Department of Veterans Affairs Medical Center, San Diego, California.
The Clinical Research, Investigation, and Systems Modeling of Acute Illness (CRISMA) Center, Department of Critical Care Medicine, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania.
Shock. 2022 Oct 1;58(4):260-268. doi: 10.1097/SHK.0000000000001980. Epub 2022 Aug 18.
Objective: To examine the risk factors, resource utilization, and 1-year mortality associated with vasopressor-resistant hypotension (VRH) compared with vasopressor-sensitive hypotension (VSH) among critically ill adults with vasodilatory shock. We also examined whether combination vasopressor therapy and patient phenotype were associated with mortality. Design: Retrospective cohort study. Setting: Eight medical-surgical intensive care units at the University of Pittsburgh Medical Center, Pittsburgh, PA. Patients : Critically ill patients with vasodilatory shock admitted between July 2000 and October 2008. Interventions : None. Measurements and Main Results: Vasopressor-resistant hypotension was defined as those requiring greater than 0.2 μg/kg per minute of norepinephrine equivalent dose of vasopressor consecutively for more than 6 h, and VSH was defined as patients requiring ≤0.2 μg/kg per minute to maintain MAP between 55 and 70 mm Hg after adequate fluid resuscitation. Of 5,313 patients with vasodilatory shock, 1,291 patients (24.3%) developed VRH. Compared with VSH, VRH was associated with increased risk of acute kidney injury (72.7% vs. 65.0%; P < 0.001), use of kidney replacement therapy (26.0% vs. 11.0%; P < 0.001), longer median (interquartile range [IQR]) intensive care unit length of stay (10 [IQR, 4.0-20.0] vs. 6 [IQR, 3.0-13.0] days; P < 0.001), and increased 1-year mortality (64.7% vs. 34.8%; P < 0.001). Vasopressor-resistant hypotension was associated with increased odds of risk-adjusted mortality (adjusted odds ratio [aOR], 2.93; 95% confidence interval [CI], 2.52-3.40; P < 0.001). When compared with monotherapy, combination vasopressor therapy with two (aOR, 0.91; 95% CI, 0.78-1.06) and three or more vasopressors was not associated with lower mortality (aOR, 0.93; 95% CI, 0.68-1.27). Using a finite mixture model, we identified four unique phenotypes of patient clusters that differed with respect to demographics, severity of illness, processes of care, vasopressor use, and outcomes. Conclusions: Among critically ill patients with vasodilatory shock, VRH compared with VSH is associated with increased resource utilization and long-term risk of death. However, combination vasopressor therapy was not associated with lower risk of death. We identified four unique phenotypes of patient clusters that require further validation.
研究与血管加压素敏感性低血压（VSH）相比，血管扩张性休克危重症成人中血管加压抵抗性低血压（VRH）的相关风险因素、资源利用和 1 年死亡率。我们还研究了联合血管加压素治疗和患者表型是否与死亡率相关。
回顾性队列研究。
匹兹堡大学医学中心的 8 个内科-外科重症监护病房，宾夕法尼亚州匹兹堡。
2000 年 7 月至 2008 年 10 月期间接受血管扩张性休克治疗的危重症患者。
无。
定义 VRH 为需要大于 0.2μg/kg/分钟的去甲肾上腺素等效剂量的血管加压素连续输注超过 6 小时，而 VSH 定义为在充分液体复苏后需要 ≤0.2μg/kg/分钟以维持 MAP 在 55 至 70mmHg 之间的患者。在 5313 例血管扩张性休克患者中，1291 例（24.3%）发生 VRH。与 VSH 相比，VRH 与急性肾损伤风险增加（72.7%比 65.0%；P < 0.001）、需要肾脏替代治疗（26.0%比 11.0%；P < 0.001）、中位数（IQR）更长的重症监护病房住院时间（10 [IQR，4.0-20.0]比 6 [IQR，3.0-13.0]天；P < 0.001）和 1 年死亡率增加（64.7%比 34.8%；P < 0.001）相关。血管加压抵抗性低血压与风险调整后死亡率增加相关（调整后的优势比[aOR]，2.93；95%置信区间[CI]，2.52-3.40；P < 0.001）。与单药治疗相比，两种（aOR，0.91；95%CI，0.78-1.06）和三种或更多种血管加压素的联合血管加压素治疗并未降低死亡率（aOR，0.93；95%CI，0.68-1.27）。使用有限混合模型，我们确定了四个具有不同人口统计学、疾病严重程度、护理过程、血管加压素使用和结局的患者群独特表型。
在血管扩张性休克的危重症患者中，与 VSH 相比，VRH 与资源利用增加和长期死亡风险增加相关。然而，联合血管加压素治疗与较低的死亡率无关。我们确定了四个具有不同特征的患者群独特表型，需要进一步验证。
