- Journal club critique
- Open Access
Hypercapnic acidosis in ARDS: A tolerated side effect or an important therapeutic modality?
© BioMed Central Ltd 2007
- Published: 16 February 2007
Kregenow DA, Rubenfeld GD, Hudson LD, Swenson ER. Hypercapnic acidosis and mortality in acute lung injury. Crit Care Med 2006;34:1–7 .
Evidence suggests that hypercapnic acidosis may be beneficial in patients with acute lung injury, though studies have not separated the effects of HA from the effects of changes in mechanical ventilation.
We tested the hypothesis that hypercapnic acidosis is associated with reduced mortality rate in patients with acute lung injury independent of changes in mechanical ventilation.
Secondary analysis of randomized clinical trial data using hypothesis-driven multivariate logistic regression.
Randomized, multiple-center trial comparing 12 mL/kg to 6 mL/kg predicted body weight (PBW) tidal volumes previously published by the National Institutes of Health Acute Respiratory Distress Syndrome (ARDS) Network.
861 acute lung injury patients enrolled in a randomized, multiple-center trial.
Measurements and main results
The adjusted odds ratio and 95% confidence intervals (CI) for 28-day mortality rate associated with hypercapnic acidosis defined as day 1 pH <7.35 and PaCO2 >45 mm Hg were 0.14 (95% CI 0.03–0.70, p = .016) in the 12 mL/kg PBW tidal volume group and 1.18 (95% CI 0.59–2.35, p = .639) in the 6 mL/kg PBW tidal volume group. Other definitions of hypercapnic acidosis spanning a range of magnitudes suggest a dose-response association between hypercapnic acidosis and 28-day mortality in the 12 mL/kg PBW tidal volume group. None of our definitions of hypercapnic acidosis were associated with reduction in 28-day mortality in the 6 mL/kg PBW tidal volume group.
Hypercapnic acidosis was associated with reduced 28-day mortality in the 12 mL/kg PBW tidal volume group after controlling for co-morbidities and severity of lung injury. These results are consistent with a protective effect of hypercapnic acidosis against ventilator-associated lung injury that was not found when the further ongoing injury was reduced by 6 mL/kg PBW tidal volumes.
A randomized clinical trial of HA in patients with ALI/ARDS undergoing lung protective ventilation seems warranted. However, greater extremes of HA than seen in the ARDS Network low vs. high tidal volume trial will likely be needed in order to see a benefit. Until the results of such a trial are available, we cannot recommend HA as a specific therapeutic goal. For now, HA remains a tolerated side effect of lung protective ventilation.
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