Postmyocardial Infarction Cardiogenic Shock

Definition

Circulatory shock is characterized by the inability of multiorgan blood flow and oxygen delivery to meet metabolic demands. Cardiogenic shock is a type of circulatory shock resulting from severe impairment of ventricular pump function rather than from abnormalities of the vascular system or blood volume. It is important to separate the shock state, in which tissue perfusion is inadequate, from hypotension, in which tissue metabolic demands may be met by increasing cardiac output or decreasing systemic vascular resistance. The diagnosis of cardiogenic shock should include the following:

• 1.

  Systolic blood pressure less than 80 mm Hg without inotropic or vasopressor support, or less than 90 mm Hg with inotropic or vasopressor support, for at least 30 minutes

• 2.

  Low cardiac output (<2.0 L/min per m ² ) not related to hypovolemia (pulmonary artery wedge pressure <12 mm Hg), arrhythmia, hypoxemia, acidosis, or atrioventricular block

• 3.

  Tissue hypoperfusion manifested by oliguria (<30 mL/h), peripheral vasoconstriction, or altered mental status

The failure to consistently define cardiogenic shock or to hemodynamically confirm the presence of an elevated pulmonary capillary wedge pressure and low cardiac index have previously confused clinicians and confounded the literature.

Etiology

The most common cause of cardiogenic shock is acute MI. Often, anterior MI due to acute thrombotic occlusion of the left anterior descending artery results in extensive infarction. Alternatively, a smaller MI in a patient with borderline left ventricular function may be responsible for insufficient cardiac output. Large areas of ischemic nonfunctioning but viable myocardium occasionally lead to shock in patients with MI. The delayed onset of shock may result from reocclusion of a previously patent infarct artery, infarct extension, or metabolic decompensation of noninfarct-zone regional wall motion. Occasionally, right ventricular MI from occlusion of a proximal large right coronary artery in a patient with inferior MI is the cause.

Mechanical complications unrelated to infarct size account for approximately 12% of cases. The papillary muscle of the mitral valve may infarct or rupture, causing acute, severe mitral regurgitation. Rupture of the interventricular septum causing ventricular septal defect or rupture of the left ventricular free wall producing pericardial tamponade also needs to be considered.

Other causes of cardiogenic shock are not emphasized in this discussion. These include end-stage cardiomyopathy, myocardial contusion, myocarditis, hypertrophic cardiomyopathy, valvular heart disease, pericardial disease, right ventricular infarction, and post-cardiopulmonary bypass.

Incidence

Before the recent emphasis on time to treatment and primary PCI, the incidence of cardiogenic shock had remained unchanged for over 25 years, with approximately 8% of patients with ST elevation myocardial infarction (STEMI) and 2.5% of patients with non-STEMI developing cardiogenic shock. The latter group is more likely to have circumflex artery occlusion, comorbid disease, and severe three-vessel disease or left main disease. Cardiogenic shock usually develops early after onset of symptoms, with approximately half of the patients developing shock within 6 hours and 72% within 24 hours. Others first develop a preshock state manifested by systemic hypoperfusion without hypotension. These patients benefit from aggressive supportive therapy and revascularization; early intervention may abort the onset of cardiogenic shock.

Pathology

The early development of cardiogenic shock is usually caused by acute thrombosis of a coronary artery supplying a large myocardial distribution, with no collateral flow recruitment. Frequently, this is the left anterior descending artery, although shock may result from coronary thrombosis in other sites if previous MI has occurred. Multivessel disease is present in two-thirds of patients.

Autopsy studies have consistently shown that at least 40% of the myocardium is infarcted in patients who die of cardiogenic shock. Various ages of infarction reflect previous infarction, reinfarction, or infarct extension.

The infarct border zone in patients without hypotension is clearly demarcated. In patients succumbing to shock, however, it is irregular, with marginal extension. Focal areas of necrosis remote from the infarct zone are also present. These findings result from progressive cell death due to poor coronary perfusion, are reflected by prolonged release of cardiac enzymes, and contribute to hemodynamic deterioration.

Pathophysiology

Progressive hemodynamic deterioration resulting in cardiogenic shock results from a sequence of events ( Fig. 13.1 ). A critical amount of ischemic or necrotic myocardium decreases contractile mass and cardiac output. When cardiac output is low enough that arterial blood pressure falls, coronary perfusion pressure decreases in the setting of an elevated left ventricular end-diastolic pressure. The resulting reduction in coronary perfusion pressure gradient from epicardium to endocardium exacerbates myocardial ischemia, further decreasing left ventricular function and cardiac output, perpetuating a vicious cycle. The speed with which this process develops is modified by the infarct zone, remote myocardial function, neurohumoral responses, and metabolic abnormalities.

The infarct zone can be enlarged by reocclusion of a previously patent infarct artery. Alternatively, infarct extension can result from side branch occlusion from coronary thrombus propagation or embolization or by thrombosis of a second stenosis stimulated by low coronary blood flow and hypercoagulability. Infarct expansion or aneurysm formation promotes left ventricular dilation, which increases wall stress and oxygen demand in the setting of decreased oxygen supply due to low cardiac output.

Preclinical and clinical studies have demonstrated the importance of hypercontractility of remote myocardial segments in maintaining cardiac output in the setting of a large myocardial infarction. This compensatory mechanism is lost when multivessel disease is present and severe enough to produce ischemia in noninfarct segments.

A series of neurohumoral responses is activated in an attempt to restore cardiac output and vital organ perfusion. Decreased baroreceptor activity due to hypotension increases sympathetic outflow and reduces vagal tone. This increases heart rate, myocardial contractility, venous tone, and arterial vasoconstriction. Vasoconstriction is most pronounced in the skeletal, splanchnic, and cutaneous vascular beds to redistribute cardiac output to the coronary, renal, and cerebral circulations. An increase in the ratio of precapillary to postcapillary resistance decreases capillary hydrostatic pressure, facilitating movement of interstitial fluid into the vascular compartment. Increased catecholamine levels and decreased renal perfusion lead to renin release and angiotensin production. Elevated angiotensin levels stimulate peripheral vasoconstriction and aldosterone synthesis. Aldosterone increases sodium and water retention by the kidney, raising blood volume. Release of antidiuretic hormone from the posterior pituitary by baroreceptor stimulation also increases water retention. Local autoregulatory mechanisms that decrease arteriolar resistance and increase regional blood flow are stimulated by hypoxia, acidosis, and accumulation of vasoactive metabolites (e.g., adenosine).

Enhanced anaerobic metabolism, lactic acidosis, and depleted adenosine triphosphate (ATP) stores result when compensatory neurohumoral responses are overwhelmed, further depressing ventricular function. Arrhythmias may reduce cardiac output and increase myocardial ischemia as well. Loss of vascular endothelial integrity because of ischemia culminates in multiorgan failure. Pulmonary edema impairs gas exchange. Renal and hepatic dysfunction results in fluid, electrolyte, and metabolic disturbances. Gastrointestinal ischemia can lead to hemorrhage or entry of bacteria into the bloodstream, causing sepsis. Microvascular thrombosis due to capillary endothelial damage with fibrin deposition and catecholamine-induced platelet aggregation further impairs organ function.

A systemic inflammatory state with high plasma levels of cytokines (e.g., tumor necrosis factor-α, interleukin-6) and inappropriate nitric oxide production may also depress myocardial function or impair catecholamine-induced vasoconstriction, respectively. All of these factors, in turn, lead to diminished coronary artery perfusion and thus trigger a vicious cycle of further myocardial ischemia and necrosis. This results in even lower blood pressure, lactic acidosis, multiorgan failure, and ultimately death.