100+ Free FCP(SA) Part II Practice Questions

Explanation: The clinical presentation and cardiac catheterization oxygen step-up from 65% in the right atrium to 84% in the right ventricle confirm an acute post-infarction ventricular septal defect (VSD). Emergency mechanical stabilization with an intra-aortic balloon pump (IABP) combined with urgent surgical or percutaneous repair is required due to high mortality with conservative medical therapy alone. Fluid loading or pericardiocentesis is indicated for cardiac tamponade, not VSD.

Explanation: True severe low-flow, low-gradient aortic stenosis with reduced LVEF is diagnosed on dobutamine stress echocardiography when contractile reserve is demonstrated (stroke volume increases by >= 20%) and the mean gradient increases to >= 40 mmHg while the AVA remains <= 1.0 cm². If AVA increases above 1.0 cm² as flow increases, pseudo-severe aortic stenosis is present. Lack of stroke volume increase indicates absence of contractile reserve.

Explanation: Foundational quadruple therapy for HFrEF includes an ARNI (sacubitril/valsartan replacing an ACEi/ARB after a 36-hour washout), an evidence-based beta-blocker, a mineralocorticoid receptor antagonist (MRA such as spironolactone), and an SGLT2 inhibitor (dapagliflozin or empagliflozin). This combination significantly reduces all-cause mortality and heart failure hospitalizations. Digoxin and hydralazine/nitrates are second- or third-line options.

Explanation: Prosthetic valve infective endocarditis complicated by S. aureus infection, perivalvular abscess, conduction abnormality (new AV block), and heart failure constitutes a mandatory indication for emergency surgical intervention alongside systemic bactericidal antimicrobial therapy. Medical therapy alone is insufficient when perivalvular tissue destruction or invasive abscess formation is present.

Explanation: Primary prevention of sudden cardiac death (SCD) with an ICD in HCM is indicated when major risk factors are present, including maximal left ventricular wall thickness >= 30 mm, family history of premature SCD in a first-degree relative, unexplained syncope, non-sustained VT on Holter, or extensive late gadolinium enhancement (> 15% of LV mass) on cardiac MRI. Massive LVH (>= 30 mm) and family history independently confer high SCD risk.

Explanation: In patients with atrial fibrillation and moderate-to-severe rheumatic mitral stenosis or mechanical heart valves (valvular AF), Vitamin K antagonists (Warfarin targeting INR 2.0-3.0) remain the mandatory standard of care. Direct oral anticoagulants (DOACs like rivaroxaban, apixaban, and dabigatran) are contraindicated in moderate-to-severe rheumatic mitral stenosis due to lack of efficacy and increased thromboembolic risk in clinical trials.

Explanation: The patient presents with Beck's triad (hypotension, JVP elevation, muffled heart sounds) and electrical alternans, indicative of acute cardiac tamponade. Pulsus paradoxus—an abnormally large decrease in systolic blood pressure (> 10 mmHg) during normal inspiration—is a hallmark clinical finding resulting from ventricular interdependence within a non-compliant, fluid-filled pericardial sac.

Explanation: Cardiac sarcoidosis presents with heart block, ventricular arrhythmias, and heart failure. High-dose oral corticosteroid therapy (prednisone 40-60 mg daily) is the first-line disease-modifying treatment to suppress active granulomatous inflammation, preserve LV function, and prevent progression of conduction heart block.

Explanation: In patients with ischemic heart disease experiencing recurrent monomorphic VT storm refractory or recurrent despite antiarrhythmic drugs (amiodarone plus beta-blockers), emergency catheter ablation of the scar-related VT re-entry substrate significantly reduces VT recurrences and improves clinical outcomes.

Explanation: Peripartum cardiomyopathy (PPCM) is driven in part by prolactin cleavage into an anti-angiogenic and pro-apoptotic 16-kDa prolactin fragment. Addition of bromocriptine (a prolactin secretion inhibitor) to standard heart failure therapy leads to higher rates of full LV functional recovery. Prophylactic anticoagulation is mandatory when bromocriptine is given due to prothrombotic risk, and also because of her apical LV thrombus.