Chapter 38. Pharmacology of Inhalational Anesthetics

1. The most useful definition of "dose" for inhaled anesthetics is the partial pressure in alveolar gases, which is readily monitored in end-tidal gases.

2. All halogenated anesthetics break down, releasing carbon monoxide (CO) and heat when they contact desiccated alkaline chemicals, such as those in common CO2 adsorbents. Potential harm to patients from this breakdown can be avoided by proper use and maintenance of anesthesia equipment and by using less alkaline CO2 adsorbents.

3. The rate at which the alveolar anesthetic concentration (FA or Palv) approaches the inspired (circuit) concentration (FI or Pcirc) depends on minute alveolar ventilation (increased ventilation accelerates equilibration), cardiac output (increased output slows equilibration), and the blood-gas partition coefficient of the anesthetic (high solubility slows equilibration).

4. Nitrous oxide (N2O) diffuses into air-filled spaces in the body, causing expansion, increased pressure, or both.

5. The minimum alveolar concentration (MAC) is the alveolar concentration of inhaled anesthetic that blocks movement in half of subjects in response to a surgical incision. MAC is influenced by age, pharmacologic and physiologic factors (eg, temperature), and genetic factors.

6. MAC-awake is the alveolar concentration of anesthetic causing loss of response to verbal commands in half of subjects. Amnesia is produced by inhalational anesthetic concentrations lower than MAC-awake.

7. Awareness and explicit recall of intraoperative events is attributable to inadequate delivery of anesthetics for the patient's needs. Without preventive measures, awareness during anesthesia occurs in about 1 of 750 patients and may cause psychological disturbances leading to posttraumatic stress disorder.

8. All potent volatile anesthetics in current use decrease mean arterial pressure in a dose-dependent manner. Severe cardiovascular and respiratory depression can occur even at low volatile anesthetic concentrations in elderly, hypovolemic, or critically ill patients. Avoidance of these toxicities requires vigilant monitoring and anticipation of anesthetic requirements.

9. Volatile anesthetics may increase heart rate, both by a baroreceptor reflex in response to decreased arterial pressure and a direct vagolytic effect on the heart.

10. Volatile anesthetics tend to increase respiratory rate and decrease tidal volume and blunt ventilatory responses to hypercapnia and hypoxia.

11. Desflurane is very pungent, and its use can be associated with airway irritability, bronchoconstriction, and laryngospasm during induction. Among volatile anesthetics, sevoflurane causes the least amount of airway irritation.

12. Volatile anesthetics vasodilate cerebral vessels, increasing blood flow while reducing cerebral metabolic oxygen consumption. Cerebral vascular responses to altered pCO2 are maintained in the presence of volatile anesthetics. N2O increases cerebral metabolism.

13. Halothane undergoes the most hepatic metabolism of the inhaled agents. Whereas enflurane, isoflurane, and sevoflurane are also metabolized in the liver, desflurane and nitrous oxide are minimally metabolized. Oxidative metabolism of halothane and other volatile agents can induce a severe immune-mediated hepatitis.

14. All potent volatile agents may trigger malignant hyperthermia in susceptible individuals.

Experimentation with inhalation of gases and vapors for the purpose of obtunding the distress associated with surgery began in the 19th century. The administration of inhaled anesthetics spread rapidly after the successful public demonstration of ether ...