A 63-year-old man comes to the emergency department due to increasing dyspnea. He was unable to mow his lawn the previous day due to shortness of breath. The patient has a history of hypertension and a 20-pack-year smoking history. He is retired and traveled to Hawaii 2 months ago. Blood pressure is 160/86 mm Hg, pulse is 94/min, and respirations are 24/min; oxygen saturation is 94% on room air. Physical examination reveals bilateral lung crackles and occasional wheezes. Laboratory testing reveals elevated brain natriuretic peptide levels. Which of the following is the primary trigger for the release of this substance in this patient?

Question

A 63-year-old man comes to the emergency department due to increasing dyspnea.  He was unable to mow his lawn the previous day due to shortness of breath.  The patient has a history of hypertension and a 20-pack-year smoking history.  He is retired and traveled to Hawaii 2 months ago.  Blood pressure is 160/86 mm Hg, pulse is 94/min, and respirations are 24/min; oxygen saturation is 94% on room air.  Physical examination reveals bilateral lung crackles and occasional wheezes.  Laboratory testing reveals elevated brain natriuretic peptide levels.  Which of the following is the primary trigger for the release of this substance in this patient?

Quizplus · Accepted Answer

In addition to their contractile and electrical conduction properties, cardiomyocytes possess endocrine capabilities to help regulate blood volume. Volume overload leads to stretching and increased wall stress of the ventricular walls. In response, the ventricular myocardium releases brain natriuretic peptide (BNP); similarly, the atrial myocardium releases atrial natriuretic peptide (ANP) in response to atrial stretching. These natriuretic peptides stimulate both venous and arterial vasodilation to decrease cardiac preload and afterload and reduce strain on the myocardium. In addition, ANP and BNP stimulate salt and water excretion by the kidneys to facilitate diuresis. Clinically, BNP has diagnostic utility in patients with shortness of breath of unknown cause. For patients in whom the serum BNP level is not elevated, shortness of breath is unlikely to be due to heart failure. (Choice A) Alveolar juxtacapillary receptors increase respiratory rate in response to pathologic alveolar processes (eg, pulmonary edema, pneumonia). (Choice B) Decreased renal perfusion pressure triggers the juxtaglomerular apparatus to release renin; activation of the renin-angiotensin-aldosterone system stimulates vasoconstriction and fluid retention, opposing the effects of natriuretic peptides. (Choice C) Decrease in vena cava blood return reduces preload and leads to a consequent reduction in cardiac output. The reduced cardiac output is sensed by carotid baroreceptors, and an increase in sympathetic drive is triggered to stimulate vasoconstriction and increased heart rate and contractility. (Choice D) Focal myocardial necrosis causes release of troponin into the bloodstream, which acts as a sensitive marker of myocardial damage. BNP levels often increase during myocardial infarction; however, this increase is likely secondary to ventricular dysfunction leading to volume overload and myocardial stretch. (Choice F) Elevated blood pressure causes stretching of aortic baroreceptors, which triggers a reduction in sympathetic drive to alleviate vasoconstriction and reduce myocardial contractility. Educational objective: The ventricular myocardium secretes brain natriuretic peptide (BNP) in response to the ventricular stretch and strain that typically occurs with volume overload. BNP, along with atrial natriuretic peptide secreted by the atrial myocardium, stimulates vasodilation and salt and water excretion to help relieve volume overload.

A 63-Year-Old Man Comes to the Emergency Department Due to Increasing