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65 Cards in this Set

  • Front
  • Back
MAC (minimum alveolar concentration)
1) more lipid-soluble agents have lower MAC values
2) at steady state, correlates to 500 umoles per 100 ml of membrane for each agent
Unitary Theory of Narcosis
all anesthetics have a common method of action
Meyer-Overton Theory
1) strong correlation between lipid solubility and potency
2) more lipid soluble agents are more potent anesthetics
3) points to a lipophilic action in some region of the brain
4) most likely site is membrane, affecting fluidity
Meyer-Overton Theory suggests what cause the effect?
the # of molecules dissolved in the membrane, and not the specific agent which cause the effect
Critical volume hypothesis (Mullins)
1) binding of anesthetic agent into membranes causes membrane to expand
2) alters the action of receptors and/or ion channel proteins locked into membrane
other theory additions
1) larger molecule size increases membrane expansion
2) binding of agent to memb. proteins in lipophilic regions alters protein (Na ion channel) function
Membrain concentration rule
1) provides quantitative explanation
Membrain concentration rule suggests?
1) when memb. excitability is blocked, the [ ] of the agent in the memb. is 500 umoles per 100 ml of memb. volume
2) equals 3 x 10(20th) molecules per 500 umoles
problems with physical theories
impossible to explain why some entantiomers have different anesthetic potencies or effects
CNS effects r/t inhalational anesthetics
1) unconsciousness - via peripheral neurons, SC, brainstem, other brain areas
2) immobilization - by action of SC
3) unconciousness - via depression of thalamic neurons
4) amnesia - via depression of hippocampal neurons
activation of which receptors in the BRAIN triggers hyperpolarization?
GABA-mediated chlorida ionophores
cell hyperpolarization
less likely to be able to be stimulated, thus decreasing passage of signals between neurons
activation of which receptors in the BRAINSTEM and SC triggers hyperpolarization?
Glycine-mediated chloride ionophores
inhalational anesthetics inhibit?
1) glutamate-mediated excitatory calcium channels (NMDA channels)
2) inhibit postsynaptic release of some neurotransmitters
GABA A receptor complex composed of?
1) GABA site
2) Benzodiazepine site
3) Steroid site
4) Barbiturate site
5) Picrotoxin site
main structures of inhalational anesthetics
1) alkanes
2) ethers
3) chlorinated/ fluorinated
general anesthesia is?
1) the loss of all perception
2) chara. by sleep, loss of pain sensation, inhibition of visceral reflexes, and muscle relaxation
characteristics that make up a good general anesthetic
1) rapid induction
2) good muscle relaxation
3) amnesia
4) analgesia
5) rapid emergence
balanced anesthesia
the mixture of different compounds for their different required effects, thus allowing less toxic doses of any one agent to be used
anesthesia will depend on
the partial pressure of the agent in the inspired air, and it's physiochemical properties
partition coefficient (blood:gas)
used to discuss the agents solubility between the gaseous phase and solubility into blood
MAC values
1) used to compare potencies of anesthetic agents
2) are at equilibrium (steady state), and are not related to time to reach anesthesia
the onset of anesthesia is related to?
blood/gas solubility (more rapid for less soluble agents)
Ethylene and Cyclopropane
1) older agents - no longer used
2) flammable
Nitrous Oxide
1) non-irritating gas
2) slightly sweet odor
3) non-explosive or flammable
4) MAC = 104 %
advantages of N2O
1) good relaxant at 10-30 % in air
2) excellent analgesic - as good as morphine
N2O act by?
inhibiting NMDA glutamate excitatory recetors, not by GABA enhancement
solubility of N2O
very low solubility in blood, therefore rapidly reaches equilibrium, and is rapidly eliminated (excreted unchanged in lungs)
long term use of N2O lead to?
1) inactivation of vitamin B12 lead to
2) megaloblastic anemia
3) leukopenia
4) thromobocytopenia
Diethyl Ether
1) no longer used in U.S.
2) stimulate catecholamine release - maintain BP, but can cause arrythmias
3) very irritating to bronchioles (>secretions)
4) explosive
CNS effects of halogenated alkanes and ethers
1) inhibit post-syna. excitatory responses
2) enhances post-syna. inhibitory response
3) pre-syna. effects leading to inhibition of NTM release
Halothane (Fluothane)
1) pleasant smelling
2) non-irritaing
3) non-explosive
4) soluble to some extent in rubber, and thus is taken up into some parts and tubing of anes. equipment
MAC of Halothane
0.76 %
rapid induction and maintenance of Halothane
1) rapid induction = 4 % v/v of air
2) maintenance = 0.5 - 2%
elimination of Halothane
80 % cleared b lungs, with remainder undergoing liver biotransformation
SE of Halothane
1) respiratory depression
2) decreases TV (cause short rapid breaths)
3) cardiac depression (<BP)
4) some vascular smooth muscle relaxation (<BP)
5) sensitizes the heart to catecholamines (trigger arrythmias)
6) post-op hepatitis
7) trigger MH
8) poor skeletal muscle relxant
Methoxyfluorane (Penthrane)
1) D/C ed
2) liver metabolism, via P-450 2E1 isomer mainly (50% of dose) releases free fluoride, whch can lead to kedney toxicity - (this has caused it to be removed from US market)
actual cause of nephrotoxicity is belived due to?
release of free fluoride in nephron by kidney metabolism (not due to liver metabolism)
Isofluorane (Forane)
1) widely used
2) pleasant smelling
3) non-irritating
4) non-explosive
MAC of Isofluorane
1.16 %
induction and maintenance [ ] of Isoflurane
1) induction [ ] = 2-4 % (v/v)
2) maintenance [ ] = 1-2 % (v/v)
metabolism of Isoflurane
very little metabolized < 1 %
effects of Isoflurane
1) mild analgesic effects
2) mild skeletal muscle relaxation (potentiates NMB)
SE of Isoflurane
1) some cardiac depression
2) < BP
3) no sensitization of the myocardium to catecholamines (Ether structure)
Which structure of volatile anesthetics cause sensitization of the heart to catecholamines?
Alkane types
(ex) Halothane
Enflurane (Enthrane)
1) similar (isomer) to Isoflurane
2) no longer widely used in U.S.
3) MAC = 1.68 %
high doses of Enflurane stimulate
the CNS, leading to seizure-like twitching of muscles
metabolization of Enflurane
~2% metabolized, and the release of free fluoride ions in long Sx procedures may lead to kidney toxicity(?)
Desflurane (Suprane)
1) low solubility (rapid induction & emergence)
2) one of most widely used agents today
MAC of Desflurane
6.0 %
vapor pressure of Desflurane
1) high vapor pressure (~700 mmHg at 20C)
2) requires specialized vaporizer
Is Desflurane good for induction?
No! due to pungent odor
cardiac effects of Desflurane
1) < BP
2) no sensitization of heart to catecholamine (Ether)
metabolization of Desflurane
very little metabolized (~0.02 %)
Sevoflurane (Ultrane)
1) newest agent approved in U.S.
2) low solubility (rapid induction & emergence)
3) rapidly become one of the most preferred agents
MAC of Sevoflurane
1.71 %
cardiac effects of Sevoflurane
1) < BP
2) no sensitization of heart to catecholamines (Ether)
metabolization of Sevoflurane
1) ~3% metabolized
2) release free fluoride due to liver metabolism (does not appear to be as nephrotoxic as methoxyflurane)
nephrotoxicity of free fluoride
1) in nephron by kidney meta. - more toxic
2) produced by liver meta. - less toxic
Carbon dioxide absorbents
1) used in gas machine to allow rebreathing and save anesthetic
2) cause chemical breakdown of all halogenated anesthetics
3) below 40C, little breakdown of modern anesthetics except for Sevoflurane
what reaction causes CO2 absorbents to increase the temperature?
reaction of soda lime or Baralyme with water vapor and CO2 causes temp. to increase to 40-60C normally, and thur allow breakdown (due to NaOH or KOH in the absorbant)
compound A
is formed from Sevoflurane is nephrotoxic and requires higher gas flow rates and limits anesthesia times
Carbon monoxide
1) is another degradation product of halogenated anesthetics with dry absorbents
2) appears worse on Monday
carbon monoxide can lead to
which agent appears to cause the most CO production?
(not as much seen with Sevo. or Halothane)