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Inhaled anaesthetics: Difference between revisions
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Nitrous oxide (N2O) is the least potent inhaled anaesthetic. It’s used for smaller procedures where complete loss of consciousness is not necessary, like during labour or dental procedures. It may be self-administered by the patient. It’s necessary to give pure O2 for a few minutes after the operation to prevent diffusional hypoxia. N2O is the only inhaled anaesthetics that doesn’t depress respiration, and it can’t cause malignant hyperthermia. It does not induce muscle relaxation, so it should be used with a muscle relaxant. | Nitrous oxide (N2O) is the least potent inhaled anaesthetic. It’s used for smaller procedures where complete loss of consciousness is not necessary, like during labour or dental procedures. It may be self-administered by the patient. It’s necessary to give pure O2 for a few minutes after the operation to prevent diffusional hypoxia. N2O is the only inhaled anaesthetics that doesn’t depress respiration, and it can’t cause malignant hyperthermia. It does not induce muscle relaxation, so it should be used with a muscle relaxant. | ||
== Dosage == | |||
MAC is the concentration of drug in the alveolar space which prevents a motor response to pain in 50% of patients. It’s inversely proportional to the potency. During general anaesthesia, the anaesthetic machine measures the amount of anaesthetic in the exhaled air (the end-tidal sevoflurane, for example), and the dose of anaesthetic is adjusted so that an end-tidal concentration of 1,0 – 1,3 x MAC is reached. | |||
== Mechanism of action == | == Mechanism of action == | ||
The specific mechanism of action of halogenated inhaled anaesthetics is not known. However, it is known that general anaesthetics cause CNS depression by hyperpolarizing neurons, which inhibits the synaptic transmission.<section end="A&IC" /> | |||
The exact mechanism of how this is achieved depends on the exact general anaesthetic. Generally, these drugs either stimulate inhibitory receptors like the GABAA and glycine receptors or they inhibit excitatory receptors like neuronal acetylcholine and NMDA glutamate receptors. The inhibitory receptors GABAA and glycine receptors are ligand-gated Cl– channels. When these are activated by the general anaesthetics, chloride ions enter the neurons, which hyperpolarizes the membrane. | The exact mechanism of how this is achieved depends on the exact general anaesthetic. Generally, these drugs either stimulate inhibitory receptors like the GABAA and glycine receptors or they inhibit excitatory receptors like neuronal acetylcholine and NMDA glutamate receptors. The inhibitory receptors GABAA and glycine receptors are ligand-gated Cl– channels. When these are activated by the general anaesthetics, chloride ions enter the neurons, which hyperpolarizes the membrane. | ||
The excitatory receptors neuronal acetylcholine receptor and NMDA glutamate receptors are ligand-gated Na+ channels. When these are inhibited by general anaesthetics the neurons are hyperpolarized. By hyperpolarizing neurons in the thalamus, hypothalamus, cortex, spinal cord and hippocampus these drugs achieve loss of consciousness, immobility, analgesia and amnesia.<section begin="A&IC" /> | The excitatory receptors neuronal acetylcholine receptor and NMDA glutamate receptors are ligand-gated Na+ channels. When these are inhibited by general anaesthetics the neurons are hyperpolarized. By hyperpolarizing neurons in the thalamus, hypothalamus, cortex, spinal cord and hippocampus these drugs achieve loss of consciousness, immobility, analgesia and amnesia.<section begin="A&IC" /> | ||
== Pharmacokinetics == | == Pharmacokinetics == | ||