Pulmonary dead-space fraction as a risk factor for death in the acute respiratory distress syndrome.

T. Nuckton, J. Alonso, R. Kallet, et al, N Engl J Med 346, 17, 4-02, 1281-1286

Reviewer: Rose Christopherson, MD, PhD
Staff Anesthesiologist
Portland VA Medical Center
Portland, OR

Background: No single variable related to the lung has been found to independently predict the risk of death when measured early in the course of acute respiratory distress syndrome (ARDS). In this study, dead-space fraction was measured systematically early during the course of ARDS. It was evaluated as a potential independent predictor of death.

Methods: Requirement for consent was waived by the institutional review board because of the noninvasive nature of the measurement, and the fact that similar measurements are taken routinely for nutritional assessment. Dead-space fraction was measured in 179 intubated patients 10.9 +/- 7.4 (mean +/- S.D.) hours after development of ARDS. Exhaled CO2 was gathered for 5 minutes while an arterial blood gas measurement was made. Dead-space fraction was defined as (PaCO2-PECO2) / PaCO2, where PECO2 is the partial pressure of CO2 in mixed expired gas. Other clinical and physiological variables were also analyzed using multiple logistic regression. The outcome was death prior to hospital discharge.

Results: The dead-space fraction was markedly elevated (0.58 +/- 0.09) compared to a normal dead space fraction of 0.3. Dead-space fraction was higher among patients who died in hospital than among those who survived (0.63 +/- 0.10 vs. 0.54 +/- 0.09, P < 0.001). Dead-space fraction was an independent predictor of death. For every 0.05 increase in the dead-space fraction, the odds of death increased 45 % (odds ratio 1.45, 95 % confidence interval 1.15 - 1.83, P = 0.002). There were only two other independent predictors of death. They were the Simplified Acute Physiology Score II, an indicator of severity of illness (o.r. 1.06, 95 % c.i. 1.03 - 1.08, P < 0.001), and the quasistatic respiratory compliance (o.r. 1.06, 95 % c.i. 1.01 - 1.10, P = 0.01).

Conclusions: Increased dead-space fraction occurs in the early phase of ARDS. Increased values are predictive of an increased risk of death.

Discussion: The authors suggested that the mechanism of increased dead-space fraction might involve injury of pulmonary capillaries and obstruction of pulmonary blood flow in the extraalveolar pulmonary circulation. They cited a recent study in which patients who died from ARDS had higher levels of von Willebrand factor antigen, a marker of endothelial injury, in pulmonary edema fluid and plasma compared to survivors. They suggested that dead-space fraction might be measured to determine what patients are at highest risk and what patients might benefit most from particular interventions.

It is interesting to consider also whether interventions in ARDS patients should include maneuvers aimed at protecting the pulmonary vascular endothelium and reducing inflammation and thrombosis, in addition to therapies aimed at protection and healing of the gas-exchange side of the lung.

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