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INTRODUCTION AND EPIDEMIOLOGY
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Cardiogenic shock is an acute state of decreased cardiac output resulting in inadequate tissue perfusion despite adequate circulating volume. Cardiogenic shock is the leading cause of in-hospital death in patients with acute myocardial infarction (AMI).1 The true incidence of cardiogenic shock is unknown because many patients die before arrival and escape estimates. Cardiogenic shock is seen in 4% to 8% of patients with ST-segment elevation myocardial infarction (STEMI).2,3 The incidence is declining in part as a result of the increased use of percutaneous intervention for AMI.3,4,5,6 Cardiogenic shock occurs less frequently (2.5%) in those with non–ST-segment elevation myocardial infarction (NSTEMI) compared with those with STEMI.7,8 Only ~10% of AMI patients who will develop cardiogenic shock have it at ED presentation, with the median time of onset after arrival being approximately 6 hours.2,9 This underscores the therapeutic opportunity that exists by thwarting ongoing myocardial ischemia.
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During the past decade, a strategy of early revascularization by percutaneous coronary intervention or coronary artery bypass surgery improved survival of cardiogenic shock patients with acute ischemia compared to medical therapy alone.3,10,11,12 Despite these advances, the mortality remains high (~50%), with half of the deaths occurring within the first 48 hours after presentation.3,13,14,15 Early recognition of cardiogenic shock or ongoing myocardial ischemia is the key for emergency physicians. Prompt and successful efforts to restore perfusion optimize patient outcomes.
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The more risk factors that are present (Table 50-1), the greater is the amount of vulnerable myocardium and the greater is the likelihood of cardiogenic shock.
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The most common cause of cardiogenic shock is extensive myocardial infarction that depresses myocardial contractility. Additional causes are listed in Table 50-2. Regardless of the precipitating cause, cardiogenic shock is primarily "pump failure," which results in reduced cardiac output. The systolic blood pressure drops due to poor cardiac output, and vital organ perfusion is limited. Absent a rise in systemic vascular resistance, the diastolic blood pressure also drops, resulting in coronary artery hypoperfusion. This creates a cycle of worsening myocardial ischemia and pump dysfunction, and eventual decompensation.
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