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Cardiology Board Review

6.21.10
Lisa Rose-Jones, MD
CAD
MKSAP Q 1
 60 yo M present to ED w/ chest discomfort for 6
hrs. Tx w/ ASA, IV BB, and NTG. Chest pain
persists. Initial troponin and CK-MB are
elevated.
Pt taken ergently to Cath lab. Occlusion of prox
RCA. PCI is successfully. Following morning
doing well on rounds but progessively more
hypotensive. JVP elevated. Nml S1, S2. +S3,
brief systolic murmur along L sternal border.
ECG is unchanged from previous.
What is the most likely cause for this
patient’s current findings?

1. Acute Cardiac tamponade


2. Aortic dissection
3. Left Ventricular Free Wall Rupture
4. Right Ventricular MI
5. Progressive Coronary Ischemia
*Characteristic RV Infarction:
progressive hypotension (always be weary
of preload reducers like NTG), elevated
JVP, and clear lung fields. +tricuspid
regurg
~R precoridal Lead ECG will detect ST elev
in V4R
~These pt may require volume challenges
*Other MECHANICAL COMPLICATIONS
following MI:
~Ventricular Septal Rupture

~Papillary Muscle Rupture: hear acute mitral


regurg murmur

~LV Free Wall Rupture => cardiac


tamponade, hypotension and usually death
Q 23
57 yo M comes to ED w/ substernal chest pressure
that developed this AM. PMHx of HTN, stable
angina, PVD; his meds are HCTZ and ASA.
BP 110/80, HR 84. No JVP and lungs clear. Nml
S1/2. Abd exam neg, pulses diminished in LE.
Continues to have angina at rest. ECG w/
changing ST segs and T waves. Trop 0.8. The
patient is given ASA, BB, and enoxaparin, and is
transferred to the CCU to await angiography.
What additional therapy should be given in
the CCU?

1. Heparin
2. Warfarin
3. Eptifbatide
4. Bivalirudin
5. Diltiazem
Early treatment w/ Glycoprotein 2b/3a
receptor blockade improves outcomes of
PCI. *Indicated only if high risk markers
(TIMI Score >3-4, +biomarkers, ST
depression, CHF, h/o of recent PCI, or
hemodynamic instability.
-Abciximab =only if undergoing PCI
-Eptifibitide or Tirofiban (if there is no clear
inidication that PCI will be performed)

*Warfarin offers no protection for Coronary events. SYNERGY trial


showed Enoxaparin and Heparin outcomes nearly equivalent (unless
switch from LMWH -> UH). Dilitaizem doesn’t affect outcomes in
CAD.
Q 37
42 yo M @ rural ED w/ severe L shoulder &
chest pain, radiates to jaw. +diaphoresis,
dyspnea. No PMHx, no meds. +father has
CABG.
In the ED, IV Heparin, Atenolol, and an ASA
are given. BP 100/79, HR 61. No JVP.
Nml S1/2. This hospital does NOT have a
Cath lab, closest is 62 miles. Takes 2 hrs
to arrange transfer.
What is the BEST management option for
this patient?
1. Glycoprotein receptor blockade
2. Plavix
3. Esmolol
4. Fibrinolytic therapy
5. NTG
GOAL of all Reperfusion strategies for STEMI
is to achieve a patent vessel w/in 90
mins from onset of symptoms.

~4 subgroups in which PCI is preferred:


A. Contraindications of fibrinolytic therapy
B. Late arriving STEMI, > 12 hrs after onset
of chest pain w/ contd CP and ST elevs
C. H/O CABG
D. Cardiogenic Shock
REMEMBER for CAD:
 Reperfusion arrhythmias (AIVR) usually do
not req antiarrhytmics
 Do not need Cardiac Cath after Fibrinolysis
if ST seg elevation and CP have resolved
 Initial management of ACS related to
systemic process, tx the preciptating
factor 1st (ie pRBCs if GI bleeding)
 ASA allergic: give Plavix
HEART FAILURE
Q 13
55 yo M w/ CAD evaluated w/ 2 wks after
having an MI. D/C meds were: ASA,
Toprol, ISMN, Lisinopril, and Atorvastatin.
Echo revealed inferoposterior akinesis and
LVEF of 40%.
Exam: HR 60, BP 13-/70. JVP nml, lungs
clear. Regular s1/s2. Labs: K-5.7, Cr-1.0,
LDL-65. Lisinopril therapy stopped.
Which of the following medications should be
started in this patient?

1. Valsartan
2. Spironolactone
3. Amlodipine
4. Eplerenone
5. Hydralazine
SHF MEDS:
 ACEi (or if intolerant, ARB)
~will usually tolerate a K to 5.5

 B-blocker
 Hydralazine/Nitrate combo if can’t tolerate an
ACEi or ARB, or adding specifically if african-
american
 Spironolactone w/ NYHA class 3 or 4 symptoms
 Eplerenone (aldo receptor antag) is useful in
reduced EF after AMI
REMEMBER for HEART FAILURE:
 Digoxin alleviates Sx, reduceds
hospitalization 2/2 HF (not mortality)
 Diurese HF pt w/ volume overload 1st,
then beta block
 Put an AICD in a HF pt that comes in w/
unexplained syncope
 Put a Biventricular Device in HF pt on
optimal therapy w/ continued symptoms
and QRS > 120 ms
Arrhythmias
Q 14
23 yo presents w/ palpitations during
exercise. Healthy, no meds. Exam and
resting ECG nml. Stress test shows
sustained monomorphic V tach @ 201
/min. No iscemic changes until arrhythmia
developed. The V tach had a Left bundle
and infoerior axis morphology.
Terminated spontanesouly 7 mins into
rest. ECHO nml, MRI nml.
What is the most likely etiology of V tach in
this patient?
1. Coronary spasm
2. Idiopathic
3. Arrhythmogenic R ventricular
cardiomyopathy
4. Infiltrative heart disease
5. Anomalous origin of the coronary arteries
Idiopathic V Tach (no structural heart
disease) carries a good prognosis. Tx
symptoms, BB first line.

~Expect BP and ST segment elev w/ spasm.


Nml MRI/ECHO rule out infiltrative disease,
anomolaus coronaries, or arrhythogenic RV
cardiomyopathy (would see fatty
infiltration).
Q 38
 68 yo presents for routine eval. No
complaints other than lumbago. Active,
does yoga 3x/week. Meds include
Levothryoxine and HCTZ. Exam: HR 46.
On further questioning, she notes
palpitations during a yoga class. 24
Ambulatory monitoring reveals HR of 39-
82, avg of 45/min and occ pauses up to 2.9
sec. Nml TSH.
What is the BEST management option for
this patient?
1. Pacemaker implantation
2. Exercise stress test
3. Repeat 24 hr monitoring
4. Reassurance and Observation
ONLY when there is definitive
correlation b/w sinus bradycardia and
symptoms, is pacemaker warranted
Class I
1. 3rd degree heart block w/ one of following:
a. Bradycardia with symptoms
b. other medical conditions that require drugs that cause sx brady
c. Documented asystole 3.0 seconds or any escape rate <40 bpm in awake,
symptom-free patients.
d. After catheter ablation of the AV junction
e. Postoperative AV block that is not expected to resolve
f. Neuromuscular diseases with AV block

2. Second-degree AV block regardless of type or site of block, with associated symptomatic


bradycardia

Class IIa
1. Asymptomatic third-degree AV block w/ average awake ventricular rates of >/= 40
2. Asymptomatic type II second-degree AV block
3. Asymptomatic type I second-degree AV block at intra- or infra-His levels found incidentally at
electrophysiological study for other indications
4. First-degree AV block with symptoms suggestive of pacemaker syndrome and documented
alleviation of symptoms with temporary AV pacing
Q 43
68 yo F comes to the ED b/c of racing heart
for past 2 hrs. Reports 2 yr history of
similar episodes. Been told by PMDs in
past to cough/strain, usually works but not
today. No chest pain, no other cardiac
history.
Exam shows BP of 110/60, HR 165, RR 20.
Lungs clear. Carotids w/o murmurs,
attempt massage w/o effect. ECG is
shown.
Which is the drug of choice for terminating
this patient’s arrhythmia?
1. Metoprolol
2. Verapamil
3. Adneosine
4. Digoxin
Q 122
26 yo nurse is evaluated in the ED after
episode of syncope. While working
stressfull day in the ICU, developed
tachycardia and then LOC. +palpitations in
past
Exam wnl. CXR wnl. ECG initially
unremarkable. 10 mins later, developed
brief tachycardia. Repeat ECG shown.
What is the most likely diagnosis in this
patient?
1. Atrioventricular nodal reentrant
tachycardia
2. Accelerated Idioventricular tachycardia
3. Atrioventircular reentrant tachycardia
4. Multifocal atrial tachycardia
AVNRT: >50% of all SVTs. Circuit involves the
AV node, so atria and Ventricle activated
simultaneously. So “p” wave usually buried in
QRS.
AVRT: Circuit involves an accessory pathway.
Most orthodromic: travels anterograde down AV
node, retrograde up accessory path. Some pts
w/ pre-excitation phenomena: during SR, see
short PR interval and delta wave (evidence of
pre-excitation)= *WPW

=> ADENOSINE is DRUG of CHOICE,


however avoid if any evidence of pre-
excitation on ECG
REMEMBER:
 In healthy adults, PVCs at rest are common and not
cause for concern
 Procainamide is drug of choice in a preexcited A fib
 DC Cardioversion is 1st line for any unstable tachycardic
pt (hypotensive, signs of HF like diaphoresis, pulm
edema)
 REMEMBER your CHADS2 score, if >2 give warfarin
 For A FIB: 1st line is always rate control, only consider
antiarrhytmic or ablation if symptomatic from being in
controlled A fib
 A flutter often result of another acute process, consider
referral for ablation earlier as often difficult to rate
control
THE AORTA
Q 45
69 yo M presented to ED for acute onset of
substernal CP radiating to left arm.
+former smoker, h/o HTN
On exam: diaphoretic, BP of 210/95 mmHG
in R arm and 164/56 in L arm with HR 90.
There is dullness ½ way up R posterior
troax and 2/6 diasolic murmur at RUSB.
ECG shows 2-3 mm inferior ST seg
elevation.
Prior to additional diagnostic tests, which of
the following is the most appropriate
initial medication?
1. ASA
2. IV Heparin
3. Thrombolytic agent
4. Beta blocker
5. ACE inhibitor
AORTIC DISSECTION: disparate BPs b/w
arms, diastolic murmur of aortic regurg. Do
NOT given ASA, heparin, etc if suspect.
Initial treatment is w/ Beta Blockers to
decrease shear stress. Diagnostic tests
should be a TRANSESOPHAGEAL ECHO vs.
CHEST CT w/ CONTRAST.
`
Valvular Disease
Q 16
82 yo presents for annual exam. PMHx: HTN on
chronic BB. Denies all cardiac sx. Takes daily 1
mi walk, no change in exercise tolerance.
Exam shows: BP 136/86, HR 80. s1, single s2,
grade 3/6 early systolic murmur @ LUSB w/
radiation to carotids. 1+ peripheral edema. LDL
is 110. ECHO 2 yrs ago showed moderate
calcific aortic stenosis (velocity was 3.6, valve
area 1.2, gradient 30) with nml LV fxn. Now
ECHO shows jet velocity of 4.2, valve area of
1.0, and gradient of 44).
What is the most appropriate next step?

1. Reassurance
2. Begin a cardiac rehab program
3. HCTZ
4. Start statin therapy
5. Refer for Aortic valve replacement
Aortic Stenosis:
~Reassurance remains appropriate if asymptomatic
and nml exercise tolerance
~w/ severe stenosis the stiff valve doesn’t snap
shut, thus loose aortic component and get only a
single S2 (a physiologic split S2 has specificity of
72% of excluding severe AS)
~controling BP important, but use CAUTION w/ any
peripheral vasodilators b/c compensation in
Stroke Volume across a stenosed valve my be
difficult!!
~ Symptoms: Angina (5), Syncope (3), Heart
Failure (2)
Q 19
36 yo F in the ED w/ fever & dyspnea. 4 wks
of fever to 40C. +heroin use.
Exam: 39.6, 100/52, 70, 91% on RA. JVP
12. Bibasilar crackles. HR reg irregulsr. S1,
muffled s2. 2/6 diastolic murmur @ R 2nd
intercostal space. 1+ pretibial edema.
ECG shows a bifascicular block and Mobitz
II. ECHO shows 2 veges on aortic valve,
w/ leaflet perforation and severe AR.
Echoluceny in paravalvular region. Placed
on broad spectrum Abx.
What is the most appropriate treatment at
this time?
1. Esmolol IV
2. Heparin IV
3. Intraortic ballon pump (IABP)
4. Permanent pacemaker
5. Aortic Valve Replacement
Acute Aortic Regurgitation
 Whether from endocarditis or Aortic
dissection, this is a SURGICAL
EMERGENCY!
 Esmolol (short acting BB)can slow HR and
prolong diastolic filling to aid in forward
output in some pts w/ AR (this pt has sig
conduction abnml)
 IABP is CONTRAINDICATED in AR
Q 44
32 yo M comes in for annual exam. No
personal or fmHx of cardiac disease.
Exam: s1/s2, +s4, 2/6 crescendo-
decrescendo systolic murmur heard best
at LLSB w/o radiation to carotids.
Increased intensity w/ valsalva. Isometric
hand grip, passive leg raising decreases
the intensity. Rapid upstrokes of
peripheral pulses are present.
What is the most likely diagnosis?
1. Mitral Valve Prolapse
2. Hypertrophic cardiomyopathy
3. Atrial septal defect
4. Ventricular Septal Defect
5. Aortic Stenosis
Hypertrophic Cardiomyopathy
 If preload is increased (isometric hand grip,
stand-> squat) = increased systolic dimension of
LV and therefore less obstruction & diminished
murmur, Valsalva = decreased preload so
increased murmur
 Tx even asymptomatic pts w/ BB, avoid
strenuous exercise
 *different from hypertrophied athlete’s LV in
that septum is asymmetrically enlarged
REMEMBER:
 ECHO for any Diastolic Murmur,
Continuous murmur, or > grade 3/6
 Wide, Fixed split S2 think ASD
 Secundum ASD can be prepared
percutaneously

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