Objectives: Gradual, almost imperceptible transitions occur between localized infection, generalized infection, systemic manifestations of the sepsis syndrome, septic shock, and death. The aim of this study was to describe the sequential pattern of hemodynamic and oxygen transport patterns of survivors and nonsurvivors of septic shock, so as to differentiate primary from secondary and tertiary events, to evaluate possible physiologic mechanisms, and to provide a template to relate the appearance of biochemical mediators to the sequence of physiologic events.
Design: Prospective, cohort study.
Setting: University-run county hospital.
Patients: A series of 300 consecutive surgical patients with septic shock; 85 survived and 215 died.
Interventions: We used specific criteria to define stages as: a) early period, the first recorded increase in cardiac output; b) middle period, time of maximal metabolic activity defined as the highest recorded oxygen consumption (VO2); and c) late period, the time of death or recovery.
Measurements and main results: Hemodynamic and oxygen transport variables were measured at frequent intervals throughout the course of septic shock. Beginning with increased cardiac index and oxygen delivery (Do2), which were the earliest observed hemodynamic changes, there were progressive increases in cardiac index, DO2, and VO2. The values of these variables in the survivors were both greater than normal and greater than those values of the nonsurvivors at comparable time periods. These values decreased in the late stage in nonsurvivors. There were early transient reductions in VO2 that preceded the increase in temperature and the decrease in blood pressure in both survivors and nonsurvivors. Although 86% of the septic patients were hyperdynamic, there were transient hypodynamic episodes (defined as cardiac index < 2.5 L/min/m2) in < 10% of the measurements. Transient preterminal hypermetabolic periods occurred in 9% of the nonsurvivors.
Conclusions: Increased cardiac index and DO2 represent compensations for circulatory deficiencies that limit body metabolism, as reflected by inadequate VO2. Survivors have higher cardiac index, DO2, and VO2 values than those values of both the nonsurvivors and normal values. These data suggest that therapy should be directed toward increasing cardiac index to > 5.5 L/min/m2, DO2 to > 1000 mL/min/m2, and VO2 to > 190 mL/min/m2 as therapeutic goals; these supranormal values were empirically determined by the patterns of the survivors. Further studies to describe temporal relationships of biochemical mediators of these physiologic patterns are needed.