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17 Cards in this Set
- Front
- Back
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Why use inhaled anesthetics?
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Reliable
unconsciousness, amnesia, immobility constant level of anesthesia level of anesthesia can be monitored |
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Mechanism of action
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poorly understood
immobility: act on spinal cord amnesia: hippoC, amygd, cerebral cortex CNS dep: enhance GABA, block NMDA |
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Minimum Alveolar Concentration (MAC)
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Conc to suppress movement to surgical stim in 50% pts
>0.5 = amnesia, 1= surgical anesthesia Additive, decline with age (6%/decade) |
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Info gained from PA mirrors Pbr and tells us three things
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index of anesthetic depth
reflection of rate of induction and recovery measure of potency |
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Factors determining PA
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Blood-gas partition coefficient
Blood-brain partition coefficient Oil-gas partition coefficient |
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Blood-gas partition coefficient
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solubility of gas in blood
main factor controlling rate of induction/emergence N2O<des<sevo<iso less soluble = faster induction/emergence |
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Blood-brain partition coefficient
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solubility of gas in tissue
mirrors blood-gas solubility |
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Oil-gas partition coefficient
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correlates lipid solubility with potency
potency roughly equivalent to MAC N2O < des<sevo<iso |
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MAC for N20, des, sevo, iso
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N20 = 105
Desflurane = 6 Sevoflurane = 2 Isoflurane = 1.15 |
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Induction/emergency kinetic factors
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High PI accelerates induction
Increased ventilation increases induction/emergence Low CO speeds induction/emergence Low solubility speeds induction/emergence |
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Recovery from anesthesia
duration of anesthesia diffusion hypoxia |
Tissue is a reservoir. Conc depends on solubility and duration of anesthesia. (the longer on, the longer off)
Diffusion hypoxia occurs with N2O, outpouring from blood into alveoli can dilute O2. Give higher PI O2 |
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N2O tox
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Inhibit cobalt ion in B12
teratogenic in animals >24 hr = megaloblastic anemia, neuropathy |
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Malignant hyperthermia
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exposure to VA or Succinylcholine
AD, usually RYR1, -> uncontrolled Ca2+ release myocyte ischemia and cell death, metabolic acidosis Dantrolene infusion, NaHCO3, hypervent, lasixs, help! |
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effects on cardiovascular system
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VA cause decrease in MAP due to decrease in SVR
N2O has little change on MAP or SVR HR: small increase iso/des...N20 and sevo = no effect Little effect on CO, may prolong QT (sevo) VA cardioprotective: ischemic preconditioning |
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ventilatory effects
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incr. RR, decr. TV, FRC; Less response to CO2 at higher MAC (apnea); sevo and N20: non pungent (peds induction), VA cause bronchodilation (asthmatics) and depress pharyn/laryn reflex (can't protect airway)
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CNS effects
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all cause cerebral vasodil (inc CBF and ICP)
but dec CMRO2 dose dependent EEG depression N2O has some mild analgesic properties (still need Opi) |
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Other effects
NM Renal Hepatic |
VA cause sk mm relax, enhance paralytics, but too weak alone
decrease renal (decrease UO) and hepatic blood flow |
