Cardiovascular System Desflurane lowers blood pressure—primarily by decreasing systemic vascular resistance—and has a modest negative inotropic effect. Thus, cardiac output is preserved, as is perfusion of major organ beds (e.g., splanchnic, renal, cerebral, and coronary). Marked increases in heart rate often occur during induction of desflurane anesthesia and with abrupt increases in the delivered concentration of desflurane; this results from desflurane-induced stimulation of the sympathetic nervous system. The hypotensive effects of desflurane do not wane with increasing duration of administration.
Respiratory System As with halothane and enflurane, desflurane causes a concentration-dependent increase in respiratory rate and a decrease in tidal volume. At concentrations <1 MAC, the net effect is to preserve minute ventilation at concentrations >1 MAC, minute ventilation is markedly depressed, resulting in elevated arterial CO2 tension (PaCO2). Patients spontaneously breathing desflurane at concentrations greater than 1.5 MAC have extreme elevations of PaCO and may become apneic. Desflurane is a bronchodilator; it also is a strong airway irritant and can cause coughing, breath-holding, laryngospasm, and excessive respiratory secretions. Thus, desflurane is not used for induction of anesthesia.
Nervous System Desflurane decreases cerebral vascular resistance and cerebral metabolic O2 consumption. Under conditions of normocapnia and normotension, desflurane produces an increase in cerebral blood flow and can increase ICP in patients with poor intracranial compliance. The vasoconstrictive response to hypocapnia is preserved during desflurane anesthesia, and increases in ICP thus can be prevented by hyperventilation.
Muscle, Kidney, Liver, and GI Tract
Desflurane produces direct skeletal muscle relaxation and enhances the effects of nondepolarizing and depolarizing neuromuscular blocking agents. Consistent with its minimal metabolism, desflurane has no reported nephrotoxicity or hepatotoxicity.
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