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166 Cards in this Set
- Front
- Back
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3 advantages of inhaled anesthetics (over IV):
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1. Rapid onset, short duration
2. Easy to monitor end-tidal measurements (mirror brain concentration) 3. Elimination via lungs (independent of hepatic/renal function) |
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What drugs were removed from clinical practice due to flammability?
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Diethyl ether
Divinyl ether Ethylene Cyclopropane (explosive) |
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What agent disappeared due to inherent hepatotoxicity?
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Chloroform
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When were halogenated agents synthesized?
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1960-1990
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What is involved in halogenating agents?
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Addition of chlorine, bromine, fluorine
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What is a physical property of halogenated agents?
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Inflammability
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What is an advantage os using fluorine over bromine/chlorine?
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Less toxicity
Less solubility (shorter acting) |
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What was the prototype agent?
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Halothane
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What was the first agent exclusively halogenated with fluorine?
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Desflurane
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What were 3 potential limitations of Desflurane?
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1. Synthesized with elemental fluorine is a potentially explosive process
2. Saturated vapor pressure near 1 atmosphere (precluding its use with conventional vaporizers) 3. 1/5 as potent as Isoflurane |
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What is a concern with Sevoflurane?
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Potential toxicity in the presence of carbon dioxide absorbents (soda lime and Compound A)
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What was the drive for commercial development of Desflurane and Sevoflurane?
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Ambulatory/outpatient surgery centers
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What is vapor pressure?
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The pressure exerted by a gas above a liquid when the two are in equilibrium
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Gay Lussac's Law:
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As temperature increases, vapor pressure increases
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Vapor pressure and vaporizers
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Vaporizers are calibrated specifically to the vapor pressures of the agents they are designed to deliver
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What happens if a high VP agent is added to a vaporizer of a low VP agent?
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Anesthetic overdose will occur
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Vapor pressure: Desflurane
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700 mmHg
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Vapor pressure: Sevoflurane
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157 mmHg
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Vapor pressure: Isoflurane
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240 mmHg
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Present day carbon dioxide absorbents can degrade all _____ anesthetics
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Halogenated
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Why is it a concern that CO2 absorbents degrade halogenated anesthetics?
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1. Potential loss of anesthetic
2. Toxicity (end products) |
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What 2 factors does degradation depend on?
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1. Moist versus dry soda lime
2. Temperature of the soda lime |
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If you have dry soda lime, the temperature _____.
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Increases
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If you have low FGF, the temperature of the soda lime _____.
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Increases
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Desflurane degradation in moist soda lime
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40 degrees C: none (normal temp)
60 degrees C: none (normal temp) 80 degrees C: slight |
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Isoflurane degradation in moist soda lime
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40 degrees C: none (normal temp)
60 degrees C: none (normal temp) 80 degrees C: moderate |
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Halothane degradation in moist soda lime
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40 degrees C: none (normal temp)
60 degrees C: none (normal temp) 80 degrees C: moderate |
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Sevoflurane degradation in moist soda lime
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40 degrees C: slight (normal temp)
60 degrees C: considerable (normal temp) 80 degrees C: massive |
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What causes degradation of anesthetic?
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Due to the interaction between the anesthetic and the monovalent bases in the carbon dioxide absorbent
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What bases are responsible for anesthetic degradation?
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Monovalent
-NaOH -KOH |
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Do the divalent bases (CaOH, barium) cause anesthetic degradation?
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No
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What agents and at what temperature does dry (desiccated) soda lime degrade anesthetics?
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-Dry soda lime degrades desflurane and isoflurane at 40C, 60C, and 80C
-Markedly increases rate of degradation of Sevoflurane |
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Which has a higher rate of degradation? Moist or dry?
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The rate of degradation of dry soda lime exceeds that in moist soda lime by several-fold
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What are the 2 consequences of anesthetic degradation?
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1. Loss of anesthetic
2. Toxicity |
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Loss of anesthetic as a consequence of anesthetic degradation
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-Significant degradation may limit delivery of anesthetic
-Negligible impact of this when moist absorbent is used -Dry absorbents can remove large amounts of inhaled anesthetics |
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What type of reaction occurs between desiccated carbon dioxide absorbents and inhaled anesthetics?
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Exothermic (i.e. higher temperature): this process is accelerated with dry absorbents
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What gas is involved in case reports of fire in the anesthetic breathing circuit?
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-Sevoflurane (when using desiccated absorbent)
-Package insert warns against excessive heating with Baralyme (KOH) -Desflurane and Isoflurane produced significant heating but no fire |
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What are the 2 toxic agents produces as a consequence of anesthetic degradation?
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1. Compound A
2. Carbon monoxide |
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What gases are associated with Compound A and Carbon Monoxide?
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Compound A: Sevoflurane
Carbon Monoxide: Desflurane, Isoflurane |
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What is Compound A?
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-Vinyl ether produced as a result of degradation of Sevoflurane by carbon dioxide absorbents
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Where is Compound A's target of injury?
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-Corticomedullary junction of the kidney
-Dose related enzymuria, proteinuria, renal necrosis in rats -Most studies suggest no human toxicity (as long as FGF rates followed) |
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Concentrations of Compound A correlate ____ with Sevoflurane concentration
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Directly
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Concentrations of Compound A correlate _____ with absorbent temperature
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Directly
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Concentrations of Compound A correlate _____ with FGF rates
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Inversely
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What are FGF recommendations when it comes to Sevoflurane and Compound A?
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-FGF 1 LPM up to 2 MAC hours
-FGF 2 LPM after 2 MAC hours -Higher FGF rates reduce rebreathing of CO2 and less contact with absorbent |
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What is carbon monoxide?
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A breakdown product of inhaled anesthetics and desiccated (dry) absorbents
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What 2 gases are most avidly degraded to carbon monoxide?
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Desflurane and Isoflurane
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What 2 agents undergo little to no degradation to carbon monoxide?
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Sevoflurane and Halothane
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How easily does production of carbon monoxide occur?
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Production of significant amounts of carbon dioxide require near 90% desiccation of absorbent (1-2 days exposure to high gas flows)
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What reaction accounts for the formation of carbon monoxide?
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Results from the action of the monovalent bases in the absorbent
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What are the 2 monovalent bases involved in the formation of carbon monoxide?
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NaOH and KOH
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What published injury has occurred to patients due to carbon monoxide toxicity?
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No published reports of patient injury
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What is the minimum alveolar concentration?
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The minimum alveolar concentration of inhaled anesthetic that produces immobility in 50% of humans when exposed to a noxious stimulus
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True or false: There is a large difference in MAC values across a myriad of species?
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False: there is a remarkably small difference
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What does MAC measure?
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MAC is a measure of anesthetic potency
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MAC and potency are _____ related
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Inversely
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What part of the bod mediates MAC?
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Spinal cord (not brain)
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Increase or decrease MAC: temperature (hypo/hyper)
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Decrease
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Increase or decrease MAC: age (young and elderly)
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Young: increase
Elderly: decrease |
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Increase or decrease MAC: ETOH (acute and chronic)
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Acute: decrease
Chronic: increase |
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Increase or decrease MAC: hypercalcemia
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Decrease
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Increase or decrease MAC: hypernatremia
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Increase
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Increase or decrease MAC: hyponatremia
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Decrease
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Increase or decrease MAC: pregnancy
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Decrease
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Increase or decrease MAC: local anesthetics
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Decrease
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Increase or decrease MAC: Opioids, ketamine, barbiturates, benzos
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Decrease
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Increase or decrease MAC: clonidine, dexmedetomidine
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decrease
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Increase or decrease MAC: amphetamine (chronic and acute)
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Chronic: decrease
Acute: increase |
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Increase or decrease MAC: cocaine, ephedrine
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Increase
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What are the 2 most common factors that affect MAC?
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1. Drugs
2. Age |
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MAC: Halothane
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100% O2: 0.75
70% N2O: 0.29 |
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MAC: Isoflurane
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100% O2: 1.2
70% N2O: 0.50 |
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MAC: Sevoflurane
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100% O2: 2.0
70% N2O: 0.66 |
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MAC: Desflurane
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100% O2: 6.0
70% N2O: 2.8 |
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MAC: Nitrous Oxide
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100% O2: 105
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What is surgical anesthesia? (MAC value)
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1.3 MAC (assuming no other drugs)
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What is MAC Awake?
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The average concentration permitting voluntary response to command (in absence of other drugs)
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What is the MAC Awake/MAC ratio?
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For Des/Iso/Sevo, MAC Awake is approximately 1/3 (30%) of MAC
(concomitant drug administration may decrease ratio) |
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MAC Awake and amnestic point
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MAC Awake exceeds amnestic point (don't remember)
-Example: Des with 2% MAC = amnestic |
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Opioids and MAC
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-Small doses of opioids cause large reductions in MAC
-After initial dose, greater doses of opioids cause smaller reductions in MAC |
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What is MAC BAR?
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Alveolar concentration that blocks autonomic response (i.e. HR, BP)
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What does MAC BAR approximate (value)?
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1.5 MAC
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What is anesthesia?
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-Reversible, mediated by CNS
--immobility --amnesia |
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Meyer Overton hypothesis
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-Anesthetic potency correlates directly with lipid solubility
-Anesthetic disrupts neuronal transmission at hydrophobic sites in the lipid bilayer |
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5-Angstrom theory
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-Anesthetics act by an action on two sites separated by a distance of 3 angstroms
-Potency increases to a maximum at a 5 carbon length, at which time potency markedly decreases |
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Receptor-Neurotransmitter interaction
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-Inhaled anesthetics depress excitatory receptors (serotonin, ACh, glutamate)
-Inhaled anesthetics enhance inhibitory receptors (GABA, glycine) |
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What is the ultimate goal of inhalation anesthesia and how is this achieved?
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-Achieve a constant partial pressure of anesthetic in the CNS
-A constant partial pressure of anesthetic must be attained in the alveoli |
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Why does dialed anesthetic concentration not match expired anesthetic concentration?
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Uptake into blood occurs (from alveoli to pulmonary circulation)
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Anesthetic uptake from the lungs is a product of what 3 factors?
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1. Solubility (blood:gas partition coefficient)
2. Cardiac output 3. Alveolar-venous partial pressure gradient |
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What is solubility denoted by and what does it describe?
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**most important factor**
-blood:gas partition coefficient -Describes the affinity of the anesthetic for two phases at equilibrium |
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Solubility is a distribution ratio. What if the blood:gas partition coefficient is 2?
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Then at equilibrium, the concentration in the blood will be twice that in the gas phase
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A larger blood:gas partition coefficient indicates a _____ solubility and they are _____ proportional?
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-Greater
-Directly |
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A larger blood:gas partition coefficient will produce a _____ FA/FI ratio
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Lower: FA/FI narrows (equilibrates) over time during a case
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Blood:gas partition coefficient at 37 degrees C --> Desflurane
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0.42
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Blood:gas partition coefficient at 37 degrees C --> Nitrous Oxide
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0.47
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Blood:gas partition coefficient at 37 degrees C --> Sevoflurane
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0.69
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Blood:gas partition coefficient at 37 degrees C --> Isoflurane
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1.4
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Blood:gas partition coefficient at 37 degrees C --> Halothane
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2.4
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Uptake is ____ proportional to cardiac output
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-Directly
-The higher the CO, the greater the uptake -More relevant for higher solubility agents |
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Low output states and anesthetic?
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Low output states can rapidly increase alveolar concentrations (and predispose to anesthetic overdose)
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What does the alveolar-venous partial pressure gradient arise from?
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Tissue uptake throughout the body
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What 3 factors govern tissue uptake in the body?
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1. Solubility of gas in tissue
2. Tissue blood flow (***most important***) 3. Arterial-tissue partial pressure gradient |
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Tissue-blood partition coefficients in lean tissue
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-Do not differ greatly
-Lean tissues don't have significantly different capacities for anesthetic per mL of blood |
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What is the main determinant of tissue uptake?
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Tissue blood flow
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Vessel-rich group:
-Parts -Equilibrates |
-Brain, heart, lungs, liver, kidneys
-10% body mass, 75% cardiac output -Rapidly equilibrates with anesthetic (4-8 minutes; high blood flow, small volume) |
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Muscle group:
-Parts -Equilibrates |
-Muscle and skin
-1-4 hours to reach equilibrium |
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Fat group:
-Parts -Equilibrates |
-High affinity for anesthetic (large fat:blood partition coefficient)
-Up to 30 hours for equilibration |
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Vessel-poor group
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Insignificant uptake
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What 2 ways do we compensate for anesthetic uptake?
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1. Increase alveolar ventilation
2. Increase inspired concentration (FI) |
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Relationship between uptake and alveolar ventilation
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-The lowering of alveolar partial pressure by uptake can be countered by increasing alveolar ventilation
-The higher alveolar ventilation, the more rapid the "wash in" of anesthetic |
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How do we maintain alveolar partial pressure?
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-By constantly replacing anesthetic taken up by pulmonary circulation
-Most pronounced with higher solubility agents (most avidly taken up by pulmonary circulation) |
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Relationship between uptake and inspired concentration
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-Increasing the FI increases alveolar concentration and rate of rise (increases FA/FI)
-"Concentration effect" or "overpressuring" |
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What 3 factors govern FI?
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1. Fresh gas flow rates (***most important***
2. Volume of the system 3. Circuit uptake (minor) |
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Circuit uptake
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-Uptake by anesthesia breathing circuit
-Too small to influence induction/recovery from anesthesia |
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FGF and system volume affect _____
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Rebreathing
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What 2 parts is inspired gas composed of?
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-Gas delivered from anesthesia machine
-Gas previously exhaled by patient (rebreathed) |
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When does rebreathing occur?
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Rebreathing = FGF < minute ventilation (6L/min)
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An increase in rebreathing with ____ the inspired concentration
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-Lower
-"Dilutes" inspired concentration |
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How do we decrease/eliminate rebreathing?
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Fresh gas flow rates
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What is the second gas effect and when does it occur?
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-Occurs with concomitant administration of N2O and potent inhaled anesthetics
-The high volume uptake of a gas (N2O) will speed the rate of rise of the alveolar partial pressure of a second gas (potent agent) |
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What gas law does the second gas effect belong to?
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Boyle's Law: as volume decreases, pressure increases
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What is diffusion hypoxia and when does it occur?
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-The second gas effect in reverse
-Gas goes from blood to alveoli --> increase volume and decrease partial pressure of oxygen |
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Nitrous oxide solubility and net effect
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-N2O is 34x more soluble than nitrogen
-N2O will diffuse into air containing spaces much faster than air will diffuse out |
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N2O and effect on volume
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Volume is increased in highly compliant spaces:
-Bowel, pneumothorax (trauma), ETT cuff |
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N2O and effect on pressure
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Pressure is increased in poorly compliant spaces:
-Intraocular, pneumocephalus (bone flap), inner ear |
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What does recovery/emergence from anesthesia rely on?
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-Reversing the partial pressure gradients in the body
-Partial pressure gradients always drive gas movement in the body |
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Partial pressure gradient: Induction
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PI > PA > Pa >PBr
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Partial pressure gradient: Emergence
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PBr > Pa > PA > PI
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What 3 factors determine rate of recovery?
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1. Solubility
2. Alveolar ventilation 3. FGF |
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How does alveolar ventilation determine rate of recovery?
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-Influences the alveolar-venous partial pressure gradient
-Hypoventilation narrows the gradient (gas stays in the blood) |
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Biotransformation: Where are anesthetics metabolized?
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All potent inhaled anesthetics are metabolized by the liver
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Halogenated agents and biotransformation
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Anesthetics halogenated with fluorine are more resistant to hepatic degradation
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Spectrum of agents metabolized by liver (most --> least)
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Halothane--Sevoflurane--Enflurane--Isoflurane--Desflurane
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What is a breakdown product of inhaled anesthesia?
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Inorganic fluoride
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With regards to metabolism, what is a negative aspect/side effect of inorganic fluoride?
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Nephrotoxic at high serum levels
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Halo/Iso/Des and hepatotoxicity
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Halothane, Isoflurane, and Desflurane can RARELY cause hepatotoxicity via an immune-mediated reaction
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What inhaled agents is most associated with serum inorganic fluoride and toxicity?
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Sevoflurane
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Inhaled anesthetics and effect on myocardial contractility
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Cause dose-dependent decreases in myocardial contractility
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What agent produces larger decreases in myocardial contractility? When would this be indicated?
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Halothane: indicated for hypertrophic cardiomyopathy (decrease outflow obstruction)
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Proposed mechanisms of decreased contractility with inhaled anesthetics
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-Direct myocardial depression
-Inhibition of calcium ion influx |
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When is myocardial depression most profound?
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At deep levels of anesthesia
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Cardiomyopathy and inhaled anesthetics
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Cardiomyopathy increases vulnerability of myocardium to depressant effects
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Inhaled anesthetics and myocardial protective properties
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-Inhaled anesthetics exert some degree of myocardial protection during/after myocardial ischemic
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Isoflurane/Halothane and effect on post-ischemic myocardium
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Isoflurane and Halothane have been shown to enhance recovery of contractile function of postischemic, reperfused myocardium (stunned myocardium)
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How does inhaled anesthetics accelerate function recovery (myocardial protection)?
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Activation of sarcolemmal or mitochondrial ATP-sensitive potassium channels
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What is ischemic preconditioning?
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Phenomenon by which transit myocardial ischemia protects the myocardium against future ischemic episodes
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Relationship between inhaled anesthetics and ischemic preconditioning?
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Inhaled anesthetics mimic this phenomena
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How does ischemic precondition occur?
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Action on ATP-dependent potassium channels
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What is coronary steal?
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-Areas of ischemia are maximally dilated
-Inhaled anesthetics may dilate "normal" vessels, "stealing" blood away from ischemic areas -Insignificant factor r/t intraoperative myocardial ischemia |
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What is the biggest determinant of myocardial oxygen demand?
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Heart rate (also HoTN)
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Relationship between inhaled anesthetics and systemic vascular resistance
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Des/Sevo/Iso reduce systemic vascular resistance in a dose-dependent manner --> results in dose-dependent reduction in MAP
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Inhaled anesthetics, heart rate, and baroreceptor response
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Inhaled anesthetics attenuate baroreceptor response to hypotension to some degree
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Desflurane and heart rate
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Desflurane transiently increases heart rate when FI is increased rapidly > 6%
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What inhaled agent predisposes heart to ventricular dysrhythmias and in the presence of what?
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-Halothane in presence of epinephrine
-Avoid doses > 1.5 mcg/kg |
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Inhaled anesthetics and alveolar ventilation: effects and net effect
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Inhaled anesthetics produce a dose-dependent depression of alveolar ventilation:
-Decreased VT (increased dead spacE) -Increase RR -->net effect is an increased PCO2 |
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Inhaled anesthetics and hypercarbia/hypoxemia
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Decreased response to hypercarbia/hypoxemia
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Inhaled agent and broncho_____
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Potent bronchodilation
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What agent irritates the airway?
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Desflurane irritates the airway at concentrations > 6%
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What is hypoxic pulmonary vasoconstriction?
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Process by which pulmonary blood flow is directed away from hypoxic alveoli, optimizing gas exchange
(normal compensatory mechanism) |
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Is hypoxic pulmonary vasoconstriction influenced by inhaled anesthetics?
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Conflicting literature as to whether HPV is abolished by inhaled anesthetics
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Do inhaled anesthetics have analgesic properties?
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-Extremely limited analgesic properties
-0.1 MAC = hyperalgesia |
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How do inhaled anesthetics affect evoked potentials? (somatosensory and motor)
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Somatosensory: depress (increase latency, decrease amplitude)
Motor: little to no effect |
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How do inhaled anesthetics affect CVR, CBF, ICP, and CMRO2?
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CVR: decrease
CBF: increase ICP: increase CMRO2: decrease |
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At what point do inhaled anesthetics produce amnesia?
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Produce amnesia at MAC levels approximating MAC Awake (30%)
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What is the assumed relationship between immobility and amnesia?
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If you have immobility, you have amnesia
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What drug is involved with seizures and when?
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Sevoflurane
-High dose mask induction with alveolar hyperventilation -Seen with pediatrics -Tonic clonic and focal events -With or without prior seizure history |
