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Recent advances in perioperative anesthetic management update on the role of vasopressin and its effects on outcomes.

机译:围手术期麻醉管理的最新进展更新了加压素的作用及其对预后的影响。

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The vasoconstrictive and antidiuretic physiologic properties of vasopressin (antidiuretic hormone) have long been known. Until recently however, vasopressin was mostly used for diabetes insipidus and noctournal enuresis. This review summarizes the growing body of evidence regarding the perioperative use of vasopressin and its analogues in the management of certain forms of cardiovascular collapse. Physiologically, vasopressin is involved in regulating osmotic, volemic, and cardiovascular homeostasis. It acts via several specific vasopressin receptors that are variably distributed in the heart, kidneys and vasculature etc. Under normal conditions, its antidiuretic effect predominates and vasopressin only induces vasoconstriction at high concentrations. Regarding catecholamine-resistant vasodilatory shock, current evidence suggests that with adequate volume resuscitation, exogenous vasopressin in low "physiologic" doses (0.01- 0.04 units/min) safely supports mean arterial pressure without adversely affecting myocardial function and splanchnic circulation. One possible explanation is that metabolic acidosis impairs the function of alpha-adrenergic (but not vasopressin) receptors, thus diminishing the response to catecholamines. Although there is yet no clear cut mortality benefit, vasopressin is now recommended as a second-line agent in septic shock for its catecholamine-sparing effect and as an alternative to epinephrine in cardiopulmonary resuscitation. It has also demonstrated efficacy in ameliorating vasoplegia after cardiopulmonary bypass as well as perioperative hypotension in patients on reninangiotensin system antagionists preoperatively. In summary, accumulating clinical experience and formal studies indicate that vasopressin has a role in restoring vascular tone in refractory vasodilatory shock states with minimal adverse effects provided that euvolemia is assured.
机译:血管加压素(抗利尿激素)的血管收缩和抗利尿生理特性早已为人所知。然而,直到最近,加压素仍主要用于尿崩症和夜尿性遗尿症。这篇综述总结了越来越多的证据表明围术期使用加压素及其类似物可治疗某些形式的心血管衰竭。在生理上,加压素参与调节渗透,血栓和心血管稳态。它通过几种特定的血管加压素受体起作用,这些受体在心脏,肾脏和脉管系统等中可变分布。在正常情况下,其抗利尿作用占主导,而加压素仅在高浓度时诱导血管收缩。关于耐儿茶酚胺的血管舒张性休克,目前的证据表明,以足够的体积复苏,低“生理”剂量(0.01-0.04单位/分钟)的外源加压素可安全地支持平均动脉压,而不会不利地影响心肌功能和内脏循环。一种可能的解释是,代谢性酸中毒会损害α-肾上腺素(而非加压素)受体的功能,从而减少对儿茶酚胺的反应。尽管尚无明确的死亡率益处,但现在仍推荐使用加压素作为败血性休克的二线药物,因为它具有保留儿茶酚胺的作用,并可以替代肾上腺素用于心肺复苏。在术前使用肾血管紧张素系统拮抗剂的患者中,它还显示出改善体外循环后血管痉挛和围手术期低血压的功效。总之,积累的临床经验和正式研究表明,加压素可在难治性血管舒张性休克状态下恢复血管紧张度,且只要能确保血容量正常,其不良反应最小。

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