Journal of applied physiology
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Tidal volumes used in high-frequency ventilation (HFV) may be smaller than anatomic dead space, but since gas exchange does take place, physiological dead space (VD) must be smaller than tidal volume (VT). We quantified changes in VD in three dogs at constant alveolar ventilation using the Bohr equation as VT was varied from 3 to 15 ml/kg and frequency (f) from 0.2 to 8 Hz, ranges that include normal as well as HFV. ⋯ At tidal volumes less than 7 ml/kg, the data deviated substantially from the conventional alveolar ventilation equation [f(VT - VD) = constant] but fit well a model derived previously for HFV. This model predicts that gas exchange with volumes smaller than dead space should vary approximately as the product of f and VT2.
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Values of the classical Haldane coefficient, i.e, the change in the concentration of total CO2 in whole blood per unit of change in the concentration of total O2 at constant PCO2, have been calculated at different combinations of plasma pH (range 7.25-7.50), erythrocyte 2,3-diphosphoglycerate (DPG) concentration (range 3.5-6.5 mM), PCO2 (range 25.0-65.0 Torr), initial hemoglobin O2 saturation (range 0.50-0.80), and erythrocyte volume fraction (range 0.25-0.55). The principle of the calculations is to utilize the so-called reciprocity relations to determine the amount of protons and CO2 released from hemoglobin on oxygenation and to estimate the resulting change in the concentration of total CO2 from published data on the interaction coefficient for the binding of O2 and protons to hemoglobin, the interaction coefficient for the binding of O2 and CO2 to hemoglobin, the distribution of protons across the erythrocyte membrane, the equilibrium constants for the reactions between CO2 and H2O, and CO2 and oxyhemoglobin, the buffer capacity of oxygenated erythrolysate, and the buffer capacity of plasma. ⋯ Furthermore, the coefficient depends on the hemoglobin O2 saturation and the erythrocyte volume fraction. The dependency of the Haldane coefficient on the O2 saturation and the PCO2 causes an increase in the O2-linked CO2 flux across the alveolar membrane by more than 30% in patients with respiratory insufficiency.