Posthyperventilation hypoxemia after methacholine inhalation.

The hypothesis of this study was that hypoxemia after methacholine (MTH) inhalation is related not only to ventilation/perfusion inhomogeneity, but also to posthyperventilation hypoxemia. To test the hypothesis, we paid special attention to changes in gas exchange and ventilation parameters after MTH inhalation. Six stable asthma patients were investigated, and SaO2, minute ventilation (V.E), oxygen uptake rate in the lung (V.O2), carbon dioxide output rate in the lung (V.CO2), and respiratory exchange ratio (R) were measured. The SaO2 level decreased from a baseline level (before MTH inhalation) of 96.8 +/- 1.0% (mean +/- SD) to the lowest level (the nadir SaO2) of 89.8 +/- 2.1% (p < 0.01) in 200 +/- 50 s after MTH inhalation and gradually increased toward the baseline level. V.CO2 increased just after MTH inhalation (post-MTH) with increased V.E, and decreased at the nadir SaO2 with baseline V.E and PaCO2, indicating a decrease in breath-by-breath V.A and an increase in dead space minute ventilation at the nadir SaO2, but V.O2 remained close to constant. R increased post-MTH, decreased at the nadir SaO2, and thereafter increased gradually toward the baseline level with a time constant of 5.6 min. The addition of CO2 to inspired air partially suppressed hypoxemia. The consensus is that hypoxemia after MTH is solely attributable to the ventilation/perfusion inhomogeneity, but posthyperventilation hypoxemia is another reasonable interpretation of the hypoxemia after MTH with decreased V.A, V.CO2, and R. It is speculated that posthyperventilation normoventilation in respect to V.CO2 with baseline PaCO2 after MTH inhalation resulted in posthyperventilation hypoxemia as a result of relative hypoventilation in respect to V.O2.