Association of Arterial pH With Hemodynamic Response to Vasopressin in Patients With Septic Shock: An Observational Cohort Study.
Association of Arterial pH With Hemodynamic Response to Vasopressin in Patients With Septic Shock: An Observational Cohort Study.
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DOI：
10.1097/cce.0000000000000634
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发表时间：
2022-03
影响因子：
--
通讯作者：
Vachharajani V
中科院分区：
文献类型：
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作者：
Bauer SR;Sacha GL;Siuba MT;Lam SW;Reddy AJ;Duggal A;Vachharajani V
据报道，血管加压素保留血管收缩活性的酸血症的设置，但临床前模型是不一致的，研究还没有评估血管加压素的基础上动脉pH值的临床有效性。本研究旨在确定动脉pH值和血压之间的关联后，血管加压素开始在感染性休克。这项回顾性、多中心、观察性队列研究评价了加压素治疗开始时动脉pH值与加压素血流动力学反应和加压素治疗开始后儿茶酚胺剂量变化的相关性。血流动力学反应定义为加压素开始后6小时，儿茶酚胺剂量降低，平均动脉压大于或等于65 mm Hg。对来自卫生系统八家医院的患者进行了评价。筛选了2012年1月至2017年11月期间开始使用加压素作为儿茶酚胺辅助治疗的脓毒性休克患者。没有。共纳入1,350例患者。在开始使用加压素时，患者病情严重，动脉pH值为7.28 ± 0.13，序贯器官衰竭评估为14.1 ± 3.5，乳酸为5.6 ± 4.6 mmol/L，去甲肾上腺素当量儿茶酚胺剂量为32.3 ± 25.4 µ g/min。采用多变量logistic回归校正乳酸和序贯器官衰竭评估后，较低的动脉pH值与血管加压素的血流动力学反应较低的比值独立相关（动脉pH值每低于7.40 0.1单位，反应比值比为0.79; 95% CI，0.72 - 0.87）。对于每0.1单位，在加压素开始时pH低于7.40，去甲肾上腺素当量的儿茶酚胺剂量在加压素开始后1小时增加1.5 µ g/min（95% CI，0.5 - 2.5 µ g/min），在加压素开始后6小时增加2.5 µ g/min（95% CI，1.4 - 3.5 µ g/min）。与动脉pH值较高的患者相比，感染性休克和动脉pH值较低的患者在开始使用加压素后，加压素反应的几率较低，而儿茶酚胺的剂量较高。与其他血管加压药相似，在酸血症的情况下，血管加压素的临床有效性似乎受损。
Vasopressin is reported to retain vasoconstrictive activity in the setting of acidemia, but preclinical models are inconsistent and studies have not evaluated the clinical effectiveness of vasopressin based on arterial pH. This study sought to determine the association between arterial pH and blood pressure after vasopressin initiation in septic shock. This retrospective, multicenter, observational cohort study evaluated the association of arterial pH at the time of vasopressin initiation with hemodynamic response to vasopressin and change in catecholamine dose after vasopressin initiation. Hemodynamic response was defined as a catecholamine dose decrease with mean arterial pressure greater than or equal to 65 mm Hg at 6 hours after vasopressin initiation. Patients from eight hospitals in a health system were evaluated. Patients with septic shock initiated on vasopressin as a catecholamine adjunct between January 2012 and November 2017 were screened for inclusion. None. A total of 1,350 patients were included. At the time of vasopressin initiation patients were severely ill with arterial pH 7.28 ± 0.13, Sequential Organ Failure Assessment 14.1 ± 3.5, lactate 5.6 ± 4.6 mmol/L, and norepinephrine-equivalent catecholamine dose 32.3 ± 25.4 µg/min. After adjusting for lactate and Sequential Organ Failure Assessment with multivariable logistic regression, lower arterial pH was independently associated with lower odds of hemodynamic response to vasopressin (for each 0.1 unit arterial pH was below 7.40, response odds ratio 0.79; 95% CI, 0.72–0.87). For each 0.1 unit the pH was below 7.40 at vasopressin initiation, the norepinephrine-equivalent catecholamine dose increased by 1.5 µg/min (95% CI, 0.5–2.5 µg/min) at 1 hour, and increased by 2.5 µg/min (95% CI, 1.4–3.5 µg/min) at 6 hours after vasopressin initiation. Compared with higher arterial pH, patients with septic shock and low arterial pH had lower odds of vasopressin response and higher catecholamine doses after vasopressin initiation. Similar to other vasopressors, the clinical effectiveness of vasopressin appears to be impaired in the setting of acidemia.