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CARDIOVASCULAR EFFECTS

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Mean arterial pressure (MAP) decreases with the use of all volatile agents, except halothane, by decreasing systemic vascular resistance (SVR). Halothane decreases cardiac output (CO), and thus MAP, with little to no change in SVR. Nitrous oxide leads to unchanged or increased MAP.

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Heart rate (HR) increases with all volatile agents at a minimum alveolar concentration (MAC) of 0.25 for isoflurane, 1 for desflurane, and 1.5 for sevoflurane. Abrupt increases in desflurane concentrations at the initiation of therapy may result in rapidly increasing HR and blood pressure (BP). This may be attenuated with the administration of beta-blockers or opioids.

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All volatile anesthetics sensitize the myocardium to epinephrine and depress myocardial contractility.

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Sevoflurane should be avoided in patients with a known history of congenital long QT syndrome. Isoflurane has coronary vasodilating properties.

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PULMONARY EFFECTS

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All inhaled anesthetics decrease tidal volume and increase respiratory rate with little effect on minute ventilation. Paco2 also increases in proportion to anesthetic concentration. All volatile anesthetics blunt the ventilatory stimulation caused by hypoxemia and hypercarbia. Patients also experience increased atelectasis with spontaneous respiration and a decrease in functional residual capacity (FRC). All volatile anesthetics cause bronchodilation. Sevoflurane, halothane, and nitrous oxide are nonpungent, whereas desflurane and isoflurane are pungent and can lead to airway irritation with inhalational inductions and concentrations greater than 1 MAC.

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CENTRAL NERVOUS SYSTEM EFFECTS

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All inhaled anesthetics increase cerebral blood flow and decrease cerebral metabolic rate for oxygen (CMRO2). Nitrous oxide, however, will increase CMRO2. Nitrous oxide, as well as inhaled anesthetics, causes cerebral vasodilation. However, if the patient’s blood pressure drops, the increase in cerebral blood flow will be attenuated or abolished because volatile anesthetics inhibit autoregulation. Isoflurane causes the least cerebral vasodilation, maintaining autoregulation better than other volatile anesthetics. Isoflurane also has no effect on cerebrospinal fluid (CSF) production and decreases resistance to CSF absorption. Desflurane increases CSF production without significantly effecting CSF reabsorption.

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Intracranial pressure (ICP) increases with all volatile anesthetics, but this can be counteracted by hypocapnia. Narcotics, barbiturates, and hypocapnia can blunt the increase in ICP seen with nitrous oxide use.

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All volatile anesthetics and nitrous oxide depress the amplitude and increase the latency of somatosensory evoked potentials (SSEPs).

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Increasing depth of anesthesia from the awake state leads to initial increased amplitude and synchrony of EEG tracings. As doses increase, the electroencephalogram (EEG) tracing progresses to electrical silence with an isoelectric pattern at 1.5-2 MAC. Sevoflurane may be associated with epileptiform activity on the EEG with higher concentrations.

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Volatile anesthetics also produce dose-related skeletal muscle relaxation and work synergistically with neuromuscular blocking agents.

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HEPATIC EFFECTS

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Immune-mediated liver injury, though rare, can happen following anesthesia with any of the volatile anesthetics, ...

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