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KEY POINTS

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KEY POINTS

  1. The most useful definition of dose for inhaled anesthetics is the partial pressure in alveoli, which can be monitored in end-tidal gases.

  2. All halogenated anesthetics decompose when they contact desiccated alkaline chemicals in CO2 adsorbents, producing carbon monoxide (CO) and heat. Proper use and maintenance of anesthesia equipment and less-alkaline CO2 adsorbents reduce potential harm to patients.

  3. The rate at which the alveolar anesthetic concentration (FA or Palv) approaches the inspired (circuit) concentration (FI or Pcirc) depends on FI (the concentration effect), minute alveolar ventilation (increased ventilation accelerates equilibration), cardiac output (increased output slows equilibration), and the anesthetic blood-gas partition coefficient (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, physiologic, 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 are 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 about 1% of patients are at high risk for this complication. Intraoperative awareness may cause psychological disturbances leading to post-traumatic 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 all attenuate baroreceptor reflex control to a varying degree and may increase heart rate, by both indirect and direct vagolytic effect on the heart.

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

  11. Desflurane is very pungent and associated with airway irritability, bronchoconstriction, and laryngospasm when used for induction. Among volatile anesthetics, sevoflurane causes the least amount of airway irritation.

  12. Volatile anesthetics inhibit cerebrovascular autoregulation by vasodilating vessels, increasing blood flow and potentially intracranial pressure. Cerebrovascular responses to altered Pco2 are maintained. Cerebral metabolic oxygen consumption is reduced by volatile anesthetics and increased by N2O.

  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. The oxidative metabolism of halothane and other volatile agents can induce severe immune-mediated hepatitis.

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

  15. Preclinical evidence suggests that volatile anesthetics exert neurotoxic effects that may impair cognitive development in the very young or accelerate cognitive decline in the elderly. However, definitive clinical ...

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