1. General Ventilatory Effects. All volatile anesthetics decrease tidal volume but have lesser effects on decreasing minute ventilation because of an offsetting response to increase breathing frequency (Fig. 17-9: Comparison of mean changes in resting PaCO₂, tidal volume, respiratory rate, and minute ventilation in patients receiving an inhaled anesthetic). The increase in resting PaCO₂ as an index of depression of ventilation is somewhat offset by surgical stimulation. The degree of respiratory depression from inhaled anesthetics is reduced when anesthesia administration exceeds 5 hours.
2. Ventilatory Mechanics. Functional residual capacity is decreased during general anesthesia (decreased intercostal muscle tone, alterations in diaphragm position, changes in thoracic blood volume).
3. Response to Carbon Dioxide and Hypoxemia
   1. All of the inhaled anesthetics produce a dose-dependent depression in the ventilatory response to hypercarbia (Fig. 17-10: All inhaled anesthetics produce similar dose-dependent decreases in the ventilatory response to carbon dioxide).
   2. Even subanesthetic concentrations of volatile anesthetics (0.1 MAC) produce depression of chemoreceptors responsible for the ventilatory response to hypoxia.
4. Bronchiolar Smooth Muscle Tone
   1. Bronchoconstriction during anesthesia is most likely caused by mechanical stimulation of the airway in the presence of minimal concentrations of inhaled anesthetics. This response is enhanced in patients with reactive airway disease.
   2. Volatile anesthetics relax airway smooth muscle by directly depressing smooth muscle contractility and indirectly by inhibiting the reflex neural pathways. Airway resistance increases more with desflurane than sevoflurane (Fig. 17-11: Changes in airway resistance before (baseline) and after tracheal intubation were significantly different in the presence of sevoflurane compared with desflurane).
5. Pulmonary Vascular Resistance
   1. The pulmonary vasodilator action of volatile anesthetics is minimal. The effect of nitrous oxide on pulmonary vascular resistance may be exaggerated in patients with resting pulmonary hypertension.
   2. All inhaled anesthetics inhibit hypoxic pulmonary vasoconstriction in animals. Nevertheless, in patients undergoing one-lung ventilation during thoracic surgery, minimal effects on PaO₂ and intrapulmonary shunt fraction occur regardless of the volatile anesthetic being administered (Fig. 17-12: Shunt fraction (top panel) and alveolar–arterial oxygen gradient (bottom panel) before, during, and after one-lung ventilation (OLV) in patients anesthetized with desflurane or isoflurane).

Inhaled Anesthetics

1. Pharmacokinetic Principles
2. Clinical Overview of Current Inhaled Anesthetics
3. Neuropharmacology of Inhaled Anesthetics
4. The Circulatory System
5. The Pulmonary System
6. Hepatic Effects
7. Neuromuscular System and Malignant Hyperthermia
8. Genetic Effects, Obstetric Use, and Effects on Fetal Development
9. Anesthetic Degradation by Carbon Dioxide Absorbers
10. Anesthetic Metabolism
11. Clinical Utility of Volatile Anesthetics
12. Pharmacoeconomics and Value-Based Decisions