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Isoflurane & Sevoflurane

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Isoflurane is among the many anesthetic agents discovered by Ross C. Terrell in 1965. It was approved for medical use in the United States in 1979. Isoflurane, along with sevoflurane, is a widely used halogenated ether used as an anesthetic agent. Isoflurane is a clear, colorless stable liquid with a mildly pungent, musty odor. Isoflurane has the advantage of favorable blood gas distribution, low blood solubility, and rapid and smooth recovery.

Sevoflurane was discovered by Ross C. Terrell and first introduced into clinical practice by Maruishi Pharmaceutic Co., Ltd. in Japan in 1990. It is one of the most widely used anesthetic agents among halogenated ethers. Sevoflurane is a non-pungent, low flammable and non-irritant anesthetic agent that also offers the advantage of favorable blood gas distribution, low blood solubility and rapid and smooth recovery.

Isoflurane alters tissue excitability by decreasing the extent of gap junction-mediated cell-cell coupling and altering channel activity; This results in the induction of muscle relaxation and reduction of pain sensitivity. Isoflurane allows rapid induction and recovery from anesthesia. Despite its mild pungent smell, isoflurane does not stimulate tracheobronchial secretions and excessive salivation. The anesthetic agent is a profound respiratory depressant.

Isoflurane decreases blood pressure in a dose-dependent manner. Anesthetization with isoflurane maintains a stable heart rhythm. Cardiac output is maintained, under controlled ventilation and normal PaCO2, compensating for stroke reduction. Isoflurane, in certain animals, can produce coronary vasodilation at the arteriolar level.

Isoflurane has a dose-dependent effect on central nervous system depression. The agent does produce convulsive activity. Isoflurane does not prevent cerebral edema or an increase in intracranial pressure following traumatic brain injury. Further, at increased concentrations of isoflurane, the need for muscle relaxants decreases.

Sevoflurane has a lower solubility in blood and body tissues than halothane. Regarding anesthetic potency, sevoflurane is about 50% less potent than isoflurane. The agent is readily degraded by carbon dioxide absorbents leading to nephrotoxicity in rats as a result of haloalkene by-products. Sevoflurane maintains cerebral metabolism at a reduced rate during anesthesia while preserving cerebral blood responsiveness to changes in arterial carbon dioxide tension. Sevoflurane also produces cerebrovasodilation and suppresses somatosensory-evoked potentials.

Sevoflurane is a dose-dependent cardiovascular depressant and does not increase the likelihood of cardiac arrhythmias induced by epinephrine. Further, the agent does not cause sympathoexcitatory activity or rapid increase in inspired concentrations. Thus, sevoflurane allows a stable heart rate profile. The anesthetic agent permits rapid alteration of the depth of anesthesia since it produces a dose-dependent decrease in blood pressure. It has a negligible effect on coronary blood flow and is similar in effect to isoflurane on regional blood flow and systemic vascular resistance. Baroreflex function is also reduced by sevoflurane as seen in isoflurane anesthesia.

Sevoflurane has a significant dose-dependent effect on ventilatory depression that leads to a decreased minute, respiratory volume. It inhibits hypoxic pulmonary vasoconstriction and tracheal smooth muscle contraction thus permitting tracheal intubation without adjunctive neuromuscular blocking agents and laryngeal mask insertion. Sevoflurane does not cause significant irritation of the airway nor induce cough reflex.

Isoflurane has a blood gas coefficient of 1.4 which is less than other potent inhaled anesthetics. Rapid rise alveolar concentration towards inspired concentration can be observed with isoflurane due to its low blood solubility. The mild pungency of the agent can provoke breath-holding or coughing which can affect the rate at which inspired concentration can be increased. However, this effect can be minimized by premedication or nitrous oxide or by using an intravenous agent for induction.

Isoflurane’s low solubility enhances its elimination. The duration of the anesthesia affects the rate of recovery. The rapid elimination allows quick reversal of circulatory, respiratory and neuromuscular depression.

For the Sevoflurane, the anesthetic agent undergoes dose-dependent hepatic biotransformation, primarily by cytochrome P450 (CYP) 2EI, with 1 to 5% of the absorbed dose of sevoflurane undergoing metabolism to liberate inorganic fluoride ions (F) and hexafluoroisopropanol (HFIP) as the principal by-products. Sevoflurane undergoes minimal renal defluorination.

Burns WB, Eger EI 2nd (2011). Ross C. Terrell, PhD, an anesthetic pioneer. Anesth Analg. 113(2):387-9. doi: 10.1213/ANE.0b013e3182222b8a.

Delgado-Herrera L, Ostroff R.D, Rogers SA (2001). Sevoflurance: approaching the ideal inhalational anesthetic. a pharmacologic, pharmacoeconomic, and clinical review. CNS Drug Rev. 7(1):48-120.

Patel S.S, Goa K.L (1996). Sevoflurane. A review of its pharmacodynamic and pharmacokinetic properties and its clinical use in general anaesthesia. Drugs. 51(4):658-700

Burns WB, Eger EI 2nd (2011). Ross C. Terrell, PhD, an anesthetic pioneer. Anesth Analg. 113(2):387-9. doi: 10.1213/ANE.0b013e3182222b8a.

Eger EI 2nd (1981). Isoflurane: a review. Anesthesiology. 55(5):559-76.

Eger EI 2nd (1984). The pharmacology of isoflurane. Br J Anaesth. 56 Suppl 1:71S-99S.

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