Septic shock: a heart story since the 1960s
Septic shock: a heart story since the 1960s
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DOI：
10.1007/s00134-006-0142-5
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发表时间：
2006-06-01
影响因子：
38.9
通讯作者：
Mebazaa, A.
中科院分区：
文献类型：
--
作者：
Rabuel, C.;Mebazaa, A.
在肺动脉导管出现之前，已经描述了两种不同的感染性休克临床特征[1，2]。一种是以温暖、干燥的皮肤和跳动的脉搏为特征，尽管有低血压（“热”休克），另一种是以寒冷的皮肤为特征（“冷”休克）。作者的印象是，在感染性休克患者住院的初始阶段观察到“热”休克，而在患者死亡之前，更经常观察到“冷”休克。在少数患者中进行了有创测量，显示“温”休克与高心输出量（CO）相关，“冷”休克与低CO相关（图1a）。然后得出结论，脓毒性休克患者在发病后最初经历了早期高动力期，最终恢复或恶化为与脓毒症相关的心力衰竭或心肌抑制，导致低动力性休克和死亡[3]。后一种概念得到了Weil（图2）设计的动物模型的支持，该模型使用静脉推注高剂量内毒素或活生物体[4，5]（图1b），显示败血性休克的特征是CO降低和全身血管阻力（SVR）升高，导致动物死亡（图1b）。然而，Wilson et al. [6]描述了人类感染性休克主要与正常或升高的CO相关，很少与低CO相关（图1c）。他们是最早将感染性休克描述为具有高CO和低SVR的人之一，将其与低CO和高SVR相结合的心源性和出血性休克区分开来。尽管有这些数据，但Wilson等人关于感染性休克中心血管功能障碍性质的观点直到肺动脉热稀释导管的广泛使用才被接受，肺动脉热稀释导管允许测量CO和肺动脉楔压。随后认识到脓毒性休克患者的容量复苏不足[7]，随后使用肺动脉导管进行的研究一致表明，脓毒性休克中容量复苏充分的患者通常表现出高动力循环状态，伴有高CO、SVR降低、正常每搏输出量和高心率[7，8，9，10，11，12]，即使在非幸存者中也是如此[11]。使用推注或慢性内毒素输注、盲肠结扎和穿刺或感染的腹膜凝块植入的精细动物模型发现“复苏”动物中CO增加和低SVR [13，14，15，16]，而“未复苏”动物中CO低[17，18]。感染性休克患者中与低CO相关的“冷”休克的最初描述很可能是由于在低血容量的情况下进行的测量（至少是“相对”血容量减少）。现在普遍认为，在足够的容量负荷后，严重脓毒症和脓毒性休克通常与高CO有关。
Before the advent of pulmonary arterial catheter two distinct clinical profiles of septic shock had been described [1, 2]. One was characterized by warm, dry skin and a bounding pulse despite hypotension (“warm” shock) and the other by cold skin (“cold” shock). Authors were under the impression that “warm” shock was seen in the initial phase of hospitalization in septic shock patients while “cold” shock was more often observed later, before patients died. Invasive measurements were available in few patients showing that “warm” shock was associated with high cardiac output (CO) and “cold” shock with a low CO (Fig. 1a). It was then concluded that patients in septic shock initially went through an early hyperdynamic phase after the onset of illness and eventually either recovered or deteriorated into heart failure or myocardial depression related to sepsis leading to hypodynamic shock and death [3]. The latter concept was supported by animal models designed by Weil (Fig. 2) using intravenous bolus injections of high doses of endotoxin or live organisms [4, 5](Fig. 1b), showing septic shock characterized by reduced CO and elevated systemic vascular resistance (SVR) leading to animal death (Fig. 1b). However, a concomitant publication by Wilson et al.[6] described septic shock in humans as associated predominantly with normal or elevated CO and very rarely with low CO (Fig. 1c). They were among the first to provide a description of septic shock as having high CO and low SVR, distinguishing it from cardiogenic and hemorrhagic shock that both combined low CO and high SVR. Despite these data the view by Wilson et al. of the nature of cardiovascular dysfunction in septic shock did not become accepted until the widespread use of pulmonary artery thermodilution catheters, allowing measurement of both CO and pulmonary artery wedge pressure. The recognition of inadequate volume resuscitation of patients in septic shock [7] followed, and subsequent studies using pulmonary artery catheter consistently showed that adequately volume-resuscitated patients in septic shock typically manifest a hyperdynamic circulatory state with high CO, decreased SVR, normal stroke volume, and high heart rate [7, 8, 9, 10, 11, 12] even in nonsurvivors [11]. Refined animal models using bolus or chronic endotoxin infusion, cecal ligation, and puncture or infected peritoneal clot implantation found increased CO and low SVR in “resuscitated” animals [13, 14, 15, 16] and low CO in “unresuscitated” animals [17, 18].In summary, the very initial description of “cold” shock associated with low CO in septic shock patients was very likely due to measurements performed in the context of hypovolemia (at least “relative” hypovolemia). It is now generally accepted that after adequate volume loading, severe sepsis and septic shock are often associated with high CO.