Hemodynamic changes in preterm neonates with septic shock: a prospective observational study*.

OBJECTIVE: We evaluated hemodynamic changes in preterm neonates with septic shock using functional echocardiography and studied the effects of vasoactive drugs on hemodynamic variables. DESIGN: Prospective observational study. SETTING: Level III neonatal ICU. SUBJECTS AND PATIENTS: We enrolled 52 preterm neonates with septic shock (shock group) and an equal number of gestation and postnatal age-matched healthy neonates (control group). INTERVENTIONS: We measured functional hemodynamic variables (left and right ventricular output, ejection fraction, isovolumetric relaxation time, and early passive to late active peak velocity ratio) by echocardiography in the shock group during initial fluid resuscitation, before initiation of vasoactive drugs, and again 30-40 minutes after initiation of vasoactive drug infusion. Control group underwent a single assessment after enrollment. We compared various hemodynamic variables between shock group and control group using paired t test or Wilcoxon signed-rank test. MEASUREMENTS AND MAIN RESULTS: The baseline left ventricular output was significantly higher in neonates with septic shock as compared with controls (median [interquartile range], 305 mL/kg/min [204, 393] vs 233 mL/kg/min [204, 302]; p < 0.001), but ejection fraction was similar between the two groups (55% ± 12% vs 55% ± 5%, p = 0.54). Other hemodynamic variables were comparable between the two groups. After vasoactive drug infusion, there was a significant increase in heart rate (152 ± 18 to 161 ± 18 beats/min, p ≤ 0.001) and right ventricular output (median [interquartile range], 376 [286, 468] to 407 [323, 538] mL/kg/min; p = 0.018) compared with the baseline, but left ventricular output and ejection fraction did not change significantly. CONCLUSIONS: We found an elevated left ventricular output but normal ejection fraction in preterm neonates with septic shock. This suggests that septic shock in preterm neonates is predominantly due to vasoregulatory failure. Vasoactive drugs significantly increased right ventricular output, which was predominantly due to increase in heart rate.