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The structure of desflurane is very similar to that of isoflurane. In fact, the only difference is the substi-tution of a fluorine atom for isoflurane’s chlorine atom. That “minor” change has profound effects on the physical properties of the drug, however. For instance, because the vapor pressure of desflurane at 20°C is 681 mm Hg, at high altitudes (eg, Denver, Colorado) it boils at room temperature. This prob-lem necessitated the development of a special desflurane vaporizer. Furthermore, the low solubility of desflurane in blood and body tissues causes a very rapid induction and emergence of anesthesia. Therefore, the alveolar concentration of desflurane approaches the inspired concentration much more rapidly than the other volatile agents, giving the anesthesiologist tighter control over anesthetic levels. Wakeup times are approximately50% less than those observed following isoflu-rane. This is principally attributable to a blood/gaspartition coefficient (0.42) that is even lower than that of nitrous oxide (0.47). Although desflurane is roughly one-fourth as potent as the other volatile agents, it is 17 times more potent than nitrous oxide. A high vapor pressure, an ultrashort duration of action, and moderate potency are the most charac-teristic features of desflurane.
The cardiovascular effects of desflurane seem to be similar to those of isoflurane. Increasing the dose is associated with a decline in systemic vascular resis-tance that leads to a fall in arterial blood pressure. Cardiac output remains relatively unchanged orslightly depressed at 1–2 MAC. There is a moderate rise in heart rate, central venous pressure, and pul-monary artery pressure that often does not become apparent at low doses. Rapid increases in des-flurane concentration lead to transient butsometimes worrisome elevations in heart rate, blood pressure, and catecholamine levels that are more pronounced than occur with isoflurane, particularly in patients with cardiovascular disease. These car-diovascular responses to rapidly increasing desflu-rane concentration can be attenuated by fentanyl, esmolol, or clonidine.
Desflurane causes a decrease in tidal volume and an increase in respiratory rate. There is an overall decrease in alveolar ventilation that causes a rise in resting Paco2. Like other modern volatile anes-thetic agents, desflurane depresses the ventilatory response to increasing Paco2. Pungency and airway irritation during desflurane induction can be mani-fested by salivation, breath-holding, coughing, and laryngospasm. Airway resistance may increase in children with reactive airway susceptibility. These problems make desflurane a poor choice for inhala-tion induction.
Like the other volatile anesthetics, desflurane directly vasodilates the cerebral vasculature, increasing CBF, cerebral blood volume, and intra-cranial pressure at normotension and normocap-nia. Countering the decrease in cerebral vascular resistance is a marked decline in the cerebral meta-bolic rate of oxygen (CMRO2) that tends to cause cerebral vasoconstriction and moderate any increase in CBF. The cerebral vasculature remains responsive to changes in Paco2, however, so that intracranial pressure can be lowered by hyperven-tilation. Cerebral oxygen consumption is decreased during desflurane anesthesia. Thus, during periods of desflurane-induced hypotension (mean arterial pressure = 60 mm Hg), CBF is adequate to maintain aerobic metabolism despite a low cerebral perfusion pressure. The effect on the EEG is similar to that of isoflurane. Initially, EEG frequency is increased, but as anesthetic depth is increased, EEG slowing becomes manifest, leading to burst suppression at higher inhaled concentrations.
Desflurane is associated with a dose-dependent decrease in the response to train-of-four and tetanic peripheral nerve stimulation.
Th ere is no evidence of any significant nephrotoxic effects caused by exposure to desflurane. However, as cardiac output declines, decreases in urine output and glomerular filtration should be expected with desflurane and all other anesthetics.
Hepatic function tests are generally unaffected by desflurane, assuming that organ perfusion is maintained perioperatively. Desflurane undergoes minimal metabolism, therefore the risk of anes-thetic-induced hepatitis is likewise minimal. As with isoflurane and sevoflurane, hepatic oxygen delivery is generally maintained.
Desflurane undergoes minimal metabolism in humans. Serum and urine inorganic fluoride lev-els following desflurane anesthesia are essentially unchanged from preanesthetic levels. There is insig-nificant percutaneous loss. Desflurane, more than other volatile anesthetics, is degraded by desiccated CO2 absorbent (particularly barium hydroxide lime, but also sodium and potassium hydroxide) into potentially clinically significant levels of carbon mon-oxide. Carbon monoxide poisoning is difficult to diagnose under general anesthesia, but the presence of carboxyhemoglobin may be detectable by arterial blood gas analysis or lower than expected pulse oxim-etry readings (although still falsely high). Disposing of dried out absorbent or use of calcium hydroxide can minimize the risk of carbon monoxide poisoning.
Desflurane shares many of the contraindications of other modern volatile anesthetics: severe hypo-volemia, malignant hyperthermia, and intracranial hypertension.
Desflurane potentiates nondepolarizing neuromus-cular blocking agents to the same extent as isoflu-rane. Epinephrine can be safely administered in doses up to 4.5 mcg/kg as desflurane does not sensi-tize the myocardium to the arrhythmogenic effects of epinephrine. Although emergence is more rapid following desflurane anesthesia than after isoflurane anesthesia, switching from isoflurane to desflurane toward the end of anesthesia does not significantly accelerate recovery, nor does faster emergence translate into faster discharge times from the post-anesthesia care unit. Desflurane emergence has been associated with delirium in some pediatric patients.
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