Chemicals {anesthesia}| {anesthetic} can inhibit voluntary-muscle movements {immobility}, inhibit involuntary-muscle movements {muscle relaxation}, lower consciousness to sleep-like level with dreaming {narcosis, anesthesia} {hypnosis, anesthesia}, inhibit pain {analgesia, anesthesia}, cause no memory of episode {amnesia, anesthesia}, and lower brain activity {sedation, anesthesia}.
Anesthesia can be borderline anesthesia {hypesthesia}. Light anesthesia allows consciousness but blocks muscle movements.
Deep anesthesia blocks consciousness and muscle movements.
levels
Anesthesia first affects higher brain functions {anesthetic depth}. The lightest anesthesia causes analgesia, memory loss, and euphoria. Deeper anesthesia causes consciousness loss, rapid shallow breathing, sweating, and flushing. Complete anesthesia causes quiet, regular breathing, with eyeballs moving rhythmically. It does not affect reflexes. In deep anesthesia, first reflexes fail, then breathing becomes shallow, and finally people die.
levels: measurement
Inhaled anesthetics have alveoli concentrations {minimum alveolar concentration} (MAC) that block movements in response to stimuli in 50% of patients. Inhaled anesthetics have lower alveoli concentrations {minimum alveolar concentration-aware} {MAC-aware} that block stimulus awareness in 50% of patients. Intravenous anesthetics have blood-plasma concentrations {end-tidal concentration} that block movements in response to stimuli in 50% of patients.
Blood pressure, heart rate, sweating, and tear secretion combined {PRST score} indicate awareness level.
EEG power spectrum shows waves at 3 Hz below alpha-wave frequency. Stimuli cause EEG evoked potentials that appear at various times after event. Anesthesia reduces or delays evoked potentials. In anesthesia, three auditory evoked potentials typically happen 20 ms to 45 ms after stimulus {AEP index}.
local anesthesia
Local anesthesia makes body parts feel non-existent, rather than senseless or paralyzed. Local anesthesia inhibits touch and pain perception with lidocaine and similar chemicals, by injection into local nerves {nerve block}, spinal-cord epidural region {epidural anesthesia}, or subarachnoid spaces {spinal anesthesia}.
Local anesthesia does not cause amnesia and maintains consciousness. Local anesthesia can combine with benzodiazepine sedation {conscious sedation}, which causes amnesia but maintains consciousness.
biology
Anesthetics typically affect cell-membrane proteins. Anesthetics stimulate vagus nerve, which detects lung expansion.
biology: brain
Anesthesia can have prolonged brain-potential synchronization. Anesthetics seem to work on whole brain, not isolated circuits or regions [Alkire et al., 1998].
biology: drugs
Barbiturates, high-pressure nitrogen, alcohols, cleaning fluids like trichloroethene, industrial solvents, steroids, ether, chloroform, xenon, nitrous oxide, phencyclidine, opioids, and cholinergic agents can cause reversible consciousness loss.
Different drugs separately affect memory, voluntary muscles, and perception. Alfentanil, chloroform, cocaine, enflurane, ethyl p-aminobenzoate [1890], etomidate, halothane, isoflurane, ketamine, nitrous oxide, procaine, and propofol are anesthetics. Ethyl p-aminobenzoate [1890] is a local anesthetic.
Different anesthetics can have cross-tolerance.
biology: EEG
Bispectral index can measure anesthesia depth.
biology: endorphins
Perhaps, anesthetics affect enkephalin or endorphin chemistry.
biology: hippocampus
Perhaps, decreased hippocampus activity causes amnesia.
biology: receptors
Perhaps, anesthetics bind to NMDA or GABA-A receptor. Some anesthetics bind to microtubules. Anesthetics inhibit signal transfer between neurons [Alkire et al., 1997] [Alkire et al., 1999] [Antkowiak, 2001] [Franks and Lieb, 1994] [Franks and Lieb, 1998] [Kulli and Koch, 1991] [Lamme et al., 1998] [Logothetis et al., 1999] [Logothetis et al., 2001] [Rosen and Lunn, 1987] [Sennholz, 2000] [Tamura and Tanaka, 2001].
procedure
Before operations, patients have sedative, intravenous benzodiazepine, and oxygen.
Next comes intravenous thiopental or propofol, whose effects wear off quickly, followed by intravenous muscle relaxant {rapid sequence induction}, for quick anesthesia. Alternatively, next comes inhaled nitrous oxide and oxygen then inhaled halothane, desflurane, or sevoflurane {inhalation induction} {mask induction}, for slow anesthesia. Alternatively, next comes intravenous sufentanyl or propofol {intravenous anesthesia}.
After surgery, neostygmine allows muscle movement, and morphine inhibits pain.
High air pressures aid recovery from anesthesia.
results: amnesia
Anesthesia can cause no memory of surgery.
results: immobility
Anesthesia can cause no reaction to stimuli and no voluntary-muscle movement. Immobility can result from inhibition at spinal-cord GABA receptors.
results: memory
After anesthesia at level that precludes consciousness, patients can remember things that happened in surgery. Intense stimuli can cause memory without consciousness [Kihlstrom, 1996] [Levinson, 1965] [Merikle and Daneman, 1996].
Lipid solubility determines anesthetic effect {Myer-Overton rule}. Solubility allows binding to membrane proteins.
Muscle relaxers act quickly, so if tourniquets stop blood flow to arms, arms later have no paralysis {isolated forearm technique}.
Intravenous hypnotic drugs, such as propofol, barbiturates, and benzodiazepines, increase inhibition by keeping chloride channels open, because they enhance receptor inhibitory neurotransmitter effects {gamma-aminobutyric acid, drugs} (GABA) [Franks and Lieb, 2000]. Humans have more than 15 GABA-receptor types, which have different binding constants and connect to different pathways.
Drugs {etomidate} can enhance GABA-A receptors [Franks and Lieb, 2000].
Intravenous drugs {propofol} can affect GABA reception and correlate with low blood flow to midbrain and thalamus.
Intravenous barbiturates and sedatives {thiopental} {sodium pentothal} can affect GABA receptors [1930 to 1940].
Inhaled CH3Cl [3 is subscript] anesthetic {chloroform} is toxic.
Inhaled anesthetic {enflurane} can replace chloroform and ether. It affects nitric-oxide synthesis.
William Morton [? to 1868] used inhaled gas {ether} [1846] for surgery October 16 {Ether Day}. Ether is too volatile.
Inhaled anesthetic {halothane} can replace chloroform and ether. It affects nitric-oxide synthesis.
Inhaled anesthetic {isoflurane} can replace chloroform and ether. It affects nitric-oxide synthesis.
Humphrey Davy noted [1800] inhaled anesthetic {nitrous oxide} {laughing gas}. Horace Wells used it in dentistry [1844]. Nitrous oxide prevents glutamine binding at NMDA-receptor complexes [Flohr, 2000]. It reduces felt time.
Amines {curare} can block acetylcholine transmission across synapses and inhibit involuntary and reflex motions [1940 to 1950].
Curare substitutes {succinyl choline} can block acetylcholine transmission across synapses and inhibit involuntary and reflex motions.
Curare substitutes {tubocurarine} can block acetylcholine transmission across synapses and inhibit involuntary and reflex motions.
Curare substitutes {vecuronium} can block acetylcholine transmission across synapses and inhibit involuntary and reflex motions.
Ap5, CPP, CGS 19755, and D-CPP-ene {NMDA antagonist} compete for NMDA receptor but have no metabolic effect themselves.
Anesthetics {ketamine} can prevent glutamine binding at NMDA receptor complexes. Ketamine can cause hallucinations and dissociation. Ketamine does not affect GABA-A receptors [Franks and Lieb, 2000] [Flohr, 2000] [Flohr et al., 1998] [Hardcastle, 2000].
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Date Modified: 2022.0225