Physiology of capnography
(a-ET)PCO2 reflects Alveolar Dead Space
(a-ET)PCO2 reflects alveolar dead space as a result of a temporal, a spatial and an alveolar mixing defect in the normal lung.
Normal values of (a-ET)PCO2 is 2-5 mm Hg.
(a-ET)PCO2 as an index of alveolar dead space
There is a positive relationship between alveolar dead space and (a-ET)PCO2. There is an exception to this rule (See text below)
(a-ET)PCO2 increases with age, emphysema, and in circumstances where alveolar dead space increases such as in low cardiac output states, hypovolemia, and pulmonary embolism.
(a-ET)PCO2 decreases in pregnancy and children (-0.65-3 mm Hg).
Decreased cardiac output increases alveolar dead space and thus increases (a-ET)PCO2
*This animation has been based on the concept as in reference 2.
(a-ET)CO2 gradient as an index of alveolar dead space:
Under normal circumstances, the PETCO2 (the CO2 recorded at the end of the breath which represents PCO2 from alveoli which empty last) is lower than PaCO2 (average of all alveoli) by 2-5 mmHg, in adults.1-8 The (a-ET)PCO2 gradient is due to the V/Q mismatch in the lungs (alveolar dead space) as a result of temporal, spatial, and alveolar mixing defects. In healthy children, the (a-ET)PCO2 gradient is smaller (-0.65-3 mm Hg) than in adults.9-14 This is due to a better V/Q matching, and hence a lower alveolar dead space in children than in the adults.9 The (a-ET)PCO2 / PaCO2 fraction is a measure of alveolar dead space, and changes in alveolar dead space correlate well with changes in (a-ET)PCO2.4 An increase in (a-ET)PCO2 suggests an increase in dead space ventilation. Hence (a-ET)PCO2 is an indirect estimate of V/Q mismatching of the lung.
However, (a-ET)PCO2 does not correlate with alveolar dead space in all circumstances. Changes in alveolar dead space correlate with (a-ET)PCO2 only when phase III is flat or has a minimal slope. In this case, the area (blue shaded color in the figure above) rectangular and PaCO2 > PETCO2. However, if phase III has a steeper slope, the terminal part of phase III may intercept the line representing PaCO2, resulting in either zero or negative (a-ET)PCO2 even in the presence of alveolar dead space. Therefore, the (a-ET)PCO2 is dependent both on alveolar dead space as well as factors that influence the slope of phase III. This implies that an increase in the alveolar dead space need not be always be associated with an increase in the (a-ET)PCO2. The (a-ET)PCO2 may remain the same if there is an associated increase in the slope of the phase III. For example, it has been observed during cardiac surgery that alveolar dead space was increased at the end of cardiopulmonary bypass but as the slope of phase III was also increased, there was no change in (a-ET)PCO2.15,16
Cardiac output and (a-ET)PCO2
Reduction in cardiac output and pulmonary blood flow result in a decrease in PETCO2 and an increase in (a-ET)PC02. Increases in cardiac output and pulmonary blood flow result in better perfusion of the alveoli and a rise in PETCO2.17,18 Consequently alveolar dead space is reduced as is (a-ET)C02 The decrease in (a-ET)PC02 is due to an increase in the alveolar C02 with a relatively unchanged arterial C02 concentration, suggesting better excretion of C02 into the lungs. The improved C02 excretion is due to better perfusion of upper parts of the lung.18 Askrog found an inverse linear correlation between pulmonary artery pressure and (a-ET)PC02.18 Thus, under conditions of constant lung ventilation, PETCO2 monitoring can be used as a monitor of pulmonary blood flow.17,19
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