“Global warming is not the only downside of elevated CO₂ concentration”

Respiratory complications are common events in the postanesthesia care unit (PACU) — as many as 7% of patients require upper-airway support of some kind during their PACU course. Although pulse oximetry provides excellent monitoring of arterial oxygen saturation, it is an anesthesia truism that reduced arterial oxygen saturation due to hypoventilation in patients receiving supplemental oxygen is a late finding. The physiologic manifestations of hypercapnea are truly protean, and although central nervous system effects are noticeable in patients who are awake, these findings, and others, may be masked by the shifting perioperative milieu. Hypercapnea both results from and causes respiratory arrest and is usually easily reversible in the PACU patient if caught in time.

Carbon dioxide (CO₂) is an odorless, colorless, heavier-than-air gas, which, apart from oxygen and water, may be the most ubiquitous drug in medicine. Anesthesiologists routinely manipulate the CO₂ content of blood to achieve physiologic goals. It is endogenously produced as a byproduct of energy production by degradation of carbohydrates in the Krebs cycle. Although physiologic investigation of the effects of CO₂ began during the Enlightenment, its toxic effects were known in antiquity from the occasional (sometimes intentional) lethal encounter between living beings and caves with elevated CO₂ concentration. Indeed, CO₂ is itself a general anesthetic; it is currently used for laboratory animal euthanasia and sedation of livestock before slaughter. Experimentation in the 1960s using monkeys and cats breathing a 50:50 mix of CO₂ and oxygen demonstrated electroencephalogram (EEG) slowing to isoelectricity after initial activation. Unlike the mechanism of conventional inhalational anesthetics, the mechanism of CO₂ anesthesia is thought to be an effect of locally induced brain acidosis. In an elegant paper published in 1967, Eisele et al. measured the PaCO₂ at which response to surgical stimulus was abolished in 50% of experimental dogs as 222 mmHg; this is, in essence, the MAC in dogs of CO₂. Thirtypercent CO₂, in oxygen administered by mask to human beings, produces
anesthesia, but produces a foul acidic taste in the mouth and feelings of anxiety and dyspnea. As PaCO₂ rises above 90 mmHg, human beings exhibit stupor and, ultimately, loss of consciousness.

CO₂, whether exogenously or endogenously sourced, has significant physiologic effects apart from those on consciousness. Hypercapnea increases cerebral blood flow and, thus, intracranial pressure. CO₂ is a pulmonary vasoconstrictor, however, and causes a predictable increase in pulmonary-artery pressures at elevated levels. Because of the Bohr effect, hypercapnea decreases hemoglobin affinity for oxygen. An increased CO₂ level also causes systemic hypertension, both from increased cardiac output and arteriolar vasoconstriction. An elevated PaCO₂ is proarrythmic, particularly in the presence of halothane. Hyperkalemia can result from release of cellular potassium stores, and at a very high PaCO₂, glomerular filtration rate is reduced by afferent arteriolar vasoconstriction. Interestingly, a brief review of the literature reveals multiple cases of PaCO₂ levels of more than 200; these patients (mostly children) were stuporous or comatose but, in the absence of hypoxemia, recovered without permanent deficit.