Parrillo J E, Parker M M, Natanson C, Suffredini A F, Danner R L, Cunnion R E, Ognibene F P
Rush-Presbyterian-St. Luke's Medical Center, Chicago, IL 60612.
Ann Intern Med. 1990 Aug 1;113(3):227-42. doi: 10.7326/0003-4819-113-3-227.
Septic shock is the commonest cause of death in intensive care units. Although sepsis usually produces a low systemic vascular resistance and elevated cardiac output, strong evidence (decreased ejection fraction and reduced response to fluid administration) suggests that the ventricular myocardium is depressed and the ventricle dilated. In survivors, these abnormalities are reversible. Failure to develop ventricular dilatation in nonsurvivors suggests that dilatation is a compensatory mechanism needed to maintain adequate cardiac output. With a canine model of septic shock that is very similar to human sepsis, myocardial depression was confirmed using load-independent measures of ventricular performance. Endotoxin administration to humans simulates the qualitative, cardiovascular abnormalities of sepsis. The pathogenesis of septic shock is extraordinarily complex. Diverse microorganisms can generate toxins, stimulating release of potent mediators that act on vasculature and myocardium. A circulating myocardial depressant substance has been closely associated with the myocardial depression of human septic shock. Therapy has emphasized early use of antibiotics, critical care monitoring, aggressive volume resuscitation, and, if shock continues, use of inotropic agents and vasopressors. Pharmacologic or immunologic antagonism of endotoxin or other mediators may prove to enhance survival in this highly lethal syndrome.
感染性休克是重症监护病房中最常见的死亡原因。尽管脓毒症通常会导致全身血管阻力降低和心输出量增加，但有力证据（射血分数降低以及对液体输注反应减弱）表明心室心肌功能受到抑制且心室扩张。在幸存者中，这些异常情况是可逆的。非幸存者未出现心室扩张表明扩张是维持足够心输出量所需的一种代偿机制。通过一种与人类脓毒症非常相似的犬类感染性休克模型，使用不依赖负荷的心室功能测量方法证实了心肌抑制。给人类注射内毒素可模拟脓毒症在心血管方面的定性异常。感染性休克的发病机制极其复杂。多种微生物可产生毒素，刺激强效介质的释放，这些介质作用于血管系统和心肌。一种循环性心肌抑制物质与人类感染性休克的心肌抑制密切相关。治疗重点在于早期使用抗生素、重症监护监测、积极的容量复苏，以及在休克持续时使用强心剂和血管升压药。对内毒素或其他介质进行药理或免疫拮抗可能会提高这种高致死性综合征的生存率。
