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Classification of general anaesthetics and pharmacokinetics
 

Classification of general anaesthetics and pharmacokinetics

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    Classification of general anaesthetics and pharmacokinetics Classification of general anaesthetics and pharmacokinetics Presentation Transcript

    • CLASSIFICATION OF GENERAL ANAESTHETICS
    • 1.INHALATIONAL Gases: N 2 O,Cyclopropane,Xenon Liquids: Ether, Halothane, Enflurane, Desflurane, Isoflurane, Sevoflurane, Methoxyflurane
    • 2.INTRAVENOUS Inducing Agents : Thiopentone sodium, Methohexitone sodium, Propofol, Etomidate Dissociative Anaesthesia: Ketamine Neuroleptanalgesia: Fentanyl+Droperidol (Analgesic)(Neuroleptic) BZDs: Diazepam,Lorazepam,Midazolam
    • Pharmacokinetics
      • Rapidly diffuse across the alveoli
      • Alveoli blood brain
      • Depth of anaesthesia-potency & pp
      • Induction & Recovery-rate of change of pp
    • Minimum Alveolar Concentration
      • Conc of the inhalational GA that renders 50% of the subjects immobile when exposed to a strong noxious stimulus
      Halothane 0.75% Ether 1.9% Enflurane 1.68% Isoflurane 1.2% Desflurane 6% Sevoflurane 2% Nitrous oxide 105%
      • 0.3 MAC ->mild analgesia
      • 0.5 MAC->amnesia
      • 1.0 MAC->50% patients immobile even after stimulation
      • 1.3 MAC->sympathetically mediated response blunted
      • 2.0 MAC->potentially lethal
      • MAC α 1 / Potency
    • Minimum Alveolar Concentration limitations
      • Leaves 50% subjects
      • At 1.3MAC awareness & recall may still exist
      • Large no. of patients receive muscle relaxants
      • Other indicators of awareness-highly suggestive when present but not definitive when absent
      • A patient who moves with incision is not necessarily awake &one who does not move is not necessarily unconscious
    • Factors affecting pp of anaesthetic in brain
      • PP of anaesthetic in inspired air
      • Pulmonary ventilation rate
      • Alveolar exchange
      • Solubility of anaesthetic in blood
      • Solubility of anaesthetic in tissues
      • Cerebral blood flow
    • 1.PP of the anaesthetic in inspired air
    • PP of the anaesthetic in inspired air
      • Increase in inspired anaesthetic conc increases the rate of induction of anaesthesia by increasing the rate of transfer into blood according to Fick’s Law
      • Used for mod soluble-halothane- 3-4% ->1-2%
    • Fick’s Law of Diffusion
      • Flux= diff in conc x A x Permeability
      • Thickness of the path
    • 2.PULMONARY VENTILATION
    • 2.Pulmonary Ventilation Rate
      • The rate of rise of anaesthetic gas conc in the arterial blood is directly dependent on both rate & depth of ventilation
      • Effects- solubility
      • 4x ↑ In VR 2x T of halothane bt only 15% ↑ in T of nitrous oxide
    • 3.ALVEOLAR EXCHANGE
    • ALVEOLAR EXCHANGE
      • GAs diffuse freely across alveoli
      • Ventilation Perfusion mismatch delays the attainment of equilibrium between blood and alveoli
    • 4.SOLUBILITY IN BLOOD
    • SOLUBILITY IN BLOOD
      • One of the most important factor
      • Blood:Gas Partition co efficient –index of solubility
      • When an anaesthetic with low solubility diffuses from alveoli into arterial blood, relatively few molecules are required to raise its partial pressure and therefore its arterial tension rises rapidly
    • 5.SOLUBILITY IN TISSUES
    • SOLUBILITY IN TISSUES
      • Relative solubility of the anaesthetic in blood and tissue determines its conc in the tissue at equilibrium
      • expressed as tissue : blood pc
      • =ly soluble in lean tissue & blood. More soluble in fat
      • Conc ↑ in white than in grey matter
    • 6.CEREBRAL BLOOD FLOW
    • CEREBRAL BLOOD FLOW
      • Brain is highly perfused
      • GAs are quickly delivered
      • CO 2 inhalation
    • Second gas effect
      • When certain gases like nitrous oxide are administered in high conc, the other anaesthetic gases are also pulled in and their alveolar tension rises more rapidly
      • Eg: halothane when given with N 2 O, delivered at same rate
    • Concentration effect
      • When an anaesthetic is administered in high conc, its alveolar tension rises more rapidly than when the same gas is inhaled in lower conc.
    • e Elimination
      • gradients reversed
      • Through lungs- unchanged,
      • Metabolism-halothane>20% in liver
      • Lipid soluble anaesthetic-delayed recovery