Abstract

IntroductionLung-protective ventilation in patients with ARDS and multiorgan failure, including renal failure, is often paralleled with a combined respiratory and metabolic acidosis. We assessed the effectiveness of a hollow-fiber gas exchanger integrated into a conventional renal-replacement circuit on CO2 removal, acidosis, and hemodynamics.MethodsIn ten ventilated critically ill patients with ARDS and AKI undergoing renal- and respiratory-replacement therapy, effects of low-flow CO2 removal on respiratory acidosis compensation were tested by using a hollow-fiber gas exchanger added to the renal-replacement circuit. This was an observational study on safety, CO2-removal capacity, effects on pH, ventilator settings, and hemodynamics.ResultsCO2 elimination in the low-flow circuit was safe and was well tolerated by all patients. After 4 hours of treatment, a mean reduction of 17.3 mm Hg (−28.1%) pCO2 was observed, in line with an increase in pH. In hemodynamically instable patients, low-flow CO2 elimination was paralleled by hemodynamic improvement, with an average reduction of vasopressors of 65% in five of six catecholamine-dependent patients during the first 24 hours.ConclusionsBecause no further catheters are needed, besides those for renal replacement, the implementation of a hollow-fiber gas exchanger in a renal circuit could be an attractive therapeutic tool with only a little additional trauma for patients with mild to moderate ARDS undergoing invasive ventilation with concomitant respiratory acidosis, as long as no severe oxygenation defects indicate ECMO therapy.

Highlights

  • Lung-protective ventilation in patients with ARDS and multiorgan failure, including renal failure, is often paralleled with a combined respiratory and metabolic acidosis

  • These ventilation specifications often lead to respiratory acidosis, the concept of permissive hypercapnia and concomitant acidosis is presently widely

  • Whereas evidence has been provided for immunologic, redox, and vasoactive protective effects, acidosis has been associated with higher hemodynamic instability [4,5,6,7]

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Summary

Introduction

Lung-protective ventilation in patients with ARDS and multiorgan failure, including renal failure, is often paralleled with a combined respiratory and metabolic acidosis. Ventilation itself, in particular with the use of high tidal volumes and high airway pressures, has been shown to be deleterious for patient outcomes [1,2], and protective ventilation strategies, including lower tidal volumes, have been implemented into clinical practice [1,3]. These ventilation specifications often lead to respiratory acidosis, the concept of permissive hypercapnia and concomitant acidosis is presently widely. In the recent Xtravent study by Bein et al [13], pumpless CO2 removal enabled efficient low-tidal ventilation (about 3 ml/kg PBW) without severe acidosis, which was associated with more ventilator-free days for patients having a severe oxygenation deficit

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