Pharmacology · General Anesthesia
Comparative pharmacokinetics, distinguishing properties, and clinical selection
Comparative Pharmacokinetics
Ranked by Blood:Gas Partition Coefficient
Inhalational Agent Profiles
| Agent | Blood:Gas Coefficient | Minimum Alveolar Concentration | Induction Speed | Key Distinguishing Feature |
|---|---|---|---|---|
| Desflurane | ~0.42 | ~6–7% | Fastest | Airway irritant — maintenance only; sympathetic surge on rapid increase; heated vaporizer required |
| Nitrous oxide | ~0.47 | ~104% | Very fast | Cannot produce surgical anesthesia alone; analgesic (N-methyl-D-aspartate antagonism); not a malignant hyperthermia trigger |
| Sevoflurane | ~0.65 | ~2.0% | Fast | Preferred pediatric induction agent; best bronchodilator; compound A at low flow; emergence agitation in children |
| Isoflurane | ~1.4 | ~1.17% | Moderate | Most widely used worldwide; vasodilation + reflex tachycardia (contrast halothane bradycardia) |
| Enflurane | ~1.9 | ~1.68% | Slow | Only epileptogenic volatile agent — contraindicated in seizure disorders |
| Halothane | ~2.4 | ~0.75% | Slowest | Catecholamine sensitization; immune hepatitis on re-exposure; bradycardia; myocardial depression |
High-Yield Hazards by Agent
Halothane
Unique Adverse Effects
Nitrous Oxide
Unique Adverse Effects
Sevoflurane
Profile and Cautions
Clinical Selection
Malignant hyperthermia susceptibility: avoid ALL volatile halogenated agents — use nitrous oxide or total intravenous anesthesia only.
Seizure disorder: absolutely avoid enflurane; sevoflurane and isoflurane preferred.
Pediatric induction: sevoflurane (non-pungent, fast, hemodynamically stable).
Fastest emergence (long/obese cases): desflurane (lowest tissue solubility, minimal accumulation).
Asthma / reactive airways: sevoflurane preferred; halothane acceptable where sevoflurane unavailable.
Air-filled space (pneumothorax, bowel obstruction, intraocular gas): avoid nitrous oxide.
Suggested References
| Author / Organization | Title | Source |
|---|---|---|
| Katzung BG, ed. | Basic and Clinical Pharmacology. 15th ed. | McGraw-Hill; 2021 |
| Brunton LL, Knollmann BC, eds. | Goodman & Gilman's The Pharmacological Basis of Therapeutics. 14th ed. | McGraw-Hill; 2023 |
| Miller RD, ed. | Miller's Anesthesia, 8th ed. Chapters 26, 27 | Philadelphia: Elsevier; 2015 |
| Eger EI 2nd | Anesthetic Uptake and Action | Baltimore: Williams & Wilkins; 1974 |
| Johnston RR, Eger EI 2nd, Wilson C | A comparative interaction of epinephrine with enflurane, isoflurane, and halothane in man | Anesth Analg. 1976;55(5):709–712 |
| Emmanouil DE, Quock RM | Advances in understanding the actions of nitrous oxide | Anesth Prog. 2007;54(1):9–18 |
| Stoelting RK, Hillier SC | Pharmacology and Physiology in Anesthetic Practice, 4th ed. | Philadelphia: Lippincott Williams & Wilkins; 2006 |
| Weiskopf RB, et al. | Rapid increase in desflurane concentration is associated with greater transient cardiovascular stimulation than with rapid increases in isoflurane concentration in humans | Anesthesiology. 1994;80(5):1035–1045 |
| Voss LJ, et al. | The howling cortex: seizures and general anesthetic drugs | Anesth Analg. 2008;107(5):1689–1703 |
| Kharasch ED | Sevoflurane and renal toxicity | Curr Opin Anaesthesiol. 1998;11(4):377–381 |
| Njoku D, et al. | Biotransformation of halothane, enflurane, isoflurane, and desflurane to trifluoroacetylated liver proteins | Anesth Analg. 1997;84(1):173–178 |
| Rosenberg H, et al. | Malignant hyperthermia: a review | Orphanet J Rare Dis. 2015;10:93 |
| Peyton PJ, Wu CY | Nitrous oxide-related postoperative nausea and vomiting depends on duration of exposure | Anesthesiology. 2014;120(5):1137–1145 |
| Franks NP | Molecular targets underlying general anaesthesia | Br J Pharmacol. 2006;147(Suppl 1):S72–S81 |
| Flood P, Rathmell JP, Shafer SL, eds. | Stoelting's Pharmacology and Physiology in Anesthetic Practice, 5th ed. | Philadelphia: Wolters Kluwer; 2015 |