Hypotension thresholds that provoke renal injury, myocardial injury, and mortality in critical care patients remain unknown. We primarily sought to determine the relationship between hypotension and a composite of myocardial injury (troponin T ≥ 0.03 ng/mL without nonischemic cause) and death up to 7 postoperative days. Secondarily, we considered acute kidney injury (creatinine concentration ≥ 0.3 mg/dL or 1.5 times baseline).
Surgical ICU at an academic medical center.
Two-thousand eight-hundred thirty-three postoperative patients admitted to the surgical ICU.
A Cox proportional hazard survival model was used to assess the association between lowest mean arterial pressure on each intensive care day, considered as a time-varying covariate, and outcomes. In sensitivity analyses hypotension defined as pressures less than 80 mm Hg and 70 mm Hg were also considered.
There was a strong nonlinear (quadratic) association between the lowest mean arterial pressure and the primary outcome of myocardial injury after noncardiac surgery or mortality, with estimated risk increasing at lower pressures. The risk of myocardial injury after noncardiac surgery or mortality was an estimated 23% higher at the 25th percentile (78 mm Hg) of lowest mean arterial pressure compared with at the median of 87 mm Hg, with adjusted hazard ratio (95% CI) of 1.23 (1.12–1.355; p < 0.001). Overall results were generally similar in sensitivity analyses based on every hour of mean arterial pressure less than 80 mm Hg and any mean arterial pressure less than 70 mm Hg. Post hoc analyses showed that the relationship between ICU hypotension and outcomes depended on the amount of intraoperative hypotension. The risk of acute kidney injury increased over a range of minimum daily pressures from 110 mm Hg to 50 mm Hg, with an adjusted hazard ratio of 1.27 (95% CI, 1.18–1.37; p < 0.001).
Increasing amounts of hypotension (defined by lowest mean arterial pressures per day) were strongly associated with myocardial injury, mortality, and renal injury in postoperative critical care patients.
1Center for Critical Care, Department of Outcomes Research, Anesthesiology Institute, Cleveland Clinic, Cleveland, OH.
2Department of Anesthesiology, Section on Critical Care Medicine, Wake Forest University School of Medicine, Wake Forest Baptist Medical Center, Winston-Salem, NC.
3Department of Outcomes Research, Anesthesiology Institute, Cleveland Clinic, Cleveland, OH.
4Department of Quantitative Health Sciences, Cleveland Clinic, Cleveland, OH.
This work was performed by the Center for Critical Care and the Departments of General Anesthesiology & Outcomes Research at the Anesthesiology Institute, Cleveland Clinic, 9500 Euclid Avenue, G-58, Cleveland, OH.
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Supported, in part, by the La Jolla Pharmaceutical Company (La Jolla, CA).
Dr. Khanna is a past awardee of the Foundation for Anesthesia Education & Research mentored research training grant in clinical and translational research; and consulted for La Jolla Pharmaceuticals. Drs. Maheshwari and Sessler consulted for Edwards Lifesciences. Cleveland Clinic received funding from La Jolla Pharmaceuticals. The remaining authors have declared that they do not have any conflicts of interest.
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