Isoflurane is a nonflammable volatile anesthetic with a pungent ethereal odor. Although it is a chemical isomer with the same molecular weight as enflurane, it has different physicochemical properties (see Table 8–3).
Isoflurane causes minimal left ventricular depression in vivo. Cardiac output is maintained by a rise in heart rate due to partial preservation of carotid baro-reflexes. Mild β-adrenergic stimulation increases skeletal muscle blood flow, decreases systemic vas-cular resistance, and lowers arterial blood pressure. Rapid increases in isoflurane concentration lead to transient increases in heart rate, arterial blood pressure, and plasma levels of norepinephrine. Isofl urane dilates coronary arteries, but not nearly as potently as nitroglycerin or adenosine. Dilation of normal coronary arteries could theoreti-cally divert blood away from fixed stenotic lesions, which was the basis for concern about coronary “steal” with this agent, a concern that has largely been forgotten.
Respiratory depression during isoflurane anesthesia resembles that of other volatile anesthetics, except that tachypnea is less pronounced. The net effect is a more pronounced fall in minute ventilation. Even low levels of isoflurane (0.1 MAC) blunt the normal ventilatory response to hypoxia and hypercapnia.
Despite a tendency to irritate upper airway reflexes, isoflurane is considered a good bronchodilator, but may not be as potent a bronchodilator as halothane.
At concentrations greater than 1 MAC, isoflurane increases CBF and intracranial pressure. These effects are thought to be less pronounced than with halothane and are reversed by hyperventilation. In contrast to halothane, the hyperventilation does not have to be instituted prior to the use of isoflurane to prevent intracranial hypertension. Isoflurane reduces cerebral metabolic oxygen requirements, and at 2 MAC, it produces an electrically silent elec-troencephalogram (EEG).
Isoflurane relaxes skeletal muscle.
Isoflurane decreases renal blood flow, glomerular fil-tration rate, and urinary output.
Total hepatic blood flow (hepatic artery and portal vein flow) may be reduced during isoflurane anes-thesia. Hepatic oxygen supply is better maintained with isoflurane than with halothane, however, because hepatic artery perfusion is preserved. Liver function tests are usually not affected.
Isoflurane is metabolized to trifluoroacetic acid. Although serum fluoride fluid levels may rise, neph-rotoxicity is extremely unlikely, even in the presence of enzyme inducers. Prolonged sedation (>24 h at 0.1–0.6% isoflurane) of critically ill patients has resulted in elevated plasma fluoride levels (15–50 µmol/L) without evidence of renal impairment. Similarly, up to 20 MAC-hours of isoflurane may lead to fluoride levels exceeding 50 µmol/L without detectable postoperative renal dysfunction. Its lim-ited oxidative metabolism also minimizes any pos-sible risk of significant hepatic dysfunction.
Isoflurane presents no unique contraindications. Patients with severe hypovolemia may not tolerateits vasodilating effects. It can trigger malignant hyperthermia.
Epinephrine can be safely administered in doses up to 4.5 mcg/kg. Nondepolarizing NMBAs are poten-tiated by isoflurane.
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