Abstract

BackgroundEarly hypercapnia is common in patients with acute respiratory distress syndrome (ARDS) and is associated with increased mortality. Fluctuations of carbon dioxide have been associated with adverse neurological outcome in patients with severe respiratory failure requiring extracorporeal organ support. The aim of this study was to investigate whether early hypercapnia is associated with impaired cerebrovascular autoregulation during the acute phase of ARDS.MethodsBetween December 2018 and November 2019, patients who fulfilled the Berlin criteria for ARDS, were enrolled. Patients with a history of central nervous system disorders, cerebrovascular disease, chronic hypercapnia, or a life expectancy of less than 24 h were excluded from study participation. During the acute phase of ARDS, cerebrovascular autoregulation was measured over two time periods for at least 60 min. Based on the values of mean arterial blood pressure and near-infrared spectroscopy, a cerebral autoregulation index (COx) was calculated. The time with impaired cerebral autoregulation was calculated for each measurement and was compared between patients with and without early hypercapnia [defined as an arterial partial pressure of carbon dioxide (PaCO2) ≥ 50 mmHg with a corresponding arterial pH < 7.35 within the first 24 h of ARDS diagnosis].ResultsOf 66 patients included, 117 monitoring episodes were available. The mean age of the study population was 58.5 ± 16 years. 10 patients (15.2%) had mild, 28 (42.4%) moderate, and 28 (42.4%) severe ARDS. Nineteen patients (28.8%) required extracorporeal membrane oxygenation. Early hypercapnia was present in 39 patients (59.1%). Multivariable analysis did not show a significant association between early hypercapnia and impaired cerebrovascular autoregulation (B = 0.023 [95% CI − 0.054; 0.100], p = 0.556). Hypocapnia during the monitoring period was significantly associated with impaired cerebrovascular autoregulation [B = 0.155 (95% CI 0.014; 0.296), p = 0.032].ConclusionOur results suggest that moderate permissive hypercapnia during the acute phase of ARDS has no adverse effect on cerebrovascular autoregulation and may be tolerated to a certain extent to achieve low tidal volumes. In contrast, episodes of hypocapnia may compromise cerebral blood flow regulation.Trial registration ClinicalTrials.gov; registration number: NCT03949738; date of registration: May 14, 2019

Highlights

  • Hypercapnia is common in patients with acute respiratory distress syndrome (ARDS) and is associated with increased mortality

  • Multivariable analysis did not show a significant association between early hypercapnia (­Arterial partial pressure of carbon dioxide (PaCO2) ≥ 50 mmHg with pH < 7.35) and impaired cerebrovascular autoregulation (CVA) (Table 3)

  • This study focused on the association between alterations of ­PaCO2 during the acute phase of ARDS and CVA

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Summary

Introduction

Hypercapnia is common in patients with acute respiratory distress syndrome (ARDS) and is associated with increased mortality. Fluctuations of carbon dioxide have been associated with adverse neurological outcome in patients with severe respiratory failure requiring extracorporeal organ support. The aim of this study was to investigate whether early hypercapnia is associated with impaired cerebrovascular autoregulation during the acute phase of ARDS. Controversy remains on the effects of hypercapnia in ARDS owing to the results of numerous experimental studies suggesting impaired immunological, alveolar epithelial, and hemodynamic function [6,7,8]. A secondary analysis of three prospective observational trials showed increased ICU mortality in patients with ARDS and early hypercapnia [9]. Aside from hypercapnia, fluctuations of carbon dioxide ­(CO2), have been associated with life-threatening neurological complications in patients requiring extracorporeal membrane oxygenation (ECMO) [10]. C­ O2 is one of the most potent vasoactive substances acting on the cerebral circulation, with hypercapnia leading to vasodilation and hypocapnia inducing vasoconstriction [11]

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