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Anesthesia

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anesthesia, pre-anesthetic medication,local anesthesia ,general anesthesia

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Anesthesia

  1. 1. PRESENTED BY: HAFSA JAMIL Facilitator : Dr.Muhammad Asadullah shahzad
  2. 2. Anesthesia
  3. 3. ANESTHESIA: • Is a temporary state consisting of unconsciousness, loss of memory, lack of pain, and muscle relaxation. • A patient under the effects of anesthesia is said to be anesthetized. • Types of Anesthesia • Local anesthesia • General anesthesia
  4. 4. Pre-Anesthetic Medication : • Drugs administered before an anesthetic to decrease anxiety and to obtain:  Smoother induction.  Maintenance.  Emergence from anesthesia.
  5. 5. These drugs are • Sedative hypnotic :: • To subside worry and tension e.g Diazepam . • Analgesics: • For smooth induction and decrease post operative pain e.g Morphine. • Anticolinergic:: • To reduce bronchial secretion e.g Atropine . • Antiemetics: • To prevent nausea and vomiting e.g Promathiazine .
  6. 6. General Anesthesia: •A drug that brings about a reversible loss of sensation along with the loss of consciousness .
  7. 7. 8 General Anaesthesia (GA) unconsciousness amnesiaanalgesia. • A variety of drugs are given to the patient that have different effects with the overall aim of ensuring unconsciousness, amnesia and analgesia.
  8. 8. Stage I: Analgesia decreased awareness of pain . Consciousness may be impaired but not lost.. Stage II: Disinhibition Excitatory stage, uncontrolled movement, irregular breathing. Goal is to move through this stage as rapidly as possible. Stage III: Surgical anesthesia return of regular respiration. Loss of blink reflex, regular respiration . Surgical procedures can be performed at this stage. Stage IV: Medullary Depression This is the stage between respiratory arrest and death due to circulatory collapse.. Stages Of General Anesthesia
  9. 9. •CLASSIFICATION
  10. 10. General Anesthetics divide into 2 classes Inhalation Anesthetics • Gasses or Vapors • Halogenated Intravenous Anesthetics • Barbiturates • Dissociative • Opioids • Benzodiazepines
  11. 11. Inhalation Anesthetics • Nitrous oxide • Cycloprapane Gas • Halothane • Isoflurane • Sevoflurane • Enflurane Halogenated agents:
  12. 12. Intravenous Anesthesia: • Thiopental • Thiamylal • MethohexitalBarbiturates • Ketamine Dissociative agents
  13. 13. • Morphine • Fentanyl citrate Opioids • Midazolam • Lorazepam • Diazepam Benzodiazipines
  14. 14. Mechanism of Action • Interaction with protein receptors. • Volatile A – increase GABA and Glycine. ( inhibitory neurotransmitters).
  15. 15. MECHANISM OF ACTION :
  16. 16. MAC(minimum alveolar concentration) •A measure of potency of inhaled anesthetics. .
  17. 17. Pharmacokinetics of Inhaled Anesthetics 1. Amount that reaches the brain Indicated by oil:gas ratio (lipid solubility) 2. Solubility of gas into blood The lower the blood:gas ratio, the more anesthetics will arrive at the brain
  18. 18. Rate of Entry into the Brain: Influence of Blood and Lipid Solubility
  19. 19. General Actions of Inhaled Anesthetics • Respiration • Depressed respiration and response to CO2. • Kidney • Depression of renal blood flow and urine output. • Muscle • High enough concentrations will relax skeletal muscle.
  20. 20. Cont’ • Cardiovascular System • Generalized reduction in arterial pressure and peripheral vascular resistance. • Isoflurane maintains CO and coronary function better than other agents. • Central Nervous System • Increased cerebral blood flow and decreased cerebral metabolism.
  21. 21. Nitrous oxide • Merits • Rapid induction and recovery • No adverse effects on circulation and respiration • Good analgesia • Demerits • Diffusion hypoxia • Post operative nausea and vomiting • Ineffective anesthetic alone. • Inadequate muscle relaxation
  22. 22. Nitrous Oxide
  23. 23. Halothane
  24. 24. • MERITS • Non irritating • Safe for children • Can be given in asthmatics. • DEMERITS • Weak analgesia and inadequate muscle relaxation. • Hepatotoxicity • CVS and respiratory disturbances . • Expensive
  25. 25. •Malignant hyperthermia (MH) is a pharmacogenetic hypermetabolic state of skeletal muscle induced in susceptible individuals by inhalational anesthetics and/or succinylcholine (and maybe by stress or exercise). Malignant Hyperthermia
  26. 26. •Signs: tachycardia, hyperthermia, muscle rigidity, sweating, arrhythmia. •May be fatal. •Treated with Dantrolene. Malignant Hyperthermia
  27. 27. ENFLURANE • Merits • Rapid inhalation and recovery . • DEMERITS • CNS excitation • May cause seizures
  28. 28. ISOFLURANE • Merits • Rapid and smooth anesthesia • No hepatic/renal toxicity • Demerits • Uterine relaxation • Progressive regulatory depression
  29. 29. Intravenous Anesthetics • Most exert their actions by potentiating GABAA receptor. • GABAergic actions may be similar to those of volatile anesthetics, but act at different sites on receptor.
  30. 30. • Most decrease cerebral metabolism and intracranial pressure. • Most cause respiratory depression. • May cause apnea after induction of anesthesia. Organ Effects
  31. 31. •They cause cardiovascular depression. Cardiovascular Effects
  32. 32. Ketamine • Merits • Short acting • Dissociative anesthesia • Can be used in children • Very good analgesic • Demerits • Post operative hallucination • Increase cerebral blood flow
  33. 33. Propofol • Merits • Rapid and smooth onset and recovery • Reduce intracranial pressure • Demerits • Poor analgesic • Excreted through kidney
  34. 34. Local Anaesthesia • DEFINITION: Local anaesthesia is drug-induced reversible local blockade of nerve conduction in a specific part of the body that does not alter consciousness.
  35. 35. Prosperities of ideal LA • Reversible action. • Non-irritant. • No allergic reaction. • No systemic toxicity. • Rapid onset of action. • Sufficient duration of action. • Potent. • Stable in solutions. • Not interfere with healing of tissue. • Have a vasoconstrictor action or compatible with VC. • Not expensive
  36. 36. Surface/topical anesthesia Local infiltration Peripheral nerve block Bier block (IV regional anesthesia) Epidural anesthesia Spinal anesthesia Six Placement Sites
  37. 37. Esters vs Amides • The ester linkage is more easily broken so the ester drugs are less stable in solution and cannot be stored for as long as amides. • Amide anaesthetics are also heat-stable. • The metabolism of most esters results in the production of para-aminobenzoate (PABA) which is associated with allergic reaction. • Amides, in contrast, very rarely cause allergic phenomena. For these reasons amides are now more commonly used than esters.
  38. 38. The mechanism of action of local anaesthetics • Disruption of ion channel function via specific binding to sodium channels, holding them in an inactive state. • Disruption of ion channel function by the incorporation of local anaesthetic molecules into the cell membrane .
  39. 39. • Small nerve fibres are more sensitive than large nerve fibres • Myelinated fibres are blocked before non-myelinated fibres of the same diameter. • Thus the loss of nerve function proceeds as loss of pain, temperature, touch, proprioception, and then skeletal muscle tone. This is why people may still feel touch but not pain when using local anaesthesia.
  40. 40. Absorption and distribution • Some of the drug will be absorbed into the systemic circulation: how much will depend on the vascularity of the area to which the drug has been applied. • The distribution of the drug is influenced by the degree of tissue and plasma protein binding of the drug. the more protein bound the agent, the longer the duration of action as free drug is more slowly made available for metabolism.
  41. 41. Metabolism and excretion • Esters (except cocaine) are broken down rapidly by plasma esterases to inactive compounds and consequently have a short half life. Cocaine is hydrolysed in the liver. Ester metabolite excretion is renal. • Amides are metabolised hepatically by amidases. This is a slower process, hence their half-life is longer and they can accumulate if given in repeated doses or by infusion.
  42. 42. Uses: • Local anesthesia. • Ventricular arrhythmia. • Decrease haemodynamic response to tracheal intubation also decrease cough. • Treatment of epileptic fits.
  43. 43. Advantages of local anaesthesia • Non inflammable. • Excellent muscle relaxant effect. • During local anesthesia the patient remains conscious. • It requires less skilled nursing care as compared to other anesthesia like general anesthesia. • Maintains his own airway.
  44. 44. • Less pulmonary complication.s • Aspiration of gastric contents unlikely. • Less nausea and vomiting. • Contracted bowel so helpful in abdominal and pelvic surgery. • Postoperative analgesia. • There is reduction surgical stress. • Earlier discharge for outpatients.
  45. 45. Advantage of using adrenaline: •Epinephrine vasoconstricts arteries reducing bleeding and also delays the resorption of lidocaine, almost doubling the duration of anaesthesia. •Bupivacaine has caused several deaths when the epidural anaesthetic has been administered intravenously accidentally.
  46. 46. Adverse Effects • CNS: excitation followed by dépression (drowsiness to unconsciousness and death due to respiratory depression. • Cardiovascular System: bradycardia, heart block, vasodilation (hypotension) • Allergic reactions: allergic dermatitis to anaphylaxis (rare, but occur most often by ester-type drugs).
  47. 47. Causes : • Accidental rapid intravenous injection. • Rapid absorption, such as from a very vascular site ie mucous membranes. • Overdose .
  48. 48. Factors reducing toxicity: • Decide on the concentration of the local anaesthetic that is required for the block to be performed. Calculate the total volume of drug that is allowed according to the table below.
  49. 49. Hope you all get it…

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