1 University of Arkansas for Medical Sciences College of Pharmacy, Little Rock, AR, USA.
2 University of Arkansas for Medical Sciences Medical Center, Little Rock, AR, USA.
J Intensive Care Med. 2019 Oct;34(10):805-810. doi: 10.1177/0885066617714209. Epub 2017 Jun 15.
Guidance for the discontinuation of vasopressors in the recovery phase of septic shock is limited. Norepinephrine is more easily titrated; however, septic shock is a vasopressin deficient state, which exogenous vasopressin endeavors to resolve. Discontinuation of vasopressin before norepinephrine may result in clinically significant hypotension.
This retrospective, cohort study compared discontinuation of norepinephrine and vasopressin in medically, critically ill patients in the recovery phase of septic shock from May 2014 to June 2016. Difference in clinically significant hypotension after norepinephrine or vasopressin discontinuation was evaluated with χ test. Linear regression was performed, examining the effect of agent discontinuation on clinically significant hypotension. Baseline variables were examined for a bivariate relationship with clinically significant hypotension; those with < .2 were included in the model.
Vasopressin was discontinued first or last in 62 and 92 patients, respectively. Sequential Organ Failure Assessment scores at 72 hours (7.9 vs 7.6, = .679) were similar. In unadjusted analysis, when vasopressin was discontinued first, more clinically significant hypotension developed (10.9% vs 67.8%, < .001). There was no difference in intensive care unit (174 vs 216 hours, = .178) or hospital duration (470 vs 473 hours, = .977). In adjusted analyses, discontinuing vasopressin first was associated with increased clinically significant hypotension (odds ratio [OR]: 13.837, 95% confidence interval [CI]: 3.403-56.250, < .001) but not in-hospital (OR: 0.659, 95% CI: 0.204-2.137, = .488) or 28-day mortality (OR: 0.215, 95% CI: 0.037-1.246, = .086).
Adult patients receiving norepinephrine and vasopressin in the resolving phase of septic shock may be less likely to develop clinically significant hypotension if vasopressin is the final vasopressor discontinued.
在脓毒性休克复苏阶段停止使用血管加压素的指南有限。去甲肾上腺素更容易滴定;然而,脓毒性休克是一种血管加压素缺乏状态,外源性血管加压素试图解决这种状态。在去甲肾上腺素之前停止使用血管加压素可能会导致临床上显著的低血压。
这项回顾性队列研究比较了 2014 年 5 月至 2016 年 6 月脓毒性休克恢复期接受医学治疗的重症患者停止使用去甲肾上腺素和血管加压素的情况。采用 χ检验评估去甲肾上腺素或血管加压素停药后临床显著低血压的差异。进行线性回归,检查药物停药对临床显著低血压的影响。检查基线变量与临床显著低血压的双变量关系;与临床显著低血压相关的变量 <.2 被纳入模型。
血管加压素分别首先或最后停用 62 例和 92 例患者。72 小时序贯器官衰竭评估评分(7.9 与 7.6, =.679)相似。在未调整的分析中,当血管加压素首先被停用,更多的临床显著低血压发生(10.9%与 67.8%, <.001)。重症监护病房(174 与 216 小时, =.178)或住院时间(470 与 473 小时, =.977)无差异。在调整分析中,首先停用血管加压素与临床显著低血压增加相关(比值比[OR]:13.837,95%置信区间[CI]:3.403-56.250, <.001),但与院内(OR:0.659,95%CI:0.204-2.137, =.488)或 28 天死亡率(OR:0.215,95%CI:0.037-1.246, =.086)无关。
在脓毒性休克缓解阶段接受去甲肾上腺素和血管加压素治疗的成年患者,如果血管加压素是最后停用的血管加压素,可能不太可能发生临床上显著的低血压。