1 intavenous anaesthetic agents dr.c.n.chandra sekhar
TRANSCRIPT
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Intavenous Anaesthetic Agents
Dr.C.N.Chandra Sekhar
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Intravenous Anaesthetic Agents
Induction with IV Anaesthetic agents is smoother and rapid than inhalational agents
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Intravenous Anaesthetic Agents
Properties of the Ideal IV Anaesthetic Agent:Rapid onset – mainly unionized at blood pH
- highly lipid solubleRapid recovery –Rapid redistributionAnalgesic at subanaesthetic ConcentrationMinimal CV and Resp. depressionNo emetic effectsNo emergence phenomenaNo Interaction with NMBD
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Intravenous Anaesthetic Agents
Properties of the Ideal IV Anaesthetic Agent:No pain on injectionNo venous sequelaeSafe if injected inadvertantly into an arteryNo toxic effects on other organsNo release of HistamineNo hypersensitivity reactionsWater soluble formulationLong shelf-lifeNo stimulation of Porphyrias.
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Intravenous Anaesthetic Agents
Pharmacokinetics of IV Anaesthetic Agents:After IV rapid in plasma conc. slower
declineAnaesthesia is produced by diffusion of drug
from arterial blood across BBB into the brain
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Intravenous Anaesthetic Agents
Rate of transfer into the brain and anaesthetic effect is regulated by:1.Protein binding2.Blood flow to the brain3.Extracellular pH & pKa of the drug4.The relative solubilities of the drug in lipid
and water5.Speed of Injection
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Intravenous Anaesthetic Agents
1.Protein Binding: Only unbound drug is free to cross the BBBLow plasma proteinDisplacement from proteins by other drugs
increase free drug conc.Hyperventilation decreases protein binding
and increases anaesthetic effect
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Intravenous Anaesthetic Agents
2.Blood Flow to the Brain:Reduced blood flow reduced delivery
of the drug.If CBF is decreased due to low Cardiac
output---initial blood conc. Higher than N, i.e Anaesthetic effect may be delayed but enhanced.
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Intravenous Anaesthetic Agents
3.Extracellular pH & pKa of the drug:Only non-ionized fraction of the drug
penetrates the lipid BBBThe potency of the drug depends on the
degree of ionization at the pH of extracellular fluid & pKa of the drug.
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Intravenous Anaesthetic Agents
4.The relative solubilities of the drug in lipid and Water:High lipid solubility enhances transfer into
brain.
5.Speed of Injection:Rapid IV adminstration high initial conc.
increases speed of induction and extent of CV and Resp.side effects
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Lean
Viscera
Fat
Pool
% of Dose
0.06 0.125 025 0.5 1 2 4 8 16 32 128 mts
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Classification of Intravenous Anaesthetics
Rapidly acting agents:Barbiturates
MethohexitalThiobarbiturates- thiopental, thiamylal
Imidazole compounds: eg.etomidateSterically hindered alkyl phenols: eg. PropofolSteroids: eg. Eltanalone, Althesin, MinaxoloneEugenol: eg. Propanidid
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Classification of Intravenous Anaesthetics
Slower- acting agents:KetamineBenzodiazepines:- Diazepam, flunitrazepam,
midazolamLarge-dose opioids:- Fentanyl, Alfentanil,
Sufentanil, remifentanilNeurolept combinations:- Opioid +
Neuroleptic
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N
C=O
N
R
C ‖O
O ‖C
C
R
R
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Thiopental Sodium
Chemical Structure:-Sodium 5-ethyl – 5(1-methylbutyl) – 2
thiobarbiturate
Physical properties & Presentation:-Sulphur analogue of pentobarbitalTaste = bitterColour = yellowishState = powderSmell = garlic
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Thiopental
Stored in Nitrogen to prevent chemical reaction with atmospheric CO2
6% anhydrous sodium carbonate to increase solubility in water
2.5% solution pH : 10.8Solution is hypotonicPrepared solution can be kept for 24 hrs.Oil/water partition coefficient 4.7pKa is 7.6
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Thiopental
Central Nervous System:-Onset <30sec after IV injection delayed if CO is lowProgressive depression of CNS and spinal cord
reflexesHypnotic action – potentAnalgesic effect – poorCMRCBF CBV ICP
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Thiopental - CNS
Recovery of consciousness occurs at high blood concentrations if a large dose is given or if the drug is injected rapidly (acute tolerance)
Consciousness regained in 5-10mts.At subanaesthetic conc.
Antanalgesic effectReduces pain threshold
Potent anticonvulsantSympathetic effect depressed more than
parasympathetic.Tachycardia
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Thiopentone
Cardiovascular System:-Myocardial contractility depressedPeripheral vasodilationHypotensionHR
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Thiopentone
Respiratory System:-Ventilatory drive In spont.Vent. Vf & Vt in bronchial muscle toneLaryngospasm
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ThiopentoneSkeletal muscle:-
tone at high blood concentrationsNo direct effect on NMJ
Uterus & Placenta:-Contractions suppressed at high dosesCrosses the placenta rapidlyFoetal blood conc. Not reach upto mother’s
Eye:-IOP by 40%Pupils = dilates first and then constrictsLight reflex present until surgical anaesthesia is reachedCorneal,conjunctival,eyelash and eyelid reflexes abolished
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Thiopentone
Hepatorenal Function:-Transient impairement of liver and kidney
functions.Hepatic microsomal enzymes are induced
metabolism & elimination of other drugs.
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Thiopentone
Pharmacokinetics:-75-85% drug is protein bound (mostly albumin)Protein binding affected by pH I.e by alkalemiaConc. Of free drug in hyperventilationDiffuses readily into CNS because of high lipid
solubility.Predominantly unionized (61%) at body pHConsciousness returns when the brain concentration
returns to a threshold value( vary from patient to patient)
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Thiopentone
Pharmacokinetics:- (contd….)Metabolism occurs in LiverMetabolites excreted in UrineTerminal elimination half-life 11.5 hrs.Metabolism is a Zero order process30% of original drug remain after 24 hrs.Hangover effect commonElimination impaired in elderlyIn obese dose should be based on lean body mass as
distribution to fat is slow.
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Thiopentone
Dosage & adminstration:-Adminstered as 2.5% solutionInitially 1-2 ml injectedHealthy adults: 4 mg/kg administered over 15-20 sec. Loss of eye reflex within 30secSupplementary dose 50-100mg slowlyChildren 6 mg/kgElderly patients 2.5 – 3 mg/kgInduction smooth, preceded by the taste of garlicNo other drugs should be mixed with Thiopentone
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Thiopentone
Adverse Effects:-HypotensionRespiratory depressionTissue necrosisIntra-arterial injectionLaryngospasmBronchospasmAllergic reactionsThombophlebitis
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Thiopentone
Indications:-Induction of AnaesthesiaMaintenance of AnaestheisaTreatment of Status epilepticusReduce intracranial pressure
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Thiopentone
Absolute Contraindications:Airway ObstructionPorphyriaHypersensitivity reaction to Baribiturates
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Thiopentone
Precautions:-Cardiovascular diseaseSevere hepatic diseaseRenal diseaseMuscle diseaseReduced metabolic rateObstetricsOutpatient anaesthesiaAdrenocortical insufficiencyExtremes of ageasthma
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Thiopentone
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Propofol
Indications:For induction and Maintenance of General
anaesthesiaSedation in Intensive Care Unit and during
Regional anaesthesia techniquesFor treatment of refractory nausea and
vomiting in patients receiving chemotherapyTreatment of status epilepticus
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Propofol
Mode of Action:- Unclear. Potentiates the inhibitory transmitters
glycine and GABA
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Propofol
Routes of Adminstration and Dose: Intravenous bolus dose 1.5 – 2.5 mg/kg for
inductionMaintenance 4-12mg/kg/hourFor children induction dose should be
increased by 50% and Manintenance infusion by 25-50%
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Propofol
Consciousness lost in 30 sec.Recovery about 10mts after a single dosePlasma concentration of 2-6mcg/ml
associated with hypnosis.Plasma conc. of 0.5 – 1.5 mcg/ml
associated with sedation.
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Propofol- pharmacodynamics
CVS: - -15-25% drop in Blood pressure and SVR without comp.
Increase in HR
-20% decrease in Cardiac output
-attenuates laryngoscopic response
-Vasodilatation due to NO release
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Propofol- pharmacodynamics
Respiratory System:Apnea for variable durationDecreased laryngeal reflexesInfusion decreases the TV and RRDepresses ventilatory response to CO2
Bronchodilatation due to direct effectPreserves the mechanism of hypoxic
pulm.vaso constriction
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Propofol- pharmacodynamics
Central Nervous System:-Smooth,rapid induction with rapid and clear headed
recoveryIntracranial pressure,cerebral perfusion pressure,
cerebral oxygen consumption reduced
GIT:-Propofol has got intrinsic antiemetic properties,
mediated by antagonism of dopamine D2 receptors.
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Propofol- Pharmacodynamics
Renal:-Causes reduction in excretion of Na+ ions
Metabolic:-Longterm use causes hypertriglyceridemia
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Propofol
Toxicity and side effects:-Pain on injection seen in 28% subjectsEpileptiform movementsFacial parasthesiasBradycardiaNeurological sequelae in children after longterm
use of propofol for sedationQuinol metabolites give green colour to urine
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Propofol-Pharmacokinetics
Distribution:-97% protein bound in plasmaVD is 700 – 1500 LDistribution half-life is 1.3 – 4.1minutes.
Metabolism:-Rapidly metabolised in the liverPrimarily to inactive glucuronide and sulphate
conjugates and the corresponding quinol.Renal and hepatic disease have no significant effect
on the metabolism.
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Propofol
Chemical:- 2,6 – diisopropylphenol
Presentation:- White oil in water emulsion containing 1 to 2% propofol
in soyabean oil and purified egg phosphatide
Main Action:- Hypnotic
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Ketamine Hydrochloride
1965Phencyclidine derivativeDissociative anaesthesiaChemical structure:-
2(o-chlorophenyl)-2(methylamino)-cyclohexanone hydrochloride
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Ketamine
Physical characteristics & presentation:-Soluble in water1% with NaCl for istonicity5 & 10% with benzothonium chloride
0.1mg/kg as preservativepH of the solution 3.5 – 5.5pKa of Ketamine 7.5
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Ketamine
Central Nervous System:-Extremely lipid soluble
After IVOnset: 30-60 secDuration: 10-15 min
After IMOnset: 3-4 mts.Duration: 15-25mts
Potent analgesic at subanaesthetic doses
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KetamineCentral Nervous System:- (contd…)
Amnesia persists 1 hr. after recovery of consciousnessInduction smoothEmergence delirium,restlessness,disorientation &
agitationEEG changes – loss of alpha activity & predominant
theta activityCMRCBF CBV ICP
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Ketamine
Cardiovascular System:-Arterial pressure by 25%HR by 20%CO may increaseMyocardial O2 consumption Myocardial sensitivity to EpinephrineVasodilatation in tissues innervated by -adrenergic
receptors & vasoconstriction in those with - receptors
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Ketamine
Respiratory System:-Transient apnoeaPharyngeal & laryngeal reflexes, patent
airway maintainedBronchial muscle is dilated
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Ketamine
Skeletal Muscle:-Muscle tone
GI system:-Salivation is increased
Uterus & Placenta:-Crosses placenta readily
Eye:-IOP
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Ketamine
Pharmacokinetics:-12% is bound to proteinInitial peak conc.after IV injection decreases
after drug distributesMetabolism is by liver demethylation &
hydroxylation of cyclohexanone ring (nor-ketamine is the active metabolite)
80% of injected drug excreted as glucuronides
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Ketamine
Pharmacokinetics:- contd……2.5% excreted unchanged in urineElimination half-life 2.5hrs.Peak conc. Achieved after 20 mts. After IM
inj.
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Ketamine
Dosage & administration:-Induction of Anaesthesia:-
2mg/kg IV, 1-1.5mg/kg required every 5-10mts.8-10mg/kg IM.0.25-0.5mg/kg or 50g/kg/min infusion for
analgesia without loss of consciousness
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Ketamine
Adverse effects:Emergence delirium,nightmares &
hallucinationsHypertension & tachycardiaProlonged recoveryIncreased salivationIncreased ICPAllergic reactions
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Ketamine
Indications:-High risk patients:- (shocked patients)Paediatric anaesthesiaDifficult locationsAnalgesia & sedationDeveloping countries
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Ketamine
Absolute contraindications:-Airway obstructionRaised ICP
Precautions:-Cardiovascular diseasesRepeated administrationVisceral stimulationOutpatient anaesthesia (not suitable for adults)
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Total Intravenous Anaesthesia
Indications:Rapid recovery and minimal hangoverMinimal cardiovascular depressionTo deliver High oxygen concentration To avoid nitrous oxide
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Methohexital Sodium
Chemical Structure:-Sodium-α-dl-5-allyl-1-methyl-5(1-methyl-2-
pentynyl) barbiturate
Physical Properties & Presentation:-Two asymmetrical carbon atomsWhite powderMixed with 6% anhydrous Na2CO3
1% solution pH 11.1 , pKa 7.9Single dose vial 100mg & multidose vials.5&2.5gm.Stable in solution for about 6 wks.(allowed only
24hrs)
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Methohexital Sodium
Pharmacodynamics:-Central Nervous System:-
Induction 15-30sec.Recovery more rapid than thio (2-3mts.)Drowsiness persists for several hoursEpileptiform activity in EEG seen in epileptic
patients.In sufficient doses acts as anticonvulsant
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Mthohexital Sodium
CVS:-Hypotension less than thioHR increases
RESP:-Moderate hypoventilation
Pharmacokinetics:-More is unionized at body pH( 75%) than thioElmination half life is shorter( appx. 4hrs)
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Methohexital Sodium
Dose & Administration:-1- 1.5mg/kg
Adverse effects:-CVS and Resp. depressionExcitatory phenomena during inductionEpileptiform activityPain on injectionTissue damageIntraarterial injectionAllergic reactionThrombophlebitis
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Etomidate
Chemical Structure:-D-Ethyl-1-(α-methylbenzyl)-imidazole-5-
carboxylate
Physical characteristics and presentation:-Soluble but unstable in waterContains 35% propylene glycol10ml ampoule contains 20mgpH is 8.1
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Etomidate
Pharmacology:-Rapidly actingDuration of action 2-3 mts.Less cardiovascular depressionLarge doses may produce tachycardiaRespiratory depression is less Impairs synthesis of cortisol from adrenal gland.Longterm infusion in ICU leads to increased
infection and Mortality.
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Etomidate
Pharmacodynamics:-76% bound to proteinMetabolised in liver mainly by esterase
hydrolysisTerminal elimination half life 75mts.
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Etomidate
Dose & administration:-0.3mg/kg
Adverse effects:-Suppression of synthesis of cortisolExcitatory phenomenonPain on injectionNausea and vomitingEmergence phenomenaVenous thrombosis
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Incidence of Adverse reactions:
Thiopentone : 1:14000-1:20000Methohexital : 1:1600- 1:7000Althesin : 1:400- 1:11000Propanidid : 1:500- 1:1700Etomidate :1: 450000Propofol :1:50000- 100000