A physician-validated, board-style question from the Active Transport QBank. Try it, then check the reasoning for every option.
A 70-year-old man comes to the physician for evaluation of worsening nocturia, fatigue, and shortness of breath on exertion. While he used to be able to walk for 15 minutes at a time, he now has to pause every 5 minutes. Recently, he has started using two pillows to avoid waking up short of breath at night. He has a history of hypertension treated with daily amlodipine and prazosin; he has difficulty adhering to his medication regimen. His pulse is 75/min, and blood pressure is 150/90 mm Hg. Physical examination shows a laterally displaced apical heartbeat and 2+ bilateral pitting edema of the lower legs. Auscultation shows an S4 gallop and fine bibasilar rales. Further evaluation is most likely to show which of the following pathophysiologic changes in this patient?
-
A
Constriction of efferent renal arteriolesCorrect. RAAS activation in CHF causes angiotensin II-mediated efferent renal arteriolar constriction, maintaining glomerular filtration despite reduced renal perfusion.
-
B
Decrease in total peripheral vascular resistanceIncorrect. Total peripheral resistance INCREASES (not decreases) in CHF due to sympathetic activation and angiotensin II.
-
C
Reduction of alveolar surface tensionIncorrect. Pulmonary surfactant production is not directly affected by heart failure; alveolar surface tension is roughly normal, though pulmonary edema raises diffusion distance.
-
D
Retention of potassiumIncorrect. Aldosterone-driven sodium retention causes potassium LOSS (hypokalemia), not retention.
-
E
Decreased plasma renin activityIncorrect. Decreased renin activity is seen in primary hyperaldosteronism; CHF causes the opposite — reduced renal perfusion stimulates renin release and RAAS activation.
↑ Tap an answer to reveal the reasoning
Answer: A. This patient has long-standing poorly controlled hypertension and now presents with orthopnea, paroxysmal nocturnal dyspnea (using two pillows), nocturia, edema, a displaced apical impulse, S4 gallop, and bibasilar rales — congestive heart failure on a background of hypertensive heart disease. The question asks what "pathophysiologic change" is most likely on further evaluation.
In heart failure, reduced effective renal perfusion activates the renin-angiotensin-aldosterone system. Angiotensin II preferentially constricts the efferent renal arteriole, which preserves glomerular filtration pressure even as renal blood flow falls. This is the central RAAS-driven response in CHF and the mechanism that ACE inhibitors and ARBs target — by blunting efferent constriction, they reduce intraglomerular pressure (and slow progression of CKD).
Pearl: in heart failure, AT-II constricts the efferent arteriole to maintain GFR; aldosterone causes sodium and water retention with potassium LOSS, raising total peripheral vascular resistance.
**Why each option:**
**A.** Correct. RAAS activation in CHF causes angiotensin II-mediated efferent renal arteriolar constriction, maintaining glomerular filtration despite reduced renal perfusion.
**B.** Total peripheral resistance INCREASES (not decreases) in CHF due to sympathetic activation and angiotensin II.
**C.** Pulmonary surfactant production is not directly affected by heart failure; alveolar surface tension is roughly normal, though pulmonary edema raises diffusion distance.
**D.** Aldosterone-driven sodium retention causes potassium LOSS (hypokalemia), not retention.