Abstract

Hypercapnic acidosis has been regarded as a tolerated side effect of protective lung ventilation strategies. Various in vivo and ex vivo animal studies have shown beneficial effects in acute lung injury setting, but some recent work raised concerns about its anti-inflammatory properties. This mini-review article aims to expand the potential clinical spectrum of hypercapnic acidosis in critically ill patients with lung injury. Despite the proven benefits of hypercapnic acidosis, further safety studies including dose-effect, level-and-onset of anti-inflammatory effect, and safe applicability period need to be performed in various models of lung injury in animals and humans to further elucidate its protective role.

Highlights

  • Management of critically ill patients has been continuously evolving

  • Fleischmann et al showed that even under high inspired oxygen concentration of 0.80 in colorectal surgery patients who were assigned to mild hypercapnia (ET PCO2 of 50 mmHg), subcutaneous tissue oxygenation increased by 38% and colon intramural oxygenation increased by about 100% compared to the patients who were assigned to normocapnia (ET PCO2 of 35 mmHg) [4]

  • In a large, randomized-controlled trial from the Acute Respiratory Distress Syndrome (ARDS) Network, Kregenow and colleagues demonstrated that permissive hypercapnia reduced 28-day mortality in patients with acute lung injury who were ventilated with 12 mL/kg predicted body weight tidal volume [30]

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Summary

Introduction

Management of critically ill patients has been continuously evolving. Technological advancement has improved the immediacy and quality of monitoring. In a prospective randomized animal study with moderate to severe ventilation-induced lung injury, hypercapnic acidosis significantly reduced stretchinduced lung injury and resulted in higher arterial PO2 compared to normocapnia It showed reduction in lung permeability as evidenced by bronchoalveolar protein concentrations and attenuated the decrease in static lung compliance in comparison with the normocapnia group [29]. In a large, randomized-controlled trial from the ARDS Network, Kregenow and colleagues demonstrated that permissive hypercapnia (pH < 7.35 and PCO2 > 45 mmHg) reduced 28-day mortality in patients with acute lung injury who were ventilated with 12 mL/kg predicted body weight tidal volume [30] This is in part due the ability of hypercapnic acidosis to attenuate physiologic and histological indices of lung injury induced by very high levels of lung stretch, [31] but not that due to the collapse and re-expansion of atelectatic lung [1].

28. Network TARDS
Findings
35. Sassoon CS
Full Text
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