A 67-year-old man is brought to the emergency department due to progressive shortness of breath. He has had decreasing exercise tolerance for several months, and over the last week he could barely walk to the bathroom without becoming short of breath. The patient has been sleeping in a semirecumbent position recently. Medical history includes type 2 diabetes mellitus, hyperlipidemia, and a myocardial infarction 3 years ago. He takes no medications. The patient does not drink alcohol or use tobacco products. BMI is 30 kg/m². Oxygen saturation is 92% on room air. The apical impulse is palpated in the 6th intercostal space along the anterior axillary line. There is 3+ bilateral pitting edema in the legs. Which of the following is most likely increased in this patient?

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11ec160b_3a83_a531_9249_b3d316cd7524_MD0001_00 This patient with progressive dyspnea, orthopnea, lower extremity swelling, and a laterally displaced point of maximal impulse has decompensated heart failure. Heart failure occurs due to either a progressive decline in myocardial contractility (systolic dysfunction) or impaired ability of the ventricular walls to relax during filling (diastolic dysfunction). Both etiologies eventually lead to decreased cardiac output and inadequate oxygen delivery to the tissues, inducing the following neuroendocrine compensatory mechanisms in an effort to restore organ perfusion: Increased sympathetic output: Baroreceptors sense decreased perfusion and stimulate epinephrine and norepinephrine release to increase heart rate and contractility. Vasoconstriction is also triggered, increasing arteriolar resistance and raising afterload. Renin-angiotensin-aldosterone system (RAAS) activation: Decreased renal perfusion (Choice D) leads to increased secretion of renin and increased circulating levels of angiotensin II, a potent vasoconstrictor that further increases afterload. Adrenal secretion of aldosterone also increases, which stimulates sodium and water retention and increases circulating blood volume (preload). Although these compensatory mechanisms initially improve organ perfusion, they are overall maladaptive. A vicious cycle is generated as the failing heart is unable to pump against increased afterload, and volume retention creates venous congestion in the kidneys that reduces glomerular filtration rate and further impairs diuresis. Atrial and ventricular stretch triggers the release of natriuretic peptides that stimulate vasodilation and fluid diuresis to counteract the vicious cycle; however, these effects are outweighed by the downward-spiraling negative effects of sympathetic drive and RAAS activation. (Choice B) Left ventricular failure leads to increased pulmonary venous pressure and transudation of fluid into the lung parenchyma, which stiffens the alveolar walls and decreases lung compliance. (Choice C) With reduced cardiac output, the tissues become starved for O₂ and increase O₂ extraction from the available capillary blood. This leads to a reduction in mixed venous O₂ content. (Choice E) Stroke volume is generally maintained early in heart failure (due to compensatory mechanisms) and decreases as decompensation takes place. Educational objective: Decreased cardiac output in heart failure triggers neuroendocrine compensatory mechanisms to maintain organ perfusion; however, the compensatory mechanisms are maladaptive over the long term. Increased sympathetic output and activation of the renin-angiotensin-aldosterone system stimulate vasoconstriction and volume retention, compounding the hemodynamic stress on an already failing heart and creating a vicious cycle of decompensation.

A 67-Year-Old Man Is Brought to the Emergency Department Due