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Cardiogenic shock and pulmonary edema are life-threatening conditions that should be treated as medical emergencies. The most common joint etiology is severe left ventricular (LV) dysfunction that leads to pulmonary congestion and/or systemic hypoperfusion (Fig. 34-1). The pathophysiology of pulmonary edema is discussed in Chap. 5.


Pathophysiology of cardiogenic shock. Systolic and diastolic myocardial dysfunction results in a reduction in cardiac output and often pulmonary congestion. Systemic and coronary hypoperfusion occur, resulting in progressive ischemia. Although a number of compensatory mechanisms are activated in an attempt to support the circulation, these compensatory mechanisms may become maladaptive and produce a worsening of hemodynamics. *Release of inflammatory cytokines after myocardial infarction may lead to inducible nitric oxide expression, excess nitric oxide, and inappropriate vasodilation. This causes further reduction in systemic and coronary perfusion. A vicious spiral of progressive myocardial dysfunction occurs that ultimately results in death if it is not interrupted. LVEDP, left ventricular end-diastolic pressure. (From SM Hollenberg et al: Ann Intern Med 131:47, 1999.)


Cardiogenic shock (CS) is characterized by systemic hypoperfusion due to severe depression of the cardiac index (<2.2 [L/min]/m2) and sustained systolic arterial hypotension (<90 mmHg) despite an elevated filling pressure (pulmonary capillary wedge pressure [PCWP] >18 mmHg). It is associated with in-hospital mortality rates >50%. The major causes of CS are listed in Table 34-1. Circulatory failure based on cardiac dysfunction may be caused by primary myocardial failure, most commonly secondary to acute myocardial infarction (MI) (Chap. 41), and less frequently by cardiomyopathy or myocarditis (Chap. 27), cardiac tamponade (Chap. 28), or critical valvular heart disease (Chap. 23).


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