Jawaban USMLE Cardiology Step 3

1. (C) The patient in question #1 is high risk for endocarditis given his aortic valve
replacement (remember prosthetic valves are quite susceptable to infection), fevers, murmur
of aortic insufficiency (which should not be present with a mechanical prostetic valve), and
elevated ESR. The ECG shown in question #1 shows normal sinus rhythm with a first degree
heart block (prolonged PR interval). This is usually the first sign of aortic valve abscess, thus
a transesophageal echocardiogram is appropriate to confirm the diagnosis. With prostetic
heart valves, transthoracic echocardiography is not sufficienct to exclude endocarditis. A
transthoracic echocardiogram is approriate if there is no prosthetic valve and the clinical
suspicion for endocarditis is low to intermediate.
The most common bacteria causing endocarditis soon after valve surgery is Staph aureus
whereas Strep species are more likely months to years after surgery. Aortic valve endocarditis
or regurgitation itself does not cause any ECG abnormality, however if an abscess develops
around the aortic valve annulus, it can compress and inflame the nearby AV node causing AV
nodal conduction disease. Remember that prolonged PR interval causes the first heart
sound to be soft since there is extra time the the mitral valve to close after atrial contraction,
thus is closes more slowly and with less force.

2. (B) The patient is question #2 presents with severe shock. His Swan-Ganz pressure
readings show a low cardiac output and elevated pulmonary capillary wedge pressure which
reflects elevated left ventricular pressures. This indicates cardiogenic shock. Late-stage septic
shock can actually appear similar when the heart begins to fail, however his presentation is
more acute and there is no sign of infection mentioned. This patient is most likely having a
large myocardial infarction causing left ventricular dysfunction and reduced cardiac output
leading to his hypotension. He must be taken emergently for cardiac catheterization to
revascularize the culprit coronary thrombosis according to the SHOCK trial.
Cardiac catheterization with stenting has been shown to be superior to thrombolytics in
patients with cardiogenic shock. Glycoprotein IIb/IIIa inhibitors are used for non-ST segment
elevation myocardial infarctions, but the new left bundle on the ECG means we should treat
this patient like an ST elevation MI (may indicated left main thrombosis). Inotropes could
sometimes be helpful to stimulate inotropy and cardiac output, however this can worsen
ongoing myocardial ischemia as well. Below is a table that summarizes the three causes of
shock, their hemodynamic abnormalities, and the treatment which is targeted at the primary
abnormality causing the shock. Remember septic shock is from massive release of cytokines
causing vasodilation and in hypovolemic shock you get massive vasoconstriction from
catecholamines.
3. (C) The ECG provided shows complete heart block (aka 3rd degree heart block) which is
an irreversible condition which results in very slow heart rates and thus reduced cardiac
output. Symptoms may include dizziness, weakness, and syncope. Note the P waves and the
QRS complexes each going at their own rate. This is known as "AV dissociation" and is a
hallmark of complete heart block. On occasion, the P wave lands on or just after the QRS
complex. Physiologically, this results in the atrium contracting at the same time as the
ventricles. Then the right atrium contracts at the same time as the right ventricle (when the
tricuspid valve is closed), the atrial blood will be forcefully ejected backwards into the
jugular veins resulting in "cannon A waves". Recall that a prolonged PR interval causes a soft
S1 heart sound (see S1 heart sound review). Since the PR intervals are varying in complete
heart block, there will be varying intensity of the S1 heart sound.
Since 2nd degree type II AV block and compete heart block are inherent problems "below the
AV node" meaning in the His Purkinje system, stopping any AV blocking medications (such
as beta-blockers or non-dihydropyridinecalcium channel blockers) will have no effect. Recall
that the AV node itself is influenced by sympathetic and parasympathetic input, however the
His Purkinje system is not, thus AV nodal blocking medications can cause 1st degree AV
block and 2nd degree type I (which are blocks within the AV node itself), but not 2nd degree
type II or 3rd degree (which are inherent, irreversible conduction disease in the His Purkinje
system). Thus, a pacemaker is indicated in this case. A defibrillator is used to treat life-
threatening ventricular arrhythmias such as ventricular tachycardia and ventricular fibrillation
which we have no indication that our patient has.

4. (D)
This case is a classic presentation of subacute endocarditis. Some pathogens are more
aggressive than others and can actually present with septic shock such as Staph aureus and
Pseudomonas auriginosa. Candidal endocarditis is rare in immunocompetent persons and the
vegetation seen are quite large (usually > 1 cm). Streptococcus viridins group is the most
common cause of endocarditis and presents in a subacute fashion (similar to Enterococcus
endocarditis). Specifically, Streptococcus bovis (a type of Strep viridins) is strongly
correlated with active colon cancer, thus if blood cultures were indeed positive for this
organism, a colonoscopy should be performed at some point. Remember that the anterior
leaflet of the mitral valve is the most common site for endocarditis. The holosystolic murmur
at the apex likely represents mitral regurgitation due to valve destruction by the organism.
Treatment includes at least 4-6 weeks of IV antibiotics which include penicillins or a third
generation cephalosporin for Strep viridins, the combination ampicillin plus gentamicin for
Enterococcus, nafcillin or oxacillin for penicillin sensitive Staph aureus, and vancomycin
plus gentamicin for methacillin resistant Staph aureus (MRSA).

5. (C) Hypertrophic obstructive cardiomyopathy or HOCM (previously called IHSS or

idiopathic hypertrophic subaortic stenosis) is the most common cause of sudden cardiac
death in young athletes. HOCM is associated with mostly exertional symptoms. During
exercise (when the heart contracts harder), the asymmetrically hypertrophied interventricular
septum obstructs blood from flowing out of the aortic valve resulting in a markedly reduced
cardiac output. This leads to dizziness and syncope. Life threatening ventricular arrhythmia
such as ventricular tachycardia also occur which can cause syncope. The murmur of HOCM
can mimic that of aortic valve stenosis: a mid-systolic crescendo-decrescendo murmur heard
at the right upper sternal border. The main differences that the murmur of HOCM increases in
intensity with Valsalva (due to decreased left ventricular volume/chamber size allowing more
obstruction to occur).

A defibrillator is indicated in any HOCM patient with syncope, documented ventricular

arrhythmias, a family history of sudden cardiac death, interventricular septal thickness of >
30 mm or systolic dysfunction. Medical management includesbeta-blockers or verapamil to
prolong diastole and improve left ventricular filling resulting in less obstruction. Dehydration
leads to reduced preload and less left ventricular filling which can worsen obstruction, this
diuretics are contraindicated. Exercise should be completely restricted.

6. (B) The patients clinical scenario and ECG findings are consistent with left ventricular
(LV) aneurysm. A left ventricular aneurysm is a complication of an anterior wall myocardial
infarction that can cause significant clinic issues includingcongestive heart failure, ventricular
arrhythmias, left ventricular thrombus formation, and left ventricular rupture leading
to cardiac tamponade. To diagnose a LV anuerysm on ECG there must be ST segment
elevation anywhere from lead V1 to lead V4 and a history of a previous anterior wall
myocardial infarction more than 6 weeks prior. The acute ECG changes seen with an anterior
wall myocardial infarction can linger for up to 6 weeks, thus an LV aneurysm is not able to
be diagnosed before then. Treatment of an LV aneurysm includes surgical resection known as
the "Dorr procedure".
In pericarditis there would be diffuse ST segment elevation (concave upward) and PR
depression. Early repolarization should "J point elevation" and occurs most commonly in
young healthy people. Cardiac tamponade is not able to be diagnosed on ECG, although you
may see low voltage due to the pericardial effusion dampening the ECG signal or "electrical
alternans" due to the heart wobbling in the pericardial effusion causing every other beat to be
dampened.

7. (D) There are only 3 causes of holosystolic murmurs: mitral regurgitation, tricuspid

regurgitation, and a ventricular septal defect. A small ventricular septal defect is quite benign
and can cause a very loud holosystolic murmur with a thrill. Think of a putting your thumb
over water coming out of a hose causing it to spray at high velocity (causing turbulence and a
loud murmur) versus not putting your thumb over the hose (causing little turbulence and a
soft murmur). Due to the loud murmur, a small VSD is frequently mistaken for significant
pathology. VSD closure is indicated for patients with symptoms or with a shunt fraction (aka
Qp/Qs or ratio of flow through the pulmonic valve to that through the aortic valve) of 1.5:1 or
greater.
In a patient with mitral regurgitation you would expect to hear a click of mitral valve
prolapse present or for there to be a history of other heart disease which may cause mitral
regurgitation (such as a previous inferior wall myocardial infarction). The murmur is
typically located at the cardiac apex and not the left lower sternal border. Symptoms of
congestive heart failure may also be present.
While the murmur of tricuspid regurgitation is heard best at the left lower sternal border
similar to a VSD, it should get louder with inspiration (Carvallo's sign). Also, tricuspid
regurgitation would result in significant "V waves" in the jugular venous pulsation due to
backward flow from the right ventricle into the jugular vein with each heart beat. Finally, it
would be very rare for isolated tricuspid regurgitation to occur in a young otherwise healthy
person.
The murmur of a patent ductus arteriosus is a continuous "machinary" murmur last is in both
systole and diastole (since the systolic and diastolic pressure in the aorta is always higher
than the systolic and diastolic pressure in the pulmonary artery causing continuous flow).

8. (A) This patient has Wolff-Parkinson-White syndrome (WPW) which occurs when an

abnormal conduction pathway connects the atrium directly to the ventricles allowing
conduction to bypass the AV node at times. This abnormal pathway is termed an "accessory
pathway" or a "bypass tract". The typical ECG finding of WPW is a short PR interval and a
"delta wave". A delta wave is slurring of the upstroke of the QRS complex. This occurs since
the action potential from the SA node is able to conduct to the ventricles very fast through the
accessory pathway, so the QRS occurs immediately after the P wave making the delta wave.

Ablation to eliminate the accessory pathway is indicated for any symptomatic patient with
WPW and tachyarrhythmias, however observation is an acceptable alternative. Medications
that block the AV node such asbeta-blockers, non-dihydropyridine calcium channel blockers,
and digoxin should be used with caution since, by blocking AV nodal conduction, allow more
conduction through the bypass tract and if the patient were to developatrial
fibrillation or atrial flutter, so many atrial action potentials can reach the ventricles via the
bypass tract that ventricular fibrillation can develop resulting in death. Remember the typical
board question of a patient with WPW presenting with atrial fibrillation and hypotension. The
answer is to give procainamide and NOT beta-blocks or calcium channel blockers.

9. (D) The patient in question #9 is clearly suffering from chest pain due to myocardial
ischemia. Since the pain occurred at rest and she has no prior history of heart disease, then
she has unstable angina. Remember that there are three categories of acute coronary
syndromes: unstable angina (UA), non-ST segment elevation MI (NSTEMI), and ST segment
elevation MI (STEMI). Also recall that there are 3 different patient presentations that can be
classified into unstable angina:
1. New onset cardiac chest pain (even if it gets worse with exertion and better with rest, the
first time it occurs it is considered UA)
2. Cardiac chest pain at rest without ST elevation on the ECG and with negative cardiac
biomarkers (troponin)
3. Worsening of known stable angina (used to be able to walk 1 block before getting chest
pain and can now only walk 1/2 block). ECG findings in unstable angina can vary from a
normal ECG to dramatic ST segment depressions.
A non-ST segment elevation myocardial infarction (NSTEMI) occurs when a patient
experiences chest pain from myocardial ischemia and the serum biomarkers of myocardial
necrosis (troponins) are significantly elevated despite not showing ST segment elevation on
the ECG. Findings on ECG in a NSTEMI can vary from a normal ECG to dramatic ST
segment depressions like in UA.
A ST segment elevation myocardial infarction (NSTEMI) occurs when a patient experiences
chest pain from myocardial ischemia, the serum biomarkers of myocardial necrosis
(troponins) are significantly elevated, and ST segment elevation is seen on the ECG.
While cardiac catheterization is reasonable to pursue at some point, there is no indication for
emergent cardiac catheterization since there is ST segment elevation. Glycoprotein IIb/IIIa
inhibitors are not indicated as a part of medical management of unstable angina, however
they can be used in NSTEMI patients. Nitroglycerine is used in acute coronary syndromes for
chest pain relief or control of blood pressure and our patient requires neither.

10. (C) There are three common heart rhythm disorders that cause an irregularly irregular
rhythm: Atrial fibrillation, atrial flutter with variable conductance and multifocal atrial
tachycardia (MAT). With atrial fibrillation, no discrete P waves can be seen, however
sometimes coarse "fibrillitory waves" are present. In atrial flutter a "sawtooth" pattern is seen.
In MAT there are at least 3 distinct P wave morphologies present.
Our patient had been drinking alcohol heavily which resulting in his atrial fibrillation. This is
known as "holiday heart" as it frequently occurs in people who do not commonly drink then
binge on a certain occasion. Treatment for atrial fibrillation is aimed at controlling the
ventricular rate versus restoring sinus rhythm and anticoagulation (based on theCHADS 2
score or CHADS 2 Vasc score). Emergent cardioversion is not needed since he is not
hemodynamically unstable. Amiodarone is not 1st line therapy in a person with a normal
structural heart. If rhythm control is needed in this situation then other antiarrhythmic
drugs such as flecainide, sotalol, or propafenone can be used. Diltiazem IV in the short term
will control the ventricular rate. Frequently in holiday heart, normal sinus rhythm returns
spontaneously and if it does not, chemical (using ibutelide or flecainide) versus electrical
cardioversion can be done safely within 48 hours of onset. After 48 hours a transesophageal
echocardiogram would be needed to confirm that no left atrial appendage clot is present
before cardioversion.