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Previous Volume 346:1281-1286 April 25, 2002 Number 17 Next

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ABSTRACT

Background No single pulmonary-specific variable, including the severity of hypoxemia, has been found to predict the risk of death independently when measured early in the course of the acute respiratory distress syndrome. Because an increase in the pulmonary dead-space fraction has been described in observational studies of the syndrome, we systematically measured the dead-space fraction early in the course of the illness and evaluated its potential association with the risk of death.

Methods The dead-space fraction was prospectively measured in 179 intubated patients, a mean (±SD) of 10.9±7.4 hours after the acute respiratory distress syndrome had developed. Additional clinical and physiological variables were analyzed with the use of multiple logistic regression. The study outcome was mortality before hospital discharge.

Results The mean dead-space fraction was markedly elevated (0.58±0.09) early in the course of the acute respiratory distress syndrome and was higher among patients who died than among those who survived (0.63±0.10 vs. 0.54±0.09, P<0.001). The dead-space fraction was an independent risk factor for death: for every 0.05 increase, the odds of death increased by 45 percent (odds ratio, 1.45; 95 percent confidence interval, 1.15 to 1.83; P=0.002). The only other independent predictors of an increased risk of death were the Simplified Acute Physiology Score II, an indicator of the severity of illness (odds ratio, 1.06; 95 percent confidence interval, 1.03 to 1.08; P<0.001) and quasistatic respiratory compliance (odds ratio, 1.06; 95 percent confidence interval, 1.01 to 1.10; P=0.01).

Conclusions Increased dead-space fraction is a feature of the early phase of the acute respiratory distress syndrome. Elevated values are associated with an increased risk of death.

Source Information

From the Departments of Medicine (T.J.N., M.D.E., M.A.M.), Anesthesia (J.A.A., R.H.K., J.-F.P., M.A.M.), and Surgery (J.-F.P.) and the Cardiovascular Research Institute (T.J.N., B.M.D., M.A.M.), University of California, San Francisco; and San Francisco General Hospital (J.A.A., R.H.K., J.-F.P.) — both in San Francisco.

Address reprint requests to Dr. Nuckton at the Cardiovascular Research Institute, University of California, San Francisco, 505 Parnassus Ave., Box 0130, San Francisco, CA 94143-0130, or at tomnuc{at}itsa.ucsf.edu.

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Pulmonary Dead Space and Survival
Feihl F., Melot C., Brimioulle S., Her C., Ho K. M., Patel S. R., Harris R. S., Malhotra A., Yoon T. S., Kupfer Y., Tessler S., Nuckton T. J., Eisner M. D., Matthay M. A.
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N Engl J Med 2002; 347:850-852, Sep 12, 2002. Correspondence

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