Anesthesia Slides 040609

8/2/2019 Anesthesia Slides 040609

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AnesthesiologyAnesthesiology

Glen T. Porter, MDGlen T. Porter, MD

Francis B. Quinn, MDFrancis B. Quinn, MD

University of Texas Medical BranchUniversity of Texas Medical Branch

Galveston, TexasGalveston, Texas

June 2004June 2004


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HistoryHistory15401540 ValeriusValerius CordusCordus synthesizes ethersynthesizes ether

1842 Dr. Crawford Long (Georgia) first1842 Dr. Crawford Long (Georgia) firstuses inhaled ether to anesthetize patientuses inhaled ether to anesthetize patient

for surgeryfor surgery1845 Dr. Horace Wells attempts to1845 Dr. Horace Wells attempts todemonstrate use of Nitrous oxide indemonstrate use of Nitrous oxide insurgerysurgery

1846 William Morton (dentist) uses ether1846 William Morton (dentist) uses etheranesthesia at Massachusetts Generalanesthesia at Massachusetts GeneralHospital (soon to become the etherHospital (soon to become the etherdome). Dr. John Warren removes a neckdome). Dr. John Warren removes a neckmass.mass.

1846 Nitrous oxide used for anesthesia1846 Nitrous oxide used for anesthesia

1847 Dr. James Simpson introduces1847 Dr. James Simpson introducesChloroform anesthesiaChloroform anesthesia

1853 Queen Victoria undergoes1853 Queen Victoria undergoesanesthesia performed by Dr. John Snowanesthesia performed by Dr. John Snow


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HistoryHistory

Crawford Long

Horace Wells W. Thomas Morton
http://www.trincoll.edu/~aallan/images/Wellsportrait1.jpg


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HistoryHistory

1878 Endotracheal tube invented1878 Endotracheal tube invented

1885 Halstead introduces nerve1885 Halstead introduces nerveblock anesthesia with cocaineblock anesthesia with cocaine

1934 Sodium thiopentone (IV1934 Sodium thiopentone (IV

anesthesia)anesthesia)1934 Curare1934 Curare

1940s clinical use of muscle1940s clinical use of muscle

relaxantsrelaxants1950s Introduction of1950s Introduction of flourinatedflourinatedinhalational anesthetic agentsinhalational anesthetic agents


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Stages of AnesthesiaStages of Anesthesia

Stage I (analgesia stage)Stage I (analgesia stage) Conscious and rationalConscious and rational

Perception of pain is diminishedPerception of pain is diminished

Stage II (delirium stage)Stage II (delirium stage) UnconsciousUnconscious

Body responds reflexively and irrationallyBody responds reflexively and irrationally

Breath holding, pupils dilatedBreath holding, pupils dilated Muscle tone intactMuscle tone intact

Stage III (surgical anesthesia)Stage III (surgical anesthesia) Increasing degrees of muscular relaxationIncreasing degrees of muscular relaxation

Unable to protect airwayUnable to protect airwayStage IV (medullary depression)Stage IV (medullary depression) Depression of cardiovascular and respiratoryDepression of cardiovascular and respiratory

centerscenters


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Inhalational AnesthesiaInhalational Anesthesia

Effect is mediated by concentration of agentEffect is mediated by concentration of agent

present in the nervous systempresent in the nervous system

Each agents anesthesia effect mediated byEach agents anesthesia effect mediated bysolubility, metabolism, alveolar ventilation,solubility, metabolism, alveolar ventilation,

cardiac output, potencycardiac output, potencyMinimum Alveolar Concentration (MAC) is aMinimum Alveolar Concentration (MAC) is ameasure of relative potencymeasure of relative potency

MAC=amount of an agent in which 50% ofMAC=amount of an agent in which 50% ofpatients do not move with surgical stimulus.patients do not move with surgical stimulus.


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Nitrous OxideNitrous Oxide

Discovered 1776 by David PriestlyDiscovered 1776 by David Priestly

Largely recreational use until mid 1800sLargely recreational use until mid 1800sColorless, tasteless, odorlessColorless, tasteless, odorless

Low potency (MAC=105%)Low potency (MAC=105%)

Usually used with additional agent to achieveUsually used with additional agent to achievesurgical anesthesiasurgical anesthesia

Weak anestheticWeak anesthetic

Powerful analgesicPowerful analgesic

Poor solubility (rapid onset/offset time)Poor solubility (rapid onset/offset time)


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Nitrous OxideNitrous Oxide

Systemic effectsSystemic effects

Mild myocardial depression (usually innocuous)Mild myocardial depression (usually innocuous)

Severe cardiac depression with underlyingSevere cardiac depression with underlying

hemodynamic compromisehemodynamic compromise

No effect on respiration/neuromuscular junctionNo effect on respiration/neuromuscular junction

Side effectsSide effects Blood:gasBlood:gas partition coefficient of nitrous oxide is 34partition coefficient of nitrous oxide is 34

times greater than that of nitrogen.times greater than that of nitrogen.

Second gas effectSecond gas effectPressure changes in airPressure changes in air--filled spacesfilled spaces

Prolonged exposure can result in megaloblastic orProlonged exposure can result in megaloblastic or

aplastic anemia, Baplastic anemia, B--12 deficiency (inhibits methionine12 deficiency (inhibits methionine

synthetase)synthetase)


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Nitrous oxideNitrous oxide


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HalothaneHalothane

Synthesized by Suckling in 1956Synthesized by Suckling in 1956

First of the fluorinated anestheticsFirst of the fluorinated anestheticsDistinctive aroma, nonDistinctive aroma, non--flammable, highlyflammable, highly

potent (MAC=0.75%)potent (MAC=0.75%)Poor analgesic propertiesPoor analgesic properties

Very soluble in blood/fatty tissues withVery soluble in blood/fatty tissues withpotential for longer offset timepotential for longer offset time


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HalothaneHalothane

Systemic EffectsSystemic Effects Reduces/eliminates sympathetic response (includingReduces/eliminates sympathetic response (including

baroresponsebaroresponse)) Depresses respiratory drive. Respiration is rapid, shallow, andDepresses respiratory drive. Respiration is rapid, shallow, and

unvaried predisposing to atelectasisunvaried predisposing to atelectasis

Decreases airway reflexesDecreases airway reflexes

Decreases myocardial contractility and heart rate resulting inDecreases myocardial contractility and heart rate resulting indecreased cardiac output and hypotensiondecreased cardiac output and hypotension

Myocardial sensitization to exogenousMyocardial sensitization to exogenous catecholeminescatecholemines

Side EffectsSide Effects HepatitisHepatitisThought to be mediated by allergic response to byproductsThought to be mediated by allergic response to byproducts

Malignant hyperthermiaMalignant hyperthermia


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EnfluraneEnfluraneIntroduced in 1972Introduced in 1972

Stable, nonflammable, pungent odorStable, nonflammable, pungent odor

MAC=1.68%MAC=1.68%

Systemic effectsSystemic effects Respiratory drive depressed (more than halothane), hypoxemiaRespiratory drive depressed (more than halothane), hypoxemia

response bluntedresponse blunted

Depresses cardiac contractility and heart rate more thanDepresses cardiac contractility and heart rate more than

HalothaneHalothane Less sensitization of myocytes to exogenous catecholaminesLess sensitization of myocytes to exogenous catecholamines

Metabolism 1/10Metabolism 1/10thth that of Halothanethat of Halothaneless hepatotoxicless hepatotoxic

Rare cases of fluoride toxicity (hyperthyroid, rifampin)Rare cases of fluoride toxicity (hyperthyroid, rifampin)

Nephrogenic diabetes insipidusNephrogenic diabetes insipidusSide effectsSide effects Similar to other fluorinated agentsSimilar to other fluorinated agents

Epileptiform EEG at deep levelsEpileptiform EEG at deep levels

Avoid in patients with seizureAvoid in patients with seizure d/od/o


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IsofluraneIsoflurane

NonflammableNonflammable

Properties similar to Halothane andProperties similar to Halothane andEnfluraneEnflurane

Pungent odorPungent odorLess soluble than Halothane/Enflurane,Less soluble than Halothane/Enflurane,

more rapid induction/recoverymore rapid induction/recoveryMAC=1.3%MAC=1.3%


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SevofluraneSevoflurane

Fluorinated ether compoundFluorinated ether compound

Similar properties to other fluorinatedSimilar properties to other fluorinatedagentsagents

Mild respiratory/cardiac depressionMild respiratory/cardiac depression

NotNot bronchoirritantbronchoirritant

Rapid onset/offset secondary to low lipidRapid onset/offset secondary to low lipid

solubilitysolubilityAs enflurane, may cause renal and hepaticAs enflurane, may cause renal and hepatic

side effectsside effects


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DesfluraneDesflurane

Newer agentNewer agent

Low blood and lipid solubility with rapidLow blood and lipid solubility with rapidonset/offsetonset/offset

High incidence ofHigh incidence of bronchoirritationbronchoirritation withwithcough, laryngeal spasm, breath holdingcough, laryngeal spasm, breath holding

Minimal metabolism resulting in few sideMinimal metabolism resulting in few sideeffectseffects


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Intravenous Anesthetic AgentsIntravenous Anesthetic Agents

Barbiturates/otherBarbiturates/other

ThiopentalThiopentalEtomidateEtomidate

KetamineKetaminePropofolPropofol

BenzodiazepinesBenzodiazepines

Narcotic agonists (Narcotic agonists (opiodsopiods)/antagonists)/antagonists


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ThiopentalThiopental

Barbiturate with alkaline formulation. May causeBarbiturate with alkaline formulation. May causesevere complications if extravasation orsevere complications if extravasation orintraarterial injection occurs.intraarterial injection occurs.

Unconsciousness within 10Unconsciousness within 10--15 seconds15 seconds

Depresses neuronal activityDepresses neuronal activitymay decrease ICPmay decrease ICPPoor analgesicPoor analgesic

Varied effect on cardiovascular systemVaried effect on cardiovascular system

Decreased ventilatory drive, short period ofDecreased ventilatory drive, short period ofapnea after bolusapnea after bolus

Short duration secondary to rapid redistributionShort duration secondary to rapid redistribution

Metabolized in liverMetabolized in liver


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Thiopental distributionThiopental distribution


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EtomidateEtomidate

Onset, elimination, ability to produceOnset, elimination, ability to produce

unconsciousness similar to Thiopentalunconsciousness similar to ThiopentalShort duration of action secondary to rapidShort duration of action secondary to rapidredistributionredistribution

Less cardiopulmonary depressionLess cardiopulmonary depression

Can cause local pain and myoclonicCan cause local pain and myoclonic

movements with injectionmovements with injectionCortisol suppression and AddisonianCortisol suppression and Addisoniancrises reported in debilitation patientscrises reported in debilitation patients


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KetamineKetamine

Similar in structure to PCPSimilar in structure to PCP

Dissociative anesthesia,Dissociative anesthesia,

intense analgesia, amnesiaintense analgesia, amnesiaSlow nystagmus with eyes openSlow nystagmus with eyes open

Systemic effects similar to sympathetic stimulationSystemic effects similar to sympathetic stimulation

Respiratory function not depressed, airway protectionRespiratory function not depressed, airway protectionnot effectednot effected

Rapid onset, lasts 10Rapid onset, lasts 10--15 minutes15 minutes

Side effect is unpleasant dreams/hallucinations duringSide effect is unpleasant dreams/hallucinations duringemergence. Benzodiazepines shown to decrease this.emergence. Benzodiazepines shown to decrease this.


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PropofolPropofol

Substituted phenolSubstituted phenol

Rapid onset, short duration (metabolized)Rapid onset, short duration (metabolized)Dilates peripheral vasculature leading toDilates peripheral vasculature leading to

decreased blood pressuredecreased blood pressuremay be significantmay be significant

in patients with blunted sympathetic responsein patients with blunted sympathetic response

Short period of apnea after administrationShort period of apnea after administration

Venous irritationVenous irritation


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BenzodiazepinesBenzodiazepines

Good for amnesia/sedationGood for amnesia/sedationvia potentiation atvia potentiation atGABA receptorsGABA receptors

Diazepam onset 2Diazepam onset 2--3 minutes (IV), Lorazepam3 minutes (IV), Lorazepam(Ativan) onset 10(Ativan) onset 10--15 minutes, both have long15 minutes, both have longhalfhalf--life (Diazepam (Valium)


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Narcotic agonists/antagonistsNarcotic agonists/antagonists

Analgesia,Analgesia, dpresseddpressed sensorium,sensorium,

respiratory depressionrespiratory depressionEffects are doseEffects are dose--relatedrelated

Minimal cardiovascular effects, thoughMinimal cardiovascular effects, thoughvasodilatory effects can be serious invasodilatory effects can be serious inpatients with hypovolemiapatients with hypovolemia

Side effects include bradycardia (doesntSide effects include bradycardia (doesntusually effect output),usually effect output), n/vn/v, chest wall, chest wallrigidity, seizure activity, decrease GIrigidity, seizure activity, decrease GI

motilitymotility


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NarcoticsNarcotics

Several receptorsSeveral receptorsMuMu: analgesia, respiratory depression, euphoria,: analgesia, respiratory depression, euphoria,

dependancedependanceKappa: spinal analgesia, sedation, meiosisKappa: spinal analgesia, sedation, meiosis

Omega: hallucinations, dysphoria, tachycardiaOmega: hallucinations, dysphoria, tachycardia

Meperidine, Morphine, Fentanyl, Sufentanil,Meperidine, Morphine, Fentanyl, Sufentanil,RemifentanilRemifentanil

Nalorphine: agonist/antagonistNalorphine: agonist/antagonistless analgesia,less analgesia,

less respiratory depressionless respiratory depressionNaloxone: reverses analgesia/respiratoryNaloxone: reverses analgesia/respiratorydepression (30 minutes)depression (30 minutes)


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Muscle RelaxantsMuscle Relaxants

Used clinically since 1940s. 1960s led toUsed clinically since 1940s. 1960s led to

the balanced anesthesia concept.the balanced anesthesia concept.Important to provide motionImportant to provide motion--free surgicalfree surgical

fieldfieldWork at neuromuscular junctionWork at neuromuscular junction

Nondepolarizing vs. DepolarizingNondepolarizing vs. Depolarizing

Competitive inhibition of endplate nicotinicCompetitive inhibition of endplate nicotinic

receptor vs. receptor binding withreceptor vs. receptor binding with

depolarizationdepolarization


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Paralytic agentsParalytic agents----AnatomyAnatomy


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Neuromuscular junctionNeuromuscular junction


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DepolarizationDepolarization


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Nondepolarizing AgentsNondepolarizing Agents

Bind to and competitively inhibit endBind to and competitively inhibit end--plateplatenicotinic receptorsnicotinic receptors

IntermediateIntermediate--acting (15acting (15--60 minutes)60 minutes)Atracurium, vecuronium, mivacuriumAtracurium, vecuronium, mivacurium

Relatively independent of renal function for clearanceRelatively independent of renal function for clearance

Less circulatory effectLess circulatory effectLongLong--acting (>60 minutes)acting (>60 minutes)Pancuronium, metocurine, dPancuronium, metocurine, d--tubocurarine, gallaminetubocurarine, gallamine

More hemodynamic effectsMore hemodynamic effectsTubocurarine blocks autonomic ganglia, may causeTubocurarine blocks autonomic ganglia, may cause

mast cell degranulationmast cell degranulation

Pancuronium inhibits vagal and muscarinic receptorsPancuronium inhibits vagal and muscarinic receptorsand produces tachycardiaand produces tachycardia


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Reversal of Muscle RelaxationReversal of Muscle Relaxation

Effect is reversed when the ratio of ACh atEffect is reversed when the ratio of ACh at

the NMJ is increasedthe NMJ is increasedNeostigmine, edrophonium, acetylcholineNeostigmine, edrophonium, acetylcholine(anticholinesterases)(anticholinesterases)

Reversal agents can cause bradycardia byReversal agents can cause bradycardia bystimulation of heartstimulation of heart muscarinicmuscarinic receptorsreceptors

PreadministrationPreadministration of muscarinic blockersof muscarinic blockersare effective in avoiding this side effectare effective in avoiding this side effect(atropine, glycopyrrolate)(atropine, glycopyrrolate)


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Depolarizing Muscle RelaxantsDepolarizing Muscle Relaxants

Bind to and depolarize endBind to and depolarize end--plate ACh nicotinic receptorsplate ACh nicotinic receptors

The depolarization continues as long as receptor isThe depolarization continues as long as receptor is

occupiedoccupiedTypically short duration of effect as drug isTypically short duration of effect as drug is hydrolysedhydrolysed bybyplasma cholinesterasesplasma cholinesterases

Patients with abnormal cholinesterase are at risk forPatients with abnormal cholinesterase are at risk forprolonged paralysisprolonged paralysis

Sustained depolarization produces transientSustained depolarization produces transient fasiculationsfasiculations

which can result in postoperative myalgias andwhich can result in postoperative myalgias andextravasation of potassium in patients with damagedextravasation of potassium in patients with damagedmyocytes. Prior administration of lowmyocytes. Prior administration of low--dose nondose non--depolarizing paralytic can attenuate incidencedepolarizing paralytic can attenuate incidence


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SuccinylcholineSuccinylcholine

Only depolarizing paralytic used clinicallyOnly depolarizing paralytic used clinically

Sinus bradycardia, junctionalSinus bradycardia, junctional arhythmiasarhythmias,,even sinus arrest can followeven sinus arrest can followadministrationadministrationlikely secondary tolikely secondary to

muscarinic receptors on heart (blockedmuscarinic receptors on heart (blockedwith atropine)with atropine)

Increased intraocular pressure, intragastricIncreased intraocular pressure, intragastricpressure, trismus reported.pressure, trismus reported.

Malignant hyperthermiaMalignant hyperthermia


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RapidRapid--Sequence InductionSequence Induction

PreoxygenationPreoxygenation

AnesthesiaAnesthesia--inducing drugs (barbiturates,inducing drugs (barbiturates,benzodiazepines,benzodiazepines, opiodsopiods, etomidate,, etomidate,

ketamine, or propofol)ketamine, or propofol)

SuccinylcholineSuccinylcholine

IntubationIntubation


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Local AnestheticsLocal Anesthetics

Reversibly inhibit the generation and conductionReversibly inhibit the generation and conductionof impulses from a particular area of the bodyof impulses from a particular area of the body

Effect is secondary to conduction blockade byEffect is secondary to conduction blockade bydecreasing permeability of nerve membranes todecreasing permeability of nerve membranes tosodiumsodium

Binds to sodium channel and blocks itBinds to sodium channel and blocks itAll but cocaine are vasodilators and thereforeAll but cocaine are vasodilators and thereforeusually are mixed with epinephrineusually are mixed with epinephrine

Ester/Amide family of drugsEster/Amide family of drugsEsters metabolized by plasma cholinesterase,Esters metabolized by plasma cholinesterase,amides metabolized by liver pamides metabolized by liver p--450 system450 system


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Lipophilic/hydrophilic endsLipophilic/hydrophilic ends

NonNon--ionized form crosses membranesionized form crosses membranesmore readilymore readily

Drugs have less effect in acidic environmentDrugs have less effect in acidic environment

(infection)(infection)

Addition of HCO3 to acidic preparations mayAddition of HCO3 to acidic preparations may

increase potency and decrease painincrease potency and decrease pain


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Local Anesthetic InjectionLocal Anesthetic Injection


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Local Anesthetic InjectionLocal Anesthetic Injection

The TargetThe Target

L l h i i j i O l i


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Local anesthetic injectionLocal anesthetic injection -- OtologicOtologic

L l h iL l th ti I lI t l


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Local anestheticLocal anesthetic -- IntranasalIntranasal

L l A h iL l A th i M illM ill


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Local AnesthesiaLocal Anesthesia -- MaxillaMaxilla

Local AnesthesiaLocal Anesthesia --


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Local AnesthesiaLocal Anesthesia

MandibleMandible

N t diti l A th iN t diti l A th i


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Nontraditional AnesthesiaNontraditional AnesthesiaAcupunctureAcupuncture Acupuncture with electrical stimulation gave 50Acupuncture with electrical stimulation gave 50--65% decrease in65% decrease in

opiodopiod use, decreased PCA use time, and decreased N/V afteruse, decreased PCA use time, and decreased N/V afterintraabdominal surgery (Wang, 1997,intraabdominal surgery (Wang, 1997, HamzaHamza, 1999,, 1999, KotaniKotani, 2001), 2001)

Decreased N/V after tonsillectomy in adults (NIH consensus,Decreased N/V after tonsillectomy in adults (NIH consensus,1998)1998)

Pain control antagonized by naloxone (Pain control antagonized by naloxone (SjolundSjolund, 1979), 1979)

Thought to stimulate large nerve fibers which changes painThought to stimulate large nerve fibers which changes painperception in the spinal cord transmitted by small fibers.perception in the spinal cord transmitted by small fibers.

Endorphins also increased.Endorphins also increased.AcupressureAcupressure

TENS (transcutaneous electrical nerve stimulation)TENS (transcutaneous electrical nerve stimulation) 1010--30% reduction in post30% reduction in post--op pain and needop pain and need

for analgesics (Tyler, 1982)for analgesics (Tyler, 1982)CapsiacinCapsiacin

HypnosisHypnosis

Tidbits, oddsTidbits, odds
http://images.google.com/imgres?imgurl=www.healthywaymagazine.com/issue16/images/acupuncture.jpg&imgrefurl=http://www.healthywaymagazine.com/issue16/06_acupuncture.html&h=170&w=170&sz=6&tbnid=spGweVn4lzoJ:&tbnh=94&tbnw=94&prev=/images%3Fq%3Dacupuncture%26start%3D200%26hl%3Den%26lr%3D%26ie%3DUTF-8%26oe%3DUTF-8%26sa%3DN


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db ts, odds,

& ends& endsMalampattiMalampatti

classificationclassification

ThyromentalThyromental distancedistance

Grading the intubationGrading the intubation

viewviewSP systemSP system

Closed systemClosed systemanesthesiaanesthesia6.5cm


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AnesthesiologyAnesthesiology

Glen T. Porter, MDGlen T. Porter, MD

Francis B. Quinn, MDFrancis B. Quinn, MD

University of Texas Medical BranchUniversity of Texas Medical BranchGalveston, TexasGalveston, Texas

Anesthesia Slides 040609

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