Trajectory of PaO2/FiO2 Ratio in Shock After Angiotensin II

Patrick M Wieruszewski; Patrick J Coleman; Andrea R Levine; Danielle Davison; Nathan J Smischney; Shravan Kethireddy; Yanglin Guo; Jason Hecht; Michael A Mazzeffi; Jonathan H Chow

doi:10.1177/08850666231174870

Trajectory of PaO₂/FiO₂ Ratio in Shock After Angiotensin II

J Intensive Care Med. 2023 Oct;38(10):939-948. doi: 10.1177/08850666231174870. Epub 2023 May 9.

Authors

Affiliations

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.

PMID: 37161301
DOI: 10.1177/08850666231174870

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 (p_interaction < 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.

Keywords: acute respiratory distress syndrome; angiotensin II; oxygenation; renin-angiotensin-aldosterone-system; sepsis; shock; vasopressor.

Publication types

Observational Study

MeSH terms

Adult
Angiotensin II / therapeutic use
Humans
Lung
Oximetry
Oxygen
Respiratory Distress Syndrome* / therapy
Retrospective Studies
Shock*

Substances

Angiotensin II
Oxygen