A call for standards on perioperative CO(2) regulation.

Abstract

To The Editor, The Journal recently published the International Standards to the Practice of Anesthesia. These Standards mandate the use of capnography, but they fail to provide guidelines for carbon dioxide management. Except under rare circumstances, carbon dioxide is inert, odourless, tasteless, invisible, and remarkably benign and beneficial. It is heavier than other atmospheric gases, so it accumulates in dependent locations, such as mines, where air circulation is lacking. Under these conditions, it displaces oxygen and causes death by drowning. Since this phenomenon was attributed to toxicity in earlier times and early gas research confused CO2 effects with carbon monoxide toxicity, carbon dioxide remains widely but mistakenly feared as toxic and narcotic. All vertebrate cells produce CO2 continuously. It saturates body tissues and fluids, and it equilibrates with the external environment. Carotid and aortic respiratory chemoreceptors gradually adapt to and maintain this equilibrium. Synergistic combinations of hypercarbia and hypoxemia exponentially increase chemoreceptor activity and respiratory drive. Hyperventilation is unnatural and abnormal in all circumstances. It confers no tangible benefits, and it may cause serious adverse events, including ‘‘shallow water blackout syndrome’’, brain damage in mountain climbers, and increased morbidity and mortality in otherwise healthy polio victims. Nowadays, its traditional use to counteract brain swelling is discouraged. Mechanical hyperventilation rapidly depletes CO2 tissue reserves, which obtunds chemoreceptors and undermines respiratory drive. Mechanical hyperventilation during anesthesia originated before pulse oximetry and capnography were available. In that bygone era, carbon dioxide was assumed to be a ‘‘toxic waste gas’’ that must be rid from the body rather than an essential element of normal physiology that is rapidly depleted by mechanical hyperventilation and requires careful conservation. It was not understood that hyperventilation damages lung tissues, impairs tissue perfusion and oxygenation, inhibits opioid clearance, traps opioids in brain tissues, and depletes CO2 reserves necessary for normal respiratory chemoreceptor activity. Moreover, it was not understood that mild hypoventilation reduces blood viscosity beneficially, increases cardiac output, promotes tissue perfusion and oxygenation, protects lung tissues, preserves tissue reserves of carbon dioxide, offsets the respiratory depressant effects of opioids, and prevents opioid ‘‘trapping’’ in brain tissues. During that past era, evidence was often misinterpreted or overlooked in favour of pre-existing beliefs about carbon dioxide toxicity. For example, Boniface and Brown mistakenly concluded that CO2 causes toxic depression of cardiac contractility, even though their study documented beneficial decreases in systemic vascular resistance that offered a simpler explanation for decreased cardiac work. Unfortunately, anesthesia hyperventilation remains entrenched, even though critical care experts have embraced the safety of permissive hypercapnia. The practice is reinforced by the routine observation that hyperventilated patients usually breathe adequately upon anesthetic emergence, provided that opioid dosage has been carefully constrained. This is because conscious awareness sustains breathing despite the absence of chemoreceptor activity, particularly in the presence of pain. L. S. Coleman, MD (&) Fresno Dental Surgery Center, 888 E. Divisadero St. #209, Fresno, CA 93721, USA e-mail: lewis_coleman@yahoo.com