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人类感染性休克死亡率的血流动力学决定因素。

Hemodynamic determinants of mortality in human septic shock.

作者信息

Groeneveld A B, Bronsveld W, Thijs L G

出版信息

Surgery. 1986 Feb;99(2):140-53.

PMID:3511560
Abstract

To assess the relative importance of cardiac versus peripheral vascular failure in patients dying of septic shock, a series of 42 patients with documented septic shock was retrospectively evaluated. Patients were included in the study if serial hemodynamic and metabolic studies had been performed: the first one within 12 hours after onset of septic shock and the last one within 12 hours (median 2 hours; range 0.1 to 12 hours) before death in nonsurvivors. Nonsurvivors were included only if they died in shock. From the patient records the first, highest, and last measured cardiac indexes (CI) (t = 1, t = 2, and t = 3) with concomitant hemodynamic and metabolic variables were obtained. Group I (n = 21) consisted of survivors and group II (n = 21) of nonsurvivors. Group II was divided into three subgroups: group IIa (n = 4) consisted of nonsurvivors with liver cirrhosis, group IIb (n = 9) patients with final CI less than 4 1 X min-1 X m-2, and group IIc (n = 8) patients with final CI greater than 4 1 X min-1 X m-2. At t = 1 no significant differences in hemodynamic variables were found between groups I and II, and all patients, whether surviving or not, were able to increase CI to similar levels. At t = 3 group II showed a marked decrease in mean arterial pressure and systemic vascular resistance index compared with group I (p less than 0.001), whereas CI did not differ significantly. The nonsurvivors showed progressive lactic acidemia. Even group IIb patients showed persistent vasodilation despite a decrease in CI. Our data suggest that many patients in septic shock die as a result of peripheral vascular rather than cardiac failure, since persistent vasodilation, irrespective of CI, was a major hemodynamic determinant in nonsurvivors, of whom 57% maintained a high CI until shortly before death.

摘要

为评估心功能衰竭与外周血管衰竭在感染性休克死亡患者中的相对重要性,我们对42例确诊为感染性休克的患者进行了回顾性评估。若患者进行了系列血流动力学和代谢研究,则纳入本研究:首次研究在感染性休克发作后12小时内进行,对于非存活患者,最后一次研究在死亡前12小时内(中位数2小时;范围0.1至12小时)进行。仅当非存活患者死于休克时才纳入研究。从患者记录中获取首次、最高及最后测量的心脏指数(CI)(t = 1、t = 2和t = 3)以及伴随的血流动力学和代谢变量。第一组(n = 21)为存活患者,第二组(n = 21)为非存活患者。第二组又分为三个亚组:IIa组(n = 4)为合并肝硬化的非存活患者,IIb组(n = 9)为最终CI小于4 l×min-1×m-2的患者,IIc组(n = 8)为最终CI大于4 l×min-1×m-2的患者。在t = 1时,I组和II组之间血流动力学变量无显著差异,所有患者,无论存活与否,均可将CI升高至相似水平。在t = 3时,与I组相比,II组平均动脉压和全身血管阻力指数显著降低(p < 0.001),而CI无显著差异。非存活患者出现进行性乳酸血症。即使IIb组患者CI降低,但仍表现为持续性血管舒张。我们的数据表明,许多感染性休克患者死于外周血管衰竭而非心功能衰竭,因为无论CI如何,持续性血管舒张是导致非存活患者死亡的主要血流动力学因素,其中57%的患者直至死亡前不久仍维持较高的CI。

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