DESFLURANE
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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