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感染性休克患者的右心室功能障碍

Right ventricular dysfunction in patients with septic shock.

作者信息

Dhainaut J F, Lanore J J, de Gournay J M, Huyghebaert M F, Brunet F, Villemant D, Monsallier J F

机构信息

Medical ICU, Cochin Port-Royal University Hospital, Paris, France.

出版信息

Intensive Care Med. 1988;14 Suppl 2:488-91. doi: 10.1007/BF00256967.

Abstract

Using a rapid computerized thermodilution method, we examined the evolution of right ventricular performance in 23 patients with septic shock. Nine survived the episode of septic shock. The other 14 patients died of refractory circulatory shock. Significant right ventricular systolic dysfunction, defined as decreased ejection fraction (-39%) and right ventricular dilation (+38%) was observed in all patients with septic shock. However, in the survivors, increased right ventricular preload may prevent hemodynamic evidence of right ventricular pump failure by utilizing the Frank-Starling mechanism to maintain stroke volume. Conversely, in the nonsurvivors, right ventricular dysfunction was more prononced two days after the onset of septic shock, leading to a fall in stroke. In the last patients, a decrease in contractility appears to be the major factor accounting for decreased right ventricular performance, as evidenced by the marked increase in end-systolic volume (+27%) without significant change in pulmonary artery pressure, during the later stage of septic shock. The observed right ventricular pump failure then appears associated with an alteration in diastolic mechanical properties of this ventricle, as suggested by a leftward displacement of the individual pressure-volume curves.

摘要

我们采用快速计算机化热稀释法,对23例感染性休克患者右心室功能的演变进行了研究。其中9例患者在感染性休克发作后存活。另外14例患者死于难治性循环休克。在所有感染性休克患者中均观察到显著的右心室收缩功能障碍,表现为射血分数降低(-39%)和右心室扩张(+38%)。然而,在存活患者中,右心室前负荷增加可通过利用Frank-Starling机制维持每搏输出量,从而防止出现右心室泵衰竭的血流动力学证据。相反,在未存活患者中,感染性休克发作两天后右心室功能障碍更为明显,导致每搏输出量下降。在最后一组患者中,收缩力下降似乎是导致右心室功能降低的主要因素,感染性休克后期收缩末期容积显著增加(+27%),而肺动脉压无明显变化,这一点得到了证实。如个体压力-容积曲线向左移位所示,观察到的右心室泵衰竭似乎与该心室舒张力学特性的改变有关。

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