Heart Murmurs USMLE Questions: 12 Valvular Heart Disease MCQs with Answers

This is classic aortic stenosis: a crescendo-decrescendo systolic ejection murmur loudest at the 2nd right intercostal space that radiates to the carotids. The narrow valve limits cardiac output, especially during exercise, so less blood reaches the brain and the patient faints. The three classic symptoms are syncope, angina and heart failure (remember “SAD”: Syncope, Angina, Dyspnea).

Why the other options are wrong:

• Mitral stenosis causes a diastolic rumble at the apex.
• Mitral regurgitation causes a holosystolic murmur at the apex that radiates to the axilla.
• Aortic regurgitation causes an early diastolic murmur.
• Pulmonic stenosis is heard at the 2nd left intercostal space and does not radiate to the carotids.

This is aortic stenosis. The left ventricle must push against a narrow valve, so it responds to the pressure overload with concentric hypertrophy (a thick wall with a normal or small cavity). Volume overload, as in aortic or mitral regurgitation, causes eccentric hypertrophy (a dilated cavity) instead.

Why the other options are wrong:

• A boot-shaped heart on chest X-ray is the sign of tetralogy of Fallot.
• A large pericardial effusion gives a “water-bottle” heart and muffled heart sounds.
• Right ventricular hypertrophy comes from pulmonary hypertension or pulmonic stenosis, not aortic stenosis.

In patients over about 70, the most common cause is age-related calcification of a normal three-leaflet valve (dystrophic calcification with normal serum calcium). In younger patients (under about 60), think of a bicuspid aortic valve, which calcifies earlier. Worldwide, rheumatic heart disease is also an important cause.

Why the other options are wrong:

• Bicuspid aortic valve causes aortic stenosis at a younger age and is linked to Turner syndrome and coarctation.
• Amyloidosis causes restrictive cardiomyopathy, not valve stenosis.
• Myocardial infarction can cause mitral regurgitation (papillary muscle rupture), not aortic stenosis.

Normally the aortic valve closes first (A2), then the pulmonic valve (P2), and the split widens on inspiration. In aortic stenosis and left bundle branch block, the left ventricle empties late, so A2 comes after P2. The split then narrows on inspiration and widens on expiration, which is “paradoxical.”

Why the other options are wrong:

• Atrial septal defect causes fixed splitting that does not change with breathing.
• Pulmonic stenosis and right bundle branch block delay P2 and cause wide splitting.

Aortic valve replacement (surgical or transcatheter, TAVR) is the only definitive treatment. Once symptoms such as syncope, angina or heart failure appear, survival drops sharply without valve replacement.

Why the other options are wrong:

• Balloon valvuloplasty gives only short-term relief because the valve narrows again; it is used as a bridge in very sick patients.
• Diuretics such as furosemide and hydrochlorothiazide lower preload, which can drop cardiac output and cause hypotension in aortic stenosis.

Hypertrophic cardiomyopathy (HCM) is an autosomal dominant disease of the sarcomere (often β-myosin heavy chain) with a thick interventricular septum that blocks the outflow tract. It is the most common cause of sudden cardiac death in young athletes. The murmur gets louder with Valsalva and standing (less preload) and softer with squatting and handgrip. Treatment includes β-blockers, avoiding dehydration and intense exercise, and an ICD for high-risk patients.

Why the other options are wrong:

• Aortic stenosis is rare at 19 (unless bicuspid) and its murmur radiates to the carotids.
• Mitral stenosis causes a diastolic murmur.
• Myocardial infarction does not cause this murmur in a healthy 19-year-old.

Mitral valve prolapse (MVP) gives a mid-systolic click followed by a late systolic murmur. Standing lowers preload, so the click comes earlier and the murmur gets longer; squatting does the opposite. Most patients have no symptoms. It is the most common valve lesion and is linked to Marfan syndrome, Ehlers-Danlos syndrome and polycystic kidney disease. Echocardiography confirms it.

Why the other options are wrong:

• Mitral stenosis causes an opening snap and a diastolic rumble.
• Aortic stenosis causes an ejection murmur at the 2nd right intercostal space.
• Tricuspid regurgitation is holosystolic and louder with inspiration.
• Dilated cardiomyopathy causes heart failure symptoms and an S3.

Dilation of the aortic root is the most dangerous complication of Marfan syndrome (fibrillin-1 defect), because it can lead to aortic dissection and aortic regurgitation. β-blockers lower heart rate and the force of ejection, which slows aortic dilation. The ARB losartan is an accepted alternative. The click in this patient comes from mitral valve prolapse, which is common in Marfan syndrome.

Why the other options are wrong:

• Lisinopril and verapamil are not the standard choice to slow aortic root growth.
• Furosemide is a diuretic and has no effect on aortic dilation.

Mitral stenosis causes an opening snap (the stiff valve snapping open in early diastole) followed by a low-pitched diastolic rumble at the apex, best heard with the bell in the left lateral position. A shorter time between S2 and the opening snap means more severe stenosis. The most common cause is rheumatic heart disease.

Why the other options are wrong:

• Aortic stenosis and pulmonic stenosis cause systolic ejection murmurs.
• Ventricular septal defect causes a holosystolic murmur at the left lower sternal border.

An irregularly irregular pulse means atrial fibrillation. Mitral stenosis raises left atrial pressure and stretches the left atrium, which is a classic cause of atrial fibrillation. These patients have a high risk of left atrial thrombus and stroke, so they need anticoagulation (warfarin is used in rheumatic mitral stenosis).

Why the other options are wrong:

• Dilated cardiomyopathy and left ventricular hypertrophy can also cause atrial fibrillation, but mitral stenosis is the classic exam answer because of the enlarged left atrium.
• Right ventricular hypertrophy is not a typical cause of atrial fibrillation.

Rheumatic heart disease follows group A streptococcal pharyngitis (molecular mimicry against M protein). It damages the mitral valve most often, then the aortic valve. Early disease causes mitral regurgitation; late disease causes mitral stenosis. Aschoff bodies and Anitschkow cells are seen on histology.

Why the other options are wrong: The tricuspid and pulmonic valves are rarely affected by rheumatic fever. The tricuspid valve is the classic valve in IV drug use endocarditis.

This is infective endocarditis in an IV drug user. Bacteria from the skin, most often Staphylococcus aureus, enter the venous blood and first reach the tricuspid valve. This causes tricuspid regurgitation: a holosystolic murmur at the left lower sternal border that gets louder with inspiration. Septic emboli to the lungs explain his cough and chest pain. Painless red spots on the palms and soles are Janeway lesions; painful nodules on the fingertips are Osler nodes.

Why the other options are wrong:

• Mitral valve involvement is more typical of subacute endocarditis from viridans streptococci on an already damaged valve.
• Stenotic lesions develop slowly over years, not in an acute infection.

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