The arterial to end-tidal PCO₂ difference is dependent on the underlying pulmonary disease. The most common reason for thoracotomy in adults is surgical treatment of lung cancer. Patients with lung cancer are almost exclusively smokers, and therefore have airways disease, and hence the PaCO₂-PETCO₂ gradient during anesthesia will be increased even in the supine position.1 In the 17 patients studied by Werner et al,2 mean PaCO₂-PETCO₂ from each lung was approximately 5 mm Hg in the supine position at a PaCO₂ of 28 mm Hg and ventilatory frequency of 10/min. The lungs receive an approximately equal share of ventilation in the supine position, whereas, the ventilation of the upper lung is increased in the lateral position.2 However, the blood flow to the lungs is gravity dependent resulting in a decreased blood flow to the upper lung. This results in a decrease in the PETCO₂ from the upper lung in the lateral position. Therefore, the PaCO₂-PETCO₂ as measured by Werner et al2 was zero for the lower lung and 11 mm Hg for the upper lung. Since the ventilation of the upper lung increases in the lateral position, it may surmised that if PETCO₂ measured in the combined expirate of both lungs, the PaCO₂-combined PETCO₂ difference would be large.1,2

An incision of the chest wall produces an increase in mean pulmonary artery pressure2 which produces an increase in the CO₂ elimination of the upper lung and a decrease in physiological dead space. The upper lung PaCO₂-PETCO₂ gradient is reduced when the mean pulmonary artery pressure increases as a result of surgical stimulation.

Furthermore, opening of the pleura increases CO₂ elimination in the upper lung and thereby decreases PaCO₂-PETCO₂. Retraction of the lung produces exactly opposite effects. The lower lung gradient is not greatly effected with these maneuvers; it remains small. If combined end-tidal CO₂ monitoring is performed, the PaCO₂-PETCO₂ would decrease when the pleura is opened, and increase again during retraction.

One lung ventilation:1,2

When the upper lung ventilation is discontinued to facilitate surgery, perfusion to the upper lung does not cease completely unless the pulmonary artery is clamped. In the absence of such clamping, there is a right to left shunt to the upper lung, the effect of which is to increase PaCO₂, thus PaCO₂-PETCO₂ increases. However, this PaCO₂-PETCO₂ may not be any greater than the original combined two lung PaCO₂-PETCO₂.

Affect of prolonged expiratory maneuvers on PaCO₂-PETCO₂ during thoracotomy:3

In 16 patients undergoing thoracoabdominal esophagectomy, the affect of two prolonged expiration maneuvers to improve prediction of PaCO₂ from PETCO₂ were studied. PCO₂ at the end of a simple prolonged expiration (PE1CO₂), and PCO₂ at the end of a prolonged expiration preceded by sustained hyperinflation of the lungs (PE2CO₂), were measured during laparotomy, in the lateral thoracotomy position during two-lung ventilation, and after transition to one lung ventilation. PaCO₂-PETCO₂ was 9.75 (SD 3) mm Hg during laparotomy and this remained stable throughout the study. Both maneuvers decreased the mean arterial to peak expired PCO₂ difference particularly during one lung ventilation. These results are in agreement with the results obtained by Bhavani-Shankar et al, where squeeze PETCO₂ decreased PaCO₂-PETCO₂ in pregnant patients undergoing laparoscopic surgery.

Table from reference 3

Measurement mean (SD) mm Hg	PaCO2-PETCO2	PaCO2-PE1CO2	PaCO2-PE2CO2
End of abdominal procedure	9.75 (3)	6 (3.7)	4.5 (3.7)
TLV for 20 min	10.5 (3.7)	7.5(4.5)	3 (4.5)
OLV for 20 min	9.75 (3)	3 (3.7)	– 0.75 (3.7)
OLV for 50 min	10.5 (3.7)	2.2 (4.5)	-1.5 (3.7)
TLV after skin closure	9 (3.7)	3.7 (5.2)	0.75 (4.5)

However, the end-expiratory PCO₂ obtained with each maneuver during laparotomy and thoracotomy agreed poorly with PaCO₂. The authors3 suggest that these maneuvers should no longer be recommended to improve estimation of PaCO₂ from PETCO₂ during anesthesia.

Arterial to end-tidal CO₂ difference after bilateral lung transplantation.

Variable

Time after lung transplantation

Mean (SD)	10 min	1 hr	3 hr	12 hr	24 hr
PaCO2-PETCO2 mm Hg	16 (5)	14 (5)	9 (4)	6 (3)	5 (3)
(PaCO2-PETCO2)/PaCO2	0.36 (0.13)	0.33 (0.13)	0.21 (0.12)	0.15 (0.07)	0.11 (0.06)

The time course of the arterial to end-tidal PCO₂ difference suggests a rapid improvement of this post-transplant ventilation/perfusion mismatch. After 24 hrs, the values were close to the physiological range, which is supposed to be 4-5 mm Hg. A possible explanation of these findings could be ischemia-reperfusion injury that affects microcirculation. An impaired distribution of pulmonary blood flow with unperfused alveoli would clinically appear as alveolar dead space as is seen immediately following lung transplantation. The ventilation/perfusion mismatch normalized in about 24 hrs indicating a redistribution of pulmonary blood flow and recovery of microcirculation.

Arterial to end-tidal carbon dioxide difference during anesthesia for thoracoscopy:

Presently, thoracoscopy is the procedure of choice in most patients requiring thoracic surgery, especially those patients with severe underlying lung disease.6,7 Srinivasa et al7 studied the difference between PaCO₂ and PETCO₂ during thoracoscopic surgery in ten patients scheduled for elective thoracoscopic procedures. All patients had general anesthesia induced by IV propofol, fentanyl and vecuronium. A double lumen endo-tracheal tube was positioned with the aid of a fiber optic bronchoscope. Anesthesia was maintained with 100% oxygen, desflurane, fentanyl and vecuronium. Ventilation was kept at, tidal volume (TV) 10 ml/kg, respiratory rate (RR) of 10 bpm and an I:E ratio of 1:2 while on two lung ventilation. TV was 7 ml/kg, RR of 10 bpm and an I:E ratio of 1:2 while on one lung ventilation (OLV). The FiO2 during all measurements was kept at 1.0. Arterial blood gas was sampled 10 min after the patient was in lateral decubitus position while on two-lung ventilation (T1). The second sample (T2) was10 min after the introduction of trocars (OLV). The last sample (T3) was taken 10 min after restarting two-lung ventilation.
Results: The mean FVC was 2.6 ± 0.8 L (79 ± 19% predicted) and the FEV1 was 1.9 ± 0.7 L (76 ± 26% predicted). Table1 shows demographic data of the patients. The mean PaCO₂ to PETCO₂ difference at times T1, T2 and T3 were 5.5 ± 4, 7.4 ± 5, 6.8 ± 4 mm Hg respectively. The lowest value noted for PETCO₂ was 27 mm Hg and the highest value for PaCO₂ was 52 mm Hg during the study (Fig.2). The difference between the PETCO₂ and PaCO₂ during the various time intervals was not statistically significant.

Time	PETCO2	PaCO2	Difference
T1	32 ± 3	38 ± 5	5.5 ± 4
T2	35 ± 4	42 ± 5	7.4 ± 5
T2	32 ± 3	39 ± 6	6.8 ±

References:

(1). Fletcher R: The Arterio-End-Tidal CO₂ difference during cardiothoracic surgery. J. cardiothorac. Anesthesiol. 4:105-117, 1990.

(2). Werner O. Malmkvist G, Beckman A, et al: CO₂ elimination from each lung during endobronchial anaesthesia. Br. J. Anaesth. 56: 995-1001, 1984.

(3). Tavernier B, Rey D, Thevenin J, Triboulet P, Scherpereel P. Can prolonged expiration manoeuvres improve the prediction of arterial PCO₂ from end-tidal PCO₂? Brit J Anaesth 1997;78:536-40.

(4). Bhavani Shankar K, Steinbrook R, Mushlin PS, Freiberger D. Transcutaneous carbon dioxide monitoring during laparoscopic surgery in pregnancy. Canadian J Anaesth 1998;45:164-9.

(5) Jellinek H, Hiesmayr M, Simon P, Klepetko W, Haider W. Arterial to end-tidal CO₂CO₂ tension difference after bilateral lung transplantation. Crit Care Med 1993;21:1035-40.

(6) Horvath KA: Thoracoscopic transmyocardial laser revascularization. Ann.Thorac.Surg. 1998; 65: 1439-41.

7) Kotloff RM, Tino G, Bavaria JE, Palevsky HI, Hansen-Flaschen J, Wahl PM, Kaiser LR: Bilateral lung volume reduction surgery for advanced emphysema. A comparison of median sternotomy and thoracoscopic approaches. Chest 1996; 110: 1399-406.

(8) Srinivasa V, Kodali BS, Bean T, Hartigan PM. Arterial to end-tidal carbon dioxide difference during thoracoscopic surgery. Anesthesiology ASA abstracts 2004;A1556.