An 84-year-old man comes to the emergency department with a 4-month history of dyspnea that recently has been getting worse. The patient is unable to lie flat and has been sleeping in a chair. Medical history includes hypertension and type 2 diabetes mellitus. He was hospitalized with an acute myocardial infarction a year ago but has not followed up with a physician. Blood pressure is 144/82 mm Hg and pulse is 98/min and regular. Physical examination shows bilateral lower extremity pitting edema. The point of maximal impulse is displaced to the left, and a holosystolic murmur is heard at the apex. Lung examination shows bibasilar crackles. ECG reveals sinus rhythm with nonspecific ST-segment and T-wave changes. Echocardiographic evaluation and cardiac catheterization are performed to determine cardiac index, systemic vascular resistance, and left ventricular end-diastolic volume. Which of the following patterns is most likely to be seen in this patient?

Question

Quizplus · Accepted Answer

Explanation: 11ec25c8_d33c_d9ef_bc81_7d527f9b2f88_MD0003_00 This patient's progressive dyspnea, orthopnea, and lower extremity swelling are consistent with decompensated heart failure (DHF). The holosystolic murmur at the cardiac apex (likely secondary mitral regurgitation) and laterally displaced point of maximal impulse suggest eccentric hypertrophy of the left ventricle with systolic dysfunction (rather than diastolic dysfunction), likely largely due to ischemic heart disease. secondary mitral regurgitation eccentric hypertrophy Left ventricular (LV) systolic dysfunction leads to the following: Stroke volume is decreased, leading to LV volume overload with increased LV end-diastolic volume (LVEDV) (ie, preload). LV stretch and eccentric hypertrophy initially compensate for increased LVEDV and help maintain cardiac output. Eventually, however, increasing wall stress leads to overwhelming LV contractile dysfunction, resulting in reduced cardiac output (or cardiac index, which is cardiac output adjusted per body surface area). In response to reduced cardiac output, there is reflexively increased systemic vascular resistance (SVR) to maintain sufficient blood pressure for organ and tissue perfusion. A vicious cycle is created: Reduced cardiac output leads to worsened renal perfusion and increased activation of the sympathetic and renin-angiotensin-aldosterone systems; this results in increased volume retention and vasoconstriction, which further worsens cardiac output. The natriuretic pathways, stimulated by atrial and ventricular stretch, attempt to counteract the decompensatory spiral but are eventually overcome. Cardiogenic shock, characterized by marked hypotension and reduced organ and tissue perfusion, represents advanced progression of DHF. Cardiogenic shock (Choice A) Reduced SVR and LVEDV with increased cardiac index is expected in the early stages of septic shock, where there is peripheral vasodilation with leakage of intravascular volume and a reflexive increase in cardiac output. Late septic shock is characterized by a drop in cardiac output, causing cold extremities and signifying a grave prognosis. septic shock (Choice B) Reduced cardiac index and LVEDV with increased SVR is expected with severe intravascular volume loss (ie, hypovolemic shock). The reduced circulating blood volume triggers compensatory vasoconstriction to increase SVR. hypovolemic shock (Choice D) Reduced cardiac index with increased SVR and normal LVEDV is expected in DHF due to diastolic dysfunction (ie, heart failure with preserved ejection fraction). LVEDV is normal (or sometimes decreased) as impaired diastolic filling increases LV end-diastolic pressure and eventually reduces cardiac output. (Choice E) Reduced SVR with normal cardiac index and increased LVEDV is seen with high-output heart failure. A reduction in SVR (eg, arterial venous fistula) increases cardiac output and allows blood to return to the heart quickly and easily, with the left ventricle eventually unable to keep up with the increased venous return. high-output heart failure Educational objective: Decompensated heart failure due to left ventricular systolic dysfunction is characterized by decreased cardiac index, increased systemic vascular resistance, and increased left ventricular end-diastolic volume. References: Cardiogenic shock. (http://www.ncbi.nlm.nih.gov/pubmed/24188221)

An 84-Year-Old Man Comes to the Emergency Department with a 4-Month