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

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Abstract
The effect of PaCOCO2 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 PaCOCO2 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 PaCOCO2 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. PaCOCO2; work of breathing; mechanical properties Submitted on June 24, 1963

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