Although there are many etiologies for cardiogenic shock, most occur from acute left ventricular (LV) infarction (see Table. .29-1). While some degree of LV dysfunction occurs with most acute infarcts, once 40 percent of the LV mass is akinetic, clinical evidence of shock is likely to ensue. This amount of LV mass loss need not have occurred with the current AMI, since there may be preexisting impairment from previous infarcts. Therefore, a patient with a past history of infarction may develop cardiogenic shock with a relatively small new MI.
In cases of cardiogenic shock after AMI, the infarct border zone appears irregular with evidence of marginal infarct extension. Myocytes in this border zone demonstrate evidence of various stages of cell death, probably due to inadequate collateral blood flow, which is exacerbated further by hypotension. Areas of focal necrosis develop throughout the right and left ventricles, suggesting widespread coronary vascular pathology and perfusion insufficiency. Resulting hypotension leads to further reduction in coronary perfusion pressure, exacerbating already compromised myocardial oxygen delivery and leading to additional loss of myocardium, additional loss of contractility, additional hypotension, and so on. This process leads to a progressive and rapid cycle of deterioration into irreversible shock. If the patient develops pulmonary edema, the hypoxia and acidosis further diminish contractility.
The severe reduction in cardiac output and the subsequent compensatory mechanisms result in acute oliguria, hepatic failure, gastrointestinal ischemia, anaerobic metabolism, lactic acidosis, and hypoxia. All these further impair myocardial contractility. Salvage of myocardium by preventing infarct extension into the border zone can prevent development of shock. Although loss of LV mass is the major predictor of shock, disease in other coronary arteries, diastolic dysfunction, and arrhythmias can amplify the negative effects of loss of LV mass and produce shock with a loss of myocardium of less than 40 percent.
Many compensatory mechanisms are recruited in the face of an AMI in an effort to maintain cardiac output and tissue perfusion. Initially, the sympathetic nervous system is activated, leading to an increased heart rate and arterial and venoconstriction. The sympathetic activity increases myocardial contractility, which can be visualized as compensatory hyperkinesis in the uninvolved myocardium by echocardiography. When the uninvolved myocardium is fibrotic or blood flow is compromised due to diffuse coronary disease, this compensatory hyperkinesis does not occur. Lack of compensatory hyperkinesis results in increased end-systolic LV volume, increasing the probability of cardiogenic shock. The renin-angiotensin system is activated by the sympathetic stimulation of renal nerves and the inadequate perfusion pressure. Increased angiotensin II activity leads to peripheral vasoconstriction and aldosterone synthesis, causing sodium and water retention and increasing blood volume. When these compensatory actions are inadequate or overwhelmed, shock may ensue.
Right ventricular (RV) infarction can occur in up to 50 percent of inferior wall infarctions. Although hypotension is not uncommon with RV infarction, shock is much less common, accounting for only 3 to 4 percent of the cases of cardiogenic shock. The major determinate of shock with RV infarction is the presence of concomitant LV dysfunction. With decreased LV contractility, the normal systolic septal function of aiding the RV to perfuse the pulmonary bed is impaired. This leads to loss of LV preload, hypotension, and a further decrease in coronary perfusion pressure.
Hemodynamic assessment of patients with AMI has disclosed four profiles based on measurement of cardiac output (either decreased or not) and LV preload (either elevated or not):
Class I: Normal cardiac output and LV preload. Infarction is tolerated without significant hemodynamic impairment; the prognosis is very good, with about a 3 percent mortality rate.
Class II: Normal cardiac output but elevated LV preload. Pulmonary edema is usually evident on clinical examination. Vasodilation and diuresis result in clinical improvement. Overall mortality is approximately 9 percent.
Class III: Decreased cardiac output but normal LV preload. There is relative or absolute volume deficiency. Cardiac output can be improved by volume infusions that increase stroke volume utilizing the Frank-Starling relationship. Overall mortality is about 23 percent.
Class IV: Decreased cardiac output and an elevated LV preload. Clinical shock is present. Overall mortality is 50 percent or greater.
Patients with occult cardiogenic shock may be clinically indistinguishable from those with stable end-stage CHF. 8 Patients at risk appear to be those with CHF duration greater than 3 months and known decreased ejection fraction of less than 30 percent.
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