Shoemaker W C, Appel P L, Kram H B, Bishop M H, Abraham E
Department of Emergency Medicine, King-Drew Medical Center, Los Angeles, CA.
Crit Care Med. 1993 Dec;21(12):1876-89. doi: 10.1097/00003246-199312000-00015.
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.
Prospective, cohort study.
University-run county hospital.
A series of 300 consecutive surgical patients with septic shock; 85 survived and 215 died.
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.
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.
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.
局部感染、全身感染、脓毒症综合征的全身表现、感染性休克和死亡之间会发生逐渐的、几乎难以察觉的转变。本研究的目的是描述感染性休克幸存者和非幸存者血流动力学和氧输送模式的连续变化模式,以区分原发性、继发性和三级事件,评估可能的生理机制,并提供一个模板,将生化介质的出现与生理事件序列联系起来。
前瞻性队列研究。
大学附属县级医院。
连续300例手术感染性休克患者;85例存活,215例死亡。
我们使用特定标准将阶段定义为:a)早期,首次记录的心输出量增加;b)中期,最大代谢活动时间定义为最高记录的氧耗量(VO2);c)晚期,死亡或恢复时间。
在感染性休克过程中频繁测量血流动力学和氧输送变量。最早观察到的血流动力学变化是心脏指数和氧输送(Do2)增加,随后心脏指数、DO2和VO2逐渐增加。在可比时间段内,幸存者这些变量的值高于正常水平,也高于非幸存者的值。非幸存者在晚期这些值下降。在幸存者和非幸存者中,VO2在体温升高和血压下降之前都有早期短暂降低。虽然86%的脓毒症患者为高动力型,但在不到10%的测量中出现短暂低动力发作(定义为心脏指数<2.5L/min/m2)。9%的非幸存者出现短暂终末期高代谢期。
心脏指数和DO2增加代表对循环缺陷的代偿,这种循环缺陷限制了身体代谢,表现为VO2不足。幸存者的心脏指数、DO2和VO2值高于非幸存者和正常值。这些数据表明,治疗应将目标设定为将心脏指数提高到>5.5L/min/m2,DO2提高到>1000mL/min/m2,VO2提高到>190mL/min/m2;这些超常值是根据幸存者的模式凭经验确定的。需要进一步研究来描述这些生理模式的生化介质的时间关系。