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Pharmacology of Anesthetics PowerPoint Presentation

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Description : Check out this medical PowerPoint presentation titled "Pharmacology of Anesthetics" by Dr Lindsey Patterson.

This medical PowerPoint presentation talks about pharmacology of anesthetics.

Anesthetics are drugs that are used to induce a state of unconsciousness, reduce pain, and provide muscle relaxation during surgical procedures. There are two main types of anesthetics: general anesthetics and local anesthetics.

General anesthetics can be administered via inhalation or injection, and they produce a reversible loss of consciousness. Inhalation agents include gases such as nitrous oxide, desflurane, sevoflurane, and isoflurane. Injection agents include propofol, etomidate, and barbiturates. General anesthetics work by altering the activity of neurotransmitters in the brain, such as gamma-aminobutyric acid (GABA), which produces a sedative effect.

Local anesthetics, on the other hand, are used to block pain in a specific area of the body without inducing unconsciousness. They are commonly used in dental and minor surgical procedures. Local anesthetics work by blocking the transmission of nerve impulses from the site of the injection to the brain. Commonly used local anesthetics include lidocaine, bupivacaine, and ropivacaine.

The pharmacology of anesthetics is complex, and their effects depend on various factors such as dose, route of administration, and individual patient characteristics. Adverse effects of anesthetics can include nausea and vomiting, respiratory depression, and cardiovascular depression. Therefore, careful monitoring of patients is necessary during anesthesia administration.

Tags : Pharmacology of Anesthetics, general anesthetics, local anesthetics, anesthesia administration, Anesthesiology

Published on : Mar 16, 2023 | Views : 972 | Downloads : 4

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Slide 1-

PHARMACOLOGY OF ANAESTHETICS Katarina Zadrazilova FN Brno, October 2010
Slide 2-

AIMS OF ANAESTHESIA
Slide 3-

Triad of anaesthesia Neuromuscular blocking agents for muscle relaxation Analgesics/regional anaesthesia for analgesia Anaesthetic agents to produce unconsciousness Why unconscious patient require analgesia ?
Slide 4-

Overview Intravenous and inhalational anaesthetics Analgesics – simple, opioids Muscle relaxants Decurarization
Slide 5-

INTRAVENOUS ANAESTETICS
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Stages of anaesthetics Induction – putting asleep Maintenance – keeping the patient asleep Reversal – waking up the patient
Slide 7-

Intravenous anaesthetics Onset of anaesthesia within one arm – brain circulation time – 30 sec Effect site brain Propofol Thiopentale Etomidate Ketamine
Slide 8-

General anaesthetic-how do they work TASK – EXPLAIN Loss of conscious awareness Loss of response to noxious stimuli Reversibility Anatomical site of action Brain : thalamus, cortex Spinal cord
Slide 9-

Linear correlation between the lipid solubility and potency Molecular theories GA – how do they work
Slide 10-

Critical volume hypothesis Disruption of the function of ionic channels Perturbation theory Disruption of annular lipids assoc. with ionic channels Receptors Inhibitory – GABA A, glycin enhance Excitatory - nAch, NMDA inhibit Molecular theories GA – how do they work
Slide 11-

GABAA receptor GA – how do they work
Slide 12-

Thiopentale Barbiturate Dose 3-7 mg/kg Effects : hypnosis, atiepileptic, antanalgesic Side effects CVS: myocardiac depression, CO Reduction in MV, apnea Intravenous anaesthetics
Slide 13-

Thiopentale Problems with use Extremely painfull and limbtreatening when given intra-arterially Hypersensitivity reactions 1: 15 000 Contraindications Porphyria Intravenous anaesthetics
Slide 14-

Phenolic derivative Dose 1- 2.5 mg/kg Effects : hypnosis Side effects CVS: myocardiac depression, SVR, CO Respiratory depression Hypersensitivity 1 : 100 000 Propofol
Slide 15-

Propofol Other effects Pain on induction Nausea and vomiting less likely Better for LMA placement then thiopentale Relative contraindications Children under 3
Slide 16-

Etomidate Ester Dose 0.3 mg/kg Effects : hypnosis Side effects CVS: very little effect on HR, CO, SVR Minimal respiratory depression
Slide 17-

Etomidate Problems with use Pain on injection Nausea and vomiting Adrenocortical suppression Hypersensitivity reaction 1: 75 000 Relative Contraindications Porphyria Intravenous anaesthetics
Slide 18-

Ketamine Phencyclidine derivative CV effects -  HR, BP, CO, O2 consumption RS -  RR, preserved laryngeal reflexes CNS – dissociative anaesthesia, analgesia, amnesia Use – analgesic in Emerg. Med
Slide 19-

Pharmakokinetics Recovery from single bolus 5-10 min Intravenous anaesthetics
Slide 20-

Choice of induction agent 1. Are any agents absolutely contraindicated ? Hypersensitivity, porphyria 2. Are there any patient related factors ? CVS status Epilepsy 3. Are there any drug related factors ? Egg allergy Intravenous anaesthetics
Slide 21-

Induction + maintenance Intravenous anaesthetics
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SUMMARY – IV anaesthetics Mechanism of action – via receptors Used for anaesthesia and sedation Used for induction Propofol used for maintenance as well Thiopentale, propofol, etomidate All cause CV and respiratory depression
Slide 23-

INHALATIONAL ANAESTETICS
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Anaesthetic gases Isoflurane Sevoflurane Halothane Enflurane Desflurane N2O – nitrous oxide Inhalational anaesthetics
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Anaesthetic gases Any agent that exists as a liquid at room temperature is a vapour Any agent that cannot be liquefied at room temperature is a gas Anaesthetic ‘gases’ are administered via vaporizers Inhalational anaesthetics
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Potency MAC – that concentration required to prevent 50 % of patients moving when subjected to standart midline incision Sevoflurane MAC 1.8 % Isoflurane MAC 1.17 % Inhalational anaesthetics
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Potency MAC – that concentration required to prevent 50 % of patients moving when subjected to standart midline incision Sevoflurane MAC 1.8 % Isoflurane MAC 1.17 % Inhalational anaesthetics
Slide 28-

Respiratory and cardiovascular effects All volatile anaesthetics cause  MV and RR Isoflurane is irritant vapour  SVR, blood pressure falls,  HR Isoflurane - ? Coronary steel Inhalational anaesthetics
Slide 29-

Metabolism and toxicity Isoflurane (0.2 %)and Sevoflurane(3.5%) are metabolized by liver F- ions are produced - ? Renal impairment Iso and Sevo trigger malignant hyperthermia N2O Megaloblastic anaemia Teratogenic PONV Inhalational anaesthetics
Slide 30-

SUMMARY – inhalational anaesthetics Mechanism of action – via receptors Used for induction (sevoflurane) And maintenance of anaesthesia Commonly used : Sevoflurane, Isoflurane Dose dependent CV and respiratory depression All, but N2O trigger malignant hyperthermia
Slide 31-

NEUROMUSCULAR BLOCKING AGENTS
Slide 32-

Neuromuscular blocking agents Exclusively used in anaesthesia and intensive care Two classes Depolarizing succinylcholine Non depolarizing Vecuronium - aminosteroid Atracurium - benzylisoquinolinium
Slide 33-

Use of NMBs Tracheal intubation Surgery where muscle relaxation is essential Mechanical ventilation Neuromuscular blocking agents
Slide 34-

Neuromuscular junction Neuromuscular blocking agents
Slide 35-

Mechanism of action Depolarizing Structurally related to Ach First activating muscle fibres, then preventing further response Non depolarizing Compete with Ach at nicotinic receptor at the neuromuscular junction Neuromuscular blocking agents
Slide 36-

Choice for tracheal intubation Neuromuscular blocking agents Intubating doses
Slide 37-

To maintain paralysis Non depolarizing muscle relaxants Neuromuscular blocking agents
Slide 38-

Succinylcholine pharmacokinetics Duration of action : 3 - 5 min Metabolism – plasma cholinesterase Cave: suxamethonium apnea Neuromuscular blocking agents
Slide 39-

Succinylcholine - adverse effects Bradycardia Muscle pain – ‘sux’ pain Transient raised pressure in eye, stomach and cranium Raise in potassium Neuromuscular blocking agents
Slide 40-

Succinylcholine - contraindications Patient related contraindications Malignant hyperpyrexia Anaphylaxis to SCh Succinycholine apnea Clinical contraindications Denervation injury Penetrating eye injury Neuromuscular blocking agents
Slide 41-

Non depolarizing muscle relaxants Choice of NMBs Personal preference Atracurium better in renal or hepatic failure Avoid atracurium in asthmatic patients Neuromuscular blocking agents
Slide 42-

Reversal Acetylcholine esterase inhibitor – neostigmine Increases concentration of Ach at NMJ Neostigmine acts at all sites where acetylcholine esterase is present including heart Neuromuscular blocking agents What effect this might have and how this can be overcome?
Slide 43-

Neostigmine Dose of neostigmine – 0.05 mg/kg In > 50 kg man 2.5 mg Given with atropine 0.5 mg Neuromuscular blocking agents
Slide 44-

Peripheral nerve stimulator Check the depth of neuromuscular blockade Determine that neuromuscular blockade is reversible Check that blockade has been reversed safisfactorily Neuromuscular blocking agents
Slide 45-

SUMMARY – muscle relaxants Mechanism of action – via acetylcholine receptor Used to facilitate tracheal intubation, mechanical ventilation and surgery Depolarizing – Succinylcholine Lots of side effects Non depolarizing – Vecuronium, Atracurium Minimal CV and Resp. effects
Slide 46-

ANALGESICS
Slide 47-

Analgesics Paracetamol, aspirin Other Non Steroid Anti Inflamatory Drugs Opioids Local anaesthetics Antidepressants Anti-epileptics Ketamine Clonidine
Slide 48-

NSAIDs - effects Antipyretic Anti-inflamatory Analgesic
Slide 49-

Simple analgesics Antipyretic agents found in white willow bark and led to development of aspirin 1899
Slide 50-

Aspirin Anti-inflamatory agent in joint disease Cardiovascular – unstable angina Antiplatelet drug - prevention of stroke Radiation induced diarrhoea Alzheimer’s disease Simple analgesics What else is aspirin used for ?
Slide 51-

NSAID – mechanism of action Inhibition of cyclo-oxigenase Simple analgesics
Slide 52-

NSAID – side effects Gastric irritation NSAID sensitive asthma Renal dysfunction – analgesic nefropathy Antiplatelet function Hepatotoxicity Drug interaction – warfarin, lithium
Slide 53-

Simple analgesics
Slide 54-

Other NSAIDs Ibuprofen – the lowest risk of GI upset Indomethacin, Diclofenac – mainly antiinflamatory effect Metamizole –Novalgin Aspirin and NSAIDs are not contraindicated for regional anesthesia
Slide 55-

SUMMARY – simple analgesics Aspirin, Paracetamol NSAID MOA – inhibition of COX Renal, gastric, hepatic side effects Can trigger NSAID sensitive asthma
Slide 56-

Opiods MORPHEUS- GREAK GOD OF DREAMS
Slide 57-

Definitions Opiate : naturally occuring substance with morphine-like properties Opioid – synthetic substance Narcotic – from greek word ‘ numb’ Opiods
Slide 58-

Opioids – mechanism of action Via opioid receptors  - receptor  - receptor  - receptor
Slide 59-

Opioids - dose – response curve
Slide 60-

Opioids - dose – response curve
Slide 61-

Uses and routes of administration Analgesics Anti - tussive Anti – diarrhoea Intravenously Intramuscularly Oral, Buccal, rectal Transdermal - Patches Epidural/intrathecal Opiods
Slide 62-

Opioids - effects Brain: Analgesia, sedation Respiratory depression Euphoria and dysphoria Addiction, tolerance Nausea and vomiting Eyes Meiosis Cardiovascular system Hypotension, bradycardia
Slide 63-

Respiratory system Anti tussive effect GI tract spastic immobility Skin Pruritus – histamine release Bladder Urinary retention Opioids - effects
Slide 64-

Commonly used opioids Opiods
Slide 65-

Naloxone Pure opioid anatagonist at ,  and  - receptors Used in opioid overdose Dose : 1- 4 g/kg Duration of action 30 – 40 min ! Often shorter then duration of action of opioid, need for repeated doses Opiods
Slide 66-

Naloxone – dose – response curve
Slide 67-

Multimodal analgesia
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SUMMARY – opioids Morphine, Fentanyl, Sufentanyl, Alfentanyl MOA – via opioid receptors Used for analgesia, anti – tussive, anti – diarrhoea Side effects : respir. depression, tolerance, constipation, nausea + vomiting Opioid overdose reversal – Naloxone Multimodal analgesia – simple analgesics + opioids
Slide 69-

SUMMARY Triad of anaesthesia Analgesia Anaesthesia Muscle relaxation Choice depends on Patient factors Type of surgery Whether the surgery is elective or emergency
Slide 70-

Questions ?