Treatment of acute myocardial infarction. 4. Other complications and rehabilitation.
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Biomedical subjects
Publications and source records attributed to P C Gazes.
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Serum total cholesterol (> or = 6.7 mmol/L) measured in 1960 in the Charleston Heart Study cohort was found to be a risk for mortality from coronary heart disease during the period of 1960 to 1988 in white men (relative risk [RR] 1.5; 95% confidence interval [CI]: 1.1, 2.2), white women (RR 1.7; 95% CI: 1.1, 2.7), and black women (RR 1.6; 95% CI: .9, 2.9) after age, systolic blood pressure, smoking status, education level, obesity, and diabetes were considered. For black men, the relative risk was .96 (95% CI, .39, 2.39). Only among white women was the relative risk (RR 2.4; 95% CI, 1.2, 4.5) increased among those in the older ages (55 to 74) in 1960. The evidence for cholesterol as a risk factor for coronary disease mortality in black men is inconclusive and requires further study.
When possible, the management of acute cardiogenic pulmonary edema should be started before the patient reaches the hospital. Simple measures such as having the patient sit up with the legs dependent, administering oxygen by nasal prongs, giving sublingual nitroglycerin and small doses of morphine, and rotating tourniquets on the limbs may reduce the need for more intensive procedures. Digoxin and other inotropic agents, aminophylline, furosemide, and vasodilators are given as appropriate during hospitalization. A minority of patients need endotracheal intubation and pressure monitoring with a Swan-Ganz catheter. If the arterial PO2 cannot be maintained at 60 mm Hg or more during face mask ventilation, the PCO2 rises, and the arterial pH declines, the patient should be intubated. Pressure monitoring with a Swan-Ganz catheter is indicated if the patient does not immediately respond to treatment or in special situations such as cardiogenic shock with pulmonary edema. Pulmonary edema caused by diastolic dysfunction is managed differently than that caused by systolic dysfunction. The cause and precipitating factors of the acute pulmonary edema should be sought and treated as early as possible to prevent recurrences.