Inotropic therapy for cardiac failure associated with acute myocardial infarction.

COMPARISON OF ACUTE AND CHRONIC FAILURE C ardiac failure is the second most common complication ofmyocardial infarction, occurring in 40-50 percent of patients, usually evident within hours of onset of symptoms, reflecting 20-25 percent involvement of the myocardium. The pathogenesis is quite distinct from that of chronic failure and requires different treatment; however, this is still not fully recognized. In most cases, the failure is transient, the underlying pathology is probably a combination of necrosis and ischemia, with the latter associated with transient ischemic dysfunction. The basic defect is sudden loss of contractile function in association with decreased ventricular compliance. The predominant relevant compensatory effects from increased catecholamines are an increase of the heart rate and myocardial contractility, the latter primarily of the remaining normal myocardium, but to some extent of the ischemic but non-necrotic myocardium. The decreased ventricular compliance results in a higher enddiastolic pressure than normal for a given end-diastolic volume. Since the pressure-volume relationship is on the ascending limb, the cardiac output is very sensitive to any decrease in circulatory volume. For example, a patient in severe failure with acute pulmonary edema from acute myocardial infarction, who has lost 500-700 ml of fluid in his/her lungs at the expense of the vascular volume, may be hypotensive and administration of a diuretic would precipitate a decrease in coronary perfusion. In contradistinction to chronic cardiac failure, such as secondary to valvular, congenital, or end-stage ischemic heart disease, institution of a diuretic would be helpful and well tolerated. The feature of acute ischemic cardiac failure and chronic failure exhibit several important differences as follows: 1) patients are normovolemic or hypovolemic as opposed to hypervolemic; 2) cardiac output is often normal; 3) sodium and water retention, a feature of chronic failure is not present in the initial days of acute cardiac failure, and in patients with inferior infarction, there is a tendency to lose salt and water; 4) cardiomegaly from either dilatation or hypertrophy is absent; 5) catecholamines are markedly elevated; 6) failure is usually transient. This refers primarily to those patients with no previous history of cardiac failure, whereas when superimposed on chronic failure the combined pathophysiology exists. It was assumed for some time that the pathogenesis ofacute failure ofischemic heart disease and of chronic failure was the same, so the traditional regimen of administration of diuretics and digoxin developed for chronic failure was considered appropriate for acute failure. The experience ofthe CCU has highlighted the lack ofhypervolemia and cardiomegaly in acute failure, but habits have changed slowly. Despite the increasing recognition ofthe different pathogenesis, only now are we beginning to change our treatment. There is widespread appreciation of the inappropriateness of therapy with digoxin and the beneficial effect of vasodilators, but the frequent use of diuretics continues despite hypovolemia and the potential for hypotension. The cardiac failure ofacute myocardial infarction is usually left ventricular, with only about 5 percent due to failure ofthe right ventricle. The clinical picture of left ventricular failure is dominated by that of pulmonary congestion, the symptoms of which are often the primary indications for treatment. In patients with mild failure, as evidenced by basal rales and no other symptoms or evidence ofhypoxemia, no specific treatment is recommended other than oxygen and morphine.