Evaluation of Vasopressor Exposure and Mortality in Patients With Septic Shock*
Evaluation of Vasopressor Exposure and Mortality in Patients With Septic Shock*
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DOI：
10.1097/ccm.0000000000004476
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发表时间：
2020-10-01
影响因子：
8.8
通讯作者：
Lat, Ishaq
中科院分区：
文献类型：
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作者：
Roberts, Russel J.;Miano, Todd A.;Lat, Ishaq
目的：本研究的目的是：1) 确定感染性休克发作后前 6 小时和前 24 小时内升压药剂量强度与 30 天院内死亡率之间的关系； 2) 确定升压药剂量强度的效果是否随液体复苏量的变化而变化； 3) 确定升压药剂量强度的效果是否因剂量滴定模式而变化。设计：2017 年 9 月至 2018 年 2 月之间的多中心前瞻性队列研究。血管升压药剂量强度定义为所有血管升压药输注的总升压药剂量，以去甲肾上腺素当量计。地点：美国 (n= 32) 和约旦 (n= 1) 的 33 个医院地点。患者：因感染性休克而需要入住 ICU 且在休克发作 24 小时内接受大于或等于 1 种血管加压药治疗的连续成人。干预措施：无。测量和主要结果：在筛选的 1,639 名患者中，纳入了 616 名患者。去甲肾上腺素（93%）是最常见的血管升压药。休克诊断后 24 小时内，患者接受的中位数为 3,400 mL（四分位数范围，1,851-5,338 mL）。休克发作前 24 小时内，中位升压药剂量强度为 8.5 μg/min 去甲肾上腺素当量（3.4-18.1 μg/min 去甲肾上腺素当量）。在前 6 小时内，增加血管加压药剂量强度与 30 天院内死亡率的比值比增加相关，且关联强度取决于伴随的液体给药。在整个 24 小时期间，血管加压药剂量强度每增加 10 μg/min 与 30 天死亡率风险增加相关（调整后的比值比，1.33；95% CI，1.16-1.53），并且这种关联不随液体给药量的变化而变化。与早期高/晚期低升压药给药策略相比，早期低/晚期高或持续高升压药给药策略与较高的死亡率相关。结论：感染性休克后 24 小时内增加血管加压药剂量强度与死亡率增加相关。这种关联随着早期输液量和升压药滴定时间的不同而变化。
Objectives: The objectives of this study were to: 1) determine the association between vasopressor dosing intensity during the first 6 hours and first 24 hours after the onset of septic shock and 30-day in-hospital mortality; 2) determine whether the effect of vasopressor dosing intensity varies by fluid resuscitation volume; and 3) determine whether the effect of vasopressor dosing intensity varies by dosing titration pattern. Design: Multicenter prospective cohort study between September 2017 and February 2018. Vasopressor dosing intensity was defined as the total vasopressor dose infused across all vasopressors in norepinephrine equivalents. Setting: Thirty-three hospital sites in the United States (n= 32) and Jordan (n= 1). Patients: Consecutive adults requiring admission to the ICU with septic shock treated with greater than or equal to 1 vasopressor within 24 hours of shock onset. Interventions: None. Measurements and Main Results: Out of 1,639 patients screened, 616 were included. Norepinephrine (93%) was the most common vasopressor. Patients received a median of 3,400 mL (interquartile range, 1,851-5,338 mL) during the 24 hours after shock diagnosis. The median vasopressor dosing intensity during the first 24 hours of shock onset was 8.5 mu g/min norepinephrine equivalents (3.4-18.1 mu g/min norepinephrine equivalents). In the first 6 hours, increasing vasopressor dosing intensity was associated with increased odds ratio of 30-day in-hospital mortality, with the strength of association dependent on concomitant fluid administration. Over the entire 24 hour period, every 10 mu g/min increase in vasopressor dosing intensity was associated with an increased risk of 30-day mortality (adjusted odds ratio, 1.33; 95% CI, 1.16-1.53), and this association did not vary with the amount of fluid administration. Compared to an early high/late low vasopressor dosing strategy, an early low/late high or sustained high vasopressor dosing strategy was associated with higher mortality. Conclusions: Increasing vasopressor dosing intensity during the first 24 hours after septic shock was associated with increased mortality. This association varied with the amount of early fluid administration and the timing of vasopressor titration.