Cardiac output during ritodrine treatment in premature labor

Unlike other β-mimetic drugs, ritodrine hydrochloride is able to inhibit uterine contractility in premature labor without producing hypotension. Based on previous studies, we have postulated that this homeostatic effect of ritodrine is caused by an increase in cardiac output. In 5 women in premature labor, the indicator dilution technique was used to check the increase in cardiac output. Arterial pressure, amniotic pressure, and heart rate were recorded electronically. The systolic blood pressure increased 12 per cent during ritodrine infusion, while the diastolic pressure decreased 10 per cent. The mean blood pressure remained stable, but the pulse pressure increased significantly at 30 minutes of infusion. A consistent increase in cardiac output was found which reached the highest value, 56 per cent over the control, at 40 minutes. There was a slight decrease in cardiac output to 35 per cent above control at 60 minutes of infusion, because of reduced venous return attributed to inhibition of uterine contractility. The significance of these findings is discussed.