Then In the early 1920s, with improved understanding of the physiological effects of carbon dioxide (CO2), its use was proposed to control respiration and facilitate recovery from ether.1,2
“De-etherization by carbon dioxid inhalations, as proposed by Henderson and Haggard, is an important factor in preventing distressing after-effects of ether anesthesia. When properly administered no ill effects have been produced.”3
“… aside from the advantages of having a patient fully awake within a short time following operation, with restoration of the circulation and the body tone to near normal, and the lessening of nausea and vomiting, CO2 therapy is of interest in its undoubted prevention of postoperative pneumonia.”4
“De-etherization with CO2 is simple and effective. It is probably an important agent in preventing postoperative pneumonia. An emergency tank of CO2 in an operating room is of more value than the usual oxygen emergency tank.”4
“The capable anesthetist with suitable apparatus and technique controls respiration to his purpose, or adapts its administration to the patient's respiration.”2
Now One of the primary goals of an ideal anesthetic technique is achieving rapid emergence after termination of anesthesia. Rapid emergence from inhaled anesthesia requires rapid removal of inhaled anesthetic from the brain, which could be achieved by increasing ventilation upon termination of anesthesia. However, increased ventilation might result in hypocapnia, which may reduce cerebral perfusion and conversely reduce removal of inhaled anesthetic from the brain. Thus, to achieve rapid emergence from inhaled anesthesia it is necessary to increase ventilation while maintaining normocarbia or mild hypercapnia.
The practice of administering CO2 at the termination of anesthesia, which was introduced in the 1920s, remained common, particularly in the United Kingdom,5 until the late 1980s when it was discontinued due to concerns of inadvertent hypercapnia.6
In recent years, there has been a resurgence in attempts to increase alveolar ventilation while maintaining normocarbia at the termination of anesthesia. One approach termed “isocapnic hyperpnea” involves administration of CO2 into the anesthesia breathing circuit while increasing alveolar ventilation. The amount of CO2 administered is proportionate to the increase in ventilation, and thus arterial CO2 concentrations are maintained within the physiological range.7,8 Another approach involves rebreathing exhaled CO2 by interposing of a reservoir tube between the breathing circuit and the tracheal tube as well as scrubbing the inhaled anesthetic.9,10 In this approach the CO2 levels can be controlled by changing the length of the reservoir tube.
It is not clear if these approaches will become a part of routine anesthesia practice. Nevertheless, the conventional practice of reducing the minute ventilation, typically the respiratory rate, at the end of surgery with the aim of increasing the end-tidal CO2 (ETCO2) levels needs to be modified. Such practice will delay washout of inhaled anesthetic. Of note, the need to increase ETCO2 at the end of surgery could be reduced if we maintain mild hypercapnia (i.e., ETCO2 40 to 45 mm Hg) throughout the intraoperative period, unless it is contraindicated (e.g., increased intracranial pressure).
Mild hypercapnia during surgery can improve tissue oxygenation through improved tissue perfusion resulting from increased cardiac output and vasodilation as well as increased oxygen off-loading from shifting the oxyhemoglobin dissociation curve to the right.11,12 Therefore, the current conventional practice of maintaining ETCO2 values between 30 and 35 mm Hg needs to be revisited, because it has no scientific merit and can be detrimental, as hyperventilation required to achieve lower CO2 levels can have significant cardiopulmonary and inflammatory adverse effects.13–15 Thus, maintaining mild hypercapnia, while using lung protective ventilation is beneficial and should come to be accepted as the standard of care. This should allow the maintenance of minute ventilation and achieve significant reduction in end-tidal inhaled anesthetic concentration while maintaining normocapnia.
Name: Girish P. Joshi, MB BS, MD, FFARSCI.
Contribution: Girish P. Joshi wrote and approved the final manuscript.
This manuscript was handled by: Steven L. Shafer, MD.
“Poison is in everything, and no thing is without poison. The dosage makes it either a poison or a remedy.”—Paracelsus (Philippus Theophrastus Aureolus Bombastus von Hohenhein), 16th century.
1. Henderson Y, Haggard HW, Coburn RF. The therapeutic use of carbon dioxide after anesthesia and operation. JAMA 1920;74:783–6
2. Henderson Y. A lecture on respiration in anaesthesia: control by carbon dioxide. BMJ 1925;2:1170–5
3. Christiansen EB, Leavitt EI. De-etherization by carbon dioxid inhalation. Anesth Analg 1924;3:168–70
4. Righetti E. De-etherization with carbon dioxid. Anesth Analg 1926;5:8–9
5. Thompson PW, Wilkinson DJ. Development of anaesthetic machines. Br JAnaesth 1985;57:640–8
6. Razis PA. Carbon dioxide-a survey of its use in anesthesia in the UK. Anaesthesia 1989;44:348–51
7. Katznelson R, Minkovick L, Beattie S, Fedoroko L, Fisher J. Accelerated recovery from sevoflurane anesthesia with isocapnic hyperpnoea. Anesth Analg 2008;106:486–91
8. Katznelson R, Naughton F, Friedman Z, Lei D, Duffin J, Fedoroko L, Wasowicz M, Van Rensburg A, Murphy J, Fisher JA. Increased lung clearance of isoflurane shortens emergence in obesity: a prospective randomized-controlled trial. Acta Anaesthesiol Scand 2011;55:995–1001
9. Sakata DJ, Gopalakrishnan NA, Orr JA, White JL, Westenskow DR. Hypercapnic hyperventilation shortens emergence time from isoflurane anesthesia. Anesth Analg 2007;104:587–91
10. Sakata DJ, Gopalakrishnan NA, Orr JA, White JL, Westenskow DR. Rapid recovery from sevoflurane and desflurane with hypercapnia and hyperventilation. Anesth Analg 2007;105:79–82
11. Akca O, Doufas AG, Morioka N, et al.. Hypercapnia improves tissue oxygenation. Anesthesiology 2002;97:801–6
12. Hager H, Reddy D, Mandadi G, et al.. Hypercapnia improves tissue oxygenation in morbidly obese surgical patients. Anesth Analg 2006;103:677–81
13. Wolthuis EK, Choi G, Dessing MC, et al.. Mechanical ventilation with lower tidal volumes and positive end-expiratory pressure prevents pulmonary inflammation in patients without preexisting lung injury. Anesthesiology 2008;108:46–54
14. Gertler R, Joshi GP. Modern understanding of intraoperative mechanical ventilation in normal and diseased lungs. Advances in Anesthesia 2010;28:15–33
15. Wrigge H, Pelosi P. Tidal volume in patients with normal lungs during general anesthesia. Lower the better. Anesthesiology 2011;114:1102–10