Hemodynamic effects of narcotics
In intact animals and nonaddicted supine patients, morphine and fentanyl and some new, as yet unreleased narcotics, e.g., sulfentanil, produce minimal changes in cardiovascular dynamics.1–3 Indeed, Lowenstein et al1 observed that the introduction of large (anesthetic) doses of morphine (as much as 1 mg/kg) intravenously as the sole or principal anesthetic did not cause significant circulatory changes in patients without cardiac disease. In patients with aortic valvular disease, stroke volume and cardiac output increased. Yet several investigators observed depression of myocardial contractility by narcotics when isolated myocardial muscle and heart-lung preparations were perfused with saline solution.4 When blood was substituted as the perfusing solution, no depressant effect was observed with as much as 30 mg/kg morphine in dog and cat heart-lung preparations.5 Apparently, fentanyl also does not change myocardial mechanics in blood-perfused preparations, whereas meperidine does cause considerable myocardial depression.6
Myocardial depression does not occur after morphine administration in intact animals or man. Schmidt and Livingston7 found no evidence of cardiac depression in awake dogs given as much as 100 mg/kg morphine. Vasco et al8 found that morphine had a positive inotropic effect in dogs, which was dependent on endogenous catecholamine release and blocked by beta-adrenergic blocking agents or previous surgical adrenalectomy. Morphine also increases the concentrations of catechol-amines in both blood and urine of human subjects.9–11 Endogenous catecholamine secretion appears to be dependent on the functional state of the cardiovascular system and plasma concentrations of morphine.9, 10 Liu et al12 have shown that elevated plasma and urinary . . .