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All anesthetic vapors affect consciousness and have analgesic effects. They depress ventilation, as judged by decreasing minute ventilation and increasing levels of arterial carbon dioxide, with increasing depth of anesthesia. A few words about generally subtle differences between these drugs:
The older halothane and the newer sevoflurane have established for themselves a special niche because they are less irritating to the upper airway than the others. Particularly in children, who abhor needle sticks (and whose veins are more easily cannulated when the child is asleep), anesthesia can be induced quite gently by inhalation of nitrous oxide/oxygen together with either one of these two drugs.
All volatile agents depress myocardial contractility and cause peripheral vasodi-latation. As long as baroreceptors function normally, heart rate will increase in response to hypotension. In deep anesthesia, this compensation will not suffice to prevent a drop in cardiac output. Here, halothane occupies an unusual position. It inhibits the baroreceptor; consequently, we see less tachycardia (even bradycar-dia in deeply anesthetized children) during halothane-induced hypotension and a greater drop in cardiac output than is true for the other agents at comparable levels of anesthesia. Another oddity regarding halothane anesthesia: otherwise well-tolerated levels of circulating catecholamines, whether injected or liberated by the body, trigger arrhythmias in the presence of halothane.
Under very deep anesthesia, ventilation stops, usually before the heart arrests. Thus, a respiratory arrest from an overdose with an inhalation anesthetic need not be fatal if discovered in time, and if ventilation of the (still perfused) lungs with oxygen can remove the volatile anesthetic.
In surgical anesthesia, spontaneous ventilation will still be maintained IF the patient was not given other drugs that depress ventilation – such as opiates – and IF the patient is not paralyzed by neuromuscular blocking drugs, so commonly used in order to relax striated muscles and thus ease the surgeon’s job.
In general, all halogenated inhalation anesthetics decrease minute ventilation by decreasing tidal volume. The compensatory increase in respiratory rate cannot prevent a respiratory acidosis (and hypoxemia when breathing room air) because any increase in respiratory rate increases the ventilation of dead space. Respir-atory depression and tachypnea are less pronounced with desflurane (Suprane®) and sevoflurane than with halothane, with isoflurane (Forane®) lying somewhere in between.
Under inhalation anesthesia, patients respond only sluggishly to rising arterial carbon dioxide levels (= respiratory depression). Even low concentrations of the inhalation agents also depress the chemoreceptor response to hypoxemia.
The inhalation anesthetics depress, in a dose-dependent manner, CNS function – as shown by clinical findings starting with a state of somnolence, during which the patient can still respond – to coma, in which external noxious (we do not call it “painful” as you have to be conscious to find something painful!) stimulation elicits no visible response. This sentence was carefully chosen, because invisible CNS responses are detectable by electroencephalography and evoked potentials; these persist long after motor responses have been abolished. Eventually, they too vanish in deep anesthesia. Halogenated inhalation agents tend to increase cerebral blood flow, which is not a desirable effect in patients at risk of brain swelling. In neurosurgical anesthesia, we rely greatly on intravenous techniques using the inhalation agents only in low doses and as adjuncts.
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