By: AMFS Physician Advisory Panel
Numerous patients unexpectedly suffer sudden respiratory arrest with catastrophic results in the immediate aftermath of surgery. (1,2) Most are elderly and recently treated with sedatives and narcotics. The problem has inspired the Anesthesia Patient Safety Foundation to convene a meeting of experts to discuss the cause and find solutions. These experts overwhelmingly recommended aggressive electronic monitoring as the best available means of detecting the problem. However, many also observed that these incidents occur so suddenly and unpredictably that electronic monitoring might generate more false alarms than effective alerts. Meanwhile, they couldn’t identify the cause. An effective solution is unlikely unless the cause can be identified.
The cause should be obvious. Modern research has long since proved that carbon dioxide is benign, beneficial, and essential for normal respiratory drive (3-11), but the common practice of hyperventilation drives carbon dioxide from the system. Hyperventilation confers no benefit and confers occult risks in all known circumstances.(12-16) Mechanical hyperventilation during anesthesia rapidly depletes tissue reserves of CO2, which paralyses the function of respiratory chemoreceptors in the aortic arch and carotid arteries.(17) These are essential for normal respiratory drive, especially during sleep and other conditions where the independent respiratory drive produced by conscious awareness is absent.(18-22) Hyperventilated patients appear to breathe normally when they emerge from anesthesia, but their respiratory drive precariously depends on conscious awareness. This condition can last for several hours, until normal metabolism has restored CO2 tissue levels and chemoreceptor function. If a patient loses consciousness during this vulnerable period he will immediately stop breathing and suffer hypoxemic brain damage within minutes, soon followed by death. Opioids and sedatives that relieve pain and promote sleep can precipitate the problem. (23)
Myth and habit often prevail over science. Critical care experts have embraced the benefits of permissive hypercarbia for more than 20 years, but anesthetists everywhere have persisted in their practice of hyperventilating anesthetized patients, based on defective old studies. Because of these outdated studies and the occult nature of the problem, most anesthesiologists mistakenly believe that hyperventilation is harmless and that it prevents harmful “respiratory acidosis” and cardiac depression. What is needed is a new set of guidelines and standards that condemn hyperventilation and promote permissive hypercarbia to avoid this disastrous problem, but such effective change is unlikely in the foreseeable future. Meanwhile, anesthesia hyperventilation can be regarded as a potentially lethal form of malpractice.
1. Overdyk FJ. postoperative Opioids Need System-Wide Overhaul. Anesthesia Patient Safety Foundation Newsletter 2010.
2. Overdyk FJ. Postoperative opioids remain a serious patient safety threat. Anesthesiology 2010;113:259-60; author reply 60-1.
3. Fothergill DM, Hedges D, Morrison JB. Effects of CO2 and N2 partial pressures on cognitive and psychomotor performance. Undersea Biomed Res 1991;18:1-19.
4. Kavanagh B. Normocapnia vs hypercapnia. Minerva Anestesiol 2002;68:346-50.
5. Laffey JG, Engelberts D, Duggan M, Veldhuizen R, Lewis JF, Kavanagh BP. Carbon dioxide attenuates pulmonary impairment resulting from hyperventilation. Crit Care Med 2003;31:2634-40.
6. Hare GM, Kavanagh BP, Mazer CD, Hum KM, Kim SY, Coackley C, Barr A, Baker AJ. Hypercapnia increases cerebral tissue oxygen tension in anesthetized rats. Can J Anaesth 2003;50:1061-8.
7. Laffey JG, O’Croinin D, McLoughlin P, Kavanagh BP. Permissive hypercapnia–role in protective lung ventilatory strategies. Intensive Care Med 2004;30:347-56.
8. Akca O, Liem E, Suleman MI, Doufas AG, Galandiuk S, Sessler DI. Effect of intra-operative end-tidal carbon dioxide partial pressure on tissue oxygenation. Anaesthesia 2003;58:536-42.
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10. Akca O. Lower tidal volumes and positive end-expiratory pressure prevents alveolar coagulation in patients without lung injury. Anesthesiology 2007;106:1065-6.
11. Akca O. Optimizing the intraoperative management of carbon dioxide concentration. Curr Opin Anaesthesiol 2006;19:19-25.
12. Jaffe MB. Infrared measurement of carbon dioxide in the human breath: “breathe-through” devices from Tyndall to the present day. Anesth Analg 2008;107:890-904.
13. Wickipedia. Shallow Water Blackout Syndrome.
14. Ainslie SG, Eisele JH, Jr., Corkill G. Fentanyl concentrations in brain and serum during respiratory acid–base changes in the dog. Anesthesiology 1979;51:293-7.
15. Albrecht RF, Miletich DJ, Ruttle M. Cerebral effects of extended hyperventilation in unanesthetized goats. Stroke 1987;18:649-55.
16. Raichle ME, Plum F. Hyperventilation and cerebral blood flow. Stroke 1972;3:566-75.
17. Nichols G, Jr. Serial changes in tissue carbon dioxide content during acute respiratory acidosis. J Clin Invest 1958;37:1111-22.
18. Corne S, Webster K, Younes M. Hypoxic respiratory response during acute stable hypocapnia. Am J Respir Crit Care Med 2003;167:1193-9.
19. Lahiri S, DeLaney RG. Stimulus interaction in the responses of carotid body chemoreceptor single afferent fibers. Respir Physiol 1975;24:249-66.
20. Prabhakar NR. O2 sensing at the mammalian carotid body: why multiple O2 sensors and multiple transmitters? Exp Physiol 2006;91:17-23.
21. Fink BR. Influence of cerebral activity in wakefulness on regulation of breathing. J Appl Physiol 1961;16:15-20.
22. Bellville JW, Howland WS, Seed JC, Houde RW. The effect of sleep on the respiratory response to carbon dioxide. Anesthesiology 1959;20:628-34.
23. Forrest WH, Jr., Bellville JW. The Effect of Sleep Plus Morphine on the Respiratory Response to Carbon Dioxide. Anesthesiology 1964;25:137-41.
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