Pharmacology of Inhaled Anesthetics
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1 Pharmacology of Inhaled Anesthetics Beverly K. Philip, M.D. Professor of Anaesthesia Harvard Medical School Founding Director, Day Surgery Unit Brigham and Women s Hospital Boston, USA Beverly K. Philip, M.D. I have received research a/o speaker support from: Abbott Merck Baxter Organon Eisai Roche GlaxoSmithKline Schering Plough Hospira Majority of Anesthetics Given USA and World Are Primarily With Inhaled Anesthetic Drugs Why? Control : Easy, reliable, available via ventilation. Administration of drug via lungs allows us to: monitor & adjust the drug concentration in Inspired gases, to obtain Continuous Control of drug s Blood concentration, hence its bioavailability to sites of drug action. Definitions Pharmacokinetics: The relationship between a drug's dose, tissue concentrations, and time - How the body affects a drug Pharmacodynamics The study of drug actions, beneficial and adverse - How a drug affects the body Pharmacokinetics of Inhaled Anesthetics Gas Man Anesthesia Simulator (relationship: dose, tissue concentrations, time) PK consists of: Uptake (absorption), from alveoli into systemic circulation Distribution, throughout the body Elimination, via lungs or metabolism
2 Factor Determining Uptake and Distribution: Partial Pressure Gradients Definition: Partial pressure = Tension: p driving force for drugs between equalizes across -- compartments {Fraction ~ Concentration, depends on solubility} Uptake and Distribution Step by Step: Transfer of Inhaled Anesthetic from Inspired to Alveoli P I P A P A determined by: P I inspired tension transfer V A alveolar ventilation characteristics of breathing system ( by FGF, by circuit volume & absorption Transfer of Inhaled Anesthetic from Alveoli to Arterial Blood P A P a. P a determined by: Blood/gas solubility - as partition coefficients Partition Coefficients at 37 C Ratio of anesthetic concentrations in the two phases at equilibrium Agent Blood/gas Brain/blood Muscle/blood Fat/Blood N2O Halothane Isoflurane Desflurane Sevoflurane Morgan, Mikhail, Murray Clinical Anesthesiology (Lange) 2006, p158 Transfer of Inhaled Anesthetic from Alveoli to Arterial Blood P A P a. P a determined by: Blood/gas partition coefficients (Tissue solubilities) Cardiac Output (Blood flow) Alveolar-venous tension difference : reflects tissue equilibration Transfer of Inhaled Anesthetic from Arterial Blood to Brain (VRG) P a P br P br determined by: Tissue/blood solubility here, Brain/blood partition coefficient Tissue blood flow here, Cerebral blood flow Arterial-venous tension difference VRG (brain, heart, liver, kidney) equilibrates with ALV 92% within 3 time constants, τ ~ 3 min.
3 Elimination Mostly, inverse of uptake, so influenced by V A Solubility CO Also influenced by: - Tissue concentrations: depend on Duration of anesthesia Solubility of agent - Metabolism: important for halothane WAKEUP occurs when P br reaches desired effect threshold Determinants of Wakeup: Rarely, Fat Solubility Agent Blood/gas Brain/blood Muscle/blood Fat/Blood N2O Halothane Isoflurane Desflurane Sevoflurane (VRG) % Cardiac Output Drug entry into fat is limited by: % CO to fat With large capacity of fat for agents (volume; sol) Fat Solubility Rarely Determines Wakeup Pharmacodynamics The study of drug actions, beneficial and adverse - How the drug affects the body Fat - A sink for anesthetic for 12 h Des, 17 h Sevo JH Philip, GasMan Clinically, Why Induction can be faster than Wakeup Overpressure! Induction - Can give 8% Sevo to body with 0% Wakeup - Can give 0% to body with 2% MAC Minimum Alveolar Concentration Alveolar partial pressure (in % atmospheric P {sea level} ) of an anesthetic that prevents movement in 50% of subjects {age} in response to a standardized surgical incision. Determined at steady state ~15 min
4 MAC = ED 50 ED MAC. Different MACs for different stimuli : MAC awake ~ 0.3 incision/surgical MAC [I,D,S] MAC intubation (ANS-blocking) ~ 2.0 MAC i [S] MACs compare potency between agents. MACs of multiple agents are ~ additive (Inh & IV) Movement is probably a spinal cord reflex Factors that Increase MAC Hyperthermia (>42ºC) Drugs that Increase CNS catecholamines: MAOI Tricyclic antidepressnts Cocaine Acute amphetamine ingestion Infants Hypernatremia Chronic ETOH abuse Factors that Decrease MAC Hypothermia CNS depressant drugs: Preop medication IV anesthetics Alpha-2 agonists; β- blockers Acute ETOH ingestion Neonates (compared w infants) Age : 6% per decade Pregnancy, 8 wks thru hr postpartum Hyponatremia Factors that Do Not Change MAC Duration of anesthesia Gender Anesthetic metabolism Thyroid gland dysfunction Hyper or hypokalemia PaCO mmhg PaO2 >38 mmhg Systolic BP >40 mmhg Spinal cord transection. Nitrous Oxide (N 2 O) Halothane Inorganic; gas at room temperature and ambient pressure Pressurized tank 750 psi with liquid N2O To reach 1 MAC, need P >atm Supports combustion Inexpensive in USA Reduces requirement for other anesthetics (MACs add) An alkane: halogen-substituted ethane derivative Non-flammable at clinically used concentrations
5 Isoflurane Desflurane Contains Ether link Substitution of Fluorine for Br & Cl - Increases chemical stability - Decreases blood solubility and anesthetic potency Similar to isoflurane : F -- atom substituting for iso s Cl -- High Vapor pressure: boils at Room T at altitude {Denver} Requires heated (boiling-liquid) vaporizer Sevoflurane Vapor P permits use of conventional vaporizer Organ Effects: N 2 O Cardiovascular Symp NS stimulation Contractility with net NC in CO - Ameliorates BP drop seen with volatile anesthetics TV, RR - NC resting PaCO2 Neuromusc: Does not provide relaxation Biotransformation & toxicities: N 2 O Not metabolized (0.004%) Inhibits enzymes that are B12 dependent: methionine and thymidylate synthetases Prolonged exposure: bone marrow depression, periph neuropathies - NOT at clinical exposures? Teratogen (myelin ; DNA) Diffuses into air-containing cavities: partial pressure N 2 O will approach alveolar -closed space -> incr P; distensible space -> incr V NOT trigger for malignant hyperthermia Organ Effects: Volatile anesthetics To some extent, all: Cerebral BF ~> ICP; autoregulation Hepatic BF Renal BF. V T, RR V A, resting PaCO2 Skeletal muscle relaxants (dose dependent); potentiate nondepolarizing NMBs All are Triggering Agents for Malignant Hyperthermia
6 Organ Effects: Halothane Direct myocardial depressant (dose-dep) HR (blunted baroreceptor reflex) Net CO. Sensitizes heart to epinephrine-induced arrhythmias Low airway pungency Good bronchodilator Biotransformation & toxicities: Halothane Metabolized 20%; TriFluoroAcetic acid (TFA) Halothane hepatitis 1:35K centrilobular necrosis Immune: Ab to TFA- liver microsomal proteins enzymes, bili; encephalopathy 1 Adults & children past puberty Sensitizes heart to catechols, esp if CO2: limits use with exogenous epi ; avoid > 1.5 ug/kg Unstable to UV: thymol preservative, amber bottle Organ Effects: Isoflurane Minimal myocardial depressant HR, dose-dep. (preserved baroreceptor reflex) NC in CO No sensitization to epinephrine-induced arrhythmias Rapid in concentration trans HR, BP, NEpi Mild irritant upper airway reflexes; bronchodilator Biotransformation & toxicities: Isoflurane Metabolized 0.2%; TFA Rare reports of immune hepatitis Prolonged exposure to anesthesia or sedation plasma F (~ 50 µmol/l) - no renal concentrating dysfunction seen Controversy re coronary steal (vasodilation) Organ Effects: Desflurane SVR, BP, Moderate HR NC in CO Dose-related HR, CVP, and PAP Rapid concentration trans HR, BP, NorEpi Attentuate by esmolol, clonidine, mod dose fentanyl Pungency; Airway irritation (coughing,laryngospasm) Biotransformation & toxicities: Desflurane Minimal metabolism 0.02% TFA One report of immune hepatitis Degraded by Dessicated alkali in CO2 absorber (esp BaOH [n/a], KOH > NaOH): reports of clinically significant Carbon Monoxide Delirium on emergence in children
7 Organ Effects: Sevoflurane contractility, SVR, BP HR only at high doses Very low airway pungency: used for airways; vital capacity induction Potent bronchodilator Good skeletal relaxant clinically higher doses Biotransformation & toxicities: Sevoflurane Metabolized 5% Not metabolized to TFA: no cases immune hepatitis Metabolized to inorganic F, w plasma F ~ 50 µmol/l - no renal concentrating dysfunction seen Degraded by alkali to form compound A Fatal nephrotoxin for rats [ ] w absorber temp~ FGF, [sevo] ; dry absorbent - no human postop renal impairment reported Sevo + Dessicated alkali ~> heat Emergence delirium in children: Tx Fentanyl 1-2 µg/kg. Inhaled Anesthetic Agents: Choices! Pharmacokinetics Uptake Distribution Elimination Pharmacodynamics Organ effects Biotransformation & toxicities To Create a Scientifically-based Optimal Anesthetic
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