KEY POINTS

1. Inhaled anesthetics affect every facet of pulmonary physiology, from the variety of forces controlling ventilation and pulmonary blood flow to surface tension, mucus secretion, and airway smooth muscle tone.
2. Volatile anesthetics are potent bronchodilators in animals and humans. This action occurs through several complex mechanisms that involve a decrease in intracellular calcium concentration and a reduction in calcium sensitivity in the presence of a bronchoconstrictive agent.
3. Volatile anesthetics increase baseline pulmonary dynamic compliance, but these agents are more effective at attenuating increases in pulmonary airway resistance due to chemical or mechanical stimuli. Inhaled anesthetics also preferentially dilate distal airways rather than proximal airways.
4. Inhaled anesthetics diminish the rate of mucus clearance by decreasing ciliary beat frequency, disrupting metachronism, or altering the characteristics of mucus.
5. Pulmonary surfactant decreases the work of breathing by reducing alveolar surface tension. Volatile anesthetics cause progressive, yet reversible, reductions in phosphatidylcholine, the main lipid component of surfactant. The roles of depressed mucociliary function and alterations in type II alveolar cell function in postoperative pulmonary complications after administration of a volatile agent are unknown.
6. The multiple sites of action of inhaled anesthetics on pulmonary parenchyma and vasculature complicate the direct assessment of anesthetic-induced alterations in PVR. Volatile anesthetics cause a biphasic, contraction-relaxation response in pulmonary vascular smooth muscle that is mediated at multiple sites in a Ca²⁺ -mediated signaling pathway. Overall, the net effect of inhaled anesthetic-induced changes in PVR is relatively small.
7. HPV is an important mechanism by which pulmonary blood is preferentially redistributed away from poorly ventilated lung regions to those with adequate alveolar ventilation. Most inhaled anesthetics attenuate HPV in vitro and exert relatively modest inhibitory effects on HPV, shunting, or oxygenation in vivo.
8. Inhaled anesthetics (with the exception of xenon) reduce tidal volume and minute ventilation and cause tachypnea in a dose-related fashion. The relative increases in arterial carbon dioxide tension (as an index of respiratory depression) occur with these agents in the following order: enflurane, desflurane, isoflurane, sevoflurane, halothane.
9. Inhaled anesthetics affect inspiratory and expiratory respiratory muscles to various degrees, possibly as a result of differential sensitivities of premotor and motor neurons.
10. All inhaled anesthetics depress the ventilatory responses to hypercarbia and hypoxia by altering central and peripheral chemoreceptor function in a dose-dependent fashion. The effects of subanesthetic concentrations of inhaled agents on hypercarbic and hypoxic responses are controversial and seem to depend on the baseline state of central nervous system arousal. Nevertheless, these findings may have important clinical implications during the perioperative period.