Responses of left ventricular function in survivors and nonsurvivors of septic shock

Abstract

In a previous study of 20 patients with septic shock, we demonstrated severe, but reversible depression of radionuclide-determined left ventricular ejection fraction. To further analyze the cardiovascular response to septic shock, we performed serial cardiovascular studies on 54 patients with blood culture-positive septic shock.The survivors had a mean initial ejection fraction (±SEM) of .40 ± .03 with a mean left ventricular end-diastolic volume index (EDVI) of 122 ± 8 mL/m 2, both significantly decreased and increased, respectively, from critically ill nonseptic control patients ( P < .02). These abnormalities persisted for two to five days and returned to normal within 2 weeks. The nonsurvivors had a mean initial ejection fraction of .47 ± .04 and a mean initial EDVI of 99 ± 9 mL/m 2; both are not different from control patients. On serial studies, the nonsurvivors exhibited one of two patterns: half of the nonsurvivors demonstrated a decreasing EDVI associated with a decreasing stroke volume index (SVI) and cardiac index, the other half of the nonsurvivors had an increasing EDVI associated with maintenance of the SVI and cardiac index. In the surviors, there a statistically significant negative correlation of the decreased ejection fraction with the increased EDVI, but no such correlation occurred in the nonsurvivors. Regarding serial cardiac performance during a 2-week period following shock onset, each patient's consecutive ejection fractions and EDVIs were correlated and the correlation coefficients were averaged. Comparing ejection fraction and EDVI, the survivors had a much greater correlation ( r= −.60) than the nonsurvivors ( r= −.14) ( P < .005). Based on the observations of these studies, the following mechanism is likely: during human septic shock, the cardiovascular system is stressed by both peripheral vascular abnormalities and direct depression of the myocardium, the latter manifested clinically by a depressed ejection fraction. In general, survivors respond on serial studies by ventricular dilation (increased preload) to maintain ventricular performance. A substantial subgroup of nonsurvivors fails to dilate, and succumbs (in part), with an inability to maintain serial ventricular function.