POSTHYPERVENTILATION HYPOXEMIA AFTER METHACHOLINE INHALATION

The hypothesis of this study was that hypoxemia after methacholine (MT H) inhalation is related not only to ventilation/perfusion inhomogenei ty, 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 inve stigated, and Sa(O2), minute ventilation (VE), oxygen uptake rate in t he lung (VO2), carbon dioxide output rate in the lung (VCO2), and resp iratory exchange ratio (R) were measured. The Sa(O2) level decreased f rom a baseline level (before MTH inhalation) of 96.8+/-1.0% (mean+/-SD ) to the lowest level (the nadir Sa(O2)) of 89.8+/-2.1% (p<0.01) in 20 0+/-50s after MTH inhalation and gradually increased toward the baseli ne level. VCO2 increased just after MTH inhalation (post-MTH) with inc reased VE, and decreased at the nadir Sa(O2) with baseline VE and Pa-C O2, indicating a decrease in breath-by-breath VA and an increase in de ad space minute ventilation at the nadir Sa(O2), but VO2 remained clos e to constant. R increased post-MTH, decreased at the nadir Sa(O2), an d thereafter increased gradually toward the baseline level with a time constant of 5.6 min. The addition of CO2 to inspired air partially su ppressed hypoxemia. The consensus is that hypoxemia after MTH is solel y attributable to the ventilation/perfusion inhomogeneity, but posthyp erventilation hypoxemia is another reasonable interpretation of the hy peremia after MTH with decreased VA, VCO2, and R. It is speculated tha t posthyperventilation normoventilation in respect to VCO2 with baseli ne PaCO2 after MTH inhalation resulted in posthyperventilation hypoxem ia as a result of relative hypoventilation in respect to VO2.