Trajectory of PaO2/FiO2 Ratio in Shock After Angiotensin II

Author:

Wieruszewski Patrick M.1ORCID,Coleman Patrick J.2,Levine Andrea R.3ORCID,Davison Danielle4,Smischney Nathan J.5ORCID,Kethireddy Shravan6,Guo Yanglin7,Hecht Jason8,Mazzeffi Michael A.9,Chow Jonathan H.4ORCID

Affiliation:

1. Department of Anesthesiology and Pharmacy, Mayo Clinic School of Medicine, Rochester, MN, USA

2. Department of Anesthesiology, Walter Reed National Military Medical Center, Baltimore, MD, USA

3. Department of Medicine, Division of Pulmonary and Critical Care Medicine, University of Maryland School of Medicine, Baltimore, MD, USA

4. Department of Anesthesiology & Critical Care Medicine, George Washington University School of Medicine and Health Sciences, Washington, DC, USA

5. Department of Anesthesiology, Division of Critical Care Medicine, Mayo Clinic School of Medicine, Rochester, MN, USA

6. Department of Medicine, Division of Pulmonary and Critical Care, Cleveland Clinic, Cleveland, OH, USA

7. Department of Medicine, Division of Pulmonary & Critical Care, University of Mississippi Medical Center, Jackson, MS, USA

8. Department of Pharmacy, St. Joseph Mercy Ann Arbor Hospital, Ypsilanti, MI, USA

9. Department of Anesthesiology, University of Virginia, Charlottesville, VA, USA

Abstract

Introduction High-dose catecholamines can impair hypoxic pulmonary vasoconstriction and increase shunt fraction. We aimed to determine if Angiotensin II (Ang-2) is associated with improved PaO2/FiO2 and SpO2/FiO2 in patients in shock. Methods Adult patients at four tertiary care centers and one community hospital in the United States who received Ang-2 from July 2018-September 2020 were included in this retrospective, observational cohort study. PaO2, SpO2, and FiO2 were measured at 13 timepoints during the 48-h before and after Ang-2 initiation. Piecewise linear mixed models of PaO2/FiO2 and SpO2/FiO2 were created to evaluate hourly changes in oxygenation after Ang-2 initiation. The difference in the proportion of patients with PaO2/FiO2 ≤ 300 mm Hg at the time of Ang-2 initiation and 48 h after was also examined. Results The study included 254 patients. In the 48 h prior to Ang-2 initiation, oxygenation was significantly declining (hourly PaO2/FiO2 change −4.7 mm Hg/hr, 95% CI − 6.0 to −3.5, p < .001; hourly SpO2/FiO2 change −3.1/hr, 95% CI−3.7 to −2.4, p < .001). Ang-2 treatment was associated with significant improvements in PaO2/FiO2 and SpO2/FiO2 in the 48-h after initiation (hourly PaO2/FiO2 change +1.5 mm Hg/hr, 95% CI 0.5-2.5, p  =  .003; hourly SpO2/FiO2 change +0.9/hr, 95% CI 0.5-1.2, p < .001). The difference in the hourly change in oxygenation before and after Ang-2 initiation was also significant ( pinteraction < 0.001 for both PaO2/FiO2 and SpO2/FiO2). This improvement was associated with significantly fewer patients having a PaO2/FiO2 ≤ 300 mm Hg at 48 h compared to baseline (mean difference −14.9%, 95% CI −25.3% to −4.6%, p  =  .011). Subgroup analysis found that patients with either a baseline PaO2/FiO2 ≤ 300 mm Hg or a norepinephrine-equivalent dose requirement >0.2 µg/kg/min had the greatest associations with oxygenation improvement. Conclusions Ang-2 is associated with improved PaO2/FiO2 and SpO2/FiO2. The mechanisms for this improvement are not entirely clear but may be due to catecholamine-sparing effect or may also be related to improved ventilation-perfusion matching, intrapulmonary shunt, or oxygen delivery.

Publisher

SAGE Publications

Subject

Critical Care and Intensive Care Medicine

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