Changes in left ventricular function in shocked newborns.

Abstract

To assess whether the change in cardiac output after volume replacement is due to elevation of stroke volume or heart rate and to determine the effect of mechanical ventilation on the hemodynamic situation. Prospective study. A ten-bed neonatal intensive care unit (level III) at a university hospital. 15 consecutive newborns with blood pressure below the 10th percentile related to age and weight. Volume replacement with Ringer's lactate 20 ml/kg body weight. Before and after volume replacement, arterial pressure recordings, blood gas analysis, and an echocardiographic study were carried out. Left ventricular and aortic diameters were measured by the two-dimensional M-mode technique and velocity time integral of aortic flow by the pulsed color Doppler technique. From these data, stroke volume and cardiac output were calculated. Cardiac output (703 +/- 204 vs 826 +/- 166 ml/ min, p < 0.005) and cardiac index (267 +/- 69 vs 302 +/- 55 ml/min per kg body weight, p < 0.01) changed significantly due to an appreciable elevation in stroke volume (5.2 +/- 1.7 vs 5.8 +/- 1.7 ml, p < 0.05), whereas heart rate was unaltered (140 +/- 12 vs 142 +/- 20 beats/min; NS). The change in blood pressure (32 +/- 5 vs 38 +/- 8 mm Hg, p < 0.01) was also significant. Cardiac index before and after volume replacement showed a significant inverse correlation with the severity of respiratory disease expressed as alveolar-arterial oxygen difference (A-aDO2) (A-aDO2 vs cardiac index before volume replacement: r = -0.77, p < 0.001; after volume replacement: r = -0.73, p < 0.005) or oxygenation index (oxygenation index vs cardiac index before volume replacement: r = -0.73, p < 0.005; after volume replacement: r = -0.73, p < 0.005). Changes in left ventricular diastolic diameter, left ventricular systolic diameter, and fractional shortening were not significant. These results indicate that the major regulator of left ventricular output in newborns with hypovolemic or cardiogenic shock is stroke volume and not heart rate and that cardiac output depends on the severity of the respiratory disease.