Capnography has three important applications during laparoscopic surgery.

1. It serves as a non-invasive monitor of PaCO₂ during CO₂ insufflation and therefore can be used to adjust ventilation.

2. It may help in the detection of accidental intravascular CO₂ insufflation.

3. It may help in the detection of complications of CO₂ insufflation such as pneumothorax and hemorrhage.

Hemodynamic and ventilatory changes during CO₂ insufflation

 

PETCO₂ as a non-invasive monitor of PaCO₂:

Prolonged intra-abdominal insufflation with CO₂ in anesthetized and mechanically ventilated patients during upper abdominal laparoscopic surgery does not significantly affect the reliability of PETCO₂ monitoring in predicting PaCO₂ in healthy ASA I and II subjects and elderly patients.1-3 However, in ASA III and IV patients, PETCO₂ may not reflect changes in PaCO₂ during insufflation due to changes in alveolar dead space consequent to reduced cardiac output, increased ventilation-perfusion mismatching, or both.4,5 Therefore, direct arterial PaCO₂ monitoring is recommended in patients with significant cardiorespiratory diseases. An arterial line is reasonable to monitor PaCO₂ in ASA III and IV patients for three reasons: (1) end-tidal PCO₂ is not a reliable index of PaCO₂, (2) the normal gradient of 3 to 5 mm Hg between PaCO₂ and PETCO₂ is increased, and (3) even with normal PETCO₂, achieved by increasing minute volume, PaCO₂ may be as high as 50 mm Hg resulting in respiratory acidosis.

Pregnant patients:

The Society of American Gastrointestinal Endoscopic surgeons (SAGES) published guidelines for laparoscopic surgery during pregnancy that include perioperative monitoring of arterial blood gases as well as perioperative fetal and uterine monitoring.6 This belief has been echoed by other authorities.7-9 Amos etal,7 documented four fetal deaths in seven pregnant women who underwent laparoscopic cholecystectomy or appendectomy (in these patients the ventilation was adjusted to maintain PETCO₂ in low-to mid-30’s). Although Amos et al, did not perform arterial blood gases, respiratory acidosis was stated as a possible factor contributing to fetal loss.10 Based on studies in pregnant ewes, 12,13 these concerns stem from previous studies indicating that elevation in maternal PaCO₂ could impair fetal CO₂ excretion across the placenta and could exacerbate fetal acidosis. Other risk factors were present for fetal loss in this series, including perforated appendix and pancreatitis.7

The pregnant sheep model gives further credence to these concerns. Hunter et al9 and Cruz et al8 both observed that CO₂ pneumoperitoneum resulted in a PaCO₂-PETCO₂ gradient of 16 to 25 mm Hg. The resulting fetal hypercarbia correspondeds to to fetal hypertension, acidosis, and tachycardia. Hunter’s group also demonstrated that the PETCO₂ lagged behind the PaCO₂ by approximately 60 minutes, and hyperventilation was not able to prevent hypercarbia and acidosis. Because of the large changes in PaCO₂ levels, these two groups reported that capnography might underestimate and is therefore not a reliable indicator of respiratory acid-base status during CO₂ insufflation. They recommended arterial blood gas monitoring for all parturients undergoing laparoscopic surgery; however, Bhavani-Shankar and Mushlin10 challenged the appropriateness of the ewe model for this purpose. Subsequently, Bhavani-Shankar et al11 prospectively evaluated the PaCO₂-PETCO₂ difference in eight parturients undergoing laparoscopic cholecystectomy with CO₂ pneumoperitoneum. The intra-abdominal pressures were maintained around 15 mm Hg. These women underwent surgery with general anesthesia during the second and third trimester of their pregnancies. Adjusting minute ventilation to maintain PETCO₂ at 32 mm Hg, the arterial blood gases were measured at fixed surgical phases: preinsufflation, during insufflation, postinsufflation, and after completion of anesthesia. The authors found no significant difference in either mean PaCO₂-PETCO₂ gradient or PaCO₂ and pH during the various phases of laparoscopy as shown below.

	Pre-insufflation	During insufflation	Post-insufflation	Post-extubation	Post-Anesth. Care unit
PETCO2 (mmHg)	32.1 (1.6) N =17 [31.3-32.8]	32.4 (1.1) N =28 [31.9-32.8]	32.7(1.4) N =12 [31.9-33.5]
PaCO2 (mmHg)	34.5 (2.6) N =17 [33.2-35.7]	35 (1.7) N =28 [34.3-35.6]	34.6 (2.5) N =12 [33.1-36]	37.9 (2.8) N =4 [35.1-40.6]	36.2 (2.9) N =8 [34.1-38.2]
PaCO2-PETCO2 (mmHg)	2.4 (1.5) N =17 [1.6-3.1]	2.6 (1.2) N =28 [2.1-3]	1.9 (1.4) N =12 [1.1-2.6]

This is in contrast to results obtained by Cruz et al (9 pregnant ewes) and Hunter et al (4 pregnant ewes) where the difference increased by a mean of 10 mmHg during insufflation.12,13 Among the twenty-eight observations obtained in 8 patients during CO₂ insufflation in our study, the highest PaCO₂-PETCO₂ observed was 5.1 mmHg as against 16 and 25 mmHg observed by Cruez et al and Hunter et al in ewes.8.9 The results observed in our study are consistent with our earlier observations of derived PaCO₂-PETCO₂ of 6-7 mmHg from tcPCO₂ monitoring in laparoscopic surgery in a parturient.12 Therefore, the physiologic consequences of pneumoperitoneum are different in humans from those in pregnant ewes as seen by a lowered PaCO₂-PETCO₂ during insufflation in pregnant patients.

Although the sheep model is used for obstetric research, there could be physiological differences between the two species. For example, the preinsufflation PaCO₂-PETCO₂ in pregnant ewes range from 6 to 15 mmHg,8,9 whereas they are lower in pregnant humans (0.6 mmHg, range -2.5-5.1 mmHg; occasionally PETCO₂ exceeds PaCO₂).13-15 In our study, they varied from 0 to 5 mmHg. These values are similar to the values reported by the author in pregnant subjects undergoing cesarean section and in women during postpartum sterilization.13,14 The smaller pre-insufflation arterial to end-tidal PCO₂ difference in humans translates into a lower preinflation alveolar deadspace in pregnant patients than in pregnant ewes.15 A lower preinsufflation alveolar deadspace in pregnant patients probably results in a smaller subsequent changes in alveolar deadspace during CO₂ insufflation, and thus to a smaller PaCO₂-PETCO₂ in pregnant patients than in pregnant ewes.

Hence it appears that arterial blood gas monitoring during laparoscopy in pregnant patients with healthy lungs may not be necessary.

Infants and children

Rosinoso-Barbero et al concluded that capnography proved to be an excellent guide to adjust ventilation during CO₂ insufflation in infants and children.18 However, Laffon et al concluded that PETCO₂ monitoring may overestimate PaCO₂ and consequently can result in hyperventilation during laparoscopic surgery.19 Arterial to end-tidal carbon dioxide differences were studied in sixty-one children undergoing pneumoperitoneum under general anesthesia.19 At a steady state, before pneumoperitoneum, the mean (a-ET)PCO₂ was -1.2 (SD)2.2, (confidence interval -5.6 to +3.4) Hg. At a steady state during CO₂ insufflation, the mean difference was -2.0(SD),(confidence interval -8.8 to +4.8) mm Hg although PaCO₂ and PETCO₂ increased by about 14% from baseline values. The incidence of negative gradients increased from 54% at pre-insufflation to 67% during CO₂ insufflation. The authors concluded that PETCO₂ often overestimates PaCO₂ during laparoscopy in children, by up to 8.8 mm Hg and therefore concluded that arterial blood gas analysis should be performed during long procedures to avoid hyperventilation. A limited data presented in a study by Bozkurt et al shows no changes in (a-ET)PCO₂ at 30 during CO₂ insufflation compared to baseline levels.20

Negative (a-ET)PCO₂:

Occasionally, during the course of laparoscopic surgery, the gradient may be negative in adults, in which case PETCO₂ overestimates PaCO₂.1 The incidence of negative gradients is higher in infants and children undergoing laparoscopic surgery.19 Low frequency, high tidal volume ventilation will open hitherto closed alveoli, whose CO₂ will now be seen as an increase in the slope of phase III of the capnogram and PETCO₂ will be close or exceed the PaCO₂ line. Low FRC coupled with increased CO₂ delivery to the alveoli can exacerbate this response thereby increasing the frequency of occurrences of negative (a-ET)PCO₂ values during laparoscopic surgery.13-15

References:

1. Wabha RWM, Mamazza J. Ventilatory requirements during laparoscopic cholecystectomy. Can J Anaesth 1993;40:206-210.

2. Nyarwaya JB, Mazoit JX, Samii K. Are pulse oximetry and end-tidal carbon dioxide tension monitoring reliable during laparoscopic surgery? Anaesthesia 1994;49:775-778.

3. Baraka A, Jabbour S, Hammoud R et al. Can pulse oximetry and end-tidal capnography reflect arterial oxygenation and carbon dioxide elimination during laparoscopic cholecystectomy? Surg Laparosc Endosc 1994;4:353-356.

4. Feig BW, Berger DH,Dougherty TB et al. Pulmonary effects of CO₂ abdominal insufflation (CAI) during laparoscopy in high-risk patients. Anesth Analg 1994;78(supplement):S108.

5. Monk TG, Weldon BC, Lemon D. Alterations in pulmonary function during laparoscopic surgery. Anesth Analg 1993;76(Supplement):S274.

6. Guidelines for laparoscopic surgery during pregnancy. Surg Endosc 1998;12:189.

7. Amos JD, Schorr SJ, Norman PF, et al. Laparoscopic surgery during pregnancy. Am J Surg 1996;171:435.

8. Cruez AM, Southerland LC, Duke T, et al. Intra-abdominal carbon dioxide insufflation in the pregnant ewe. Anesthesiology 1996;64:790.

9. Hunter JG, Swanstrom L, Thronburg K. Carbon dioxide pneumoperitoneum induces fetal acidosis in pregnant ewe model. Surg Endosc 1995;9:272.

10. Bhavani-Shankar K, Mushlin P. Arterial to end-tidal gradients in pregnant subjects. Anesthesiology 1997;87:1596.

11. Bhavani shankar K, Steinbrook R, Brooks D, Datta S. Arterial to end-tidal carbon dioxide difference during anesthesia for laparoscopic surgery in pregnancy. Anesthesiolgy 2000;93(2):370-3.

12. Bhavani Shankar K, Steinbrook RA, Mushlin PS, Freiberger D. Transcutaneous PCO₂ monitoring during laparoscopic cholecystectomy in pregnancy. Canadian J Anaesth 1998;45(2):164-9.

13. Bhavani Shankar K, Moseley H, Kumar Y, Vemula V, Krishnan A. Arterial to end-tidal carbon dioxide tension difference during anaesthesia for tubal ligation. Anaesthesia 1987;42:482-6.

14. 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.

15. Bhavani Shankar K, Moseley H, Kumar Y, Delph Y. Capnometry and anaesthesia. Can J Anaesth 1992;39:6:617-32.

16 Wahba RW, Beique F, Kleiman SJ. Cardiopulmonary function and laparoscopic cholecystectomy. Review article. Can J Anaesth 1995;42:1:51-63.

17 Joris JL, Noirot DP, Legrand MJ, Jacquet NJ, Lamy ML. Hemodynamic changes during laparoscopic cholecystectomy. Anesth Analg 1993;76:1067-71,

18 Resinoso-Barbero F, Diez A Paz JA, et al. Physiopathologic implications of the anesthesiologic management of pediatric laparoscopic surgery. Rev Esp Anesthesiol Reanim 1995;42:277-82.

19. Laffon M, Goucher A, Sitbon P et al. Differences between arterial to end-tidal carbon dioxide pressures during laparoscopy in paediatric patients. Can J Anaesth 1998;45:561-3.

20. Bozkurt P, Kaya G et al. The cardiorespiratory effects of laparoscopic procedures in infants. Anaesthesia 1999;54:831-4.