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INTRODUCTION AND EPIDEMIOLOGY

Cardiogenic shock results from decreased cardiac output, leading to inadequate tissue perfusion despite adequate circulating volume, and it carries an in-hospital mortality rate of 27% to 51%.1,2 The true incidence is unknown because many patients die before hospital arrival. Cardiogenic shock occurs in 4% to 8% of patients with ST-segment elevation myocardial infarction (STEMI) and is the leading cause of in-hospital death in patients with acute myocardial infarction (AMI).3-6 Cardiogenic shock occurs less frequently (2.5%) in those with non–ST-segment elevation myocardial infarction (NSTEMI).7,8 Only approximately 10% of AMI patients who will develop cardiogenic shock have it at initial ED presentation, with the median time of onset after arrival being 6 hours.9 This highlights the therapeutic opportunity possible with rapid treatment of myocardial ischemia. Over the past decade, a strategy of early revascularization by percutaneous coronary intervention or coronary artery bypass surgery has improved the survival of cardiogenic shock patients with acute ischemia compared to medical therapy alone.3,10-13 As more risk factors for cardiogenic shock exist (Table 50-1), a greater amount of vulnerable myocardium and greater likelihood of cardiogenic shock also exist.

TABLE 50-1Risk Factors for Cardiogenic Shock

PATHOPHYSIOLOGY

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.14 The systolic blood pressure drops due to poor cardiac output, causing hypoperfusion of vital organs. Without a rise in systemic vascular resistance, the diastolic blood pressure drops, resulting in coronary artery hypoperfusion. This creates a cycle of worsening myocardial ischemia and pump dysfunction and eventual decompensation.

TABLE 50-2Causes of Cardiogenic Shock

Both increased afterload and systolic/diastolic dysfunction of the heart can lead to increased left ventricular end-diastolic pressures (LVEDP) and pulmonary edema. Pulmonary edema leads to hypoxia and hypoxemia, which worsens ischemia and ...

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