A physician-validated, board-style question from the Active Transport QBank. Try it, then check the reasoning for every option.
A 33-year-old woman schedules an appointment at an outpatient clinic for the first time after moving to the US from Peru a few months ago. She complains of easy fatigability and shortness of breath with minimal exertion for the past 6 months. She further adds that her breathlessness is worse when she goes to bed at night. She is also concerned about swelling in her legs. As a child, she says she always had sore throats. She does not smoke or drink alcohol. Medical records are unavailable, but the patient says that she has always been healthy apart from her sore throats. The blood pressure is 114/90 mm Hg, the pulse is 109/min, the respiratory rate is 26/min, and the temperature is 36.7°C (98°F). On examination, she is icteric with distended jugular veins. Bilateral basal crepitations are audible on auscultation of the lungs. Also, a high-pitched apical holosystolic murmur is audible that radiates to the left axilla. A transthoracic echocardiogram reveals mitral regurgitation with an ejection fraction of 25%. Treatment should focus on which of the following?
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A
Decrease total peripheral resistanceCorrect. afterload reduction decreases regurgitant fraction in mitral regurgitation, improves forward output, and is foundational therapy for systolic heart failure with reduced EF.
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B
Increase inotropy of cardiac muscleIncorrect. Increasing inotropy with positive inotropes (dobutamine, milrinone) is a short-term bridge for cardiogenic shock — long-term inotrope use worsens mortality in chronic systolic HF.
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C
Increase the rate of SA node dischargeIncorrect. Increasing SA node rate would worsen her already-elevated heart rate (109) and shorten diastolic filling, harming a failing heart.
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D
Increase coronary blood flowIncorrect. Increased coronary blood flow addresses ischemic disease — irrelevant to her valvular/heart-failure pathology from rheumatic mitral regurgitation.
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E
Increase preload to improve cardiac outputIncorrect. Increasing preload in a patient with mitral regurgitation and EF 25% would worsen pulmonary congestion and regurgitant volume — diuresis and afterload reduction are preferred.
↑ Tap an answer to reveal the reasoning
Answer: A. A young woman with childhood recurrent sore throats (suggesting prior streptococcal pharyngitis with rheumatic fever sequelae) now presenting with dyspnea, orthopnea, edema, jugular venous distension, an apical holosystolic murmur radiating to the axilla, and EF 25% has chronic mitral regurgitation from rheumatic heart disease, now decompensated with systolic heart failure. In MR, the regurgitant fraction depends on the gradient between LV and LA — and that gradient is driven by afterload (systemic vascular resistance). Decreasing total peripheral resistance (afterload reduction with ACE inhibitors, ARBs, hydralazine/nitrates) reduces the regurgitant fraction, improving forward stroke volume and reducing pulmonary congestion.
For systolic heart failure with reduced EF, the foundational therapies (GDMT) all reduce afterload or preload or favorably remodel the heart: ACE inhibitors/ARBs/ARNIs (afterload reduction), beta-blockers (anti-remodeling, not for acute decompensation), spironolactone (anti-remodeling), and SGLT2 inhibitors.
Distractors: increasing inotropy (dobutamine, milrinone) is a short-term bridge in cardiogenic shock but worsens long-term mortality. Increasing SA node rate would worsen tachycardia (already 109). Increasing coronary flow is irrelevant — her problem is valvular, not ischemic.
**Why each option:**
**A.** Correct — afterload reduction decreases regurgitant fraction in mitral regurgitation, improves forward output, and is foundational therapy for systolic heart failure with reduced EF.
**B.** Increasing inotropy with positive inotropes (dobutamine, milrinone) is a short-term bridge for cardiogenic shock — long-term inotrope use worsens mortality in chronic systolic HF.
**C.** Increasing SA node rate would worsen her already-elevated heart rate (109) and shorten diastolic filling, harming a failing heart.
**D.** Increased coronary blood flow addresses ischemic disease — irrelevant to her valvular/heart-failure pathology from rheumatic mitral regurgitation.