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INHALATION ANESTHETICS

INHALATION ANESTHETICS. Prof. Ayman Hussein Kahla Prof. of Anesthesia Technology Public Health & Health Informatics Faculty UMM ALQURA UNIVERSITY. Anesthesia.

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INHALATION ANESTHETICS

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  1. INHALATION ANESTHETICS Prof. Ayman Hussein Kahla Prof. of Anesthesia Technology Public Health & Health Informatics Faculty UMM ALQURA UNIVERSITY

  2. Anesthesia • A state of temporary & reversible loss of awareness and reflex reactions induced by drugs to render surgery painless, possible & comfortable. • General anesthesia for surgical procedure to render the patient unaware / unresponsive to the painful stimuli.

  3. Receptor Theory of Anesthesia • GABA: major inhibitory neurotransmitter (point of action of anesthetic drugs) • Membrane structure and function: future of the anesthesiology • Glutamate: major excitatory neurotransmitter • Endorphins: analgesia. • Unitary hypothesis of the inhalation agents.

  4. MECHANISM OF ACTION • Act in different ways at the level of the central nervous system. • Disrupt normal synaptic transmission - interfering with release of neurotransmitters from pre-synaptic nerve terminal (enhance or depress excitatory or inhibitory transmission). - altering re-uptake of neurotransmitters, - Changing the binding of neurotransmitters to the post-synaptic receptor sites or - Influencing the ionic conductance change that follows activation of the post-synaptic receptor by neurotransmitters.

  5. Meyer-Overton Theory postulates that it is the number of molecules dissolved in the lipid cell membrane. • Protein Receptor Hypothesis postulates that protein receptors in the central nervous system. • Activation of GABA receptors. • may inhibit certain calcium channels and therefore prevent the release of neurotransmitters and inhibit glutamate channels.

  6. Inhalation Anesthetic Agents • Nitrous oxide • Halothane (Fluothane) • Methoxyflurane (Penthrane) • Enflurane (Ethrane) • Isoflurane (Forane) • Desflurane (Suprane) • Sevoflurane (Ultane)

  7. STRUCTURE OF DIETHYL ETHER

  8. F H F – C – C* – Br F Cl F F F Cl – C* – C – O – C – H H F F N=N=O Nitrous Oxide Halothane Enflurane F F H H C F C O C F F C H F F F H F F – C – C* – O – C – H F F F F H F F– C – C* – O – C – H F Cl F Desflurane Sevoflurane Isoflurane

  9. Obsolete Volatile Anesthetics - Aliflurane - Chloroform - Cyclopropane - Diethyl ether - Enflurane - Ethylene - Halothane - Methoxyflurane - Methoxypropane - Roflurane - Teflurane - Trichloroethylene - Vinyl ether

  10. DEFINITION • It is a chemical compound possessing general anesthetic properties that can be delivered via inhalation. • They are administered by anesthetists (anesthesiologists, nurse anesthetists, and anesthesiologist assistants) through an anesthesia mask, LMA or ETT connected to some type of anesthetic vaporizer and an anesthetic delivery system.

  11. Inhalational Anesthetic Agents • Inhalational anesthesia refers to the delivery of gases or vapors from the respiratory system to produce anesthesia • Pharmacokinetics-- uptake, distribution, and elimination from the body. • Pharmacodyamics- MAC value.

  12. Inhaled anesthetic agents remain popular for maintenance and induction of anesthesia. • Inhalation induction is the technique of choice for: • Predicted difficult airway. • Difficult intravenous access. • Needle phobia, including children.

  13. History of Anesthesia • 1845 - Horace Wells- N2O • 1846 - William Morton- Ether • 1847 - Simpson- Chloroform • 1934 - Cyclopropane • 1956 - Halothane

  14. Pharmacokinetics and Pharmacodymanics • Pharmacokinetics: how the body affects the drug • Pharmacodymanics: how the drugs affects the body

  15. Anesthetic Uptake • Solubility in blood • Alveolar blood flow • Differences in partial pressure between alveolar gas and venous blood • Therefore: low output states predispose patients to overdosage of the soluble agents

  16. ELIMINATION • Biotransformation: cytochrome P- 450 (specifically CYP 2EI) • Transcutaneous loss or exhalation • Alveolus is the most important in elimination of the inhalation agents • Diffusion hypoxia” and the nitrous oxide

  17. Elimination • Redistribution from brain to blood to air • Anesthetics that are relatively insoluble in blood and brain are eliminated faster

  18. Pharmacokinetics • The concentration of a gas in a mixture of gases is proportional to the partial pressure. • Inverse relationship between blood : gas solubility and rate of induction.

  19. Pharmacokinetics • Increase in inspired anesthetic concentration will increase rate of induction • Direct relationship between ventilation rate and induction rate • Inverse relationship between blood flow to lungs and rate of onset • MAC = minimum concentration in alveoli needed to eliminate pain response in 50% of patients

  20. Hallmark of Anesthesia • Amnesia / Unconsciousness • Analgesia • Muscle relaxation

  21. Basic Principles of Anesthesia • Anesthesia defined as the abolition of sensation • Analgesia defined as the abolition of pain “Triad of General Anesthesia” • Need for Unconsciousness • Need for Analgesia • Need for Muscle relaxation

  22. STAGES OF ANESTHESIA • Stage I : Analgesia • Stage II : Excitement, combative behavior – dangerous state • Stage III : Surgical anesthesia • Stage IV : Medullary paralysis – respiratory and vasomotor control ceases.

  23. Anesthetics are associated with - Decrease in systemic blood pressure – myocardial depression and direct vasodilatation. - Blunting of baroreceptor control and decreased central sympathetic tone.

  24. Side Effects • Reduce metabolic rate of the brain • Decrease cerebral vascular resistance thus increasing cerebral blood flow = increase in intracranial pressure

  25. The main target of inhalation anesthetics is the brain.

  26. The important characteristics of Inhalational anesthetics which govern the anesthesia are : • Solubility in the blood (blood : gas partition co-efficient) • Solubility in the fat (oil : gas partition co-efficient)

  27. Agents with low solubility in blood quickly saturate the blood. The additional anesthetic molecules are then readily transferred to the brain. BLOOD GAS PARTITION COEFFICIENT

  28. Blood gas partition co-efficient affecting rate of induction and recovery

  29. OIL GAS PARTITION CO-EFFICIENT Higher the Oil: Gas Partition Co-efficient lower the MAC . E.g., Halothane 0.8 1.4 220

  30. Oil: gas partition co-efficient: • It is a measure of lipid solubility. • Lipid solubility - correlates strongly with the potency of the anesthetic. • Higher the lipid solubility – potent anesthetic. e.g., halothane

  31. Ideal Inhaled Anesthetic • Pleasant odor • Non-irritant • Low blood gas solubility. • Chemically stable. • Non inflammable. • Potent. • Inert. • Not metabolized. • Non-toxic. • Analgesic. • No Cardiovascular & respiratory depression.

  32. Minimal Alveolar Concentration (MAC) • Concentration of inhaled anaesthetics in the alveolar gasthat prevents movements in 50% of patients in response to a standardized stimulus (eg surgical incision) • MAC is important to compare the potencies of various inhalational anesthetic agents. • 1.2-1.3 MAC prevent movement in 95% of patients.

  33. MAC • MAC value is a measure of inhalational anesthetic potency. • It is defined as the minimum alveolar anesthetic concentration ( % of the inspired air) at which 50% of patients do not respond to a surgical stimulus. • MAC values are additive and lower in the presence of opioids.

  34. MAC TYPES • MAC awake:MAC allowing voluntary response to command in 50% of patients • MAC 95%: MAC that prevents movement in 95 % of patients • MAC intubation:MAC that allows intubation without muscle relaxant, coughing or bucking in 50% of patients. • MAC-BAR(1.7-2.0 MAC), which is the concentration required to block autonomic reflexes to nociceptive stimuli.

  35. Increase MAC • Hyperthermia. • Chronic drug abuse (Ethanol). • Acute use of amphetamines. • Hyperthyroidism. • Reducing age.

  36. Decrease MAC • Increasing Age. • Hypothermia. • Other anesthetic (Opioids). • Acute drug intoxication (Ethanol). • Pregnancy. • Hypothyroidism. • Other drugs ( Clonidine ,Reserpine).

  37. No Effect on MAC • Gender • Duration of anesthesia • Carbon dioxide tension (21-95 mmHg) • Metabolic Acid base status • Hypertension • Hyperkalemia

  38. MAC • N2O = 105% • Halothane = 0.75% • Isoflurane = 1.15% • Euflurane = 1.68% • Sevoflurane = 2% • Deslurane = 6% • N2O alone is unable to produce adequate anesthesia ( require high conc. )

  39. Inhalational Agent Reaches The Alveoli • Increasing the delivered concentrations of anesthetic • The gas flow rate through the anesthetic machine • Increasing minute ventilation MV = Respiratory Rate × Tidal volume

  40. Inhalational Agent Reaches The Brain • The rate of blood flow to the brain • The solubility of the inhalational agent in the brain • The difference in the arterial and venous concentration of the inhalational agent

  41. Inspiratory Concentration (Fi) • Increase FGF rate. • Decrease Breathing System Volume. • Decrease absorption of the breathing system of the anesthetic machine. • All closer inspired gas concentration to the fresh gas concentration.

  42. Alveolar Concentration (FA) • The greater uptake of an anesthetic agent; the lower rate of rise of FA • The greater difference between Fi and Fa; the slower the rate of induction • The higher the blood gas solubility coefficient; the greater the anesthetic solubility, and the slower the onset of induction and recovery. • Increased alveolar blood flow increases anesthetic uptake.

  43. Solubility in blood • Alveolar blood flow • Partial pressure difference between alveolar gas & venous blood (PA- PV)

  44. Arterial Concentration (Fa) • Mainly ventilation perfusion mismatching • Normally, alveolar and arterial anesthetic pressures are assumed to be equal. • Presence of ventilation perfusion mismatching increases alveolar arterial differences

  45. Anesthetic delivery to alveoli • Ventilation • Concentration • Apparatus Dead Space

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