close attention design: Because of the gradual insidious transitions between localized infection.

close attention design: Because of the gradual insidious transitions between localized infection, generalized infection, and septic brunt it is difficult to compare data of patients in various stages and to differentiate primary from secondary and tertiary marked occurrences The aim of the existing study was to describe the sequential pattern of hemodynamic and oxygen transport patterns of survivors and nonsurvivors of septic stroke in order to evaluate possible physiologic mechanisms and to provide a template to relate the order of succession of physiologic events to biochemical mediators.

Procedure: A previously described defined protocol was used prospectively to inquiry the sequence of physiologic terminations 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 ([Vosub2]); and (c) late period, the time of death or recuperation In addition, three time lines were defined as the first time mean arterial compressing fell below 70 mm Hg the first time temperature rose above 38 [degrees]C and the earliest fall in [Vosub2] 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 influences arterial and mixed venous gas plains cardiac output, and derived calculations were made at resort to frequently intervals and keyed to the time of the cardiac output; each risk of measurements in turn was clewed to the aforementioned time periods to describe the early, middle, and late periods.

Results: Beginning with increased cardiac index and oxygen delivery ([Do.sub.2]) as the early physiologic changes, there were progressive increases in cardiac index, [Do.sub.2], and [Vosub2] from beginning to end the early and middle periods. They were maintained above the normal range in the late stage of survivors, if it were not that fell in the last 16 h in nonsurvivors. These values were greater in survivors than in nonsurvivors from end to end There were early transient reductions in [Vosub2] that preced the rise in temperature and the fall in mean arterial hurry (MAP). Although 84 percent of the septic patients were hyperdynamic, there were transient hypodynamic episodes defined as cardiac index of les than 25 L/min.[m.sup.2] in approximately 10 percent of the measurements. There were also transient preterminal hypermetabolic periods in about 8 percent of the nonsurvivors. Conclusion: We bring to an end that increased cardiac index and [Do.sub.2] portray compensations for circulatory inadequacies that limit carcass metabolism as reflected by [Vosub2] Cardiac index, [Do.sub.2], and [Vosub2] values of survivors were higher than those of nonsurvivors and normal values. Therapy directed toward increasing cardiac index to supranormal values empirically determined through survivors has been reported to improve issue Additional studies to describe temporal relationships of biochemical mediators of these physiologic patterns are needed

(Chest 1993; 104:1529-36)

[Do.sub.2] = oxygen delivery; MAP = mean artery pressure; PaOP = pulmonary artery occlusion pressure; Sa[O.sub.2] = arterial oxygen saturation; Sv[Osub2] = mixed venous oxygen saturation; [Vosub2] = oxygen consumption

Clinical aspects of sepsis and the septic clash syndrome are well described,[1,2] nevertheless physiologic descriptions are varied and somewhat contradictory. principally early studies described only hemodynamic measurements in rather small heterogeneous series, still recent studies have reported oxygen transport changes in relation to hemodynamic changes.

High mortality as well as high cardiac output values were reported in principally clinical series of septic shock[2-17] However, reduc cardiac output was reported in near patients with septic shock and hypovolemia. Cardiac puzzles and low blood volume were incriminated as major determinants of mortality in septic patients.[4,18-20] Reduc myocardial performance in answer to fluid repletion was demonstrated in patients with septic percussion by Rackow et al.[13] Moreover, Parker et al[18] showed reduc cardiac function and reduc left ventricular ejection fraction, while Vincent et al[17] reported increased cardiac function in septic shock

In experimentally induced conflict produced by intravenously injected endotoxin, there was hypotension, decreased cardiac output inadequate tissue perfusion, and acidosis similar to the pattern of many patients in the late stage of exact septic shock. When the bacteria were infused into animals across prolonged periods, or when the animals were not well hydrated, the hyperdynamic state did not occur[21-24] Reduc cardiac performance was attributed to reduc preload from venous pooling.[13]

Interpretation of reported hemodynamic data is difficult because greatest in number studies have reported data without regard to the time of attack of septic shock and frequently as though values occurred at a single time frame. Moreover, the following of time-related measurements to each other, to the attack of sepsis, to the time of late-stage septic onset and to the time of death or convalescence has not been addressed. Furthermore, frequently it is unclear that the patient had merely sepsis without other associated shock-producing conditions, like as hemorrhage, trauma, cardiac conditions, and posttraumatic or postoperative states.

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