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小剂量血管加压素治疗血管舒张性感染性休克

Low-dose vasopressin in the treatment of vasodilatory septic shock.

作者信息

Malay M B, Ashton R C, Landry D W, Townsend R N

机构信息

Allegheny General Hospital, Division of General Surgery, Pittsburgh, Pennsylvania 15212, USA.

出版信息

J Trauma. 1999 Oct;47(4):699-703; discussion 703-5. doi: 10.1097/00005373-199910000-00014.

DOI:10.1097/00005373-199910000-00014
PMID:10528604
Abstract

BACKGROUND

Despite appropriate therapy, refractory hypotension often occurs in septic shock. A double-blinded placebo controlled clinical trial was performed to assess the role of low-dose vasopressin (VP) as a pressor agent in septic shock.

METHODS

Patients admitted to a trauma intensive care unit with vasodilatory septic shock were randomized to receive either VP at 0.04 U/min (n = 5) or placebo (n = 5). Vasodilatory septic shock was defined as a need for catecholamine agents to maintain a mean arterial pressure more than or equal to 70 mm Hg, despite a cardiac index more than 2.5 L/min and a minimal pulmonary artery wedge pressure more than 12 mm Hg. After 1 hour of initiation of the study drug, attempts to discontinue norepinephrine, phenylephrine, and/or dopamine, in respective order, were undertaken provided that the mean arterial pressure remained more than or equal to 70 mm Hg.

RESULTS

A vasopressin infusion increased systolic arterial pressure (98 +/- 5 to 125 +/- 8 mm Hg, p < 0.008) because of peripheral vasoconstriction (systemic vascular resistance increased from 878 +/- 218 to 1,190 +/- 213 dynes/s per cm(-5) p < 0.05). Arterial pressure and systemic vascular resistance were statistically unaffected in the placebo group. Before study termination, measured at 24 hours after drug initiation, two patients in the placebo group died of refractory hypotension. However, all patients receiving VP survived the 24-hour study period and had all other catecholamine pressors withdrawn and blood pressure maintained solely with a low-dose VP infusion.

CONCLUSION

A VP infusion improved arterial pressure and permitted the withdrawal of catecholamine vasopressors. VP is a useful agent in the treatment of refractory septic shock.

摘要

背景

尽管进行了适当治疗,但难治性低血压仍常发生于感染性休克。开展了一项双盲安慰剂对照临床试验,以评估小剂量血管加压素(VP)作为升压药在感染性休克中的作用。

方法

因血管舒张性感染性休克入住创伤重症监护病房的患者被随机分为两组,分别接受0.04 U/分钟的VP(n = 5)或安慰剂(n = 5)。血管舒张性感染性休克的定义为:尽管心脏指数大于2.5 L/分钟且肺动脉楔压最小值大于12 mmHg,但仍需要使用儿茶酚胺类药物来维持平均动脉压大于或等于70 mmHg。在开始使用研究药物1小时后,若平均动脉压仍大于或等于70 mmHg,则依次尝试停用去甲肾上腺素、去氧肾上腺素和/或多巴胺。

结果

由于外周血管收缩(全身血管阻力从878±218增加至1190±213达因/秒·厘米⁻⁵,p < 0.05),血管加压素输注使收缩压升高(从98±5 mmHg升至125±8 mmHg,p < 0.008)。安慰剂组的动脉压和全身血管阻力在统计学上未受影响。在研究结束前,即药物开始使用24小时后测量,安慰剂组有两名患者死于难治性低血压。然而,所有接受VP治疗的患者均存活至24小时研究期结束,且停用了所有其他儿茶酚胺类升压药,仅通过小剂量VP输注维持血压。

结论

VP输注可改善动脉压,并允许停用儿茶酚胺类升压药。VP是治疗难治性感染性休克的有效药物。

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