In adults, blood pressure is decreased by SNP due to arteriolar and venous dilating effect; however, its actions have not been established in newborn infants. To elucidate the latter, we examined the changes in heart rate, arterial and central blood pressures, echo and electrocardiograms, and pH. Tissue perfusion was evaluated using skin surface unheated PCO2 electrodes. 5 infants developed left heart failure and refractory hypertension after severe fetal distress and neonatal asphyxia and were treated with digitalis and intravenous SNP (2-6 umg/kg/hr.). Before therapy all infants had: tachycardia, cardiomegaly, pulmonary edema, high central venous and arterial blood pressures. Increased left ventricular internal diameter and LA/Ao ratio, ECG ST depression, elevated CPK-MB2 isoenzymes, acidosis and elevated skin tissue PCO2 with increased skin-arterial PO2 gradients. Hemodynamic changes observed within 20 minutes of therapy were compared to values before therapy by paired t tests. With therapy, there were no increase in heart rate, and a significant decrease in arterial and central venous blood pressures. Increases in local perfusion, tissue PO2, and arterial pH, with simultaneous decrease in skin PCO2 were observed. These data suggest that, afterload reduction with SNP in infants with post-asphyxic hypertension and acute heart failure, produces improvement of cardiac pump function, tissue perfusion and oxygenation.
Infants with acute heart failure due to perinatal asphyxia may have elevation of systemic blood pressure from adrenergic stimulation. This afterload elevation is probably deleterious for myocardial function and tissue perfusion. Treatment needs to be directed towards increasing cardiac contractility and reducing afterload. Dopamine and chlorpromazine were given at 2-8 and 1-2 ugm/kg/min respectively, to 6 preterm infants with hypertension following severe perinatal asphyxia. This therapy improved hemo-dynamics in all infants: the heart rate did not increase significantly, mean arterial pressure decreased from 52±4 to 46±4, and skin PCO2, obtained with an unheated electrode, decreased by 8%. These results suggest that improvement in hemodynamics and tissue perfusion occurred without production of myocardial stress by tachycardia or hypotension. The use of an inotropic agent alone for heart failure in the presence of hypertension, may worsen the condition. The combination of dopamine, inotropic and moderate chronotropic agent with chlorpromazine, rapidly active, short acting vasodilator, successfully treated acute hypertension and transient left ventricular dysfunction. The association of hypertension and heart failure in asphyxiated preterm infants may be neurogenic or of vascular origin. In both, appropriate choice of therapy may be significant determinor of outcome.