Desflurane cardiovascular effects

Inhaled anesthetics change heart rate either directly by altering the rate of sinus node depolarization or indirectly by shifting the balance of autonomic nervous system activity. Bradycardia is often seen with halothane, probably through vagal stimulation. In contrast, enflurane, and sevoflurane have little effect, and both desflurane and isoflurane increase heart rate. In the case of desflurane, cardiovascular responses include a transient sympathetic activation that can lead to marked increases in heart rate and blood pressure when high inspired gas concentrations are administered. 

Recovery is sufficiently rapid with most intravenous drugs to permit their use for short ambulatory (outpatient) surgical procedures. In the case of propofol, recovery times are similar to those seen with sevoflurane and desflurane. Although most intravenous anesthetics lack antinociceptive (analgesic) properties, their potency is adequate for short superficial surgical procedures when combined with nitrous oxide or local anesthetics, or both. Adjunctive use of potent opioids (eg, fentanyl, sufentanil or remifentanil see Chapter 31) contributes to improved cardiovascular stability, enhanced sedation, and perioperative analgesia. However, opioid compounds also enhance the ventilatory depressant effects of the intravenous agents and increase postoperative emesis. Benzodiazepines (eg, midazolam, diazepam) have a slower onset and slower recovery than the barbiturates or propofol and are rarely used for induction of anesthesia. However, preanesthetic administration of benzodiazepines (eg, midazolam) can be used to provide anxiolysis, sedation, and amnesia when used as part of an inhalational, intravenous, or balanced anesthetic technique. 

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. 

Cardiovascular System The hypotensive effect of sevoflurane primarily is due to systemic vasodilation, although sevoflurane also produces a concentration-dependent decrease in cardiac output. Unlike isoflurane or desflurane, sevoflurane does not produce tachycardia and thus may be a preferable agent in patients prone to myocardial ischemia. 

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