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

References:

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.