Tissue CO 2 enters capillary blood by simple diffusion resulting from a pressure gradient. 4 Regardless of its origin, CO 2 has to leave the tissues, be transported in blood, and be eliminated in the lungs, or respiratory acidosis will develop.ĬO 2 transport in blood is complex. Tissue P CO 2 can also increase as a consequence of bicarbonate (HCO 3 −) buffering of non-volatile acids (eg, lactate) during tissue dysoxia, 1, 2 which can result in a respiratory quotient of > 1 3 lipogenesis can also produce a respiratory quotient of > 1 under aerobic conditions. In aerobic metabolism, the respiratory quotient varies from 0.7 to 1 as a function of the substrate being burned to produce energy. The respiratory quotient shows the relationship between oxygen consumption (V̇ O 2) and CO 2 production (V̇ CO 2): respiratory quotient = V̇ CO 2/V̇ O 2. In normal conditions, CO 2 is produced at the tissue level during pyruvate oxidation as a result of aerobic metabolism. Measuring physiologic dead space and alveolar ejection volume at admission or examining the trend during mechanical ventilation might provide useful information on outcomes of critically ill patients with ARDS. When PEEP recruits collapsed lung units, resulting in improved oxygenation, alveolar dead space may decrease however, when PEEP induces overdistention, alveolar dead space tends to increase. Alveolar dead space is potentially large in pulmonary embolism, COPD, and all forms of ARDS. Lung areas that are ventilated but not perfused form part of the dead space. Lung heterogeneity creates regional differences in CO 2 concentration, and sequential emptying raises the alveolar plateau and steepens the expired CO 2 slope in expiratory capnograms. In steady-state conditions, CO 2 output equals CO 2 elimination, but during non-steady-state conditions, phase issues and impaired tissue CO 2 clearance make CO 2 output less predictable.
Alveolar P CO 2 (P ACO 2) depends on the balance between the amount of CO 2 being added by pulmonary blood and the amount being eliminated by alveolar ventilation (V̇ A). The diffusion of gases brings the partial pressures of O 2 and CO 2 in blood and alveolar gas to an equilibrium at the pulmonary blood-gas barrier.
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