Augmentation of cardiac output with intravenous catecholamines in unanesthetized hypoxemic newborn lambs

We compared the effects of three different sympathetic-type agonist drugs upon cardiac output (pump function) and its determinants during hypoxemia, a condition of increased endogenous catecholamines. At 1-3 days after birth, 15 lambs were instrumented with catheters in the aorta, the left atrium, and a vein, and thermistors were placed in the abdominal aorta for cardiac output sampling. In eight animals, a pressure transducer was placed in the left ventricle. After a 2- to 3-day recovery, sequential measurements were made of blood gases, cardiac output, aortic and left atrial pressure and left ventricular maximal first derivative of pressure with respect to time (LV dP/dtmax) in room air and in hypoxemia (F1O2=0.08-0.10). Measurements were repeated during continued hypoxemia with increasing doses of isoproterenol (0.1, 0.4, 0.7, and 1.0 μg/kg/min) and dopamine and dobutamine (10, 20, 40, and 80 μg/kg/min). Hypoxemia alone was associated with no significant change in cardiac output, but cardiac output rose significantly during continued hypoxemia with each drug (maximum increases—dobutamine 58%, isoproterenol 51%, dopamine 31%, all p < 0.05). Studies with continued hypoxemia alone showed no rise in cardiac output over time. Augmentation of contractility, demonstrated by a doubling of LV dP/dtmax by each of the drugs, contributed to the increases in cardiac output. Differences in cardiac output responses could not be explained by contractile effects of the drugs alone, since LV dP/dtmax increased in similar fashion for all three. The relatively limited cardiac output response and downward trend at the highest dosage of dopamine occurred with a reduction in heart rate and an increase in systemic vascular resistance. Dobutamine and isoproterenol, in contrast, lowered systemic vascular resistance at the highest doses. Sympathetic-type adrenergic agents are highly effective in augmenting cardiac pump function when endogenous catecholamines are elevated. These “inotropic” agents do not appear to augment cardiac output by cardiac contractile mechanisms alone.