11780314.ppt
- 1. What is Anesthesia? Franklin Scamman, MD
- 2. Topics to Cover This Lecture 1. What is “anesthesia” 2. History and mechanism of anesthesia 3. Uptake and distribution of inhaled anesthetics 4. CNS effects of anesthesia 5. Minimal alveolar concentration (MAC) 6. Properties of inhaled anesthetics 7. System effects of inhaled anesthetics 8. Delivery systems for inhaled anesthetics
- 3. “Anesthesia” • Insensitivity to pain • May be from local or general agents • Term introduced by Oliver Wendell Holmes in 1847 in response to work by WTG Morton using ether
- 4. History of Anesthesia • Greeks and Romans: aware of opium and derivatives; oral ethanol • Japan: 1820s, mandrake causing cholinergic crisis and unconsciousness • TWG Morton, MGH, October 16, 1846 using diethyl ether • However, Crawford Long in 1849 described his use of it in 1842
- 5. MGH “Ether Dome” 1846
- 6. Mechanisms of Anesthesia • No single macroscopic site of action • Specific brain areas affected by inhalational Anesthetics causing amnesia – Reticular activating system, – Cerebral cortex – Cuneate nucleus – Olfactory cortex – Hippocampus • Anesthetics depress excitatory transmission in the spinal cord supressing movement
- 7. Mechanisms of Anesthesia • General anesthetic action could be due to alterations in any one of several cellular systems including ligand-gated ion channels, second messenger functions, or neurotransmitter receptors. • Many anesthetics (the potent agents) enhance (GABA) inhibition of the central nervous system. • Other agents (nitrous oxide and xenon) are NMDA agonists with good pain relief, just like ketamine • Potency of inhalation agents correlates directly with their lipid solubility (Meyer–Overton rule)
- 10. Rate of Rise of Alveolar Concentration
- 11. Factors Determining the Speed of Induction • Vaporizer setting (concentration) • Fresh gas flow • Alveolar minute ventilation • Blood-gas partition coefficient (solubility) • Cardiac output • Alveolar-to-venous partial-pressure difference • Brain-blood partition coefficient • Cerebral blood flow
- 12. How fast do you go asleep? The higher the blood/gas coefficient The greater the anesthetic's solubility The greater its uptake by the pulmonary circulation. Alveolar partial pressure rises more slowly Slow induction
- 13. Many of the factors that speed induction also speed recovery • Elimination of rebreathing • High fresh gas flows, • low anesthetic-circuit volume, • low absorption by the anesthetic circuit, • Decreased solubility, • High cerebral blood flow, • Increased ventilation.
- 14. Minimal Alveolar Concentration • Percent alveolar concentration to prevent purposeful movement in 50% of individuals • Corresponds to the ED-50 of oral or IV drugs • Lower at extremes of age • Lower with other depressant drugs • Lower in pregnancy • Maximum at 37-39 degrees • Maximum age 2-24 (roughly)
- 15. Properties of the Vapors Desflurane Nitrous Oxide Isoflurane Sevoflurane Blood/Gas 0.42 0.47 1.43 0.69 Brain/Blood 1.29 1.1 1.57 1.70 Fat/Blood 27.2 2.3 44.9 47.5 MAC % 6.0 104 1.2 2.0
- 16. Depth of Anesthesia • Anesthesia depth can be assessed by – Lack of movement in non-paralyzed state – Respiration rate and pattern – Respiratory depression (ET CO2 and VE ) – Eye signs – BP and P less valuable – BIS and Entropy analysis
- 17. Respiratory Effects • Abolish the hypoxic response at less than half MAC concentrations • Fantastic bronchodilators by direct action on smooth muscle
- 18. Cardiovascular Effects (1) • All cause cardiac depression • Cardiac depression causes an increased rate of concentration rise • An increased concentration causes more cardiac depression • Positive feedback -> cardiac arrest if not careful
- 19. Cardiovascular Effects (2) • Isoflurane and desflurane cause increased heart rate which may mask depression • Systemic vascular resistance – Isoflurane and desflurane decrease (great for starting IVs) – Halothane and nitrous oxide do not change
- 20. Renal Effects • All decrease arterial pressure • RBF and GFR will be maintained until threshold of autoregulation, absent other influences (sympathetic tone, renin) • Urine output is variable, depending on ADH and aldosterone and other humeral agents • Creatinine clearance not effected by UO