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326: Cardiogenic Shock and Pulmonary Edema

Judith S. Hochman; David H. Ingbar

INTRODUCTION

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. 326-1). The pathophysiology of pulmonary edema and shock is discussed in Chaps. 47e and 324, respectively.

FIGURE 326-1

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.)

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CARDIOGENIC SHOCK

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 326-1. Circulatory failure based on cardiac dysfunction may be caused by primary myocardial failure, most commonly secondary to acute myocardial infarction (MI) (Chap. 295), and less frequently by cardiomyopathy or myocarditis (Chap. 287), cardiac tamponade (Chap. 288), or critical valvular heart disease (Chap. 283).

TABLE 326-1Etiologies of Cardiogenic Shock (CS)a and Cardiogenic Pulmonary Edema
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TABLE 326-1 Etiologies of Cardiogenic Shock (CS)a and Cardiogenic Pulmonary Edema
Etiologies of Cardiogenic Shock or Pulmonary Edema
Acute myocardial infarction/ischemia
 LV failure
 Ventricular septal rupture
 Papillary muscle/chordal rupture–severe MR
 Ventricular free wall rupture with subacute tamponade
 Other conditions complicating large MIs
Hemorrhage
 Infection
 Excess negative inotropic or vasodilator medications
 Prior valvular heart disease
 Hyperglycemia/ketoacidosis
Post-cardiac arrest
Post-cardiotomy
Refractory sustained tachyarrhythmias
Acute fulminant myocarditis
End-stage cardiomyopathy
LV apical ballooning
Takotsubo’s cardiomyopathy
Hypertrophic cardiomyopathy with severe outflow obstruction
Aortic dissection with aortic insufficiency or tamponade
Severe valvular heart disease
 Critical aortic or mitral stenosis
 Acute severe aortic regurgitation or mitral regurgitation
Toxic/metabolic
 β blocker or calcium channel antagonist overdose
Other Etiologies of Cardiogenic Shockb
RV failure due to:
 Acute myocardial infarction
 Acute cor pulmonale
Refractory sustained bradyarrhythmias
Pericardial tamponade
Toxic/metabolic
 Severe acidosis, severe hypoxemia

aThe etiologies of CS are listed. Most of these can cause pulmonary edema instead of shock or pulmonary edema with CS.

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