The neurological mechanism of action for inhaled anesthetics is unknown.
This acronym represents halothane, enflurane, isoflurane, sevoflurane, methoxyflurane, nitrous oxide
Respiratory depression occurs with all inhalational anesthetics due to blunted medullary respiratory drive. Furthermore, these drugs are usually combined with mechanical ventilation, making mechanical respiration necessary.
Inhaled anesthetics lead to myocardial depression by causing reduced cardiac contractility and depression of the SA node. Blood pressure is also reduced.
These drugs significantly lower cerebral metabolic demand. Inhaled anesthetics also affects cerebral blood vessels by causing cerebral vascular vasodilation, increasing cerebral blood flow.
Halothane, due to oxidative reactions in the liver, can cause severe liver injury, termed "halothane hepatitis." This drug is rarely used in adults or children, as safer drugs have replaced it.
Methoxyflurane is broken down in the liver and kidney, and its metabolites lead to irreversible, dose-dependant nephrotoxicity. It has also been linked to hepatotoxicity. This drug's use has been largely abandoned due to newer inhaled anesthetics.
Enflurane is known to lower the seizure threshold and used should cautioned in patients with epilepsy. Enflurane can also cause nephrotoxicity in patients.
With exception to nitrous oxide (N2O), inhaled anesthetic drugs can trigger malignant hyperthermia, a severe side effect. Malignant hyperthermia is a life-threatening condition with symptoms of increased temperature, CO2 production, respiration and O2 consumption, as well as acidosis and rhabdomyolysis.
Nitrous oxide leads to expansion of trapped gas when blood containing NO equilibriates with closed air-containing spaces in the body. This is not a problem with compliant tissues (gut lumen), but may cause increased pressure and trauma if the space cannot expand (sinuses, middle ear).
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