Types and modes of anaesthesia

DR.NADIR MEHMOOD

Asst professor

Department ofSurgery, RMC

LEARNING OBJECTIVES

At end of this discussion, a student will be able to,• Enumerate the types of anesthesia• Describe techniques of G/A and L/A• Enlist the advantages and indications of each type

of anesthesia• Outline management plan in case of adverse effect

of technique or overdose of L/A, S/A, OR Bier’s A• Technique and Video of spinal anesthesia

TYPES OF ANESTHESIA

• G/A- TIVA, I/M, RECTAL, INTRAPERIT,DISSO A, INHALA A

• SPINAL, EPIDURAL, CAUDAL,• REGIONAL A • NERVE BLOCK A• BIER’S A• LA- SURFACE,INFILT, NERVE BLOCK,

COMBINATION

General Anaesthesia (GA)• complete loss of perception & consciousness

• fundamental attributes of GA

– loss of consciousness – does not block autonomic reflexes to

painful stimuli (perspiration, arrhytmia, hypertension, bronchoconstriction, bronchial hypersecretion)– vegetative stabilisation– analgesia – loss of pain sensation, suppression of

autonomic reactions– muscle relaxation

• induction of all the GA attributes facilitated by mosaic assembly of partial effects of many substances such as anaesthetics, analgetics, tranquillizers, myorelaxants

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

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Overview

• General anaesthesia is a complex procedure involving :– Pre-anaesthetic assessment – Administration of general anaesthetic drugs – Cardio-respiratory monitoring – Analgesia– Airway management – Fluid management – Postoperative pain relief

Techniques

• History and physical examination• Induction• Maintenance• Emergence

Types of GA according to the entry into organism

• inhalational

• intravenous

• intramuscular

• rectal – especially in children

• intraperitoneal – in animals

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Pre-anaesthetic evaluation

•medical history, current medications. •previous anaesthetics.History•age, weight, teeth condition.•Airway assessment, neck flexibility and head extension

Examination.

•Relevant to age and medical conditions.

Investigations.

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Pre-anaesthetic evaluationThe plan

best combination , drugs and dosages and the degree of how much

monitoring is required .fasting time

If airway management is deemed difficult, then

alternative placement methods such as fiberoptic intubation

may be used.

GA – premedication

Purpose of premedication

– satisfactory rest at night before operation (premedication)– calm down– basal analgesia– supression of readines to allergic reactions– supression of vegetative reflexes (bradycardia, hypersalivation, bronchial hypersecretion)

e.g: sedatives, hypnotics, anxiolytics, vagolytics (atropine), atihistaminics

Ideal Characteristics of Inhalational Anesthetics

• Rapid & pleasant induction & recovery• Rapid changes in depth of anesthesia• Adequate relaxation of smooth muscle• Wide margin of safety• Absence of toxic effect

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Induction

intravenous

Faster onset

avoiding the excitatory phase of anaesthesia

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Maintenance

• In order to prolong anaesthesia for the required duration (usually the duration of surgery), patient has to breathe a carefully controlled mixture of oxygen, nitrous oxide, and a volatile anaesthetic agent. This is transferred to the patient's brain via the lungs and the bloodstream, and the patient remains unconscious.

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Maintenance

• Inhaled agents are supplemented by intravenous anaesthetics, such as opioids (usually fentanyl or morphine).

• At the end of surgery the volatile anaesthetic is discontinued.

• Recovery of consciousness occurs when the concentration of anaesthetic in the brain drops below a certain level (usually within 1 to 30 minutes depending upon the duration of surgery).

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Maintenance

• Total Intra-Venous Anaesthesia (TIVA): this involves using a computer controlled syringe driver (pump) to infuse Propofol throughout the duration of surgery, removing the need for a volatile anaesthetic.

• Advantages: faster recovery from anaesthesia, reduced incidence of post-operative nausea and vomiting, and absence of a trigger for malignant hyperthermia.

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Neuromuscular-blocking drugs

• Block neuromuscular transmission at the neuromuscular junction.

• Used as an adjunct to anesthesia to induce paralysis.

• Mechanical ventilation should be available to maintain adequate respiration.

GA muscle relaxants

depolarising muscle relaxants

• cholinergic receptor -> depolarisation -> generation AP

• fasciculations• antagonisation is not possible• e.g.: Suxametonium (succinylcholine)

non-depolarising muscle relaxants

• competetive block of cholinergic receptors without generation of AP

• so called curariform medicaments, e.g.: Pancuronium, Atracurium

• antagonist: neostigmin (decurarization)

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Monitoring

• ECG• Pulse oximetry (SpO2)• Blood Pressure Monitoring (NIBP or IBP)• Agent concentration measurement• Low oxygen alarm• Carbon dioxide measurement (capnography) • Temperature measurement • Circuit disconnect alarm

Monitoring depth of GA

• concentration inhalational anaesthetics

• bispectral index (computerized EEG analysis)

• vegetative response (perspiration, pupils, blood pressure, pulse rate)

• clinical status, esp. waning muscle tonus (not available when muscle relaxants are used)

TOXICITY OF INHALATIONAL AGENTS

1. Hepatotoxic agent Isoflurane2. Nephrotoxic agent Barbiturate3. Cardiotoxic agent Enflurane

Halothane4. Flammable agent Ether

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Mortality rates• Overall, about five deaths per million.• Most commonly related to surgical/anesthesia factors or

pre-existing medical conditions ( haemorrhage, sepsis).• Common causes of death directly related to anaesthesia

include: 1- aspiration of stomach contents 2- suffocation (due to inadequate airway management) 3- allergic reactions to anaesthesia 4- human error 5- equipment failure

Local Anesthetics

• Followed general anesthesia by 40 years• Koller used cocaine for the eye surgery in 1884• Halsted used cocaine as nerve block• First synthetic local-- procaine in 1905• Lidocaine synthesized in 1943

Local Anesthetics

• Mechanism of action is by reversibly blocking sodium channels to prevent depolarization

• Anesthetic enters on axioplasmic side and attaches to receptor in middle of channel

Mechanism of the effect of LA

• blockade of the inner oriffice of sodium channel -> influenced depolarisation

• non-ionized form – penetration throuhg connective tissue, myelin sheet and cell membrane, intracellularly ionization and attachment to the sodium channel (competetive antagonism)

• ionizoed vs. non-ionized form ratio dependent on pH– healthy tissue: slightly alkaline pH -> more non-ionized form

-> easy penetration of LA into cells -> quick effect onset

– inflammatory focus: acid pH -> less non-ionized form -> -> poor penetration intracellularily -> weak LA effect

• Vasoconstrictive addition agents (adrenaline/epinephrine) – reduction of absorbtion ->longer lasting effect, lowered

toxicity, less bleeding

Classified into

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

mepivacaine, dibucaine, prilocainec. Long acting – tetracaine, bupivacaine,

etidocaine

Properties of a Desirable Local Anesthetic

•contrary to general anaesthesia, consciousness is preserved sites of action• should not be irritating to tissues• should not cause permanent damage to

nerves• have low systemic toxicity• must be effective • should have rapid onset but long duration of

action

ROUTES OF ADMINISTRATION:

1. Topical (skin, mucosal)2. Local Infiltration3. Nerve Block4. Spinal or Intrathecal injection5. Epidural 6. Caudal

LOCAL ANESTHETICS

Local anaesthesia

topic

infiltrativecunduct

epidural

subarachnoid

scheme by J.Cendelín

Effects of LA on nerve fibers

1. block of sympathetic division (warming of skin)

2. loss of sensation of heat and pain

3. loss of sensation of touch and pressure

4. loss of motorics

Local Anesthetic Toxicity• Central nervous system– initially-- lightheadedness, circumoral numbness,

dizziness, tinnitus, visual change– later-- drowsiness, disorientation, slurred speech, loss

of consciousness, convulsions– finally-- respiratory depression

Local Anesthetic Toxicity

• Cardiovascular– myocardial depression and vasodilation--

hypotension and circulatory collapse

• 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– ABC’s

Treatment of Toxicity

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