3877479 lecture presentation on anasthetics

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Lecture Presentation

N STHETICS

Prof. S.V. Tembhurne

Department of Pharmacology

S.N.I.O.P, Pusad. India



Categories of Anesthetics

General anesthetics

Central nervous system (CNS) depressants used to

produce loss of pain sensation and consciousness Local anesthetics

Used to cause loss of pain sensation and feeling in a

designated area of the body

Does not produce the systemic effects associatedwith severe CNS depression



Important difference between general

and local anesthetic are as fallows

Local anesthetics General anesthetics

Site of action CNS Peripheral nerve

Area of body involved Whole body Restricted area

Consciousness Lost Unaltered

Care of vital function Essential Usually not need

Physiological trespass High Low

Poor health patient Risky Safer

Use in non cooperative

patient

Possible Not possible

Major surgery Preferred Cannot be use

Minor surgery Not preferred preferred



Agents Involved in Balanced

Anesthesia

Preoperative medications

Sedative–hypnotics

Antiemetics

Antihistamines

Narcotics



Local Anesthetics



Local Anesthetics L As )

Followed general anesthesia by 40 years

Koller used cocaine for the eye in 1884

Halsted used cocaine as nerve block

First synthetic local-- procaine in 1905

Lidocaine synthesized in 1943



Local Anesthetics LAs)

Local anesthetic can be produced bycooling. Clinically used LAs have no/minimal local irritant

action and block sensory nerve endings, nervetrunks, neuromuscular junction, ganglionic synapse

and receptor (non selective) i.e. structures whichfunction through increased sodium permeability.

They also reduced release of acetylcholine frommotor nerve endings. Injected around a mixednerve they cause anesthesia of skin and paralysis

of voluntary muscle supplied b that nerve.



Classification

Injectable:

1) Low potency, short duration:-Procaine, Chloroprocaine2) Intermediate potency and duration: - Lignocaine, prilocaine

3) High potency, long duration: - Tetracaine (Amethocaine),Bupivacaine.Ropivacaine Dibucaine (Cinchocaine)

Surface anesthetics

A) Soluble: Cocaine

Lignocaine

Tetracaine

Benoxinate

B) Insoluble: Benzocaine

Butylaminobenzoate (Butamben)

Oxethazaine.



Occasionally use local anesthetics in other

countries:-

Mepivacaine, Etidocaine, cyclomethycaine, Dyclonine,Proparacaine.

Anesthetics which having local irritancy and

other prominent systemic activity:-

Propranolol, Chlorpromazine, H1 antihistamine, Quinine.

Estered linked local anesthetics: Cocaine,

procaine, Chloroprocaine, Tetracaine, and Benzocaine.

Amide linked Local anesthetics: Lignocaine, Bupivacaine, Dibucaine, Prilocaine, and Ropivacaine.



Mechanism of action

Mechanism of action is by reversibly blocking

sodium channels to prevent depolarization

Anesthetic enters on axioplasmic side andattaches to receptor in middle of channel



Mechanism



Characteristics

Linear molecules that

have a lipophilic and

hydrophilic end

(ionizable) low pH-- more in

ionized state and

unable to cross

membrane

adding sodium bicarb--

more in non-ionized

state



Characteristics

Two groups: esters and amides

esters metabolized by plasma cholinesterase

amides metabolized by Liver microsomes by

dealkylation and hydrolysis.



Features of Amide LAs

compared to ester LAs)

Produced more intense and longer lasting anesthesia

Bind to α1 acid glycoprotein in plasma.

Not hydrolyzed by plasma esterase. Rarely cause hypersensitivity reaction; no cross

sensitivity with ester LAs.

Because of their short duration, less intense analgesiaand higher risk of hypersensitivity, the ester linked LAs

are rarely used for infiltration or nerve block, but are stillused on mucous membrane.



Structure



Pharmacokinetic of Local

Anesthetics:

Soluble surface anesthetics are rapidly

absorbed from mucous membranes and

abraded areas; but absorption from intact

skin is poor. Procaine is negligible bound toplasma protein, but amide LAs are bound to

plasma protein.

After oral ingestion both procaine and

Lignocaine have high first pass metabolism

in the liver. Thus they are not effective orally

for antiarrhythmic purpose.



Toxicity Profile



Local Anesthetic Action/Toxicity

Central nervous system initially-- lightheadedness, circumoral numbness,

dizziness, tinnitus, visual change

later-- drowsiness, disorientation, slurred speech,loss of consciousness, convulsions

finally-- respiratory depression.Cocaine having more potent action on CNS.

Blood vessels:Fall in blood pressure due to sympathetic

blockage, relaxation of arteriolar smooth muscle.Toxic doses of Las produce cardiovascular

collapse.



Cardiovascular myocardial depression and vasodilation-- hypotension

and circulatory collapse

They have quinidine like antiarrhythmic action.

Procaine cannot used as a antiarrhythmic agentbecause of short duration of action and propensity tocause CNS effect, but its amide derivative

procainamide is a classical anti-arrhythmic action. At high dose they induce arrhythmias.

Bupivacaine is more cardiotoxic

Lignocaine is used as an antiarrhythmic

Allergic reactions-- rare (less than 1%) preservatives or metabolites of esters

rash, bronchospasm



Prevention and Treatment of

Toxicity

Primarily from intravascular injection or

excessive dose -- anticipation

aspirate often with slow injection

ask about CNS toxicity

have monitoring available

prepare with resuscitative equipment, CNS-depressant drugs, cardiovascular drugs



Treatment of Toxicity



Individual compounds

Cocaine- Obtained from Erythroxylem coca) South American Indians used to induce

euphoria, reduce hunger, and increase worktolerance in sixth century

Many uses in head and neck-- strong

vasoconstrictor, no need for epinephrine Mechanism is similar-- blocks sodium channel,

also prevents uptake of epinephrine andnorepinephrine

May lead to increased levels of circulatingcatecholamine-- tachycardia, peripheralvasoconstriction

Safe limits (200-400 mg)-- use with epinephrineclinically



Procaine

It is the first synthetic local anestheticsintroduced in 1905.

It is not surface anesthetics.

PABA is released on hydrolysis ofprocaine which can antagonized theantibacterial action of sulfonamide given totreat the infection.

Procaine penicillin injected i.m. acts for 24hours.



Lignocaine

Introduced in 1948

Lignocaine hydrochloride is used both topically and byinjection.

It block the conduction within 3 min. where as procainemay take15 min.

Cross sensitivity with ester LAs is not seen. Central effect of Lignocaine are drowsiness, mental

clouding, altered taste and tinnitus.

Overdose may cause muscle twitching, convulsion,cardiac arrhythmias, fall in BP,coma and respiratoryarrest

It is rapidly metabolized in liver by dealkylation to formmonoethylglycinexylidide and glycine xylidide.

Lignocaine is a popular antiarrhythmic



Prilocaine

It is similar to Lignocaine but does notcause vasodilation at the site of infiltration

and has lower CNS toxicity due to larger

volume of distribution. It is readily metabolized in liver and

kidneys. The principal metabolite excreted

in the urine is o-toluidine. This is believed

to cause methaemoglobinaemia.



Eutectic Lignocaine/Prilocaine

It can anesthetize the intact skin after

surface application.



Tetracaine (Amethocaine)

A PABA ester, more potent and more toxic

due to slow metabolism. It is used for surface anesthesia and spinal

anesthesia.



Bupivacaine

It is a potent and long acting (180-360 min.)

amide linked LA: used chiefly for infiltration and

regional nerve block, epidural and spinal

anesthesia.

It has high lipid solubility; distributed in tissue orethan in blood after spinal and epidural injection.

It is more prone to prolong QT interval and also

cause cardiac depression.

Should not used for intravenous regional

analgesia.



Ropivacaine

It is a congener of Bupivacaine, equally

long acting but less cardiotoxic.

It block the fiber involved in pain

transmission

Used for postoperative and labour pain, it

can also be employ for nerve block.



Dibucaine (Cinchocaine)

It is a most potent, most toxic and longest

acting LA (180-600 min.).

Used as a surface anesthetics on lessdelicate mucous membrane (anal canal)

and occasionally for spinal anesthesia of

long duration.



Benoxinate

It is a good surface anesthetics for the

eye; has little irritancy.

0.4 percent solution rapidly producecorneal anesthetics



Benzocaine and

Butylaminobenzoate Butamben)

Both are PABA derivative –can antagonisesulphonamide locally.

It is hydrolysed by esterases in the plasma to 4-aminobenzoic acid.

It has very low aqueous solubility, these are notsignificantly absorbed from mucous membraneor abraded skin.

Produce long lasting effect without systemic

toxicity. Is often used in combination with other drugs for

temporary local relief of pain associated withdental procedures, sore throat, hemorrhoids andpruritis.



Oxethazaine

Topical anasthetics,unique in ionizing to avery small extent even at low PH values.

Effective in anaesthetising gastric mucosa

despite acidity of the medium. swallowedalong with antacid it afford symptomatic

relief in gastric, drug induced gastric

irritation,gastroesophageal reflex andheartburn of pregnancy



Methods of Administering Local Anesthetics

Topical/Surface anesthesia

Infiltration anesthesia (infiltered under the skin in the area ofoperation)

Conduction block (injected around nerve trunk)

Field block

Nerve block

Spinal anesthesia (injected in subarachnoid space)

Drug used in spinal anesthesia are: Lignocaine, Tetracaine,Bupivacaine, Dibucaine

complication of spinal anesthesia:

Respiratory paralysis -Pulmonary complication

Hypotension due to sympathetic blocker.

HeadacheNeurological complication

septic meningitis

Nausea and vomiting



Intravenous regional anesthesia -mainly used forupper limb and orthopedic procedure.

Epidural anesthesia: Lignocaine and Bupivacaine aremost popular epidural Anastasia. It divided into 3category depending on the site of injection.

Thoracic-used generally for pain relief from thoracic/upper abdominal surgery.

Lumber: produce anesthesia of lower abdomen,pelvis and hind limb.

Caudal :given in sacral can produce anesthesia ofpelvic and peripheral region-used mostly for vaginaldelivery,anorectal,and genitourinary operation.

Duration of action of both anesthesia is prolong by

adrenaline. Cardiovascular complication are similar tospinal anesthesia but neurological and headache areless.



Goals of General

Anesthetics

Analgesia

Loss of pain perception

UnconsciousnessLoss of awareness of one’ s surroundings

Amnesia

Inability to recall what took place



History of Anesthesia

Ether synthesized in 1540 by Cordus

Ether used as anesthetic in 1842 by Dr.

Crawford W. Long

Ether publicized as anesthetic in 1846 by

Dr. William Morton

Chloroform used as anesthetic in 1853 byDr. John Snow



History of Anesthesia

Endotracheal tube discovered in 1878

Local anesthesia with cocaine in 1885

Thiopental first used in 1934

Curare first used in 1942 - opened the

“Age of Anesthesia”



Basic Principles of Anesthesia

Anesthesia defined as the abolition of

sensation

Analgesia defined as the abolition of pain

“Triad of General Anesthesia”

need for unconsciousness

need for analgesia

need for muscle relaxation



Potent CNS depressantsGeneral anesthesia = most severe state of

intentional drug-induced CNS depression

= opioid narcotic + volatile anesthetic (no pain +unconsciousness)

Depression of all CNS functions

- sedation, sleep, depressed reflexes,amnesia, unconsciousness



Risk Factors Associated With

General Anesthetics

CNS factors

Cardiovascular factors

Respiratory factors

Renal and hepatic function



Mechanism



Mechanism

The research finding that the anesthetics act on ligandgated ion channels (but not voltage sensitive ionchannels) are the major target of anesthetics action. TheGABA A receptor gated chloride channel is the mostimportant of these. Many inhalation anesthetics,

barbiturates, benzodiazepines and propofol potentiatethe action of inhibitory transmitter GABA to open chloridechannels.

Action of glycine (activate chloride channels) in thespinal cord and medulla is augmented by barbiturates,

propofol and many inhalation anesthetics. This actionmay block responsiveness to painful stimuli resulting influorinated anesthetics and barbiturates, in addition,inhibit neuronal cation channel gated by nicotiniccholinergic receptor.



Stages of Anesthesia

Stage 1: The analgesia stage

Stage 2: The excitement stage

Stage 3: Surgical anesthesia

Stage 4: Medullary paralysis



Stage 1: The analgesia stageStart from beginning of anesthetic inhalation and lastsupto the loss of consciousness. Pain is progressively

abolished during these stage patient remains abolishedduring this stage. Patient remains conscious, can hearand see, and fees a dream like state. Reflexes andrespiration remain normal. Though some minor and evenmajor operation can be carried out during this stage, it israther difficult to maintain-use is limited to shortprocedure.

Stage 2: The excitement stage/ Stageof Delirium:From loss of consciousness to beginning of regular respiration.Excitement is seen-patient may shout, struggle and hold his breath;muscle tone increases, jaw are tightly closed, breathing is jerkey;vomiting, involuntary micturition or defecation may occur. Heart rateand BP may rise and pupils dilate due to sympathetic stimulation.

No stimulus should be applied or operative procedure carried out

during this stage.



Elimination

When anesthetic administration is

discontinued, gradient are reversed and

the channel of absorption (pulmonary

epithelium) becomes the channel of

ellimination.

Most of general anesthetics are eliminated

unchanged. metabolism is significant only

for halothane. Other are practically notmetabolized



Inhalational Anesthetic Agents

Inhalational anesthesia refers to thedelivery of gases or vapors from the

respiratory system to produce anesthesia

Pharmacokinetics--uptake, distribution,and elimination from the body

Pharmacodyamics- MAC value



Nitrous Oxide

Prepared by Priestly in 1776

Anesthetic properties described by Davy in 1799

Characterized by inert nature with minimal

metabolism

Colorless, odorless, tasteless, and does not

burn.

Simple linear compound

Not metabolized Only anesthetic agent that is inorganic



Major difference is low potency

MAC value is 105%

Weak anesthetic, powerful analgesic

Needs other agents for surgical

anesthesia

Low blood solubility (quick recovery)



Nitrous Oxide Systemic Effects

Minimal effects on heart rate and blood

pressure

May cause myocardial depression in sickpatients

Little effect on respiration

Safe, efficacious agent



Nitrous Oxide Side Effects

Manufacturing impurities toxic

Hypoxic mixtures can be used Large volumes of gases can be used

Beginning of case: second gas effect

End of case: diffusion hypoxia

Inhibits methionine synthetase (precursor toDNA synthesis)

Inhibits vitamin B-12 metabolism

Dentists, OR personnel, abusers at risk



Ether

It is highly volatile liquid, produces irritating vapors which

are inflammable and explosive. Ether is a potent anesthetics, produce good analgesia

and marked muscle relaxation by reducing Ach outputfrom motor nerve ending

It is highly soluble in blood-induction is prolonged and

unpleasant with struggling, breath holding, salivation andmarked respiratory secreations(atropine must be givenas premedication to prevent the patient from drowsing inhis own secretion.

Post anesthetics nausea, vomiting and retching aremarked.

It does not sensitize the heart to adrenaline and is nothepatotoxic.



Halothane Systemic Effects

Inhibits sympathetic response to painfulstimuli

Inhibits sympathetic driven baroreflex

response (hypovolemia) Sensitizes myocardium to effects of

exogenous catecholamines- ventricular

arrhythmias



Halothane Systemic Effects

Decreases respiratory drive-- centralresponse to CO2 and peripheral to O2

• Respirations shallow-- atelectasis

• Depresses protective airway reflexes

Depresses myocardium by reducingintracellular calcium concentration-- lowersBP and slows conduction

Mild peripheral vasodilation



Halothane Side Effects

Halothane Hepatitis” -- 1/10,000 cases• fever, jaundice, hepatic necrosis, death

• metabolic breakdown products are hapten-protein conjugates

• immunologically mediated assault

• exposure dependent.

Malignant Hyperthermia due to intracellular release ofcalcium from sarcoplasmic reticulum causingpersistent muscle contraction and heat production--1/60,000 with succinylcholine to 1/260,000 without halothane in 60%, succinylcholine in 77%

Classic-- rapid rise in body temperature, musclerigidity, tachycardia, rhabdomyolysis, acidosis,hyperkalemia, DIC



Malignant Hyperthermia (continued)

• treatment--early detection, d/c agents,

hyperventilate, bicarb, IV dantrolene (2.5

mg/kg), ice packs/cooling blankets,

lasix/mannitol/fluids. ICU monitoring

• Susceptible patients-- preop with IV

dantrolene, keep away inhalational agents

and succinylcholine



Enflurane

Developed in 1963 by

Terrell, released for

use in 1972

Stable, nonflammable

liquid

Pungent odor

MAC 1.68%



Enflurane Systemic Effects

Potent inotropic and chronotropic depressant

and decreases systemic vascular resistance--lowers blood pressure and conductiondramatically

Inhibits sympathetic baroreflex response

Sensitizes myocardium to effects of exogenouscatecholamines – arrhythmias.

Respiratory drive is greatly depressed-- centraland peripheral responses

increases dead space widens A-a gradient

produces hypercarbia in spontaneously breathingpatient



Enflurane Side Effects

Metabolism one-tenth that of halothane-- doesnot release quantity of hepatotoxic metabolites

Metabolism releases fluoride ion-- renal toxicity

Epileptiform EEG patterns

Stimulates salivary and respiratory secretion.



Isoflurane

Synthesized in 1965 byTerrell, introduced intopractice in 1984

Isomer of enflurane Not carcinogenic

Nonflammable, pungent

Less soluble than

halothane or Enflurane MAC of 1.30 %



Isoflurane Systemic Effects

Depresses respiratory drive and ventilatory responses--less than enflurane

Myocardial depressant-- less than enflurane

Inhibits sympathetic baroreflex response-- less thanenflurane

Sensitizes myocardium to catecholamines -- less thanhalothane or enflurane.

Produces most significant reduction in systemic vascularresistance-- coronary steal syndrome, increased ICP

Excellent muscle relaxant-- potentiates effects ofneuromuscular blockers



Desflurane has distinct property in their highvolatility, lower oil: gas partition coefficient and

very low solubility in blood and tissue because of

which induction and recovery are very fast.

Patient can discharge few hours after surgery. Sevoflurane is polyfluronated anesthetic which

is intermediate between isoflurane and

desflurane,no problem in induction.

Sevoflurane does not cause sympathetic

stimulation and airway irritation even during

rapid induction.



Intravenous Anesthetic

Agents

First attempt at intravenous anesthesia by

Wren in 1656-- opium into his dog

Use in anesthesia in 1934 with thiopental Many ways to meet requirements-- muscle

relaxants, opoids, nonopoids

Appealing, pleasant experience



Inducing agent:

Thiopental

Barbiturate

Water soluble

Alkaline

Dose-dependentsuppression ofCNS activity--decreased

cerebralmetabolic rate(EEG flat)



Thiopental Systemic Effects

Rapid onset of action; ultrashort recovery period Varied effects on cardiovascular system in

people-- mild direct cardiac depression-- lowers

blood pressure-- compensatory tachycardia

(baroreflex) Dose-dependent depression of respiration

through medullary and pontine respiratory centers

IV route: Onset 1 min; duration 20–

30 min T½: 3–8 hours; metabolized in the liver, excreted

in the urine



Thiopental Side Effects

Noncompatibility

Tissue necrosis--gangrene

Tissue stores

Post-anesthetic course Laryngospasm occur generally when respiratory

secretion or other irritant are present it can preventedby atropine premedication and administration ofsuccinylcholine immediately after thiopentone.

Succinylcholine and thiopentone react chemically-should not mixed in same syringe.



Other uses

Occasionally used for rapid control of

convulsion.

I.V infusion of subanasthetic doses can be

used to facilated psychiatric verbal

communication with psychiatric pateint.



Etomidate

Structure similar to

ketoconozole

Direct CNS depressant(thiopental) and GABA

agonist

Redistribution



Etomidate Systemic Effects

Little change in cardiac function in healthy and

cardiac patients

Mild dose-related respiratory depression Decreased cerebral metabolism.

it suppress the production of steroid from

adrenal and is not suited for continuous i.v. use.

It is poor analgesic



Etomidate Side Effects

Pain on injection (propylene glycol)

Myoclonic activity

Nausea and vomiting (50%)

Cortisol suppression



Propofol

Rapid onset and short duration of action

Myocardial depression and peripheral

vasodilation may occur-- baroreflex notsuppressed

Not water soluble-- painful (50%)

Minimal nausea and vomiting



Slower acting drugs

Benzodiazepine

Produce sedation and amnesia

Potentiate GABA receptors

Slower onset and emergence

BZDs are poor analgesic: an opoids pr nitric oxide is usually added if theprocedure is painful



BZDs decrease muscle tone by central action,

but require neuromuscular blocking drugs for

muscle relaxation of surgical grade.

They donot provoke postoperative nausea or

vomiting.

Involuntary movement are not stimulated.

The anesthetic action of BZDs can be reversedby flumazenil



Diazepam

Often used as premedication or seizureactivity, rarely for induction

Minimal systemic effects-- respirations

decreased with narcotic usage Not water soluble-- venous irritation

Metabolized by liver-- not redistributed



Lorazepam

Slower onset of action (10-20

minutes)-- not used for induction

Used as adjunct for anxiolytic

and sedative properties

Amnesia are more profound

Not water soluble-- venous

irritation



Midazolam

More potent than diazepam or

lorazepam

Induction slow, recoveryprolonged

May depress respirations when

used with narcotics

Minimal cardiac effects

Water soluble: non irritating



Dissociative anesthesia:

Ketamine

Pharmacologically related to the hallucinogen phencyclidine

Interrupts cerebral association pathways -- “Dissociativeanesthesia”

Stimulates central sympathetic pathways

Primary site of action is the cortex and subcortical area; not inreticular activating system.



Ketamine has been recommended for

operation on the head and neck, in patient

who have bled, in asthamatic(relieves

bronchospasm).

It is good for repeated use; particularly

suitable for burn dressing.

It may dangerous for hypertensive and in

ischemic heart but is good for hypovolemic

patient.



Ketamine Systemic and Side Effects

Characteristic of sympathetic nervous

system stimulation-- increase HR, BP, CO

Maintains laryngeal reflexes and skeletalmuscle tone

Emergence can produce hallucinations

and unpleasant dreams (15%)



Clonidine

It is selective α2 adrenergic agonist used as a

antihypertensive.

Stimulation of central α2

adrenoceptors producessedation and analgesia.

Administered before surgery, clonidine reduce

the dose of anesthetic/analgesic drug, resulting

in less overall depression of cardiovascularfunction for the same level of anesthesia.



Narcotic agonists opiods)

Used for years for analgesic action-- civil war forwounded soldiers

Predominant effects are analgesia, depressionof sensorium and respirations

Mechanism of action is receptor mediated

Minimal cardiac effects-- no myocardial



Minimal cardiac effects no myocardial

depression

Bradycardia in large doses Some peripheral vasodilation and histamine

release -- hypotension

Side effects nausea, chest wall rigidity,

seizures, constipation, urinary retention

Meperidine, morphine, alfentanil, fentanyl,

sufentanil are commonly used

Naloxone is pure antagonist that reversesanalgesia and respiratory depression

nonselectively- acts 30 minutes, effects may

recur when metabolized



Muscle Relaxants

Current use of inhalational and previous

intravenous agents do not fully providecontrol of muscle tone

First used in 1942-- many new agents

developed to reduce side effects andlengthen duration of action

Mechanism of action occurs at theneuromuscular junction



Muscle Relaxants

Neuromuscular Junction

Non-depolarizing Muscle



Relaxants

Competitively inhibit end plate nicotinic

cholinergic receptor

Intermediate acting (15-60 minutes):atracurium, vecuronium, mivacurium

Long acting (over 60 minutes):

pancuronium, tubocurarine, metocurine Difference-- renal function



Non-depolarizing Muscle

Relaxants

Tubocurare-- suppress sympathetics, mast

cell degranulation

Pancuronium-- blocks muscarinics Reversal by anticholinesterase-- inhibit

acetylcholinesterase

neostigmine, pyridostigmine, edrophoniumside effects muscarinics stimulation



Depolarizing Muscle Relaxants

Depolarize the end-plate nicotinic receptor

Succinylcholine used clinically

short duration due to plasma cholinesteraseside effects-- fasiculations, myocyte rupture,

potassium extravasation, myalgias

sinus bradycardia-- muscarinic receptormalignant hyperthermia



Techniques

History and physical examination

Induction

Maintenance Emergence



Agents Involved in Balanced



Anesthesia

Preoperative medications

Sedative–hypnotics

Opiods

Antiemetics Anticholinergics

Antihistamines

Neuroleptics

Narcotics

Why there is need to give



preoperative medication

For relief of anxiety and facilated smooth induction.

Amnesia for pre- and postoperative events.

Supplement analgesic action of anesthetics andpotentiate them so that less anesthetics is needed.

Decrease the secretion and vagal stimulation caused byanesthetics.

Antiemetics effect extending to the postoperative period.

Decrease acidity and volume of gastric juice so that it is

less damaging if aspired.

Sedative-antianxiety drugs: BZDs have become popular drug forth ti b th d t ilit d th



preanesthetics because they produce tranquility and smootheninduction, there is loss of recall of preoperative events. Theycounteract CNS toxicity of anesthetics. Barbiturate is absolute.

Promethazine: is an antihistaminic with sedative, antiemetic and Anticholinergics properties. It is particularly use in children.

Anticholinergics: Atropine or hyoscine have been used, primarilyto reduce salivary and bronchial secretions. The main aim of theiruse now is to prevent vagal bradycardia and hypotension, andprophylaxis of laryngospasm which is precipitated by respiratorysecretion. they dilate pupils, abolish the pupilary sign and increasesigns and increase chances of gastric reflex by decreasing tone oflower esophageal sphincter.

Glycopyrrolate: Is a longer acting quaternary atropine substitute. it isa potent antisecretory and antibradycardiac drug; acts rapidly andless likely to produce central effect.

Neuroleptics: chlorpromazine,triflupromazine or haloperidol arefrequently used in premedication. They allay anxiety, smootheninduction and have antiemetic action. however they potentiaterespiratory depression and hypotension caused by the anestheticsand delay recovery.

Involuntary movement and muscle dystonias can occur, specially inchildren.

Antihistamines: H2 blockers patient undergoing prolonged



Antihistamines: H2 blockers, patient undergoing prolongedoperations, obese patients are at increased risk of gastricregurgitation and aspiration pneumonia.Ranitidine or Famotidinegiven night before and in the morning benefit by raising PH of gastric

juice; may also reduce its volume and thus chances of regurgitation.prevention of stress ulcer is another advantage.

Antiemetics:metaclopramide preoperatively is effective in reducingpost operative vomiting. By enhancing gastric emptying and tone ofLES, it reduces the chance of reflux and its aspiration.Extrapyramidal effect and motor restlessness can occur.

Domperidol is nearly as effective and does not produceExtrapyramidal side effect.

Opiods: Morphine or pethidine ally anxiety and apprehension of theoperation, produce pre- and post operative analgesia, smootheninduction, reduce the dose of anesthesia required and supplementpoor analgesic(thiopentone, halothane) or weak nitrous oxide

anesthetics. Use of opiods is now mostly restricted to those having preoperative

pain. When indicated fentanyl is mostly injected just beforeinduction.



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3877479 lecture presentation on anasthetics

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