peri anaesthesia pharmacology

8/14/2019 Peri Anaesthesia Pharmacology

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Peri-Anaesthesia Pharmacology

By

Hyder Gulam,FRCNA


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OVERVIEW:

Introduction

Overview of General Anaesthesia

Inhalational Agents

Neuromuscular Blockade

Intravenous Agents Benzodiazepines

Intravenous Agents HypnoticsSummary


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Anaesthesia first used by Plato in 400 BC todescribe absence of emotions.

Other terms commonly used in association withanaesthesia include:

-Analgesia: without pain-Hypnosis: sleep

-Narcosis: dulling of consciousness

-Paralysis: without movement

A typical GA now includes a premedication, ananalgesic agent, iv induction, and the combinationof a volatile and gaseous agent (with or without amuscle relaxant) as a maintenance anaesthesia.


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There are 4 clinical stages of anaesthesia, whichrecognise a progressive loss of cortical, sensoryand motor function.

The stages predict progressively decreasingresponses to surgical stimuli with increasinganaesthesia. Depth of anaesthesia can therefore begauged by progressive loss of respiratoryresponse, reflexes such as coughing and

hiccuping, eyelid and gag reflexes, and finallyloss of cardiovascular responses such astachycardia, hypertension and diaphoresis.



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Clinical Stages of Anaesthesia

Stage 1 Begins with the initiation of anaesthesia and

ends with loss of consciousness. Protective reflexes remainintact. NURSING ACTION: Close OR doors, keep roomquiet, stand by patient to assist, rest and reassure.

Stage 2 Starts with loss of consciousness with the onsetof regular pattern of breathing and disappearance of the lidreflex. Patient may appear agitated and excited reactions tostimuli (noise, being touched suddenly). NURSINGACTION: Be ready to restrain patient.

Stage 3 equated to the surgical stage of anaesthesia asat this level of anaesthesia there is depression of nervoussystem function so that there is absence of cardiovascular

or respiratory responses to surgical stimulation. Eyelashresponse, blink and swallowing reflex are absent. PREP

Stage 4 (over dosage) extends from diaphragmaticparalysis, apnoea, and loss of all reflex activity.Circulatorycollapse


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Triad of Anaesthesia

Reflex Suppression

(Analgesia)

Hypnosis/Amnesia (Unconsciousness)

Paralysis (Muscle Relaxation)


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Inhalational Agents

MAC Minimum Alveolar Concentration, the term usedto compare concentrations of inhalational agents. Refers tothe lowest concentration of the inhalational agents thatprevents movement in 50% of the patients when subjected

to a painful stimulus.All inhalational agents depress the myocardium anddepress ventilation.

Either gases or liquids that evaporate at room temp to formvapours that may be inhaled

These agents use the respiratory system for their uptake,and to a large extent, their elimination form the body.


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Relatively weak anaesthetic agent used inconjunction with other volatile agents to lowerconcentrations and decrease negative effects ofvolatile agents.

Non-irritating to the respiratory tract

Analgesic properties

Depresses CNS. CO, SV, HR & BP remainrelatively constant

May increase cerebral blood flow and ICP

Always administered with approx.30% oxygen toprevent hypoxia

Nitrous Oxide (gaseous inhalation agent)


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Isoflurane (Forane)

Stabilising effects on CV system

Does not increase sensitivity to catecholamines less incidence of arrhythmias

Reduces cerebral metabolic requirements,maintains carbon dioxide responsiveness, andcauses a lesser degree of cerebral vasodilation agent of choice for neurosurgical procedures dueto degree of cerebral protection.

May be irritative to the respiratory systemRapid recovery and emergence.

Isoflurane (Forane)


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Sevoflurance

More rapid induction and emergence that

isoflurane

No predisposition to arrhythmias

Less airway irritation

Increased ICP

Emerging as the agent of choice for ambulatory

and paediatric surgery.

Expensive $300-$400 per bottle.


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Used as an adjunct to inhalational agents to facilitate

intubation, provide relaxation of skeletal muscles

(abolishes laryngeal spasm), and enhance optimal surgical

conditions.

Normal Neuromuscular Transmission Action potentialtravels along the axon of a motor neuron. Motor nerve

releases an enzyme Acetylcholine (ACh). ACh acts on the

receptor site at the muscle surface resulting in polarization

(contraction). ACh is then metabolised by the enzyme

acetylcholinesterase and the muscle repolarises (relaxes).

Neuromuscular Blockade


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Suxamethonium (Depolarizing muscle relaxant)

Onset: Rapid (30-60secs)

Duration: Short 3-5min

Causes muscular fasciculation keeps muscle in a

depolarised state until metabolised bypseudocholinesterase (found in the plasma). Noreversal required. Stored in fridge.

Side Effects: Bradycardia, myalgia, hyperkalemia(fatal in burns, spinal injuries or massive trauma),

Sux apnoea, increased ICP. Hypothermiaincreases duration.

Triggering agent for Malignant Hyperthermia,


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Compete with ACh for receptor sites, therebyblocking the action of ACh resulting inneuromuscular blockade.

Mivacurium (short acting 6-10min, minimal CVeffects, dose related histamine release),Atracurium (intermediate acting 45min CV stable,slight histamine release, used in ICU settings),Vecuronium (power form, intermediate acting 20-

40min, no histamine release), Rocuronium (rapidonset 60-90secs alternative to SUX for rapidsequence induction, Pancuronium (long acting 60-80min, tachycardia).

Non-Depolarizing Block


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Do not cause muscular fasciculation.

Reversed by Neostigmine anticholinesterase drug),restore neuromuscular transmission by displacing the

neuromuscular blocking agent from the receptor site.Anticholinesterase drug bind with Acetylcholinesterasepreventing the hydrolysis of ACh. This increases theconcentration of ACh and allows the ACh to reclaim thereceptor site, thus preventing the blockade.

NEOSTIGMINE Onset: 6-8mins, Duration 60min,

Usual Dose 0.5-2.5mg IV. Causes muscarinic effects iebradycardia, bronchoconstriction, hypotension, nausea,vomiting, salivation, lacrimation and urinal urgency.

Non-Depolarizing Block-cont


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Anticholinergic drugs are given concurrently with

anticholinesterase drugs to counteract these

muscarinic side effects.

ATROPINE Duration: 40mins, Dose: 2mg IV.Tachydysrhythmias common.

GLYCOPYRROLATE Duration 80min, Dose:

1mg IV. More expensive, lower incidence of

dysrhythmias, slow change in heart rate betterfor the elderly and cardiac compromised.

Non-Depolarizing Block-cont


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Factors that may contribute to prolonged

neuromuscular blockade

Hypothermia

Hypercarbia

AcidosisHypokalemia

Renal disease, hepatic disease

Mycin antibiotics - tetracycline


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Clinical Assessment for adequate reversal

Opens eyes

Sustain hand grasps

Sustains head lift for 5 secsAdequate respirations and depth

Tidal Volume 5ml/kg

Monitor vital signs, assess secretions


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Wide variety of uses including premedicationbefore surgery, induction and anaesthetic ivsedation for hypnosis, amnesia and suppression ofseizure activity.

DIAZEPAM(Valium) produces calming effect,and skeletal muscle relaxation. Minimaldepressant effects on ventilation and circulation.

Dosage: 2-10mg IV; 0.4 mg/kg IM

Onset 1-3min IV, IM 20min - Duration 1 hourBurns when given IV note Dizac (Diazepam inEmulsion) does not burn (decreasedthrombophlebitis)


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MIDAZOLAM (Versed): Short acting CNS Depressant.Possesses antianxiety, sedative, (retrograde) amnesic,anticonvulsant and skeletal muscle relaxant effects. 3xpotent that diazepam

Dosage: 0.5-5mg IV titrated to effectOnset: 1-5min - Duration 2-6 hours

Water Soluble does not burn on injection.

FLUMAZENIL Benzodiazepine antagonist

Dosage 0.2mg IV (Max dose 1mg/15min or 3mg/hour)

Onset 1-2min Duration 1-3 hoursMay cause nausea/vomiting.



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Intravenous Agents Hypnotics

THIOPENTONE 4-6mg/kg IV

Action: CNE Depressant, shortacting IV barbiturate. Noanalgesic properties.

Onset: Rapid 15-40secs

Duration: 3-8mins, initialhypnotic action is intense,followed by mild sedation forup to 24hrs

Uses: IV induction, briefsurgical procedures

Side Effects: Resp depression(apnoea), hypotension,laryngospasm, anaphylaxis,arrhythmias, tissue necrosis

PROPROFOL Diprivan2mg/kg

Action: CNS Depressant. Shortacting anaesthetic agent

Onset: Rapid 15-40secs

Duration: 5-10min, withminimal residual sedation

Uses: IV Induction,Maintenance via infusion, briefsurgical procedures. ReducesICP and cerebral metabolic rate

Side Effects:Minimal, pain upon injection,hypotension, Resp depression(apnoea), anaphylaxis, hiccup.

Used for anaesthetic, induction, sedation and maintenance


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References:

Aitkinson, R.S., Rushman, G.B. and Lee, J.A. 1987,ASynopsis of Anaesthesia, Wright, Bristol.

Drain, C.B. 1994, The Post Anesthesia Care Unit (3rdedn),W.B. Saunders,Philadelphia, P.A.

Litwack, K. 1995,Post Anesthesia Care Nursing (2ndedn.), M.O. Mosby, St Louis.

Morgan, E.G. & Mikhail, M.S. 1996, ClinicalAnesthesiology, Appleton & Lange, California.

Rosewarne, F., Harley, I. And Hore, P. (eds) 1994,

Introductory Notes on Anaesthesia Australia (3rd

Edn),Royal Melbourne Hospital Anaesthetic Department.

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