THE EFFECTS OF MORPHINE ON THE ARTERIAL AND MIXED VENOUS BLOOD GAS STATE AND ON THE HEMODYNAMICS IN PATIENTS WITH CLINICAL PULMONARY CONGESTION

. The arterial and mixed venous blood gases and the pressures in the systemic and pulmonary circulation have been determined before and after an injection of 1.5 cg of morphine chloride intramuscularly in eight patients with left heart failure and auscultatory and roentgenologic signs of pulmonary congestion. Before morphine all patients showed clearly elevated mean pulmonary artery pressure (PAP), while only two of them showed markedly increased mean pulmonary capillary venous pressure (PCVP). All patients showed normal PaCO2, low PaO2, and low SaO2, except the two patients with high PCVP, who showed markedly reduced PaCO2 and normal PaO2. All patients showed clearly reduced PvO2 and SvO2, and an abnormally high a-vO2 difference, suggesting poor myocardial function or cardiac output response to hypoxia. The base excess was, however, slightly increased, indicating that there was no tendency to metabolic acidosis. After morphine the two patients with increased PCVP showed a clear fall in mean PAP, mean systemic arterial pressure (FAP) and heart rate, while only one of them showed a transient fall in PCVP. In the other patients there was no change in any of these parameters. There was a slight increase in PaCO2, reaching maximum about 60 min after the injection, and a relatively smaller decrease in PaO2, indicating some respiratory depression, but no further impairment of the alveolar/arterial gas exchange. PvO2 and SvO2 remained unchanged and a-vO2 was thus reduced. The base excess remained unchanged. The constancy of the base excess and SvO2 showed that no impairment of tissue oxygenation occurred after morphine, not even in the two patients with high PCVP and a marked fall in FAP after morphine. The data suggest that morphine led to a reduction of the cardiac work in the two patients with high PCVP. The remarkable constancy of PvO2 throughout the investigation, even in the presence of substantial fluctuations in PaO2, SaO2 and systemic blood pressure, suggests some O2-dependent regulation of the peripheral circulation on the venous side.