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Cardiogenic shock (CS) and pulmonary edema are life-threatening high acuity conditions that require treatment as medical emergencies, usually in an intensive care unit (ICU) or cardiac intensive care unit (CICU). The most common joint etiology is severe left ventricular (LV) dysfunction from myocardial infarction (MI) that leads to pulmonary congestion and/or systemic hypoperfusion (Fig. 298-1). The pathophysiology of pulmonary edema and shock are discussed in Chaps. 33 and 296, respectively.

FIGURE 298-1

Pathophysiology of cardiogenic shock and potential treatment targets. The pathophysiological concept of the expanded cardiogenic shock spiral and treatment targets. CABG, coronary artery bypass grafting; eNOS, endothelial nitric oxide synthase; iNOS, inducible nitric oxide synthase; LVEDP, left ventricular end diastolic pressure; NO, nitric oxide; PCI, percutaneous coronary intervention; SIRS, systemic inflammatory response syndrome; SVR, systemic vascular resistance; TNF, tumor necrosis factor. (Reproduced and adapted, with permission, from H Thiele et al: Shock in acute myocardial infarction: The Cape Horn for trials? Eur Heart J 31: 1828, 2010.)


CS is a low cardiac output state resulting in life-threatening end-organ hypoperfusion and hypoxia. The clinical presentation is typically characterized by persistent hypotension (<90 mmHg systolic blood pressure [BP]) unresponsive to volume replacement and is accompanied by clinical features of peripheral hypoperfusion, such as elevated arterial lactate (>2 mmol/L). Objective hemodynamic parameters such as cardiac index or pulmonary capillary wedge pressure can help confirm the diagnosis, but are not mandatory. The in-hospital mortality rates range from 40 to 60%, depending on shock severity and the associated underlying cause. Acute MI with LV dysfunction remains the most frequent cause of CS with other causes listed in Table 298-1. Circulatory failure based on cardiac dysfunction may be caused by primary myocardial failure, most commonly secondary to acute MI (Chap. 269), and less frequently by cardiomyopathy or myocarditis (Chap. 254), cardiac tamponade (Chap. 265), arrhythmias (Chap. 249), or critical valvular heart disease (Chap. 256).

TABLE 298-1Etiologies of Cardiogenic Shock (CS)a and Cardiogenic Pulmonary Edema

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