Effect of alterations in end-tidal CO₂ tension on flow resistance

The effect of PaCO CO2 on flow resistance and on the mechanical work of ventilating the lung was studied in five normal subjects during sustained voluntary hyperventilation. Hypocapnia caused a consistent increase in flow resistance. Thus, for a minute volume of approximately 30 liters/ min the mean inspiratory flow resistance was 133% greater and the mean respiratory work of ventilating the lungs 68% greater at PaCO CO2 20–25 mm Hg compared to values at 45–50 mm Hg. End-expiratory pressure and compliance were unaffected. Atropine and isoproterenol each markedly diminished the responsiveness of the airways to low PaCO CO2 levels and, given together, blocked the effect completely. These findings could largely account for the increase in oxygen cost of breathing, and in cardiac output associated with voluntary (i.e., hypocapneic) hyperventilation. PaCO CO2 ; work of breathing; mechanical properties Submitted on June 24, 1963