Volumetric capnography in acute respiratory distress syndrome: is the era of day-to-day monitoring finally here?

Acute lung injury (ALI) and the acute respiratory distress syndrome (ARDS) affect 4.5–7.1% of the patients admitted to the intensive care unit with acute respiratory failure.1,2 In our population, we found that ARDS affects 15.3 per 100,000 persons per year.3 Although the reported mortality of patients with ALI and ARDS has improved, it remains high among the causes of death in the intensive care unit. Affected patients usually die secondary to sepsis and multisystem organ dysfunction. Some predictive factors associated with mortality include the triggering disease, the severity of the respiratory illness, and the presence of dysfunction of the right ventricle.4 Although hypoxemia is the protean gas exchange abnormality in ALI and ARDS (it is part of the definitions),5 the degree of hypoxemia does not predict outcome.6 As a matter of fact, patients treated with lower tidal volume (VT) in the ARDS Network trial had a lower ratio of PaO2 to fraction of inspired oxygen in the first 3 days of therapy but still had a lower mortality and a higher number of ventilator-free days.7 In this issue of RESPIRATORY CARE, Kallet et al8 demonstrate that using volumetric capnography to calculate the physiologic dead space in patients with ARDS gives values that correlate with those obtained by the metaboliccart method used in their important 2002 paper.9 Kallet et al showed a statistically strong correlation between the 2 techniques in terms of the expired carbon dioxide tension and physiologic dead-space-to-VT ratio, with a fair bias and precision. However, the sample of patients was small and it will be important to independently confirm these exciting findings. These results are important because they simplify the technique of a bedside measurement that can predict survival in patients with ARDS.9 Enghoff defined the physiologic dead space in 1938 as the “wasted ventilation.”10 He modified the Bohr’s equation by replacing the alveolar CO2 concentration with the PaCO2, adding to the anatomic dead space the alveolar units that are either completely nonventilated or subject to varying degrees of ventilation-perfusion mismatch. The physiologic dead space is therefore a measure of the efficiency of ventilation. In 2002, Nuckton et al identified the physiologic dead-space fraction measured within several hours of the onset of respiratory failure as the first lung-specific predictor of mortality in ARDS.9 To calculate the physiologic dead space they used a metabolic monitor, also known as indirect calorimetry cart, that allows the collection of the exhaled VT in the cart’s built-in mixing chamber. An infrared censor then measures the expired CO2 fraction in the collected gas, which in turns allows the calculation of the partial pressure of CO2 in the exhaled VT. The technique is accurate if water vapor pressure is well controlled, the system is relatively free of leaks, and the exhaled VT is collected for several cycles to average the breath-to-breath variation in CO2 composition. The bedside metabolic monitor has been validated against the classic method of collecting exhaled gases in a Douglas bag and measuring the CO2 partial pressure in an arterial blood gas analyzer.11 The metabolic cart is less cumbersome than the Douglas bag, and it allows a minute-tominute bedside evaluation.