Norepinephrine exerts an inotropic effect during the early phase of human septic shock

Background: We conducted this study to investigate whether norepinephrine increases cardiac contractility when administered during the early phase of septic shock. Methods: We studied 38 patients with septic shock who had been resuscitated for <3 h and whose mean arterial pressure (MAP) remained <65 mm Hg. Echocardiographic variables were obtained before (T-0) and after either initiation or an increase in the dose of a norepinephrine infusion to increase MAP to >= 65 mmHg (T-1). We collected left ventricular ejection fraction (LVEF), velocity-time integral of the left ventricular outflow tract (VTI), tissue Doppler imaging of mean systolic velocity of the lateral tricuspid annulus (S-a) and of the lateral mitral annulus (S-m), and tricuspid annular plane systolic excursion (TAPSE). Results: There were significant (P<0.05) increases from T-0 to T-1 in MAP [mean (SD): from 56 (7) to 80 (9) mmHg], LVEF [from 49 (13) to 56 (13)%], VTI [from 18 (5) to 20 (6) cm], S-m [from 10.8 (5.1) to 12.1 (5.0) cm s(-1)], TAPSE [from 1.8 (0.5) to 2.0 (0.5) cm], and S-a [from 13.0 (5.6) to 15.1 (6.4) cm s(-1)]. In the subgroup of 15 patients with LVEF <= 45%, significant increases in VTI [from 16 (8) to 18 (7) cm] and in LVEF [from 36 (7) to 44 (10)%] were observed. Conclusions: Norepinephrine administration during early resuscitation in patients with septic shock increased the cardiac systolic function despite the presumed increase in left ventricular afterload secondary to the increased arterial pressure. Whether such an effect persists over time remains to be evaluated.