Inhaled anesthetics are delivered and eliminated via pulmonary ventilation. The most useful definition of “dose” for these drugs is the partial pressure in alveolar gases, which is readily monitored in end-tidal expired gases.
Volatile anesthetics tend to increase respiratory rate, decrease tidal volume, and blunt ventilatory responses to hypercapnia and hypoxia. Volatile anesthetics depress respiration through both central medullary and peripheral muscular effects. Inhaled anesthetics dose dependently decrease tidal volume. The concomitant increase in respiratory rate is more pronounced with halothane, desflurane, and sevoflurane than with isoflurane. Compensatory tachypnea maintains minute ventilation with desflurane up to alveolar concentrations of 1.6 x MAC. Nonetheless, alveolar ventilation is reduced by all volatile anesthetics, resulting in an increased PaCO2. N2O also causes tachypnea and decreased tidal volume, but alone it causes minimal changes in PaCO2. N2O depression of ventilation is additive when given in combination with other inhalational agents. Factors that contribute to hypoxia and hypercarbia during inhalational anesthesia include hypoventilation, atelectasis, airway closure, decreased functional residual capacity, and ventilation–perfusion mismatch. Volatile anesthetics blunt hypoxic and hypercarbic respiratory drive, increasing the risk of severe hypoxia and hypercarbia in spontaneously breathing patients. Depression of hypoxic and hypercarbic ventilatory drives occurs even at subanesthetic doses. N2O blunts the respiratory drive to hypoxia and hypoventilation, but its clinical effects are minimal because of its low potency.