Cardiovascular Medicine Flashcards

A 58-year-old man with hypertrophic obstructive cardiomyopathy (HOCM) presents with worsening exertional syncope. Echo shows a resting LVOT gradient of 55 mmHg. He is already on metoprolol 200 mg/day. Which of the following interventions is MOST appropriate at this stage?

Answer: Add disopyramide to his current regimen

Disopyramide is a class IA antiarrhythmic with strong negative inotropic properties that reduces LVOT obstruction in HOCM. When a maximally tolerated beta-blocker fails to adequately control symptoms or LVOT gradient, adding disopyramide is the preferred pharmacologic escalation before considering invasive therapies (septal myectomy or alcohol septal ablation). Verapamil is an alternative to beta-blockers but should not be combined with them due to risk of heart block and hypotension. Digoxin is contraindicated in HOCM as it increases inotropy, worsening obstruction. Diuretics reduce preload and can dangerously worsen obstruction in HOCM.

A 72-year-old woman undergoes right heart catheterization. Results: RA 8 mmHg, RV 42/10 mmHg, PA 42/22 mmHg (mean 30 mmHg), PCWP 18 mmHg, cardiac output 4.2 L/min. What is the pulmonary vascular resistance (PVR) and the correct classification of her pulmonary hypertension?

Answer: PVR ≈ 2.9 Wood units; combined pre- and post-capillary pulmonary hypertension

PVR = (mean PA pressure − PCWP) / CO = (30 − 18) / 4.2 ≈ 2.86 Wood units. A PVR ≥ 3 Wood units defines a pre-capillary component. Her PCWP of 18 mmHg (>15 mmHg) indicates post-capillary hypertension (elevated left-sided filling pressures). However, the diastolic pressure gradient (DPG = diastolic PA pressure − PCWP = 22 − 18 = 4 mmHg; 20 mmHg, PCWP >15 mmHg, and PVR ≥2 WU classifies as combined pre- and post-capillary PH (CpcPH), reflecting intrinsic pulmonary vascular remodeling on top of left heart disease.

A 45-year-old woman with systemic lupus erythematosus presents with progressive exertional dyspnea. Echo shows preserved EF, impaired relaxation, and a pericardial effusion. Right heart catheterization demonstrates equalization of diastolic pressures across all four chambers (within 5 mmHg of each other). During inspiration, her systolic BP drops from 118 to 98 mmHg. Which hemodynamic finding would BEST distinguish constrictive pericarditis from cardiac tamponade in this patient?

Answer: Kussmaul sign on physical exam

Kussmaul sign — a paradoxical rise (or failure to fall) in jugular venous pressure with inspiration — is classically associated with constrictive pericarditis, not tamponade. In tamponade, venous return increases with inspiration but the fixed pericardial volume prevents RV filling, so JVP falls normally or exaggerates. In constriction, the thickened pericardium prevents the RV from accommodating increased venous return, causing JVP to rise with inspiration. Pulsus paradoxus occurs in both conditions. A prominent y-descent is characteristic of constrictive pericarditis (rapid early ventricular filling then abrupt halt — 'square root sign'), while tamponade blunts the y-descent. Equalization of diastolic pressures occurs in both.

A 63-year-old man with known coronary artery disease presents with chest pain. ECG shows new ST elevations in leads V1–V4. He is taken for emergent PCI. Angiography reveals a total occlusion of the proximal LAD. After successful recanalization, the patient develops progressive hypotension and hypoxia. Repeat echo shows new severe right ventricular dilation and paradoxical septal motion. Which mechanism BEST explains the hemodynamic compromise?

Answer: Ventricular interdependence causing LV underfilling from acute RV failure

The proximal LAD supplies the RV free wall via the right ventricular branches (especially the first diagonal and septal perforators). Acute proximal LAD occlusion can cause concomitant RV infarction. The dilated, failing RV shifts the interventricular septum leftward into the LV cavity (paradoxical septal motion), physically restricting LV filling — this is ventricular interdependence. The shared pericardial space means the dilated RV compresses LV diastolic volume, reducing preload and CO. Management requires volume loading to maintain RV preload, avoidance of vasodilators, and consideration of mechanical support. This is distinct from no-reflow (which causes persistent ST elevation but not the echo findings described), MR (which would show a flail leaflet), or pulmonary edema (which would cause LV dysfunction signs).

A 51-year-old woman is referred for evaluation of a diastolic murmur. Echo reveals a severely calcified aortic valve with a mean gradient of 20 mmHg and an AVA of 0.85 cm². However, her LVEF is 25% and stroke volume index (SVI) is 30 mL/m². Low-dose dobutamine stress echo is performed. With dobutamine, AVA increases to 1.1 cm² and the mean gradient increases to 30 mmHg. Which of the following best characterizes her condition?

Answer: Pseudo-severe aortic stenosis (low-flow artifact)

This is a classic presentation of pseudo-severe or paradoxical low-flow, low-gradient aortic stenosis. In true severe AS, the valve area is fixed and does not change significantly with increased flow. When the AVA increases to ≥1.0 cm² with dobutamine (reflecting a flow-dependent reduction in calculated area at low states), this suggests the baseline low AVA was a calculation artifact of low transvalvular flow, not true anatomic stenosis. True severe AS with contractile reserve would show a persistent small AVA with an increasing gradient. The AVA normalizing to >1.0 cm² with dobutamine is the key discriminator. These patients often benefit from medical optimization rather than valve replacement.

A 38-year-old competitive marathon runner presents with recurrent pre-syncope during peak exertion. His resting ECG shows sinus bradycardia at 42 bpm, early repolarization in inferior and lateral leads, and T-wave inversions in V1–V3. Cardiac MRI shows mild RV dilation (RV end-diastolic volume index 114 mL/m²) with a small area of subepicardial late gadolinium enhancement at the RV insertion points. 24-hour Holter shows 850 PVCs with LBBB morphology and inferior axis. Which diagnosis MOST warrants urgent evaluation?

Answer: Arrhythmogenic right ventricular cardiomyopathy (ARVC)

This clinical picture meets multiple 2010 Task Force Criteria for ARVC: (1) minor structural criterion — mild RV dilation (RVEDVI 114 mL/m²; major >110 in women, this is borderline minor), (2) minor repolarization criterion — T-wave inversions V1–V3 in absence of RBBB, (3) minor depolarization criterion — late potentials potentially, and (4) minor arrhythmia criterion — LBBB-morphology PVCs (>500/24h) with inferior axis (superior RVOT vs inferior free wall axis must be distinguished). RV insertion point LGE is an early ARVC finding. RVOT tachycardia would have PVCs with superior axis (LBBB + superior axis), not inferior. Athlete's heart does not explain T-wave inversions in V1–V3 or LGE. Brugada shows a distinct coved ST pattern. ARVC is a primary ion channelopathy/desmosomal gene disorder that is a leading cause of SCD in young athletes, and competitive exercise accelerates disease progression — advising cessation of competitive sport is critical.