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43 Cards in this Set
- Front
- Back
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General anesthesia |
amnesia, immovility to noxious stimuli, analgesia, unconsciousness, attenuation of autonomic responses to noxious stim |
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Diethyl Ether |
relatively safe, flammable, prolonged induction, delayed emergence, N/V high rate |
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Chloroform |
associate w/ unexplained intraop deaths, hepatotoxicity |
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Ethylene
Divinyl ether-variation of ether |
-Cycloproane toxicity, - faster/more pleasant induction/faster awakening compared to older anesthetics -HIGHLY FLAMMABLE & TOXIC |
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Modern Inhalents -2 types |
Halogenated hydrocarbons-volatile -transition from L to G at room temp Halogenated partly/entirely w/ fluorine -greater stability(less flammable) less toxic |
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Halogenated hydrocarbons -n20 not halogenated hydro- |
anesthetic vapor delivered by variable bypaass vapes- calibrated to vape pressure of each drug |
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perfect inhalent |
non flammable, easily vaporized, potent, low solubilty, minimal metabolism, nonarrhythmogenic compatible with epi, provides skelatol muscle relaxation |
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3 stages of anesthesia |
intoxication, excitement, narcosis |
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Stage 1 analgesia |
slow regular breathing- with the diaphragm w/ intercostal muscles -presence of the lid reflex Complete amnesia, analgesia, & sedation |
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Stage 2 -delerium |
excitement, unconscousness, dream state(uninhibited activity) -Ventilation: irregular/unpredictable Reflex dilation of pupils- lid reflex intact Risk w/ reflex activity ^(vomit, laryngospasm, arrhythmias)
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stage 3 - surgical anesthesia plane 1 & 2 |
plane 1- slight somatic relaxation, regular periodic breathing, active ocular muscles Plane 2: breathing changes, inhalation< exhalation, slight pause seperates in/exhale, eyes become immobile |
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surgical anesthesia stage 3 & 4 |
plane 3: abdo muscles completely relax/ diaphragmatic breathing prominent, eyelid reflex absent Plane 4: intercostal muscles completely parlalyzed, paradoxical rib cage movement, irregular breathing, dilated pupils |
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STAGE IV paralysis |
muscles flaccid, eyes dilated, CV/ respiratory arrest, cardiovascular collapse |
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Signs of anestehsia |
use of ether, cycloproane, chloroform -small dose muscle relaxant- mask signs anesthesia except pupil size & lacrimation -masked in straight inhalation induction-kids -premed hastens passing through stage 2 |
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ETHERS which ones? Flourine replaces _________ ISO And enflurane |
-all inhalational general anesthetics except N20 & halothane -all other halogens -nearly identical |
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Volatility |
able to change L to G at low temp. -must be vaporized before administered -gas molecules create saturated vapor pressure ^ temp=^vapor pressure= ^volatility |
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volatility and BP temperature? Altitude? low Bp? |
temp at which Vp is = to atm pressure high altitudes(low atm p) BP decreases agents with low bP more like variations in barometric p. -Desflurane lowest-boils at room temp(heated container) |
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MAC what is it? |
minimum alveolar concentration: measure of inhalation anesthetic that prevents movement in response to surgical stimulation in 50% subjects -varies per drug 1:MAC=50% 1.2 MAC=95% no move 1.3 MAMC 99% no move - additive |
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things that ^ MAC |
decreased age- acute ^ in CNS- ^temp ^na- alcohol, inc CNS catacholamine leves |
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decrease MAC |
metabolic acidosis, increased age, hypoxia, induced lowBP, multiple drugs, dec. temp/Na/osmolality, progesterone(preg), ketamine, pancuronium, neo/physostimine, lido, opioids, barbiturates, diazepam, verapamil,anemia |
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meyer oberton rule mech of inhalent |
lipid theory of anesthesia- ^solublity =dec onset -can hyperpolarize neurons reduce excitability -inhibit excitatory synapse /enhance inhib synap inhibit presynaptic release and alter response of post synaptic receptors |
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anesthesia mechanisms-molecular -GABA
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CL- channels gated by inhibitory GabaA receptors> sensitive to halogenated inhalation agents ^ senstivity of GabaA receptor to Gaba> nehanced inhib transmission/dep NS activity -due to binding on GABAa reeceptor protein |
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molecular Glycine mechanism w/ anesthesia |
glycine & neuronal nicotinic acetylcholine recepotors -enhance capacity of glycine to activate glycine-gated Cl- channels(glycine receptors) -role inhib transmission in brain/spinal cord inhibit some nicotinic receptors> mediate analgesia/amnesia |
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N20/cyclopropane/xenon effects on gaba/glycine |
no effects selectively inhibit N-methyl-D-aspartate(NMDA) receptor> inhibit NMDA activated currents |
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Anesthesia and inhibition of CNS activity |
global reduction in cerebral metabolic rate/cerebral blood flow -suppress metab/excitability of thalamic neurons -relay by which sensory input from periphery ascends to the cortex -suppression of thalamic activity may act as switch btwn awake state cerebral cortex suprresd b4 thalamus- cortical suppresion via corticothalamic fibers leads to thalamic suppresion>cortex |
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anesthesia affect on sleep/amnesia |
inhalant agents with GabaA activity -can^ inhib effects of ventrolateral preoptic(VLPO) nuclei> suppress consciousness Depress hypocampal transmistter> probable locus of amnesia |
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Fresh gas flow determined by? Fresh inspired gas concentration? fresh alveolar gas concentration? fresh arterial gas concentration? |
-vaporizer & flowmeter I-FGF rate, breathing circuit volume, circuit absoprtion Fa-uptake, ventilation, concentration effects/2nd gas effect arterial- ventilation/perfusion mismatching |
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Solubility of sevo & ISO |
less soluble sevoflurane time constant=2> complete equiplibrium 6min -more soluble isoflurane- time constant 3-4min> complete equilibration in 10-15min
(constant= circulation time) |
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pharm principles solubility, equilibrium |
Pp inspired gas= Pp End tital alveolar gas low sol in blood = equil. fast vice versa fat: blood parititon coefficient n20=2.3vs halothane 51 |
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GG coefficients for N20, HaL/ISO/DES/SEVO |
N2O=0.47 Halothane=2.4 Isoflurane=1.4 Desflurane=0.42 Sevoflurane =0.65 |
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speeds of induction
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brain PP= aleveolar + blood pp in minutes anestheisa= after alveolar pp=MAC |
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CO and uptake HIGH vs LOW CO |
high CO= more rapid uptake- rate of ^ in PA and induction of anesthesia are slowed LOW CO= shock speeds rate of Increase of PA -less uptake into the blood |
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Rate at which PA decreases with time depends on increased solubility order 4 gases |
Halothane>isoflurane>desflurane>sevoflurane |
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reate of decrease of PA for Halothane vs iso/des/sevo |
halothane-metabolism & alveolar ventilation ISO/DES/SEVO- principally from alveolar ventilation |
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what doesn't trigger MH |
N20 & xenon |
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ADR halogenated anesthetics CO Bronchoconstriction |
CO preserved in ISO/DES -each causes lowBP -direct stim of laryngeal & tracheal areas -histamine relase /noxious stimuli activate reflex response > in light anesthesia spon vent < min volume in dose manner( ^ CO2 tension, Differences among agents modest) |
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Halothane - room temp? flammable? |
volatile liquid @ room temp- stored in sealed container -light senstive (can breakdown) amber bottle with THYMOL preservative -not flammable or explosive with O2/air |
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Halothane Pharm- sluble, elim, coefficient |
^ blood: gas & fat:blood partition (INDUCTION SLOW) alveolar conc. < inspired con. (long uptake) SOluvle in fat/tissues: accumulate in long admin. -speed recovery depends on duration admin 60-80% elimn unchanged by lungs 1st 24hr biotransform hepatic CYP: metab Trifluouracetic acid) FULMINANT HALOTHANE INDUCED HEPATIC NECROSIS |
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halothane clinical use |
first modern inhaled anesthetic not pungent-kids tolerate it Anesthesia @ end-tital concentration .7-1%
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halothane ADR cardiac |
cardiac- predictable dose dep. reduction ABP -MAP dec. 20-25% @ MAC -dec HR or Normal HR w/ low BP(disppear after hours) attenuation of baro reflex(dec. chron/ionotrop) HR ^ in light anesthesia -sensitize heart to epi(PVC, sustained VT) ^ epi levels (exogenous/endogenous) |
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HALOTHANE ADR autoregulation |
alters resistance of specific vascular beds/redistributes blood flow(skin & brain dilate> ^ CBF/skin perfusion -autoreg: renal/splanhi=nic & CBF inhibited> reduced perfusion w/ dec BP -inhibits hypoxic pulm. vasoconstrictoin(HPV)--> inc. perfusion of poor vent regions - |
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Respiratory HALOTHANE ADRs |
spont RR are rapid /shallow(dec. alveolar vent) ^ in art CO2 tension w/o compensate ^ in vent. -inhibits peripheral chemoreceptors response to arterial hypoxemia -potent bronchodilator |
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HALOTHANE NS effects |
dilates cerebral vasculature(^ CF/CB volume- ^ ICP) attenuates autoreg of CBF> dose dep. -CBF ^ w/ reduction in ABP reduce ABP< lower limit of autoreg-->cbf dec sig. suppreses cerebral metaolism and cerebral metabolic rate |
