Free USMLE Step 2 CK Cardiology practice questions

This man has chronic aortic regurgitation. The murmur is an early diastolic, high-pitched decrescendo murmur at the left sternal border, accentuated by sitting forward in end-expiration. Chronic volume overload produces a large stroke volume ejected into a leaky aorta, causing a wide pulse pressure (here 122 mm Hg) and the peripheral signs that follow from it: bounding water-hammer (Corrigan) pulses, head bobbing (de Musset sign) and nail-bed pulsations (Quincke sign). The dilated, eccentric hypertrophied ventricle displaces the apical impulse laterally. The apical mid-diastolic rumble is the Austin Flint murmur, caused by the regurgitant jet striking the anterior mitral leaflet and producing functional mitral obstruction. Echocardiography should follow to quantify severity and measure LV ejection fraction and end-systolic dimension, which guide timing of surgery.

A. Mitral stenosis causes an apical diastolic rumble, but it follows an opening snap, is accompanied by a loud S1, and does not produce a wide pulse pressure or bounding pulses; the rumble here is an Austin Flint murmur.

B. Patent ductus arteriosus can widen the pulse pressure, but its murmur is continuous and machinelike at the left infraclavicular area, not purely diastolic.

C. Pulmonic regurgitation causes an early diastolic murmur at the left upper sternal border that increases with inspiration and is usually due to pulmonary hypertension; it does not cause peripheral signs of wide pulse pressure.

E. Aortic stenosis produces a systolic crescendo-decrescendo murmur and a narrow pulse pressure with a weak, delayed carotid upstroke.

This is pulseless electrical activity (PEA), and the bedside clues point to massive pulmonary embolism: recent orthopedic surgery with immobilization and held prophylaxis, sudden dyspnea before collapse, distended neck veins with clear, equal breath sounds, and ultrasound showing an acutely dilated right ventricle with septal shift and an underfilled left ventricle and no effusion. In PEA the cause is the treatment; for suspected or confirmed PE during arrest, systemic thrombolysis is reasonable (with CPR continued for 60 to 90 minutes after the lytic is given), and surgical or catheter embolectomy are options in experienced centers.

A. Cardiac tamponade also causes PEA with distended neck veins, but the ultrasound shows no pericardial effusion; tamponade typically follows cardiac surgery, trauma, malignancy, or dissection.

B. Tension pneumothorax causes distended neck veins with absent breath sounds on one side and tracheal deviation; her breath sounds are equal and the trachea is midline.

D. Hypovolemia from hemorrhage causes PEA with flat neck veins and a small, hyperdynamic or empty heart on ultrasound, the opposite of these findings.

E. Acute myocardial infarction more often presents with chest pain and VF or a regional wall motion abnormality of the left ventricle; isolated right ventricular dilation with clear lungs after immobilization points to PE.

This man has subclavian steal physiology: a high-grade proximal left subclavian stenosis with retrograde left vertebral flow, a 28-mm Hg systolic gap between the arms, and a weak left radial pulse. Reversed vertebral flow is often found incidentally, and most such patients never develop symptoms because the circle of Willis compensates. Because he has no vertebrobasilar symptoms and no disabling arm claudication, revascularization is not indicated. He does, however, have atherosclerotic disease in a major arterial bed, which marks a high risk of myocardial infarction and stroke. Management is guideline-directed risk-factor modification: antiplatelet therapy with aspirin (or clopidogrel), a high-intensity statin, smoking cessation, diabetes control, and blood pressure treatment. Revascularization by stenting or carotid-subclavian bypass or transposition is reserved for disabling arm claudication, vertebrobasilar attacks, coronary-subclavian steal in a patient with a left internal mammary artery graft, or the need to protect inflow before planned coronary bypass or dialysis access.

B and C. Endovascular and open revascularization carry procedural risk and are not justified for an asymptomatic steal; either becomes appropriate if disabling symptoms develop. D. Warfarin has no role in atherosclerotic subclavian stenosis without another indication and adds bleeding risk. E. Blood pressure must be measured and treated using the higher-reading arm, here the right arm; titrating to the falsely low left-arm readings would leave him undertreated.

This patient's HEART score is low. History is moderately suspicious (1 point: nonexertional pressure with some anginal features), the ECG shows a nonspecific repolarization change (1), age is under 45 (0), she has one risk factor, smoking (1), and troponin is normal (0), for a total of 3. With a score of 0 to 3 and negative serial high-sensitivity troponins obtained on a validated 0/2-hour pathway, her risk of a major adverse cardiac event over the next 30 days is about 1 to 2%.

The 2021 AHA/ACC chest pain guideline classifies such patients as low risk and recommends discharge with outpatient follow-up without urgent or routine pre-discharge diagnostic testing. Testing in this group produces many false-positive results, downstream invasive procedures, radiation and cost without improving outcomes. Smoking cessation counseling and primary care follow-up are appropriate, with return precautions for recurrent or exertional symptoms.

B. Observation with a stress test before discharge is appropriate for an intermediate HEART score (4 to 6), not for a score of 3 with negative troponins. C. Coronary CT angiography is a good choice for intermediate-risk patients without known coronary disease, but routine testing adds little in low-risk patients. D. Early invasive angiography is reserved for a high HEART score (7 or more), a dynamic troponin diagnostic of NSTEMI, or ongoing ischemia. E. Prolonged telemetry monitoring is indicated for arrhythmia concerns or ongoing ACS evaluation and is unnecessary once ACS has been excluded.

The ECG shows multifocal atrial tachycardia (MAT): an irregular rhythm above 100/min with at least three P-wave morphologies, varying PR intervals and an isoelectric baseline, which distinguishes it from atrial fibrillation. MAT arises from several automatic atrial foci driven by hypoxemia, hypercapnia, acidosis, beta-agonists, theophylline and electrolyte depletion, and it occurs mainly in older patients with acute pulmonary disease, as in this COPD exacerbation.

The cornerstone of management is to treat the underlying cause: titrated (controlled) oxygen to a saturation of 88% to 92%, inhaled bronchodilators, systemic glucocorticoids, antibiotics for a likely bacterial trigger, and ventilatory support if needed. IV magnesium (useful even with a low-normal level) and potassium repletion help suppress atrial automaticity. If the rate remains fast after correction of hypoxemia, verapamil or diltiazem (or a beta-1 selective blocker if there is no active bronchospasm) can be used.

A. Synchronized cardioversion is ineffective because MAT is driven by multiple automatic foci rather than a single reentrant circuit that a shock can reset. C. Adenosine causes only transient AV block, does not terminate MAT, and can provoke bronchospasm in a patient who is already wheezing. D. Digoxin is ineffective for rate control in MAT and its toxicity is promoted by hypoxemia and hypokalemia. E. MAT itself does not carry the thromboembolic risk of AF and does not require anticoagulation.

This man has Eisenmenger syndrome: a large unrepaired VSD caused pulmonary overcirculation that remodeled the pulmonary arterioles until pulmonary vascular resistance reached systemic levels and the shunt reversed. The clues are cyanosis, clubbing, a loud P2 with an RV heave, disappearance of the childhood murmur, secondary erythrocytosis and a fixed, nonreactive pulmonary vascular bed on catheterization. Defect closure is contraindicated. For symptomatic patients (WHO functional class II to III), the ACC/AHA adult congenital heart disease guideline recommends a pulmonary arterial hypertension-targeted therapy; the endothelin receptor antagonist bosentan is the agent with randomized evidence (BREATHE-5), improving exercise capacity and hemodynamics without worsening oxygen saturation. A phosphodiesterase-5 inhibitor such as sildenafil is an alternative or add-on. Liver enzymes are monitored monthly with bosentan, and it is teratogenic, a concern largely moot here but central in women.

A. Calcium channel blockers help only the small subset of PAH patients with a positive vasoreactivity test; he had none, and systemic vasodilation increases right-to-left shunting and can cause syncope.

B. ACE inhibitors lower systemic resistance, which worsens shunt reversal and cyanosis without improving pulmonary hemodynamics.

C. Hydroxyurea is used for sickle cell disease and myeloproliferative neoplasms; erythrocytosis in Eisenmenger syndrome is a compensatory response and should not be suppressed.

E. Routine anticoagulation is not recommended in Eisenmenger syndrome because of hemoptysis and bleeding risk; it is reserved for specific indications such as atrial fibrillation or thrombus.

This man has stable exertional angina (predictable, brief, relieved by rest, unchanged pattern) and needs a noninvasive test to confirm ischemia and stratify risk. Two features choose the test. First, his resting ECG is uninterpretable for ischemia: left ventricular hypertrophy with a repolarization (strain) pattern and more than 1 mm of resting ST depression means that further ST depression during exercise cannot be reliably attributed to ischemia. Other baseline abnormalities with the same implication are left bundle branch block, a paced rhythm, pre-excitation, and digoxin effect. Second, he can exercise well. When a patient can exercise but the ECG cannot be read, the recommended test is exercise with imaging, either stress echocardiography or nuclear perfusion imaging. Exercise is preferred over pharmacologic stress whenever possible because it adds prognostic information such as workload, heart rate response, and blood pressure response.

A. A plain exercise ECG relies on ST changes, which his baseline LVH with strain makes uninterpretable; a high false-positive rate would result.

C. Dobutamine stress echocardiography is reserved for patients who cannot exercise adequately; he walks miles a day.

D. Invasive angiography is appropriate after high-risk noninvasive findings or for angina refractory to medical therapy, neither of which is present yet.

E. Serial troponins are used to evaluate possible acute coronary syndrome; his pattern is stable, with no rest or crescendo symptoms, and troponin does not rise in stable angina.

Grip myotonia, distal weakness, early cataracts, frontal balding, temporal wasting, ptosis and a DMPK CTG expansion establish myotonic dystrophy type 1. Its main cardiac manifestation is progressive degeneration and fibrosis of the conduction system, and sudden cardiac death from complete heart block or ventricular tachyarrhythmia is a leading cause of death, often while the ejection fraction is still normal; his father's sudden death at 50 fits this. A PR interval above 240 ms and a QRS of 120 ms or more mark the highest-risk patients. Guidelines (2018 ACC/AHA/HRS bradycardia and conduction delay guideline and the 2017 ventricular arrhythmia guideline) recommend a yearly ECG for all patients, a low threshold for electrophysiologic study and permanent pacing (or an ICD when indicated) for progressive conduction disease, even before symptoms. This patient should be referred for electrophysiology evaluation now.

A is wrong because aortic root dilation and dissection are features of Marfan, Loeys-Dietz and Turner syndromes, not myotonic dystrophy. C is wrong because outflow obstruction is a feature of hypertrophic cardiomyopathy, which among neuromuscular diseases is associated with Friedreich ataxia. D is wrong because pericardial constriction is unrelated to this disorder. E is wrong because tricuspid regurgitation with pulmonic stenosis is the classic lesion of carcinoid heart disease.