General Anaesthetics - drdhriti


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A Power point presentation on General anaesthetics suitable for UG MBBS level students

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  • KWI- essence.
  • LOW solubility in blood= fast induction and recovery
    HIGH solubility in blood= slower induction and recovery.
  • Lower anesthetic solubility  in blood results in the "blood" compartment becoming saturated with the drug following fewer gas molecules transferred from the lungs into the blood.  
    Once the "blood" compartment is saturated with anesthetic, additional anesthetic molecules are readily transferred to other compartments, the most important one of which is the brain.
  • Imagine two cups of warm water: into one you put a spoon of sugar and into the other a spoon of sand. Which will be in higher concentration in the bottom of the cup? The sand is insoluble, the sugar dissolves, so very little reaches the bottom. For bottom of cup read brain.
    The blood:gas partition coefficient is the ratio of the concentrations of anesthetic gas in the blood and gas phases at equilibrium. In general, the blood:gas partition coefficient represents the capacity of the blood or a specific tissue to absorb the anesthetic. A higher blood:gas partition coefficient (e.g., 2.0 equals a 2% blood concentration and a 1% lung concentration at equilibrium) shows greater affinity for the blood. An anesthetic that has a blood concentration of 3% and a lung concentration of 6% at equilibrium would have a partition coefficient of 0.5, showing a greater affinity for the gas phase.
    The blood/gas partition coefficient describes how the gas will partition itself between the two phases after equilibrium has been reached. Isoflurane for example has a blood/gas partition coefficient of 1.4. This means that if the gas is in equilibrium the concentration in blood will be 1.4 times higher than the concentration in the alveoli. A higher blood gas partition coefficient means a higher uptake of the gas into the blood and therefore a slower induction time. It takes longer until the equilibrium with the brain partial pressure of the gas is reached
    Agents with low blood solubility require few molecules to dissolve into the blood to raise the partial pressure to equilibrium.
  • This agent was used previously, but not now. It is faster acting substitute of Halothane. The features include -
  • These drugs are used as inducing agents and given via iv route. Produces loss of consciousness in one arm-brain circulation time (11 secs). These are not used for maintenance for the reasons – 1. Administration of multiple doses by i.v. injection or a continuous i.v. infusion can result in drug accumulation and delays in recovery from anesthesia. 2. The higher cost of i.v. therapy compared with the cost of inhaled therapy also is a consideration. 3. The lack of a means for continuously measuring the depth of anesthesia the most important reason for avoiding the use of i.v. anesthetics for anesthesia maintenance.
  • General Anaesthetics - drdhriti

    1. 1. General AnestheticsGeneral Anesthetics Dr. D. K. Brahma Associate Professor Department of Pharmacology NEIGRIHMS, Shillong
    2. 2. General AnesthesiaGeneral Anesthesia
    3. 3. AnaesthesiaAnaesthesia • AnesthesiaAnesthesia – is a reversible condition of comfort, quiescence and– is a reversible condition of comfort, quiescence and physiological stability in a patient before, during and afterphysiological stability in a patient before, during and after performance of a procedure.performance of a procedure. • General anesthesiaGeneral anesthesia – for surgical procedure to render the patient– for surgical procedure to render the patient unaware / unresponsive to the painful stimuli.unaware / unresponsive to the painful stimuli. Drugs producing G. Anaesthesia – are called general anaestheticsDrugs producing G. Anaesthesia – are called general anaesthetics • Local anesthesia - reversible inhibition impulse generation and propagation in nerves. In sensory nerves, such an effect is desired when painful procedures must be performed, e.g., surgical or dental operations. Drugs producing L. Anaesthesia – are called local anaesthetics
    4. 4. Local anaesthesiaLocal anaesthesia • Some terms related to LocalSome terms related to Local anaesthesia:anaesthesia: 1.1. Surface anaesthesiaSurface anaesthesia: Ointment / jelly / solutions applied on: Ointment / jelly / solutions applied on mucous membrane.mucous membrane. 2.2. Infiltration anaesthesiaInfiltration anaesthesia: Injection of the LA to produce: Injection of the LA to produce analgesia over an area.analgesia over an area. 3.3. Regional anaesthesiaRegional anaesthesia: spinal, epidural and IV regional: spinal, epidural and IV regional anaesthesia.anaesthesia. SpinalSpinal – sub-arachnoid space.– sub-arachnoid space. EpiduralEpidural – between spinal bone and dura matter.– between spinal bone and dura matter. IV RegionalIV Regional – limited to limbs and practically upper limbs.– limited to limbs and practically upper limbs.
    5. 5. What are GeneralWhat are General anaesthetics ?anaesthetics ? • General AnaestheticsGeneral Anaesthetics are the drugs whichare the drugs which produce reversible loss of all sensation andproduce reversible loss of all sensation and consciousness, or simply,consciousness, or simply, a drug that brings about a reversible loss of consciousness. • These drugs are generally administered by an anesthesiologist in order to induce or maintain general anesthesia to facilitate surgery. • General anaesthetics are – mainly inhalation or intravenous
    6. 6. What are the Drugs used as GA ?What are the Drugs used as GA ? (Classification)(Classification) Inhalation: • Gase: Nitrous Oxide • Volatile liquids: – Ether – Halothane – Enflurane – Isoflurane – Desflurane – Sevoflurane Intravenous: • Inducing agents: Thiopentone, Methohexitone sodium, propofol and etomidate • Benzodiazepines (slower acting): Diazepam, Lorazepam, Midazolam • Dissociative anaesthesia: Ketamine • Neurolept analgesia: Fentanyl
    7. 7. Essential components of GA:Essential components of GA: • TriadTriad of General Anesthesia:of General Anesthesia: – need for unconsciousnessneed for unconsciousness – need for analgesianeed for analgesia – need for muscle relaxationneed for muscle relaxation • Essential components of GA:Essential components of GA: – Loss of all sensations – painLoss of all sensations – pain – UnconsciousnessUnconsciousness – AmnesiaAmnesia – Immobility and muscle relaxationImmobility and muscle relaxation – Loss of somatic and autonomic reflexesLoss of somatic and autonomic reflexes
    8. 8. History - The Primitive techniquesHistory - The Primitive techniques • Club • Strangulation • Alcohol • Mesmerism • Plants
    9. 9. History / Background - GAHistory / Background - GA
    10. 10. History – contd.History – contd. • General anesthesia wasGeneral anesthesia was absent until the mid-absent until the mid- 1800’s1800’s • Original discoverer ofOriginal discoverer of general anestheticsgeneral anesthetics – Crawford Long, PhysicianCrawford Long, Physician from Georgia: 1842, etherfrom Georgia: 1842, ether anesthesiaanesthesia • Chloroform introducedChloroform introduced – James Simpson: 1847James Simpson: 1847 • Nitrous oxideNitrous oxide – Horace Wells in 1845Horace Wells in 1845 19th Century physician administering chloroform
    11. 11. History – contd.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, ether no longer used in modern practice, yet considered to be the first “ideal” anesthetic
    12. 12. Mechanism of GA(Potency)Mechanism of GA(Potency) • For inhalation anestheticsFor inhalation anesthetics –– Minimum Alveolar ConcentrationMinimum Alveolar Concentration (MAC) – 1(MAC) – 1 (one) MAC is defined as the minimum alveolar concentration that prevents(one) MAC is defined as the minimum alveolar concentration that prevents movement in response to surgical stimulation in 50% of subjects.movement in response to surgical stimulation in 50% of subjects. • PracticallyPractically –– • Alveolar concentrations can be monitored continuously by measuring end-tidalAlveolar concentrations can be monitored continuously by measuring end-tidal anesthetic concentration using spectrometryanesthetic concentration using spectrometry • End point (immobilization) – can me measured.End point (immobilization) – can me measured. • Other end points – Verbal commands or memory etc.Other end points – Verbal commands or memory etc. • For Intravenous agentsFor Intravenous agents – Potency of IV agent is defined as the free plasma– Potency of IV agent is defined as the free plasma concentration (at equilibrium) that produces loss of response to surgicalconcentration (at equilibrium) that produces loss of response to surgical incision in 50% of subjects.incision in 50% of subjects. • Difficult to measureDifficult to measure:: – no available method to measure blood or plasma concentration continuouslyno available method to measure blood or plasma concentration continuously – Free concentration at site of action cannot be determinedFree concentration at site of action cannot be determined
    13. 13. Mechanism – contd.Mechanism – contd. • The unitary theory of anesthesiaThe unitary theory of anesthesia –– Meyer-Meyer- Overton rule (1901)Overton rule (1901) • Lipid : water partition coefficient (fluidization) • Potency of a gas correlated with its solubility inPotency of a gas correlated with its solubility in olive oil (olive oil : water) – lipid bilayer as theolive oil (olive oil : water) – lipid bilayer as the only target for anesthetic action.only target for anesthetic action. • Clear exceptions have been found out now.Clear exceptions have been found out now. • The unitary theory has been discarded now.The unitary theory has been discarded now.
    14. 14. Modern theory on Mechanism ofModern theory on Mechanism of general anesthesiageneral anesthesia • Major targetsMajor targets – ligand gated ion channels.– ligand gated ion channels. • Important oneImportant one –– GABAGABAAA receptor gated Clreceptor gated Cl¯¯ – Examples – Many inhalation anesthetics, barbiturates,Examples – Many inhalation anesthetics, barbiturates, benzodiazepines and propofolbenzodiazepines and propofol – Potentiate the GABA to open thePotentiate the GABA to open the ClCl¯ channels¯ channels
    15. 15. Molecular Actions: GABAMolecular Actions: GABAAA ReceptorReceptor • Ligand-gated ion channelsLigand-gated ion channels – Chloride channels gated by the inhibitory GABAChloride channels gated by the inhibitory GABAAA receptorreceptor • GABAGABAAA receptor mediates the effects of gamma-receptor mediates the effects of gamma- amino butyric acid (GABA), the major inhibitoryamino butyric acid (GABA), the major inhibitory neurotransmitter in the brainneurotransmitter in the brain – GABAGABAAA receptor found throughout the CNSreceptor found throughout the CNS Most abundant, fast inhibitory, ligand-gatedMost abundant, fast inhibitory, ligand-gated ion channel in the mammalian brainion channel in the mammalian brain Located in the post-synaptic membraneLocated in the post-synaptic membrane
    16. 16. GABAAA receptor – contd. • GABAGABAAA receptor is a 4-receptor is a 4- transmembrane (4-TM)transmembrane (4-TM) ion channelion channel – 5 subunits arranged5 subunits arranged around a central pore: 2around a central pore: 2 alpha, 2 beta, 1 gammaalpha, 2 beta, 1 gamma • Each subunit has N-terminalEach subunit has N-terminal extracellular chain whichextracellular chain which contains the ligand-bindingcontains the ligand-binding sitesite • 4 hydrophobic sections cross4 hydrophobic sections cross the membrane 4 times: onethe membrane 4 times: one extracellular and twoextracellular and two intracellular loops connectingintracellular loops connecting these regions, plus anthese regions, plus an extracellular C-terminal chainextracellular C-terminal chain
    17. 17. GABAAA receptor – contd.
    18. 18. GABAAA receptor – contd. • Receptor sits in the membrane ofReceptor sits in the membrane of its neuron at the synapseits neuron at the synapse • GABAGABA, endogenous compound,, endogenous compound, causes GABA to opencauses GABA to open • Receptor capable of binding 2Receptor capable of binding 2 GABA molecules, between anGABA molecules, between an alpha and beta subunitalpha and beta subunit – Binding of GABA causes aBinding of GABA causes a conformational changeconformational change inin receptorreceptor • Opens central poreOpens central pore • Chloride ions pass downChloride ions pass down electrochemical gradientelectrochemical gradient – Net inhibitory effect, reducingNet inhibitory effect, reducing activity of the neuronactivity of the neuron
    19. 19. Mechanism of GA – contd. Other Mechanisms: • Glycine – Barbiturates, propofol and others can activate in spinal cord and medulla • N – methyl D- aspartate (NMDA) type of glutamate receptors - Nitrous oxide and ketamine selectively inhibit
    20. 20. Signs and stages of GA • Guedel in 1920 described with ether – Guedel`s stages of GA. • Descending depression of CNS. • Higher to lower areas of brain are involved. • Vital centers located in medulla are paralyzed last. • But, in spinal chord lower segments are affected earlier than the higher segments.
    21. 21. signs & stages of GA – contd.signs & stages of GA – contd.
    22. 22. stages of GA – contd.stages of GA – contd. Stage I: Stage of AnalgesiaStage I: Stage of Analgesia • Starts from beginning of anaesthetic inhalation and lastsStarts from beginning of anaesthetic inhalation and lasts upto the loss of consciousness.upto the loss of consciousness. • Pain is progressively abolished during this stage.Pain is progressively abolished during this stage. • Patient remains conscious, can hear and see, and feelsPatient remains conscious, can hear and see, and feels a dream like state.a dream like state. • Reflexes and respiration remain normal.Reflexes and respiration remain normal. • It is difficult to maintain - use is limited to shortIt is difficult to maintain - use is limited to short procedures only.procedures only.
    23. 23. stages of GA – contd. Stage II: Stage of Delirium and Excitement:Stage II: Stage of Delirium and Excitement: • From loss of consciousness to beginning of regular respiration.From loss of consciousness to beginning of regular respiration. • Excitement - patient may shout, struggle and hold his breathExcitement - patient may shout, struggle and hold his breath • Muscle tone increases, jaws are tightly closed.Muscle tone increases, jaws are tightly closed. • breathing is jerky; vomiting, involuntary micturition or defecationbreathing is jerky; vomiting, involuntary micturition or defecation may occur.may occur. • Heart rate and BP may rise and pupils dilate due to sympatheticHeart rate and BP may rise and pupils dilate due to sympathetic stimulation.stimulation. • No stimulus or operative procedure carried out during this stage.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 – preanaestheticThis stage is not found with modern anaesthesia – preanaesthetic medication, rapid induction etc.medication, rapid induction etc.
    24. 24. stages of GA – contd. • Stage III: Stage of Surgical anaesthesiaStage III: Stage of Surgical anaesthesia • Extends 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.
    25. 25. stages of GA – contd. Stage IV: Medullary / respiratoryStage 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.
    26. 26. Phases of GA There are 3 (three) phases: • Induction • Maintenance • Recovery
    27. 27. Phases of GA – contd. • Induction: It is the period of time which begins with the beginning of administration of anaesthesia to the development of surgical anaesthesia (Induction time). Induction is generally done with IV anaesthetics like Thiopentone Sodium • Maintenance: Sustaining the state of anaesthesia. Usually done with an admixture of Nitrous oxide and halogenated hydrocarbons • Recovery: At the end of surgical procedure administration of anaesthetic is stopped and consciousness regains (recovery time)
    28. 28. Pharmacokinetics of inhalation anaesthetics: Pathway for anaesthetics:
    29. 29. Pharmacokinetic of inhalation GA – contd. • Depth of anaesthesia depends on Potency of the agent (MAC) and Partial Pressure (PP) attained in the brain. • Induction and recovery depends on rate of change of PP in brain.
    30. 30. Pharmacokinetic of inhalation GA – contd. Factors affecting PP of anaesthetics in Brain: 1. PP of anaesthetic in the inspired gas 2. Pulmonary ventilation 3. Alveolar exchange 4. Solubility of anaesthetic in blood - Blood: gas partition coefficient 5. Solubility in tissues 6. Cerebral blood flow
    31. 31. Blood : gas partition coefficient • Solubility of an anesthetic agent in blood is quantified as the blood : gas partition coefficient. • It is the ratio of the concentration of an anesthetic in the blood phase to the concentration of the anesthetic in the gas phase when the anesthetic is in equilibrium between the two phases. • Lower the blood : gas co-efficient – faster the induction and recovery – Nitrous oxide. • Higher the blood : gas co-efficient – slower induction and recovery – Halothane.
    32. 32. Rate of Entry into the Brain: Influence ofRate of Entry into the Brain: Influence of Blood and Lipid SolubilityBlood and Lipid Solubility
    34. 34. BLOOD GAS PARTITION COEFFICIENT Agents with lowAgents with low solubility in bloodsolubility in blood quickly saturate thequickly saturate the blood. Theblood. The additionaladditional anestheticanesthetic molecules are thenmolecules are then readily transferredreadily transferred to the the brain.
    35. 35. Elimination of GA • Mostly through lungs in unchanged form. • Channel of absorption (lungs) become channel of elimination • Enter and persists in adipose tissue for long periods – high lipid solubility and low blood flow. • They are not metabolized except Halothane • Second gas effect • Diffusion hypoxia
    36. 36. Techniques of inhalation GA • Open drop method • Through anaesthetic machines - Open system - Closed system - Semi-closed system
    37. 37. Continuous flow (Boyle’s) anaesthetic machine Anaesthetic Machine (Boyle’s equipment) • The anaesthetic machine • Gas source- either piped gas or supplied in cylinders • Flow meter • Vaporisers • Delivery System or circuit
    38. 38. Properties of an Ideal anaesthetic agent: • For Patient: - Pleasant, non-irritating and should not cause nausea or vomiting - Induction and recovery should be fast • For Surgeon: - analgesia, immobility and muscle relaxation - nonexplosive and noninflammable
    39. 39. Properties of GA – contd. • For the anaesthetist: - Margin of safety - Heart, liver and other organs - Potent - Cheap, stable and easily stored - Rubber tubing or soda lime - Rapid adjustment of depth of anaesthesia
    40. 40. Individual Inhalation anaesthetic agents
    41. 41. 1. Diethyl ether (C2H5 – O – C2H5) • Colourless, highly volatile liquid with a pungent odour. Boiling point – 35ºC • Produces irritating vapours and are inflammable and explosive. Pharmacokinetics: - 85 to 90 percent is eliminated through lung and remainder through skin, urine, milk and sweat. - Can cross the placental barrier.
    42. 42. Ether – contd. • Advantages - Can be used without complicated apparatus. - Potent anaesthetic and good analgesic. - Muscle relaxation. - Wide safety of margin. - Respiratory stimulation and bronchodilatation. - Does not sensitize the heart to adrenaline - No cardiac arrythmias. - Can be used in delivery. - Less likely hepato or nephrotoxicity. • Disadvantages - Inflammable and explosive. - Slow induction and unpleasant -atropine. - Slow recovery – nausea & vomiting - Cardiac arrest. - Convulsion in children. - Cross tolerance – ethyl alcohol.
    43. 43. 2. Nitrous oxide / laughing gas (N2O): • NH4NO3 (s) → 2 H2O (g) + N2O (g) • Colourless, odourless inorganic gas with sweet taste. • Noninflammable and nonirritating, but of low potency. • Very potent analgesic • Carrier and adjuvant to other anaesthetics – 70% + 25-30% + 0.2-2%
    44. 44. Nitrous oxide – contd. • Advantages: - Non-inflammable and nonirritant. - Rapid induction and recovery - Very potent analgesic (low concentration) - No nausea and vomiting. - Nontoxic to liver, kiddney and brain. • Disadvantages: - Not potent alone (supplementation) - Hypoxia. - Inhibits methionine synthetase (precursor to DNA synthesis). - Inhibits vitamin B-12 metabolism. - Dentists, OR personnel, abusers at risk. - Gas filled spaces - dangerous
    45. 45. 3. Halothane: • Fluorinated volatile liquid with sweet odour, non- irritant non-inflammable and supplied in amber coloured bottle. • Potent anaesthetic, 2-4% for induction and 0.5- 1% for maintenance. • Boiling point - 50ºC • Pharmacokinetics: 60 to 80% eliminated unchanged. 20% retained in body for 24 hours and metabolized.
    46. 46. Halothane – contd. • Advantages: - Non-inflammable and non-irritant - Pharyngeal and laryngeal reflexes – bronchodilatation - Potent and speedy induction & recovery - Controlled hypotension - Inhibits intestinal and uterine contractions • Disadvantages: - Special apparatus - Poor analgesic and muscle relaxation - Respiratory depression - Hypotension and arrythmia - Decreased urine formation - Hepatitis: 1 in 10,000 - Malignant hyperthermia: Ryanodine receptor
    47. 47. 4. Enflurane: • Non-inflammable, with mild sweet odour and boils at 57ºC • Similar to halothane in action, except better muscular relaxation. • Depresses myocardial force of contraction and sensitize heart to adrenaline. • Induces seizure in deep anaesthesia and therefore not used now - Epileptiform EEG • Metabolism one-tenth that of halothane-- does not release quantity of hepatotoxic metabolites • Metabolism releases fluoride ion-- renal toxicity
    48. 48. 5. Isoflurane: • Isomer of enflurane and have simmilar properties but slightly more potent. • Induction dose is 1.5 – 3% and maintenance dose is 1 – 2%. • By special vapourizer.
    49. 49. Isoflurane – contd. • Advantages: - Rapid induction and recovery - Good muscle relaxation - Good coronary vasodilatation - Less Myocardial depression than no myocardial sensitization to adrenaline - No renal or hepatotoxicity - Low nausea and vomiting - No dilatation of pupil and no loss of light reflex in deep anaesthesia - No seizure and preferred in neurosurgery - Uterine muscle relaxation • Disadvantages: - Pungent and respiratory irritant - Special apparatus required - Respiratory depression - Maintenance only, no induction - ß adrenergic receptor stimulation - Costly
    50. 50. Intravenous Anaesthetics: • For induction only • Rapid induction (one arm-brain circulation time • For maintenance not used • Alone – analgesic and muscle relaxants Intravenous: • Inducing agents: Thiopentone, Methohexitone sodium, propofol and etomidate • Benzodiazepines (slower acting): Diazepam, Lorazepam, Midazolam • Dissociative anaesthesia: Ketamine • Neurolept analgesia: Fentanyl
    51. 51. 1 Thiopentone sodium: • Barbiturate • Water soluble • Alkaline • Dose-dependent suppression of CNS activity • Dose: 3-5mg/kg iv (2.5%) solution – 15 to 20 seconds
    52. 52. Thiopentone sodium – contd. Pharmacokinetics: - Redistribution - Hepatic metabolism (elimination half-life 7- 12 hrs) - CNS depression persists for long (>12 hr)
    53. 53. Tiopentone – contd,. Redistribution: Blood Brain Muscle Body fat conc.ofthiopentoone Time
    54. 54. Side effects of Thiopentone: • Pre-anaesthetic course - laryngospasm • Noncompatibility - succinylcholine • Tissue necrosis--gangrene • Post-anaesthetic course - analgesic
    55. 55. Thiopentone – contd. • Advantages: - Rapid induction - Does not sensitize myocardium to adrenaline - No nausea and vomiting - Non-explosive and non-irritant - Short operations (alone) - Other uses: convulsion, psychiatric patients and narcoanalysis of criminals • Disadvantages: - Depth of anaesthesia difficult to judge - Pharyngeal and laryngeal reflexes persists - apnoea – controlled ventilation - Respiratory depression - Hypotension (rapid) – shock and hypovolemia - Poor analgesic and muscle relaxant - Gangrene and necrosis - Shivering and delirium
    56. 56. 2. Propofol • Replacing thiopentone • Oily liquid used as 1% emulsion • Rapid induction (one arm-brain circulation time): 15 – 45 seconds and lasts for 5–10 minutes • Rapid distribution – distribution half-life (2-4 min) • Short elimination half-life (100 min) • Dose: Induction - 2mg/kg bolus i.v. Maintenance - 9 mg/kg/hr i.v. • Propofol is extensively metabolized – 88% of an administered dose appears in the urine • Metabolized by hepatic conjugation of the inactive glucuronide metabolites
    57. 57. Propofol – contd. Advantages: - Rapid induction - Does not sensitize myocardium to adrenaline - No nausea and vomiting - Non-explosive and non- irritant - Total i.v. anaesthesia - Short operations (alone) Disadvantages: - Induction apnoea - Hypotension - Braddycardia - Dose dependent respiratory depression - Pain during injection: local anaesthetic combination
    58. 58. 3. Ketamine: • Phencyclidine derivative • Dissociative anaesthesia: a state characterized by immobility, amnesia and analgesia with light sleep and feeling of dissociation from ones own body and mind and the surroundings. • Site of action – cortex and subcortical areas – NMDA receptors • Dose: 5-10mg/kg im or 1-2mg i.v.
    59. 59. Ketamine – contd. • Disadvantages: - Limb movements and nystagmus - Emergence phenomenon – 50% patients - Hypertensives - Increase in IOT and ICP - Uterine stimulation - Psychosis and shizophrenia - Rare laryngospasm - Poor muscle relaxation
    60. 60. Ketamine – contd. Uses: 1. Characteristics of sympathetic nervous system stimulation (increase HR, BP & CO) – hypovolumic shock 2. In head and neck surgery 3. In asthmatics 4. Short surgical procedures – burn dressing, forceps delivery, breech extraction manual removal of placenta and dentistry 5. Combination with diazepam - angiography, cardiac catheterization 6. OPD surgical procedures
    61. 61. 4. Fentanyl • Neurolept analgesia: droperidol • 4-acylanilino derivative • Opioid analgesic • Duration of action: 30-50 min. • Uses: - in combination with diazepam used in diagnostic, endoscopic and angiographic procedures - Adjunct to spinal and nerve block anaesthesia
    62. 62. Fentanyl – contd.Fentanyl – contd. Advantages:Advantages: - Smooth onset and rapidSmooth onset and rapid recoveryrecovery - Suppression of vomitingSuppression of vomiting and coughingand coughing - Commanded operationCommanded operation - Less fall in BP and noLess fall in BP and no sensitization tosensitization to adrenalineadrenaline Disadvantages:Disadvantages: - RespiratoryRespiratory depressiondepression - Increase tone of chestIncrease tone of chest musclemuscle - Nausea, vomiting andNausea, vomiting and itching duringitching during recoveryrecovery
    63. 63. Complications of anaesthesia:Complications of anaesthesia: During anaesthesia:During anaesthesia:  Respiratory depressionRespiratory depression  Salivation, respiratorySalivation, respiratory secretionssecretions  Cardiac arrhythmiasCardiac arrhythmias  Fall in BPFall in BP  AspirationAspiration  Laryngospasm and asphyxiaLaryngospasm and asphyxia  AwarenessAwareness  Delirium and convulsionDelirium and convulsion  Fire and explosionFire and explosion After anaesthesia:After anaesthesia:  Nausea and vomitingNausea and vomiting  Persisting sedationPersisting sedation  PneumoniaPneumonia  Organ damage – liver, kidneyOrgan damage – liver, kidney  Nerve palsiesNerve palsies  Emergence deliriumEmergence delirium  Cognitive defectsCognitive defects
    64. 64. Preanesthetic medication:Preanesthetic medication: • Definition:Definition: It is the term applied toIt is the term applied to the use of drugs prior tothe use of drugs prior to the administration of anthe administration of an anaesthetic agent toanaesthetic agent to make anaesthesia safermake anaesthesia safer and more agreeable toand more agreeable to the patient.the patient. • Aim:Aim:  Relief of anxietyRelief of anxiety  Amnesia for pre and postAmnesia for pre and post operative eventsoperative events  AnalgesiaAnalgesia  Decrease secretionsDecrease secretions  Antiemetic effectsAntiemetic effects  Decrease acidity andDecrease acidity and volume of gastric juicevolume of gastric juice
    65. 65. Preanaesthetic medication –Preanaesthetic medication – contd.contd. • Drugs used:Drugs used:  Sedative-anxiolytics – diazepam or lorazepam,Sedative-anxiolytics – diazepam or lorazepam, midazolam, promethazine etc.midazolam, promethazine etc.  Opioids – Morphine and its congenersOpioids – Morphine and its congeners  Anticholinergics – AtropineAnticholinergics – Atropine  HH22 blockers – ranitidine, famotidine etc.blockers – ranitidine, famotidine etc.  Antiemetics – Metoclopramide, domperidoneAntiemetics – Metoclopramide, domperidone etc.etc.
    66. 66. The Practical approach:The Practical approach: ProtocolProtocol Preoperative assesment PreanaestheticPreoperative assesment Preanaesthetic medication Induction by thiopentonemedication Induction by thiopentone or Propofol Muscle relaxantsor Propofol Muscle relaxants Intubation Nitrous oxide +Intubation Nitrous oxide + halogenated hydrocarbon Withdrawhalogenated hydrocarbon Withdraw and recovery.and recovery.
    67. 67. Thank youThank you