anesthesia

ANESTHETICSPresented by GROUP 3

History - The Primitive techniques

• Club• Strangulation• Alcohol• Mesmerism• Plants

History – contd. General anesthesia

was absent until the mid-1800’s

Original discoverer of general anesthetics Crawford Long,

Physician from Georgia: 1842, ether anesthesia

Chloroform introduced James Simpson: 1847

Nitrous oxide Horace Wells in 1845

19th Century physician administering Chloroform

History – contd. William T. G. Morton, a Boston

Dentist and medical student - October 16, 1846 - Gaseous ether Public demonstration gained world-

wide attention Public demonstration consisted of

an operating room, “the ether dome,” where Gilbert Abbot underwent surgery for removal of a neck tumour in an unconscious state at the Massachusetts General Hospital

But, no longer used in modern practice, yet considered to be the first “ideal” anesthetic

They did it for a better tomorrow!

AnalgesicsAnalgesics is sometimes confused with anesthesia. Below is the difference between them

AnestheticA medication that causes loss of

sensation. This is sometimes used to alleviate pain or for loss of consciousness for surgical procedures.

It relieves pain by numbing nerve impulses. Its action is reversible when right dose is administered

AnesthesiaLoss of consciousnessAnalgesia (loss of pain sensation)Adequate muscle relaxation

Analgesia• Loss of sensation to pain

Types of anesthesiaGeneralRegionalLocal

GENERAL ANESTHESIAThey induce unconsciousness and eliminate pain by blocking the general body innervation usually administered by IV inhalation for the purpose of

In ophthalmology general anesthesia is rarely used but does have a place in physically or emotionally traumatic surgeries and in non co-operative children.

General anesthesia

need for unconsciousness

‘Amnesia-hypnosis’

need for analgesia‘Loss of sensory and autonomic reflexes’

need for muscle relaxation

REGIONAL ANESTHESIA Regional anesthesia is an injection of a local

anesthetics around nerves or into the trunk of a nerve so that all the areas supplied by these nerves will not send pain signals to the brain.

They anesthetized area is usually larger than the area affected by local anesthesia.

Eg: retrobulbar injection to numb all eye movents by targeting the oculomotor nerve

LOCAL ANAESTHESIA

It is an anesthetic agent given to temporarily stop the sense of pain in a particular area of the body. The entire area supplied by a nerve is not be anesthetized. Only a certain branches does.

Patient remains conscious during a local anesthetic.

Giving ametocaine to numb the cornea (only axons of the ophthalmic division are severed)

Mechanism of action GENERAL ANESTHESIA

General anesthetics have two main routes:Inhalation

Most general anesthetics target GABAA receptor channel

Intravenous

General anesthesia

Inhalational

Gas

Nitrous oxideZenon

Volatile liquids

Etherhalothaneenfluraneisofluranedesflurane

Sevofluranemethoxyflurane

Intravenous

Slower acting

Dissociative anesthesia

ketamine

opiod analgesia

fentanyl

Benzodiazepines

diazepamlorazepammidazolam

Inducing agents

Thiopentone sod.

methohexitone sod.

propofolEtomidatedroperidol

Inhaled anesthetics Two main drugs used areGases eg Nitrous oxide, cyclopropane

Halogenated anesthetics e.g. halothanes, isoflurane, desflurane and influrane

Inhaled anesthetics have varying potency in proportion to their lipid solubility.

Every inhaled anesthetic has a specific MAC value.

A MAC (minimal alveolar anesthetic concentration)

is defined as the concentration of inhaled anesthetic as a % of inspired air, at which 50% of patients will be anesthetized.

MAC is a measure of potency: ED50.

Comparison between Nitrous Oxide and the Halothanes

Facts about inhaled anesthetics Rates of onset and recovery depend on the blood-

gas ratio:

a. The more soluble the anesthetic in the blood, the slower the anesthesia.

b. Anesthetics with high blood-gas ratios are associated with slow onset.

c. Anesthetics with high blood-gas ratios are associated with slow recovery.

d. Anesthetics with low blood-gas ratios have fast onset and recovery.

Intravenous anesthetics

Their onset of action faster than the fastest of the gaseous agents so they are used for induction of anesthesia.

1. Thiopental Barbiturate used for induction Highly lipid soluble; rapid onset; short-acting

due to redistribution

Disadvantage:Severe vasospasm Cardiovascular depression Hypersensitivity reactions

Midazolam Benzodiazepine used for:

Preoperative sedation Anterograde amnesia Induction Outpatient surgery Depresses respiratory function

Propofol (Michael Jackson's Killer)

Used for induction and maintenance of anesthesia

Antiemetic CNS and cardiac depressant It can induce prolonged sedation. Similar to thiopentone, but more rapidly

metabolized (rapid induction and recovery) so it is suitable for one day surgery.

Lacks tendency to induce involuntary movement and adrenocortical suppression.

Propofol (Michael Jackson's Killer)Propofol. The onset of itsaction begins after 30 s. Aftera single dose patient recoversafter 5 min with a clear headand no hangover.

Fentanyl Opiate used for induction and

maintenance of anesthesia Depresses respiratory function – be

careful of your asthma patient

Ketamine Dissociative anesthetic NMDA-receptor antagonist Induction of anesthesia Emergent delirium, hallucinations Cardiovascular stimulation increases intracranial pressure

Disadvantages: Cerebral hemorrhage Dysphoria and hallucinations

Mechanism of action of general anesthetics

Most injectable and inhaled anesthetic agents produce anesthesia by enhancing GABA-mediated neuronal transmission, primarily at GABAA receptors. GABA is an inhibitory neurotransmitter found throughout the CNS. Some inhaled anesthesia may also act by inhibiting such excitatory ion channels as neuronal nicotinic and glutamate receptors.

Note: Ketamine does not affect GABAA it antagonizes glutamic acid on NMDA receptor

4 (Four) Stages and signs !!!

• Traditional Description of signs and stages of GA - Also called Guedel`s sign• Typically seen in case of Ether

Stages of GAStage I: Stage of Analgesia Starts from beginning of anaesthetic inhalation and lasts upto

the loss of consciousness

Pain is progressively abolished during this stage Patient remains conscious, can hear and see, and feels a dream

like state Reflexes and respiration remain normal It is difficult to maintain - use is limited to short procedures

only

Stage II: Stage of Delirium and Excitement:

From loss of consciousness to beginning of regular respiration Excitement - patient may shout, struggle and hold his breath Muscle tone increases, jaws are tightly closed. Breathing is jerky; vomiting, involuntary micturition or

defecation may occur. Heart rate and BP may rise and pupils dilate due to

sympathetic stimulation. No stimulus or operative procedure carried out during this

stage. Breatholding are commonly seen. Potentially dangerous

responses can occur during this stage including vomiting, laryngospasm and uncontrolled movement.

This stage is not found with modern anaesthesia – preanaesthetic medication, rapid induction etc.

Stage III: Stage of Surgical anaesthesiaExtends from onset of regular

respiration to cessation of spontaneous breathing.

This has been divided into 4 planes: Plane 1: Roving eye balls. This plane

ends when eyes become fixed. Plane 2: Loss of corneal and laryngeal

reflexes. Plane 3: Pupil starts dilating and light

reflex is lost. Plane 4: Intercostal paralysis, shallow

abdominal respiration, dilated pupil.

Stage IV: Medullary / respiratory paralysis

Cessation of breathing failure of circulation death

Pupils: widely dilated Muscles are totally flabby Pulse is imperceptible BP is very low.

Local anesthetics Drugs used to provide local anesthesia are also used to achieve regional anesthesia. Regional anesthesia is an injection of a local anesthetics around nerves so that the area supplied by these nerves will not send pain signals to the brain. They anesthetized area is usually larger than the area affected by local anesthesia.

Mechanism of action Mechanisms: Nonionized form crosses axonal membrane - From within, ionized form blocks the inactivated Na+ channel - Slows recovery and prevents propagation of action

potentials

When local anesthetics are applied to the area that they numb, they need to get to the axon by crossing to the membrane. Only non ionized forms R-NH2 can enter the axon through the membrane. Upon entering the axon, only the ionized forms can block the sodium channels which causes depolarization of the sodium channel consequently numbing the area.Ionized form RNH3+

Classification of Local Anesthetics based on chemical

group - Esters: procaine, cocaine, benzocaine are metabolized by plasma and tissue esterases - Amides: lidocaine, bupivacaine, mepivacaine are metabolized by liver amides

Esters

Two types 1.Esters of benzoic acid (BA)2.Esters of para amino benzoic acid.

( PABA)

Esters of benzoic acid

ButacaineCocaineEthyl aminobenzoate (benzocaine)HexylcainePiperocaineTertracaine

Esters of para-aminobenzoic acidCloroprocaineProcainepropoxycaine

AmidesArticaineBupivacaineDibucaineEtidocaineLidocaineMepivacainePrilocaineRoppivacaine

May also be classified into

a. Short acting – cocaine, procaineb. Intermediate acting –

lidocaine, mepivacaine, dibucaine, prilocaine

c. Long acting – tetracaine, bupivacaine, etidocaine

MetabolismEsters are metabolized by the

plasma by enzymes esterase

amides are metabolized by liver by the enzyme hepatic amidases

Clinical noteDon’t give amides to patients with

poor liver function. Eg. patient with any form of hepatitis! WHY?

the amides will pile up due inability of the liver to metabolize. Hence elicit a complete history in your patient. In cases where patients have liver problem; your local anesthesia should be an ester.

How do we know which cocaine derivative is an amides or ester?The trick: the letter i

in almost all cases if an i precedes the “caine” sound, the drug is an amide but if not, it is an ester.

Amides EsthersArticaineBupivacaineDibucaineEtidocaineLidocaineMepivacainePrilocaineRoppivacain

e

Butacaine Cocaine Ethyl aminobenzoate (benzocaine) Hexylcaine Tertracaine Cloroprocaine Procaine propoxycaine

Limiting local anesthetics

All local anesthetics should be co-administered with alpha-1 agonist. E.g. phenylephrine, metoximine. WHY?

Reason;The alpha-1 agonist will cause a powerful vasoconstriction and limit the access of

surrounding tissues to the local anesthetics.

The Cocaine saga

I am the only local anesthetics that does not need an alpha-1 agonist. WHY?

ANS: I am a NEP re-uptake blocker.NOTE: it causes NEP build up in the synapsis. From the synapsis NEP binds to the alpha-1 receptors and causes vasoconstriction in the surrounding tissues. Therefore you don’t need an alpha-1 agonist after administration of cocaine.

Side effect

Local anesthetics can cause allergies especially the ester groups because they form PABA. All PABA containing compounds can always cause allergic reactions.

Therefore check your creams that you buy on the market.

OCULAR FOCUSQUICK NOTES

Injection:

amide + longer acting ester = longer-acting motor and sensory anesthesia.

Targets of injectable agents

muscle cone of the orbit-blocks all motor and sensory nerves of eye

directly into orbicularis muscles into CNVII

stylomastoid foramen –these two cause a complete loss of facial nerve on that side of face

Topical anesthesia Any test requiring contact with the cornea is

made more comfortable if topical anesthetic is used first

Indeed, some of these tests would be nearly impossible for the patient to endure if the cornea was not numbed first. In addition to numbing the cornea and

conjunctiva for testing, topial anesthetic is required in procedures such as removal of a foreign body or scraping a corneal lesion

Tetracaineis the most popular topical

anesthetic. Tetracaine is unpreserved.

Proparacaine and benoxinate contain preservatives and are effective

in anesthetizing the corneal nerve endings through topical application.

These formulations are highly osmotic and therefore sting and burn when applied.

Home use?never prescribed for a patient to use at home. Frequent use interferes with the healing process and can cause corneal melting

Please don’t rub your eyes!

the cornea now lacks sensation, the patient could conceivably rub hard enough to cause a corneal abrasion.

Toxicity Potential . All anesthetics have a potential to become

toxic in higher doses. Individuals may experience lightheadedness, ringing in their ears, or blurred vision.

At even higher doses, respiratory arrest can occur, as well as convulsions, coma and death.

punctual occlusionWhen topical anesthetic is used,

punctual occlusion can reduce the amount of drug that is absorbed into the system

MUSCLE RELAXANTS Used mainly in anesthesia protocols (EMERGENCIES) or in the (Intensive Care Unit) ICU to afford muscle relaxation and/or immobility. Used to relieve symptoms such as spasms ,pain and hyperreflexia Muscle relaxants interact with nicotinic ACh receptors at the neuromuscular junction.

MECHANISM

NORMAL CHOLINERGIC TRANSMISSIONNormally, a nerve impulse arrives at the motor nerve terminal, initiating an influx of calcium ions, which causes the exocytosis of synaptic vesicles containing acetylcholine.Acetylcholine then diffuses across the synaptic cleft. It may be hydrolysed by acetylcholine esterase (AchE) or bind to the nicotinic receptors located on the motor end plate. The binding of two acetylcholine molecules results in a conformational change in the receptor that opens the sodium-potassium channel of the nicotinic receptor. This allows Na + and Ca 2+ ions to enter the cell and K+ ions to leave the cell, causing a depolarization of the end plate, resulting in muscle contraction.

Normal end plate function can be blocked by two mechanisms.

1.Nondepolarizing agents (competetive), such as tubocurarine,

block the agonist , acetylcholine, from binding to nicotinic receptors and activating them, thereby preventing depolarization.

Major Non-depolarizing MRsAtracurium Rapid recovery Safe in hepatic or renal impairment Spontaneous inactivation to laudanosine ,Laudanosine can cause seizures

Mivacurium Very short duration Metabolized by plasma cholinesterases

2.depolarizing agents, (noncompetitive)Alternatively, depolarizing agents such

as succinylcholine, are nicotinic receptor agonists which mimic Ach, block muscle contraction by depolarizing to such an extent that it desensitizes the receptor and it can no longer initiate an action potential and cause muscle contraction

MRsmainly in anesthesia

protocols (EMERGENCIES) or in the (Intensive Care

Unit)

Beware of Anesthetics!

Thank youAny question?