A physician-validated, board-style question from the Active Transport QBank. Try it, then check the reasoning for every option.
A 65-year-old African American woman with a history of untreated hypertension and obesity presents to the clinic with progressive shortness of breath over the past 3 months. She denies chest pain or syncope. Her blood pressure is 160/95 mmHg, heart rate is 78/min, and respiratory rate is 18/min. A cardiac examination reveals an S4 gallop, but no murmurs. An ECG shows left ventricular hypertrophy. Which of the following best explains the pathophysiology behind her symptoms?
-
A
Decreased myocardial oxygen demandIncorrect. Decreased oxygen demand contradicts LVH physiology, which raises demand from increased muscle mass.
-
B
Decreased cardiac output due to bradycardiaIncorrect. Heart rate is 78, not bradycardic, and cardiac output is not the primary mechanism here.
-
C
Increased pulmonary vascular resistanceIncorrect. Pulmonary vascular resistance rises in pulmonary hypertension; no right-heart failure signs are described.
-
D
Increased left ventricular wall tensionCorrect. Chronic HTN raises LV wall tension, driving concentric hypertrophy and diastolic dysfunction symptoms.
-
E
Increased right ventricular afterloadIncorrect. Right ventricular afterload increases in pulmonary disease, not in left-sided pressure overload from HTN.
↑ Tap an answer to reveal the reasoning
Answer: D. The vignette indicates LVH secondary to longstanding hypertension. The key pathophysiological mechanism leading to her symptoms is increased left ventricular wall tension due to the compensatory hypertrophy from chronic pressure overload. This increased tension can lead to diastolic dysfunction, explaining her dyspnea. The closest wrong answer, 'Increased pulmonary vascular resistance', is eliminated by the absence of right-sided heart failure symptoms.