(a-ET)CO2 difference and Alveolar dead space
Physiology of capnography
Bhavani Shankar Kodali MD
(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
Air embolism increases alveolar dead space and thus increases(aET)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
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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.
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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.
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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.
PETCO2 and Cardiac output
Physiology of capnography
Bhavani Shankar Kodali MD
How does cardiac output affect PETCO2
Increases in cardiac output and pulmonary blood flow result in better perfusion of the alveoli and a rise in PETCO2.
Under conditions of constant lung ventilation, PETCO2 monitoring can be used as a monitor of pulmonary blood flow
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)PC02.1,2 The percent decrease in PETCO2 directly correlated with the percent decrease in cardiac output (slope= 0.33, r2=0.82 in 24 patients undergoing aortic aneurysm surgery with constant ventilation).3 Also, the percent decrease in CO2 elimination correlated with the percent decrease in cardiac output similarly (slope=0.33, r2=0.84).3 The changes in PETCTO2 and CO2 elimination following hemodynamic perturbation were parallel. These findings suggest that decrease in PETCO2 quantitatively reflect the decreases in CO2 elimination.3
Increases in cardiac output and pulmonary blood flow result in better perfusion of the alveoli and a rise in PETCO2.1,2 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.2 Relationship between PETCO2 and pulmonary artery blood flow was studied during separation from cardiopulmonary bypass.4 This showed that PETCO2 is a useful index of pulmonary blood flow. A PETCO2 greater than 30 mm Hg was invariably associated with a cardiac output more than 4 L/min or a cardiac index > 2 L/min.4 Furthermore, when PETCO2 exceeded 34 mm Hg, pulmonary blood flow was more than 5 L/min (CI > 2.5 L).4
Thus, under conditions of constant lung ventilation, PETCO2 monitoring can be used as a monitor of pulmonary blood flow.4-8
Recently, using Fick's Principle, attempts were made to determine cardiac output non-invasively implementing periods of CO2 rebreathing during which CO2 partial pressure of oxygenated mixed venous blood was obtained from the measured exponential rise of the PET value. In addition, oxygen uptake, carbon dioxide elimination, end-tidal PCO2, oxygen saturation, and tidal volume were determined. The results are encouraging in patients with healthy lungs.9 Whereas the results are controversial when the lungs are diseased.10
1. 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.
2. Askrog V. Changes in (a-A)CO2 difference and pulmonary artery pressure in anesthetized man. J Appl Physiol 1966;;21:1299-1305.
3 Shibutani K, Muraoka M, Shirasaki S, Kabul K, Sanchala VT, Gupte P. Do changes in end-tidal PCO2 quantitatively reflect changes in cardiac output? Anesth Analg 1994;79:829-33.
4. Maslow A, Stearns G, Bert A, Feng W, Price D, Schwartz C, Mackinnon S, Rotenberg F, Hopkins R, Cooper G, Singh A, Loring SH. Monitoring end-tidal carbon dioxide during weaning from cardiopulmonary bypass in patients without significant lung disease. Anesth Analg 2001;92:306-13.
5. Weil MH, Bisera J, Trevino RP, Rackow EC. Cardiac output and end-tidal carbon dioxide. Crit Care Med 1985;13:907-9.
6. Ornato JP, Garnett AR, Glauser FL. Relationship between cardiac output and the end-tidal carbon dioxide tension. Ann Emerg Med 1990;19:1104-6.
7. Jin X, Weil MH, Povoas H, Pernat A, Xie J, Bisera J. End-tidal carbon dioxide as a noninvasive indicator of cardiac index during circulatory shock. Crit care Med 2000;28:2415-9.
8. Isserles SA, Breen PH. Can changes in end-tidal PCO2 measure changes in cardiac output? Anesth Analg 1991;73:808-14.
9. Gedeon A, Krill P, Kristensen J, Gottlieb I. Noninvasive cardiac output determined with a new method based on gas exchange measurements and carbon dioxide rebreathing: A study in animals/pigs. J Clin Monit 1992;8:267-78.
10. Pianosi P, Hochman J. End-tidal estimates of arterial PCO2 for cardiac output measurements by CO2 rebreathing: a study in patients with cystic fibrosis and healthy controls. Pedatr Pulmonol 1996;22:154-60.