachycardia and loud S3 gives a characteristic cadence to

the heart sounds described as gallop rhythm / triple rhythm
 In any clinical setting presence of S3 indicates abnormal LV filling with
high end diastolic pressure

ii. S4 (refer table above)

iii. Opening snap

 High pitched sound
 Heard all over precordium
 Best heard with diaphragm just Medial to the Apex
 Easily mistaken for split S2
 Accentuated by exercise & Widens on standing
 Persists despite atrial fibrillation & even after mitral valvulotomy
 Occurs in MS when the stenosed valve moves forward towards the left
ventricle at the beginning of systole
 Absent in MS in the following conditions
o mild MS
o Calcified / markedly Fibrosed valve
o Associated significant MR

Mechanism:
The sound is due to sudden / sharp tensing of the cusps of the mitral valve as it tries to
open during early diastole, when the left Atrial pressure > left ventricle pressure

iv. Ejection clicks

 High pitched sounds closely following S1
 Due to opening of semilunar valves
 Mimic the split S1
 Types
2. aortic ejection click (EC)
3. pulmonary EC
4. mid systolic click

Cause Character Clinical conditions

Aortic EC Abnormality of Well heard thru out precordium, Congenital AS – bicuspid
aortic valve cusps best heard at apex aortic valve
Pulmonar Abnormality of Heard at pulmonary area Commonly in valvular PS
y EC pulmonary valve Only right sided event that Also in dilatation of
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cusps becomes softer on inspiration pulmonary artery due to

but loud & sharp on expiration
Mid arise from halting  Loud clicks occurring in mid
systolic of mitral leaflet as systole in association with
click it prolapses into MVP
the left atrium  Mimics S3 but differentiated
during systole by its high frequency (S3 is
of low frequency)
 Late systolic murmur
(sometimes absent)
idiopathic nature /
pulmonary HT
Mitral valve prolapse
(MVP)
Also in Tricuspid vale
prolapse, aneurysm of
interatrial / interventricular
septum, Severe AR

v. Pericardial rub
 Character - Scratching / grating / creaking
 Triphasic (mid systolic, mid diastolic & presystollic)
 Evanescent, vary with time & posture
 Best heard – along left sternal edge in 3rd & 4th spaces
 Heard in
1. pericarditis – viral / pyogenic / tuberculous
2. acute MI
3. acute rheumatic fever & rheumatoid arthritis
 Mechanism: Produced due to sliding of the 2 inflamed layers of
pericardium
vi. Pericardial knock
 Loud, High frequency diastolic sound
 Heard in constrictive pericarditis
 Produced due to abrupt halt of early diastolic filling

Murmurs
 Def: relatively prolonged series of auditory vibrations of variable intensity, Quality,
Frequency due to turbulence arising when blood velocity increases due to increased flow via a
constricted / irregular orifice

 Note the following features

o Area over precordium where best heard, conduction
o Systolic / diastolic
o Timing & character,
o Intensity (grading)
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 Grading of SYSTOLIC murmurs (Lance & Freeman’s grading)

I Very soft (heard in a quiet room)
II Soft
III Moderate
IV Loud with thrill
V Very loud
VI Very loud (heard even when
stethoscope is away from chest wall)

 Grading of DIASTOLIC murmurs (Lance & Freeman’s grading)

I Very soft
II Soft
III Loud
IV Loud with Thrill

o Pitch
o Better heard with bell / diaphragm
o Variation with respiration, posture, dynamic auscultation

Classification of murmurs

Type Causes
Systolic (from S1 to S2)
1. Early systolic …. VSD, acute severe TR, acute severe MR
2. Mid systolic …... AS, PS, hypertrophic cardiomyopathy(HOCM)
3. Late systolic…… Mitral Valve Prolapse (MVP), TVP
4. Pan systolic……. MR, TR, VSD
Diastolic
1. Early …………. AR, PR
2. Mid …………... MS, TS (other rare causes given below)
3. Late ………….. MS, TS, Atrial myxomas, complete heart block
(presystolic)
Continuous Refer below

Diagnosis of the MDM (mid diastolic murmur)

 Mitral stenosis (low pitched, rough, rumbling, Long drawn MDM with
presystolic Accentuation ending in loud S1 with / without Opening snap,
heard in left lateral position, Bell of the stethoscope Breath held in
Expiration)
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Differential diagnosis of MDM

1. Austin flint murmur
2. Flow murmur in ASD,VSD, PDA,
3. Carey – Coombs murmur (soft, low- pitched MDM in Acute
rheumatic mitral valvulitis; usually Transient)
4. Left Atrial Myxomas
5. Ball valve thrombus
6. Tricuspid stenosis (best heard in left sternal edge; Increases in
Inspiration; exaggerated “a” wave in JVP)

Comparison of Mitral Stenosis & Austin Flint Murmur

Opening snap Present Absent
S! Loud Normal
S3 Absent Present
Left Ventricular lift Absent Common
Right ventricular heave Present Absent
Rhthym Atrial Fibrillation Sinus rhythm
Palpitation Common Uncommon
Hemoptysis Common Uncommon
Thrill Common Uncommon
Peripheral signs of AR Absent Present

Diagnosis of pan systolic murmur

 Mitral regurgitation
It is a high pitched, Soft, Pan systolic murmur, well heard in the mitral area, in
left lateral position with diaphragm, breath held in expiration conducted to axilla
& back.
o The conduction of the murmur depends on the leaflet involved

Anterior leaflet Axilla & back

Posterior leaflet Base

Differential diagnosis of pan systolic murmur

Best heard over Associated
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conditions
1. Tricuspid Left lower strnal edge Severe pulmonary
regurgitation Increases with inspiration HT, pulsatile liver
2. VSD (Loud& Left 3rd & 4th ICS Thrill
harsh)

Diagnosis of ejection systolic murmur

 Aortic stenosis
Rough crescendo – decrescendo well heard in sitting position with breath
held in expiration conduction to carotids

Differential diagnosis of ejection systolic murmur

i. Hypertrophic cardiomyopathy
ii. Stenosis- Sub-valvular aortic, Supra-valvular aortic, Pulmonary
iii. ASD
iv. Pulmonary arterial hypertension
v. Thyrotoxicosis

vi. Physiological
1. Innocent systolic murmur,
2. Anemia,
3. Pregnancy,
4. chest wall deformity (pectus excavatum)

Diagnosis of EDM
 AORTIC regurgitation-
high pitched, blowing, decrescendo, early diastolic murmur, well heard in
aortic area & Erb’s area, patient sitting & leaning forward, breath held in
expiration
Etiology of AR EDM (best heard)
Rheumatic etiology Left 2nd ICS
Aortic root dilatation Right 2nd ICS

Differential diagnosis of early diastolic murmur

Pulmonary regurgitation (Graham – Steell murmur)

In case of a murmur better heard along rt side of sternum search for non-
rheumatic etiology
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Conditions resulting in AR murmur best heard on right side of sternum

i. Aortic aneurysm – cystic medial necrosis, Syphilis, Idiopathic,
Marfan’s
ii. Sinus of Valsalva aneurysm,
iii. Aortic dissection

Comparison of AORTIC & PULMONARY incompetence

Peripheral Present Absent
signs
Chamber Left ventricle Right ventricle
enlargement
Apical Hyperdynamic Normal
impulse
Murmur Right 2nd ICS & Left 2nd ICS
Erbs area
Relation of On expiration On inspiration
respiration

CONTINUOUS murmur
 Begins in systole, overlaps the S2 & spills over to diastole for a variable period
generated by flow of blood from zone of high resistance to a zone of low
resistance without interruption during both systole & diastole
 Differentiated from Systolico – diastolic murmurs and To & fro murmurs by
prominent S2.

Systolico- diastolic murmur To & Fro murmur

Definition Occupies both systole & diastole but
the murmur occurs thru different
channels and doesn’t peak around
S2
Seen in VSD with AR- systolic murmur
originates across VSD & diastolic
murmur across aortic valve
Occupies both systole and
diastole but both
components originate
across a single channel
AS with AR; PS with PR;
MS with MR

Differential diagnosis of continuous murmur-

PDA, Aorto- pulmonary window, Rupture of sinus of Valsalva,
Artereio venous (AV) fistula, Coronary AV fistula,
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Anomalous origin of Left Coronary Artery from Pulmonary Artery (ALCAPA),

Venous hum,
Mammary soufflé

VENOUS HUM
 Continuous Bruit heard over neck veins due to increased velocity of flow OR
diminished viscosity
 Patient – sitting position
 Bell of steth used lightly Between the 2 heads of Sternomastoid
 Disappears with compression of root of neck
 Occurs in Anemia, Thyrotoxicosis, Intracranial AV fistula

Examination of other systems

RS- look for bilateral basal crackles

Pleural effusion, CCF, Bronchiectasis, commonly on left side in MS

Abdomen- look for hepatosplenomegsaly, free fluid,in abdomen, CCF, infective

endocarditis,
CNS- look for any focal neurological deficit due to emboli in the form of stroke
Clinical diagnosis of common cardiovascular diseases

1. MITRAL STENOSIS
 Pulse Low volume with regular / irregular rhythm, tapping in character
 BP is normal
 Palpable P2 with variable Parasternal heave
 Diastolic thrill
 loud S1with / without opening snap
 mid diastolic murmur
o low pitched, rough, rumbling, Long drawn
o presystolic accentuation
o Heard in left lateral position
o Bell of the stethoscope
o Breath held in Expiration

 Assessment of severity:
1. Duration of murmur : shorter the duration, less severe the stenosis
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2. A2 – OS interval :
Severe MS 0.05 – 0.07 sec
Mild MS 0.10 – 0.12 sec
3. Intensity doesn’t correlate with Severity
4. Valve Area
Normal 5 sq. cm
Asymptomatic >2.5 sq. cm
Mild 1.5 – 2.5 sq. cm
Moderate 1 – 1.5
Severe < 1 sq. cm

2. MITRAL REGURGITATION
 Pulse - Normal / large volume pulse with / without AF
 Hyperdynamic AI – thrill rarely made out
 Left Parasternal lift,
 Soft S1
 Audible S3,
 Evidence of pulmonary HT
 Pan systolic murmur
o High pitched soft
o well heard in mitral area
o in left lateral position
o with diaphragm
o breath held in expiration
o conducted to axilla & back

 Assessment of dominant lesion in combined MS & MR

Positive signs Mitral Stenosis Mitral regurgitation

S1 Loud Soft
Thrill Diastolic Systolic
Apical Impulse Tapping Hyperdynamic
S3 Absent Present

3. AORTIC STENOSIS
Slow Rising pulse
Carotid thrill
Apical impulse – heaving
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S3 – heard all over aortic area

S4 may be heard
Rough, crescendo- decrescendo ejection systolic murmur
Best heard in sitting position
Breath held in expiration
Conducted to the carotids
Assessment of severity
1. according to Valve area
4 sq. cm Normal
< 0.75 sq. cm Severe
< 0.5 sq. cm Critical

2. according to S2
A2 followed by P2 Mild
Single S2 Moderate
Reversed Split S2 Severe

3. long drawn murmur with Late Peaking =>severe

4. presence of S4 & absence of A2 => severe

4. AORTIC REGURGITATION
 Peripheral signs of Aortic Regurgitation

1. lighthouse sign – alternate flushing & blanching of forehead

2. landolfi’s sign – change in papillary size inaccordance to cardiac cycle and not
related to light
3. de musset sign – head nodding with each heart beat
4. mullers sign – pulsatin uvula
5. quinke sign – capillary pulsation
6. Corrigan sign – dancing carotids
7. water hammer pulse – collapsing pulse
8. pulsus bisferians – double peaking pulse, both peaks in systole
9. traube sign – pistol shot sound over femoral artery
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10.durozeiz sign - systolic murmur heard over femeral artery with proximal
compression and diastolic murmer with distell compression
11. hill signs – popliteal cuff systolic BP exceeds brachial cuff pressure by >20
mmHg

< 20 mmHg Normal

20 to 40 mmHg Mild AR

40 to 60 mmHg Moderate AR

> 60 mmHg Severe AR

12.Bosenbach sign – pulsatile liver

13.Grehadt sign- pulsatile spleen
14.Becker sign – retinal arteriolar pulsation

 Cardiovascular findings
 Large volume pulse
 High Systolic BP with very Low Diastolic BP
 Hyperdynamic Apical Impulse
 Heart sounds – Soft S1 + presence of S3
 EDM
o high pitched, blowing, decrescendo, early diastolic murmur
o well heard in aortic area & Erb’s area
o patient sitting & leaning forward
o breath held in expiration

 Assessment of severity
1. Marked peripheral signs
2. Bisferians pulse
3. Hill’s sign >60 mmhg
4. Duration of Murmur – occupying > 2/3 rd of the Diastole
5. Austin flint murmur

Assessment of dominant lesion in presence of combined AS & AR

Positive signs For AR & For AS
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Peripheral signs / Peripheral signs Slow rising pulse

slow rising pulse
Pulse pressure Wide Narrow
Systolic thrill in Absent Present
Aortic area
BP High systolic BP & low Systolic Decapitation
diastolic BP

5. Ventricular Septal Defect (VSD)

 Palpitation, Dyspnoea on exertion, Frequent respiratory infections
 Normal / wide pulse pressure
 Hyperdynamic precordium with systolic thrill in left 3rd & 4th ICS
 S1 & S2 masked by murmur at the left sternal border
 Wide split S2 with variable attenuation of P2
 S1 may be heard at the apex
 PSM over left Para sternal area, not conducted to axilla
 Flow MDM may be heard over apex
Comparison of murmurs of MR, TR & VSD
Features MR TR VSD
Best heard Apex Tricuspid area Left para-asternal area
Thrill Rare Absent Common
Conduction Axial and back Not conducted Absent
Character Soft blowing Soft blowing Rough harsh
Relation to Expiration in lying Inspiration in sitting Unrelated
respiration position
Associated LV hypertrophy RV hypertrophy Biventricular
features Soft S1 Signs of Pulmonary HT hypertrophy
Low volume S3 Elevated JVP – “v” Apical MDM

Symptoms & signs of

ASD PDA Tetrology of Fallot
1. Symptoms Generally Symptomatic since Symptomatic since
asymptomatic childhood childhood, Anoxic spells,
Palpitation, Effort Dyspnoea on exertion,
intolerance, Frequent chest Exercise intolerance,
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infections squatting episodes,

2. Impulse Left parasternal Hyperkinetic LV apical -
impulse
3. S1 Normal / accentuated Accentuated Normal
4. S2 Wide & Fixed split Narrow / paradoxically spit Single S2
with PHT fixity
maintained but
becomes narrow
5. Thrill Usually no thrill Systolic / continuous thrill Usually no thrill
over left 2nd ICS /
Infraclavicular area
6. Murmurs ESM in left 2nd & 3rd Continuous murmur masking ESM in pulmonary area
ICS S2
Flow MDM may be Flow MDM may be heard in
heard apical area
7.Associated MR may be heard With development of PHT Cyanosis, clubbing
Signs Mild cardiomegaly diastolic componnt slowly
gets diminished with
accentuated P2