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Cardiogenic shock occurs when there is insufficient cardiac output to meet the metabolic demands of the tissues. It is most commonly due to an acute myocardial infarction (AMI) that is extensive, impairs right ventricular contractility, or causes a rupture of a papillary muscle. Other etiologies to consider include cardiotoxic drug effects, infection (myopericarditis, endocarditis), and mechanical dysfunction (valvular disease, pulmonary embolism, cardiac tamponade, myocardial contusion). Early stabilization and treatment are critical, as mortality approaches 50% for AMI complicated by cardiogenic shock.

The hallmark of all shock states is hypoperfusion. Cardiogenic shock generally presents with hypotension (systolic blood pressure [SBP] <90 mm Hg), although SBP may be greater than 90 mm Hg if there is preexisting hypertension or a compensatory increase in systemic vascular resistance. Sinus tachycardia is frequently seen, but may be absent in the setting of preceding calcium channel or beta-blockade. Evidence of hypoperfusion may include cool, mottled skin, oliguria, or altered mental status due to decreased cerebral perfusion and hypoxemia. Left ventricular failure may present with evidence of pulmonary edema: tachypnea, rales, wheezing, and frothy sputum. Jugular venous distention without pulmonary edema in the setting of hypotension should raise the suspicion of right ventricular failure due to infarction, tamponade, or pulmonary embolism. It is crucial to listen for the presence of a murmur that may represent acute valvular dysfunction (papillary muscle dysfunction or chordae rupture) or new ventricular septal defects as these findings may prompt life-saving surgery.

The key task is to differentiate cardiogenic shock from shock due to hypovolemia or distributive causes (sepsis, neurogenic). A search for GI bleeding, obvious sources of infection, and focal neurologic deficits may establish an alternate diagnosis.

The first and most important test to order is an electrocardiogram (ECG). The ECG will aid in the detection of ischemia or infarction, arrhythmias, electrolyte abnormalities, or drug toxicity. ST-segment depression in the lateral leads should prompt consideration of a right ventricular infarction, which may occur without ST-segment elevation in the standard twelve lead ECG. Right ventricular infarction increases mortality from approximately 6% to 31%. A chest radiograph also should be obtained to look for pulmonary edema, abnormally wide mediastinum, or other abnormalities of the cardiac silhouette, or suggest alternate/confounding diagnoses such as pneumonia or pneumothorax.

There is no single laboratory test that is diagnostic for shock. A complete blood count and chemistries (including liver function tests) should be obtained. In the absence of ST-segment elevation, cardiac markers such as troponin may establish the diagnosis of non-ST-segment elevation MI (NSTEMI); in addition, they add prognostic value in non-AMI states such as acute heart failure and sepsis. Given their high negative predictive value, natriuretic peptides, such as BNP or n-terminal pro-BNP, should prompt a search for a noncardiac etiology if normal. Serum lactate will indicate the degree of hypoperfusion present. Blood gas measurements will provide insight into acid-base status and CO2 retention. The decision to obtain toxicology testing should be ...

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