No abstract

Doppler estimates of cardiac output have been shown to correlate closely with invasive measurement of cardiac output in hemodynamically stable adults and children. However, this method has not been validated in hemodynamically unstable pediatric patients. To assess the accuracy of continuous wave Doppler echocardiography in pediatric patients with unstable hemodynamics, we performed 27 simultaneous Doppler and thermodilution comparisons in 12 pediatric patients receiving inotropic support and afterload-reducing agents. Doppler cardiac output was calculated using aortic diameter measured from long-axis two-dimensional echocardiograms at three different sites: the aortic valve anulus, the aortic root at the sinuses of Valsalva, and the ascending aorta. For all measurements, there was a close correlation between Doppler and thermodilution techniques. However the site of measurement of aortic diameter had a significant impact on the strength on the correlation and the variability between Doppler and thermodilution. The best correlation and least variability were obtained using the aortic valve anulus diameter (r = 0.94). On serial determinations, percent change in Doppler stroke volume correlated well with thermodilution stroke volume (r = 0.87) and was useful in detecting both direction and magnitude of change in thermodilution stroke volume. Despite the administration of positive inotropic and afterload-reducing agents, Doppler cardiac output is a useful method for estimating cardiac output in hemodynamically unstable pediatric patients.

A B S T R A a . We evaluated the hypothesis that increased endogenous opioid activity mediates part or all of the left ventricular contractile and pump dysfunction previously demonstrated in HC1-induced metabolic acidemia. Eighteen Western newborn lambs were catheterized and instrumented; pacing wires were sutured to the right atrial ap~endafze: a catheter mounted micromanometer Dressure iransdvucer was inserted into the left ventricle; and a 2.5 F thermistor was inserted into the distal abdominal aorta. The lambs were studied 3 days after surgery. Metabolic acidemia was produced with an infusion of 0.5 N HCl into the inferior vena cava. Inhibition of endogenous opioids was achieved with a bolus of 2 mg/kg of intravenous naloxone, which was demonstrated to inhibit morphine sulfate-induced myocardial dysfunction. The effects of opioid inhibition were contrasted with our previously published results after restoration of a normal arterial pH with intravenous sodium bicarbonate. In agreement with our previous study, we found that reducing the arterial pH from 7.41 f 0.01 to 6.97 f 0.04 was associated with a 45% reduction in cardiac output which resulted from a 50% reduction in stroke volume. These changes in turn were mediated by a 35% reduction in the maximal first derivative of left ventricular pressure and/or a 63% increase in systemic vascular resistance which we used to estimate contractility and afterload, respectively. Left ventricular end diastolic pressure increased during acidemia. Although opioid inhibition produced a consistent increase in the maximal first derivative of left ventricular pressure, this increase was relatively small and was not associated with a significant change in cardiac output, stroke volume, or systemic vascular resistance. In contrast, restoration of a normal arterial pH was associated with increases in cardiac output, heart rate, stroke volume, and dP/dt to greater than control values, as well as a normalization of systemic vascular resistance. These hemodynamic changes were not attributable to direct effects of naloxone. Herein we suggest that although opioids may exert a small role in mediating the contractile dysfunction that occurs during HC-induced metabolic acidemia, there is no apparent influence of opioids on pump performance. Opioids participate very little in the myocardial dysfunction of this model of metabolic acidemia in lambs. (Pediatr Res 23: 643-646, 1988) Abbreviations IV, intravenous LVEDP, left ventricular end diastolic pressure dP/dt, first derivative of left ventricular maximal pressure Received October 23, 1987; accepted February 23, 1988 Supported by a grant from the American Heart Association, Texas Affiliate.Myocardial dysfunction has occurred in conjunction with the metabolic acidemia of birth asphyxia in human newborns (1-5). To examine the effects of metabolic acidemia on neonatal cardiovascular function, we recently used an IV HC1 infusion to produce a metabolic acidemia in unanesthetized lambs (6). In this model, metabolic acidemia was associated wi...