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179 Cards in this Set
- Front
- Back
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the present day use of N2O can be credited to who?
|
Edmund Andrews
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what was one of the earliest complete anesthetic agents used?
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diethyl ether
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where and when was the first ether anesthetic used and by whom?
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Georgia in March 1842 by C. W. Long
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what were some unfavorable characteristics of the first ether anestheic agents?
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-excessive secretions w/ inh. indxn
-laryngospasm -excessive depths of anesthesia |
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in 1930's reserach into potential anesthetic agents was based on what principle?
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the principle of a structure-activity relationship
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when and by who was Halothand introduced into clinical practice?
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1956 by Bryce-Smith and O'Brien in Oxford and Johnstone in Manchester
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what were clinical characteristic of halothane that were absent from previous inhaled anesethtics?
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-sweet odor
-nonflammability -high potency |
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what remains as a significant variable in determining use of sevo and des vs iso?
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cost
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what are some properties that would make and "ideal" anesthetic?
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-pleasant odor
-nonirritating to resp tract -rapid indx of anesthesia -low blood/gas solubility -chemically stable in storage -not interact w/ material of AM and circuits w/ soda lime -capable of producing unconsciousness w/ anaglesia and preferable some degree of muscle relaxation -not be metabolized in the body -no systemic toxicty (see rest on pg 100 box 9-1) |
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all commonly used inh agents are ____ or ____ with no more than ____carbon atoms?
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ethers or
aliphatic hydrocarbons with no more than 4 carbon atoms |
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why is the length of the anesthetic molecule important?
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immobility (anesthetic effect) is attenuated or lost if carbon atom chain length exceeds a distance of 4 or five carbon atoms (5 angstroms)
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|
what is the molecular shape of the anesthetic agents?
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spherical or cylinidrical with a length less than 1.5 times the diameter
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halogenation of hydrocarbons and ethers with addition of Fluorine, chlorine, bromine or iodine influences what?
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-anesthetic potency
-arrhythmogenic properties -flammability -chemical stability (oxidation during storage and reactions w/ bases) |
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the potency of volatile agents correlates with the physical property of what?
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lipid solubility
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in increase in MAC is assoc. with a proportional decrease in what?
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oil/gas partition coefficient values
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in regard to arrhythmogenic properties increasing the number of halogen atomis w/in a volatile agent favors the genesis of what?
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cardiac dysrhythmias
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ether molecules contain what which reduces arrhythmogenic effects?
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oxygen
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flammability is reduced and chemical stability enhanced by substituting ______atoms with ______.
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hydrogen, halogens
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des contains what ion as its only halogen thus strongly resists biodegradation?
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fluorine
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what determines the extent to which each volatile agent is metabolized?
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the chemical structure
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T or F des has been shown to resist biodegradation?
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true
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how are all current inh anesthetics biodegraded?
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by way of hepatic metabolism through oxidation (phase I)
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why is halothane metabolism unique?
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b/c it can also be metabolized by an alternative reductive pathway
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what is the Meyer-Overton rule?
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lipid solubility is directly proportional to potency
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T or F a reduction in body temperature lowers anesthetic requirements
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true
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the more lipid soluble an agent the greater/less its potency?
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greater
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what is definition of inh. anesthesia?
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compounds that produce amnesia and immobility in response to noxious stimuli
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how is amnesia defined?
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being unaware of one's environment or the inability to recall a previous episode of awareness
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any agent that produces both amnesia and immobility is termed what?
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full anesthesia
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drugs that cause amnesia alone are called what?
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-nonimmobilizers and nonanesthetics
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the other traditional characteristics of anesthetic state (analgesia and skeletal muscle relaxation) are viewed as what?
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side effects
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what part of body brain or sp cord is known to mediate immobility to a painful stimulus?
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spinal cord
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what mechanisms are known of the spinal cord to mediate immobility to painful stimulus?
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1-enhancing background K+ currents in tandem-pore-domain, weak inward-rectifying K+ channels (TWIK)
2- reducing spontaneous action potential firing of spinal neurons via glycine receptors and GABA receptors |
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how is the anesethetic effect of immobility is modulated in teh spinal cord and supraspinal?
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spinal and cerebral GABA receptors were shown to contribute to volatile anesthetics ability to produe immobility
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what are other specific sites where volatile anesthetics produce an effect?
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-reticular formation w/in brainstem
-cerebral cortex -hippocampus |
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evidence of changes in cortical activity by volatile agents includes alterations in what?
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EEG
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how do volatile agents affect EEG?
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cause a dose-dependent change in EEG
(an initial increase in voltage and decrease in frequency, then a peak, followed by a decline) |
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what do deeper levels of anesthetia produce on EEG?
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burst suppression and eventually a flat EEG
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T or F nonspecific EEG changes may persist for several days postoperatively
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True
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in addition to supraspinal effects modulation of _______ and ___________ impulses within the spinal cord has occured w/ volatile anesthetics?
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afferent, efferent
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on molecular level researchers found that most likely site of action for volatile anesthetics involves interactions of what?
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interactions with membrane proteins in specific receptors and not perfusion of lipid bilayers
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the primary receptor w/in CNS believed to modulate anesthetic effects is what receptor?
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GABA receptor, specifically subtype A
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where is GABA receptor located abundantly?
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in CNS and is a ligand gated chloride channel
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agonism of GABA receptor subtype A by full anesthetics results in what?
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enhanced chloride conductance which leads to inhibitory actions on local neurons
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do nonimmobilizers work on GABA receptors subtype A?
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no-nonimmoblizers do not enhance the effect of GABA on these receptors
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What other receptors have also been shown to be highly sensitive to inh anesthetics and are believed to infuence several stages of anesthesia?
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neuronal nicotinic acetylcholine receptors (nAChRs)
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inh agents have also been shown to block morphologic plasticity of what?
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dendritic spines
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the volatile agents strongly inhibit actin motility which blocked changes in what?
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dendritic spine shape
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what do denritic spines serve as ?
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excitatory postsynaptic contact sites
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where are dendritic spines very abundant?
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in cerebral cortex (greater than 10^13)
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where are dendritic spines also located in large numbers?
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cerebellum
basal ganglia olfactory bulb |
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what is MAC?
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minimum alveolar concentration at equilibrium in which 50% of subjects will not respond to painful stimulus
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what receptors are likely not involved in producing immobility?
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-potassium
-AMPA and kainate -GABA -opiod -5HT -Ach (these are more involved in amnestic and anesthetic effects in CNS) |
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what is a response to painful stimulus defined as ?
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gross purposeful movment of the head or extremeties
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what is the MAC of halothane?
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0.75
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with increasing age what happens to MAC?
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it decreases
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how is MAC-awake define?
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as the minimum alveolar concentration at which 50% of subjects will respond to command "open your eyes"
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the end-tidal concentration is usually assoc. w/ what?
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a loss of recall and encompasses approx. one third of MAC values
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what does the MAC-BAR parameter represent?
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the MAC necessary to block the adrenergic response to skin incision
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what are the adrenergic responses that can occur in relation to skin incision?
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changes in plasma norepinephrine conc., HR, MAP, rate-pressure product
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what is AD95?
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values which represent the anesthetic dose that inhbits somatic evidence of light anesthesia in 95% of subjects in response to skin incision
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what is the MAC-BAR50 for sevo in 66% N2O is?
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2.2
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what are the traditional signs of anesthetic depth the anesthesia provider must also use?
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-changes in HR, BP
-pupillary size -sweating |
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pupillary changes can be affectd by what two agents over time?
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1-opiods (miosis)
2-volatile agents (mydriasis) |
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the anesthesia provider is to estimate anesthetic depth bason on what collection of variables?
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-HR
-BP -synergistic and additive effects of anesthetic adjuvants -volume status -physiologic reserve -MAC -MAC-BAR -MAC intubation values |
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T or F MAC intubation is similar to MAC BAR in that its values exceed the anesthetic requirements for surgical skin incisions?
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True
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what are factors that reduce MAC?
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-increase in age
-hypothermia -administration of depressant meds -alpha-agonists -acute ETOH consumption -metabolic acidosis -hypoxemia -anemia -hypotension -hyponatremia -pregnancy |
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what are some medications that can reduce MAC?
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-N2O
-ketamine -verapamil -lidocaine -clonidine -alpha-methyldopa -reserpine -chronic dextroamphetamine use -lithium -levodopa |
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what are some factors that increase MAC?
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-decrease in age
-hyperthermia -hyperthyroidism -hypernatremia -chronic alcohol consumption -acute administration of dextramphetamine -MAOI's -cocaine, levodopa |
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what are factors that have no effect on MAC?
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-duration of anesthesia
-gender -redheaded females -hypocarbia and hypercarbia -metabolic alkalosis -HTN |
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what are some medications that have no effect on MAC?
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-propranolol
-isoproterolol -promethazine -naloxone -aminophyilline -neuromuscular blocking agents |
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how do volatile agents affect CMRO2?
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decrease in dose-dependent manner
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when vascular resistance is descreased what happens to CBF?
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CBF, CBV, and CSFP all increase
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the order of potency for increasing CBF varies and is affected by what?
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-the dose of volatile anesthetic
-administration of other drugs -rate of change in end-tidal concentration of agent |
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when does uncoupling occur?
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when decreases in CMRO2 are accompanied by increases in CBF
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what can produce an uncoupling effect?
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volatile anesthetics
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what agent reduces cerebrovascular tone significantly?
|
nitrous oxide
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how does N2O affect CMRO2?
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N2O increases CMRO2
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is N2O use in neurosurgical procedures acceptable?
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Yes-as long as provider recognizes that its vasodilatory effects might adversely affect surgical outcome in pts w/. reduced intracranial compliance
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what can be done to help attenuate the increase in CBF that accompanies the use of N2O?
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hyperventilation
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the normal physiologic response of the cerebral vasculature to CO2 is to ________in the presence of hypocapnia?
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vasoconstrict
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the normal physiologic response of the cerebral vasculature to CO2 is to ________in the presence of hypercarbia?
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vasodilate
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the usual goal for pts in which a reduction in intracranial volume is desired is a PaCO2 of ___-____mmHg w/ duration of effectiveness being no more than ___-___hours?
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30-35 mmHg
4-6 hrs |
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what are some variables that can affect the differences of volatile agents responsiveness to CO2?
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-the type of surgical procedure
-associated pathophysiology -presence of coexisting disease(s) |
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what volatile agent is less vasoactive and recommended as good alternative to propofol in pts w/ normal intracranial pressure?
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sevo
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increases in CBF produced by iso, des and sevo can be prevented by what measures?
|
-hyperventilation
-using concentrations less than 1.5 MAC |
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what are some possible etiologic factors of pediatric emergence delirium?
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-rapid emergence
-intrinsic characteristics of an aneshetic -post-op pain -surgery type -age -preoperative anxiety -child temperament -adjunct medication |
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for those procedures requiring monitoring of integrity of the spinal cord or mapping of cortical regions of the brain inh agents can skew what?
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-coritcal somatosensory
-motor -brainstem -auditory -and visual evoked potentials |
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what evoked potentials are most sensitive to the inh. agents?
|
visual evoked potentials
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what evoked potentials are the least sensitive to the inh. agents?
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brainstem evoked potentials most resistant
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how do inh agents and N2O affect evoked potentials?
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dose-dependent reduction in evoked potentials
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what are two evoked potential variables commonly assessed?
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latency
amplitude |
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what can an increase in latency or decrease in amplitude of evoked potentials reflect?
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- ischemia or be secondary to volatile agent
|
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what is latency?
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the time between the initiation of a peripheral stimulus and onset of the evoked potential recorded by scalp electrodes
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what volatile agent has been shown to interfere w/ recording of cortical somatosensory evoked potentials at light planes of anesthesia (0.5 MAC w/ N2O)?
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iso
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what levels do des and sevo affect coritical somatosensory evoked potentials?
|
1.5 MAC no N2O
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of iso, des, and sevo what agent produces the greatest reduction in cSSEP amplitude?
|
iso
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what is the effect on cSSEP latency of the three agents?
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no difference exists among the volatile anesthetics' effect on latency
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T or F the addition of N2O can produce a significant reduction in teh amplitude of cSSEP's?
|
True
|
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what agent can predispose pediatric and adult pts to epileptic activity?
|
sevo
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what kind of consequences can a delayed emergence from a neurosurgical procedure have for a pt?
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-makes it difficult to perform initial post-op neuro exam
-can add unnecessary therapeutic or diagnositc intervention and predispose pt to respiratory complications |
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what can you run for a TIVA on a neuro pt for rapid awakening?
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propofol and remifentanyl
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what two inh agents are associated with emergence agitation or delirium in children?
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sevo and des
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what are some preventive measures for emergence delirium?
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-reduce preop anxiety
-reduce postop pain -provide quiet stress-free environment -small doses of midazolam, fentanyl, clonidine, or dexmedetomidine -reunite child w/ parent post-op |
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what are some preop and intraop factors that can affect how inh agents alter hemodynamics?
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-ASA status
-coadministration of vasoactive drugs -opioids, barbiturates |
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how do inh agents affect MAP?
|
all decrease MAP
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how do inh agents affect CO and CI?
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decrease in dose-dependent manner
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how do des, iso and sevo decrease MAP?
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via a reduction in SVR
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which agent has least affect on SVR?
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sevo
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how does halothane decrease MAP?
|
direct myocardial depression versus a reduction in preload
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how does N2O affect SVR?
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N2O activiates sympathetic nervous system and increases SVR which can also lead to increase in CVP and arterial pressure
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in general N2O used in combination w/ inh agents _____SVR and helps support _____blood pressure?
|
increases, arterial
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What happens if N2O is used w/ opioids?
|
N2O augments cardiac depression instead of supporting it, N2O produces a direct negative inotropic effect
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what agent best supports CI?
|
Des
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what happens to CI and HR as MAC hours of anesthesia increase?
|
increase slightly
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at the cellular level how do iso, des, and sevo affect intracellular calcium concentrations??
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reduce intracellular calcium concentrations in cardiac and vascular smooth muscle
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what is the mechanism for the reduced intracellular free calcium?
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reducting in ca+ influx through the sarcolemma and a depression of depolarization activated Ca+ release from sarcoplasmic reticulum
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what are other reported cellular effects of volatile agents?
|
-augmentation and attenuation of endothelium derived relaxation factor
-inhibition of acteylcholine-induced vascular relaxation -attenuation of Na+-Ca+ exchange that leads to reduction in quantity of intracellular Ca+ |
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alterations in HR are result of what variables?
|
-antagonism of SA node
-automaticity -modulation of baroreceptor reflex activity -sympathetic nervous system activation via activation of tracheopulmonary and systemic receptors |
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what two agents increase the HR?
|
iso and des
|
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why can des's steep dose-response to HR potentially be problematic?
|
-diminishing the reliability to of HR as guide to anesthetic depth
-predisposing pts at risk for CAD to myocardial ischemia secondary to increased myocardial oxygen demand |
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what can be given as pretreatment five minutes before an increase in end-tidal des concentration?
|
fentanyl
|
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when is optimal use for fentanyl w/ des to keep HR down?
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during steady-state periods of anesthesia when actue adjustments of des are desired
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what other agent has been used to attenuate HR response but does not affect MAP and may be less desrable than fenatnyl?
|
esmolol
|
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what does coronary steal mean?
|
a reduction in perfusion of ischemic myocardium with simultaneaous improvement of blood flow to nonischemic tissue
|
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what two agents have been proven to produce a coronary steal with relevant concentrations?
|
des and iso
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an important qualifier to iso's ability to maldistribute coronary blood flow is presence of what?
|
hypotension
|
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reduced blood flow to ischemic myocardium can be reversed if normtension is reestablished withwhat?
|
phenylephrine administration
|
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If ECG monitoring demonstrates ST segment or Twave changes suggestive of myocardial ischemia in absence of abnormal hemodynamics what may be warranted?
|
a change in primary anesthetic technique
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what is anesthetic preconditioning (APC)?
|
a cascade of intracellular events that help protect the myocrdium from ischemic and reperfusion insult, potentially limiting infarct size
|
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what is the mechanism for APC?
|
-improving contractile function
-preventing the down-regulation of major sarcoplasmic reticulum Ca+ cyclic proteins (thereby reducing calcium overload in myocardial cells) |
|
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administration of volatile agents during myocardial reperfusion activates what group?
|
prosurvival kinsases called teh reperfusion injury salvage kinase (RISK)
|
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what do the prosurvival kinases produce?
|
potent cardioprotective effects
|
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what other factors have been identified with preconditioning?
|
-protein kinase C activation of Katp channel opening
-adenosine receptors -inhibitory G proteins |
|
|
sulfonylurea oral hyperglycemic drugs should be discontinued ___-___hours prior to elective surgery and why?
|
24-48, their ability to close Katp channels
|
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inh agents can be conducive to bradycardia and disturbances where to cause this?
|
disturbances in AV nodal conduction
|
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when myocardial fibers become ischemic or injured the volatile agents are prone to produce what?
|
reentrant excitation
|
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what is the oral and nasal submucosal ED50 dosage of epi for volatile agents?
|
- 2.11 +/- 0.15mcg/kg for halothane
- 6.72 +/- 0.66mcg/kg for iso |
|
|
what are variables that effect epi ED50 values?
|
-differences in systemic absorption
-route of administration -existing plasma catecholamine levels -preexisting atrial or ventricular dysrhythmias -previous administration of indx agents (thiopental, ketamine) |
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in ASA I or II pts fewest difficulties w/ dysrhythmias if submucosal epi dose remains ___mcg/kg or less, w/ ___-___MAC des, or ___mcg/kg or less w/ ___-___MAC sevo or iso?
|
7.0 mcg/kg, 1.0 -1.3 MAC des
5.0 mcg/kg, 1.0-1.3 MAC sevo or iso |
|
|
people who are on what antiarrythmic agent and are given GA can have significant dyshythmias intraop and post-op?
|
amiodarone
|
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|
amidarone and its metabolite are detectable in plasma for up to ____months after discontinuation of therapy?
|
9 mos
|
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|
in adults w/ normal PVR what happens to PVR when using N2O?
|
PVR is increased
|
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how do volatile agents affect pulmonary artery pressure?
|
decrease pulmonary artery pressure
|
|
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what happens if administer Des at 1.6 MAC to pulmonary artery pressure?
|
it increases
|
|
|
the pulmonary vasculature minimizes changes to alveolar-arterial oxygen tension gradient via what?
|
HPV-hypoxic pulmonary vasoconstriction
|
|
|
what agents attenuate the normal phsyiologic response to atelectasis or hypoxia?
|
halothane
iso N2O |
|
|
the volatile agents exert a dose dependent effect on the respiratory system primarily the _____?
|
tidal volume
|
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what is response to CO2 and TV when volatile agents are used?
|
decreased response to CO2 and TV reduces as concentrations of teh agents are increased
|
|
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what is the compensatory mechanism for the diminshed TV with volatile agents?
|
increased respiratory rate
|
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is the increase in RR in response to decreased TV sufficient enough to prevent elevations in arterial CO2 tension?
|
NO
|
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what variable helps to over-come the respiratory depressant effects of volatile agents?
|
surgical stimulation
|
|
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emergence from an anesthetic can be associated w/ what if Minute volume is not adequately supported?
|
hypercarbia
|
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what represents an increase in the apneic threshold?
|
hypercarbia
|
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patients should be closely monitored during emergence from an anesthetic to avoid what two things?
|
acidemia or
hypercarbia |
|
|
the smoothness of an inhalation induction is directly related to the ability of an agent to avoid what?
|
provoking an irritant response
|
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|
what 3 agents are considered standards by which other agents are measured b/c of low incidence of breath holding, coughing, secretions, and laryngospasm during inh. indxn?
|
halothane
N2O sevo |
|
|
volatile agents do what to airway smooth muscle and bronchioles?
|
relax airway smooth muscle and produce bronchodilation
|
|
|
what happens to autoregulation of renal circulation during administration of inh. agents?
|
it remain intact
|
|
|
reduction in systolic blood pressure are accomanied by what to renal vascular resistance?
|
decreases in renal vascular resistance
|
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|
compensatory reduction in renal vascular resistance can lead to what w/ regard to GFR? and what effect can this have?
|
decline in glomerular filtration rate
-intraoperative reduction in urinary output |
|
|
the potential for a volatile agent to produce renal damage is assessed by what?
|
to which it elevates creatinine, BUN, and serum inorganic Fluoride
|
|
|
what current agent affects renal integrity the least?
|
Des
|
|
|
what protein has been shown to be a specific marker for indicating the presence of tubular damage of any cause?
|
retinol-binding protein
|
|
|
current FDA guidelines recommend sevo be used w/ caution in pts w/ renal insuff. w/ Cr > ___mg/dL?
|
1.5
|
|
|
what 3 variables increase compound A content?
|
1-low fresh gas flows
2-high conc of sevo 3-drying of soda lime CO2 absorbant |
|
|
one way to eliminate compound A is to replace soda lime with what?
|
Amsorb
|
|
|
how do volatile agents affect liver?
|
decrease total hepatic blood flow
|
|
|
iso, sevo, and des have been shown to increase what?
|
hepatic artery blood flow
|
|
|
what factors can cause hepatocyte hypoxia?
|
-volatile agents
-surgical manipulation -enzyme induction |
|
|
what is one significant outcome of liver hypoxia?
|
increased reductive metabolism of halothane, which has been linked to halothane hepatitis
|
|
|
what are two clinical forms of halothane hepatitis?
|
1-mild hepatic reaction that occurs secondary to direct hepatic effect (low morbidity/mortality)
2-fulminant hepatic failure w/ high mortality rate (multiple anesthetic exposures precede its onset) |
|
|
what predominant P-450 isoform is responsible for the oxidation of halothane?
|
cytochrom P-450 2E1
|
|
|
what are some factors identified for development of halothane hepatitis?
|
-fatty liver infiltration
-having multiple anesthetics -isoniazed and ethanol use |
|
|
what is the only volatile agent that is not biodegraded to TFA-protein molecules?
|
sevo
|
|
|
N2O can lead to inactivation of Vit b12 component of methionine synthetase which can disrupt DNA synthesis and caution should be exercised in what types of patients?
|
-pregnant
-those who receive GA more than once a week -have problems w/ wound healing |
|
|
all volatile agents produce a dose-dependent relaxation of what as well as potentiation of what?
|
skeletal muscle, potentiation of the effects of depolarizing and nondepolarizing muscle relaxants
|
|
|
what is dose of IV dantrolene that should be given if MH occurs?
|
2.5mg/kg repeated every 5 min up to 10mg/kg
|
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|
is it acceptable to use N2O in pt's susceptible to MH?
|
yes
|
