Fig. 2. The upper figure (A ) illustrates the closed apparatus used to measure the rate of increase in alveolar carbon dioxide (CO2) in preoxygenated, anesthetized (thiopental) normocapnic or hypocapnic (previously hyperventilated) patients. Exchange of gases was ensured by intermittent compression of the rubber bag. Volume constancy was assured by adjustment of the inflow of oxygen (O2) (∼200 ml/min). The gas volume, primarily the 300-ml rubber bag, was too small to act as a significant reservoir, and thus the increasing carbon dioxide in the apparatus, as measured by the carbon dioxide analyzer, reflected the rate of increase in alveolar carbon dioxide. The lower figure (B ) provides the results. In both the normocapnic and hypocapnic patients, carbon dioxide increased by 10-12 mmHg in the first 30-60 s, reflecting the change in the alveoli from equilibration with arterial blood gases to venous blood gases. It also probably resulted partly from initial ventilation/perfusion inequalities. The subsequent 3-5 mmHg/min increase in carbon dioxide reflected the rate of filling of the body with carbon dioxide—the buffering by the body. The figures are reprinted from figs. 1 and 2from Anesthesiology 1961; 22:419-25.2

Fig. 2. The upper figure (A ) illustrates the closed apparatus used to measure the rate of increase in alveolar carbon dioxide (CO2) in preoxygenated, anesthetized (thiopental) normocapnic or hypocapnic (previously hyperventilated) patients. Exchange of gases was ensured by intermittent compression of the rubber bag. Volume constancy was assured by adjustment of the inflow of oxygen (O2) (∼200 ml/min). The gas volume, primarily the 300-ml rubber bag, was too small to act as a significant reservoir, and thus the increasing carbon dioxide in the apparatus, as measured by the carbon dioxide analyzer, reflected the rate of increase in alveolar carbon dioxide. The lower figure (B ) provides the results. In both the normocapnic and hypocapnic patients, carbon dioxide increased by 10-12 mmHg in the first 30-60 s, reflecting the change in the alveoli from equilibration with arterial blood gases to venous blood gases. It also probably resulted partly from initial ventilation/perfusion inequalities. The subsequent 3-5 mmHg/min increase in carbon dioxide reflected the rate of filling of the body with carbon dioxide—the buffering by the body. The figures are reprinted from figs. 1 and 2from Anesthesiology 1961; 22:419-25.2 

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