Bhavani Shankar Kodali MD

(a-ET)PCO₂ reflects alveolar dead space as a result of a temporal, a spatial and an alveolar mixing defect in the normal lung.
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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

 

 

Pulmonary thrombo-embolism increases alveolar dead space and thus increases (a-ET)PCO₂

(a-ET)PCO₂ may not reflect Alveolar Dead Space when phase III has a steeper slope

 

* (a-ET)PCO₂ could be zero or negative even in the presence of alveolar dead space

*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

Reference:

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2. Fletcher R. The single breath test for carbon dioxide. Thesis, Lund 1980.

3. Bhavani shankar K, Kumar AY, Moseley H, Hallsworth RA. Terminology and the current limitations of time capnography. J Clin Monit 1995;11:175-82.

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5. Fletcher R, Jonson B. Deadspace and the single breath test carbon dioxide during anaesthesia and artificial ventilation. Br J Anaesth 1984;56:109-19.

6. Shankar KB, Moseley H,Kumar Y, Vemula V. Arterial to end-tidal carbon dioxide tension difference during Caesarean section anaesthesia. Anaesthesia 1986;41:698-702.

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8. Bhavani Shankar K, Mosely H, Kumar AY, Delph Y. Capnometery and anaesthesia. Review article. Can J Anaesth 617-32.

9. Fletcher R. Invasive and noninvasive measurement of the respiratory deadspace in anesthetized children with cardiac disease. Anesth Analg 1988;67:442-7.

10 Fletcher R, Niklason L, Drefeldt B. Gas exchange during controlled ventilation in children with normal and abnormal pulmonary circulation. Anesth Analg 1986;65:645-52.

11. Stokes MA, Hughes OG, Hutton P. Capnography in small subjects. Br J Anaesth 1986;58:814P.

12. Sivan Y, Eldadah MK, Cheah TE, Newth CJ. Estimation of arterial carbon dioxide by end-tidal and transcutaneous PCO₂ measurements in ventilated children. Pediatric Pulmonology 1992;12(3):153-7

13 Burrows FA. Physiologic deadspace, venous admixture, and the arterial to end-tidal carbon dioxide difference in infants and children undergoing cardiac surgery. Anesthesiology 1989;70:219-25.

14 Cambell FA, McLeod ME, Bissonette B, Swartz JS. End-tidal carbon dioxide measurements in infants and children during and after general anaesthesia. Canadian J Anaesth 1993;41;107-10.

15. Fletcher R, Malmkvist G, Niklasson L, Jonson B. On line-measurement of gas-exchange during cardiac surgery. Acta Anaesthesiol Scand 1986;30:295-9.

16. Shankar KB, Moseley H, Kumar Y. Negative arterial to end-tidal gradients. Can J Anaesth 1991;38:260-1.

17. Leigh MD, Jones JC, Motley HL. The expired carbon dioxide as a continuous guide of the pulmonary and circulatory systems during anesthesia and surgery. J Thoracic cardiovasc surg 1961;41:597-610.

18. Askrog V. Changes in (a-A)CO₂ difference and pulmonary artery pressure in anesthetized man. J Appl Physiol 1966;;21:1299-1305.

19. Weil MH, Bisera J, Trevino RP, Rackow EC. Cardiac output and end-tidal carbon dioxide. Crit Care Med 1985;13:907-9.