A 63-year-old man comes to the emergency department due to dyspnea. Over the past several days, the patient has experienced progressively worsening shortness of breath while walking his dog around the block. In addition, he could not breathe while lying in bed last night and fell asleep only after moving to a recliner. The patient had an acute myocardial infarction 2 years ago and has been nonadherent with his medications and follow-up appointments. Temperature is 36.7 C (98 F), blood pressure is 122/74 mm Hg, pulse is 94/min, and respirations are 22/min. Physical examination shows bibasilar lung crackles, jugular venous distension, and bilateral pitting edema in the lower extremities. Chest x-ray reveals cardiomegaly and pulmonary venous congestion. Which of the following factors is most likely contributing to this patient's symptoms?

Question

A 63-year-old man comes to the emergency department due to dyspnea.  Over the past several days, the patient has experienced progressively worsening shortness of breath while walking his dog around the block.  In addition, he could not breathe while lying in bed last night and fell asleep only after moving to a recliner.  The patient had an acute myocardial infarction 2 years ago and has been nonadherent with his medications and follow-up appointments.  Temperature is 36.7 C (98 F), blood pressure is 122/74 mm Hg, pulse is 94/min, and respirations are 22/min.  Physical examination shows bibasilar lung crackles, jugular venous distension, and bilateral pitting edema in the lower extremities.  Chest x-ray reveals cardiomegaly and pulmonary venous congestion.  Which of the following factors is most likely contributing to this patient's symptoms?

Quizplus · Accepted Answer

11ec160b_3c8f_c8c9_9249_e355632db6b9_MD0001_00 This patient's progressive dyspnea, orthopnea, and lower extremity swelling are consistent with acute decompensated heart failure. Heart failure occurs when a structural or functional cardiac disorder impairs ventricular filling or ejection of blood, causing reduced cardiac output and elevated filling pressure. The reduced cardiac output causes an initial drop in blood pressure, which triggers compensatory neurohormonal activity mainly via stimulation of the sympathetic nervous system and renin-angiotensin-aldosterone system (RAAS). These adaptations function together in an effort to improve organ perfusion by increasing cardiac chronotropy and inotropy (improves cardiac output), promoting arterial and venous vasoconstriction (maintains perfusion pressure), and expanding the extracellular fluid compartment (improves circulating blood volume). However, over time, these responses lead to adverse consequences that perpetuate a downward spiral of progressive cardiac deterioration. Chronic hemodynamic stress (eg, increased preload and afterload) and prolonged exposure to sympathetic drive (catecholamines) and RAAS stimulation (angiotensin II, aldosterone) lead to deleterious remodeling with worsening cardiac function and eventual symptomatic decompensation. (Choices A and B) Decreased cardiac output in heart failure stimulates increased RAAS activity and sympathetic output, resulting in increased arteriolar resistance. (Choice C) Ventricular end-diastolic and end-systolic pressures are increased in heart failure due to increased preload and afterload. (Choice D) Heart failure triggers the myocardium to secrete natriuretic peptides (ie, atrial natriuretic peptide, brain natriuretic peptide) in response to myocardial stretch from volume overload. These peptides stimulate vasodilation and increase salt and water excretion to improve the symptoms of heart failure; however, these positive effects are overpowered by the negative effects of increased sympathetic drive and RAAS activation. Educational objective: The reduced cardiac output in heart failure triggers compensatory activation of the sympathetic nervous system and renin-angiotensin-aldosterone pathway, resulting in vasoconstriction (increased afterload), fluid retention (increased preload), and deleterious cardiac remodeling. These mechanisms perpetuate a downward spiral of cardiac deterioration, leading to symptomatic decompensated heart failure.

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