Study design: Because of the gradual insidious transitions between localized infection, generalized infection, and septic shock, it is difficult to compare data of patients in various stages and to differentiate primary from secondary and tertiary events. The aim of the present study was to describe the sequential pattern of hemodynamic and oxygen transport patterns of survivors and nonsurvivors of septic shock in order to evaluate possible physiologic mechanisms and to provide a template to relate the sequence of physiologic events to biochemical mediators.
Procedure: A previously described defined protocol was used prospectively to study the sequence of physiologic events using specific criteria to define stages as: (a) early period, the first recorded change 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. In addition, three time lines were defined as the first time mean arterial pressure fell below 70 mm Hg, the first time temperature rose above 38 degrees C, and the earliest fall in VO2. Physiologic data were aligned in actual time before or after the time these criteria were met. Invasive hemodynamic and oxygen transport variables were measured with systemic and pulmonary artery catheters; intravascular pressures, arterial and mixed venous gas levels, cardiac output, and derived calculations were made at frequent intervals and keyed to the time of the cardiac output; each set of measurements in turn was keyed to the aforementioned time periods to describe the early, middle, and late periods.
Results: Beginning with increased cardiac index and oxygen delivery (DO2) as the early physiologic changes, there were progressive increases in cardiac index, DO2, and VO2 throughout the early and middle periods. They were maintained above the normal range in the late stage of survivors, but fell in the last 16 h in nonsurvivors. These values were greater in survivors than in nonsurvivors throughout. There were early transient reductions in VO2 that preceded the rise in temperature and the fall in mean arterial pressure (MAP). Although 84 percent of the septic patients were hyperdynamic, there were transient hypodynamic episodes defined as cardiac index of less than 2.5 L/min.m2 in approximately 10 percent of the measurements. There were also transient preterminal hypermetabolic periods in about 8 percent of the nonsurvivors.
Conclusion: We conclude that increased cardiac index and DO2 represent compensations for circulatory inadequacies that limit body metabolism as reflected by VO2. Cardiac index, DO2, and VO2 values of survivors were higher than those of nonsurvivors and normal values. Therapy directed toward increasing cardiac index to supranormal values empirically determined by survivors has been reported to improve outcome. Additional studies to describe temporal relationships of biochemical mediators of these physiologic patterns are needed.