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ITE target review volatile anesthetics

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ITE target review volatile anesthetics

  1. 1. Inhalation Anesthetics Aden Bronstein, MD
  2. 2. MAC • Decreased: Hypoxia, Hypotension, Hypothermia, Anemia, Age, Acute etoh, pregnancy, chronic amphetamines • Unchanged: Thyroid function, gender, Paco2 15-95, Beta blockers • Increased: Hyperthermia, Hypernatremia, acute amphetamines, Chronic etoh
  3. 3. Alveolar Partial pressure • Alveolar partial pressure ~rate of input/removal • Rate of induction affected by: – FiAA – Alveolar ventilation – Characteristics of anesthetic breathing circuit – uptake
  4. 4. Uptake = (Λ)(Q)(PA-PV) Barometric pressure • Denver, Colorado
  5. 5. Uptake • Uptake = (Λ)(Q)(PA-PV) – Barometric pressure Λ: B.G. partition coefficient • Decreased solubility decreases uptake: anemia,hypoalbuminemia,fever – Uptake most dependent on Alveolar partial pressure difference
  6. 6. Uptake = (Λ)(Q)(PA-PV) Barometric pressure • RL Shunt – Accelerated rise of FA/FI – Slows rate of induction b/c of dilution – Uptake of highly soluble volatile anesthetics is sufficient to partially negate the dilutional effect
  7. 7. Uptake = (Λ)(Q)(PA-PV) Barometric pressure • Dead space – Profound impact on soluble anesthetic gases – Small impact on insoluble agents
  8. 8. Uptake = (Λ)(Q)(PA-PV) Barometric pressure • LR shunt – Faster increase in FA/FI due to higher partial pressure of anesthetic gas in blood returning to the lung • Clinically insignificant
  9. 9. MAC B/G solubili Vapor press Halothane 0.75 2.3 240 Enflurane 1.68 1.8 175 Isoflurane 1.15 1.4 238 Methoxyflu rare 0.15 12 22 Ether 2.0 12 450 Nitrous 105 0.47 ---- Desflurane 5.70 0.42 665 Sevoflurane 2.0 0.60-0.65 200
  10. 10. Metabolis m Deflurinati on Methoxyflu rane 40% Methoxyflu rane Halothane 20% Sevoflurane Sevoflurane 3% Halothane Enflurane 2% Enflurane Isoflurane .2% Desflurane Desflurane .02% N2O
  11. 11. Fluoride nephropathy • Diabetes insipidus: • Renal tubule damage • Fluoride and lithium in appropriate concentrations are capable of causing nephrogenic diabetes insipidus
  12. 12. Hemodynamics HR SVR CI Halothane NONE NONE Dec Sevoflurane Dec Dec Dec Desflurane Inc Dec Dec (min) Isoflurane Inc Dec None N2O Inc (min) Inc Increased
  13. 13. Hemodynamics (cont) • Mechanism of decrease BP – 1. Decreased SVR—2-3x increase in skeletal muscle blood flow – 2. Myocardial Depression/decreased C.O. – 3. Decrease sympathetic nervous system tone
  14. 14. Respiratory Affects • Rapid/shallow • Elevated PaCO2
  15. 15. Desflurane • Low B/G partition coefficient (.42)rapid induction of anesthetics • Pungency, Airway irritation • Airway irritiationcoughing, salivation, breath holding, laryngospasm • Abrupt increase in concentration increased sympathetic dischargeHTN and tachycardia – If increased slowly or prior narcotic---HTN and tachy may not occur
  16. 16. Sevoflurane • Biotransformationcompound A, fluoride renal toxicity • Compound A: Renal tubular necrosis – Sevo is degraded in a temp-dependent fashion in both sodalyme and baralyme – Factors that lead to increased concentration of Compound A: • Fresh absorbent • Baralyme>sodalyme • Higher absorbent temperatures • Higher concentrations of sevo in anesthetic system • Closed circuit or LOW FLOW anesthesia – Gas flows >2L/m prevent rebreathign
  17. 17. Nitrous Oxide • Dose dependent myocardial depressant • Sympathetic stimulation obscures myocadial depressant effects • Sympathetic stimulationIncrease in PVR, C.O. HR, circulating catecholamines • Contraindications: Air embolus, bowel obstruction, COPD, CHF, PTX/pneumocephalus, chest wall trauma, eye/ear surgery
  18. 18. Second gas effect • Alveolar uptake of a second gas (ie N2O) creates a subatmospheric intrapulmonary pressureincreased tracheal inflow • Alveolar uptake of a second gas (ie N2O) increases Alveolar Concentration of 1st gas (concentrating affect)

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