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Neuro Path (2nd Year) > Anesthesia > Flashcards

Anesthesia Flashcards

1
Q

5 primary effects of anestheisa

A 
unconsciousness
amnesia
analgesia
inhibition of automatic reflexes
skeletal muscle relaxation
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2
Q

Remifentanil is what class of drug

A

remifentanil

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3
Q

thiopental is what class of drug

A

thiopental

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4
Q

stages of anesthesia

A

induction, maintenance, recovery

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5
Q

what is induction

A

time from initiation of anesthesia until desired concentration is achieved in brain

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6
Q

What drug and what route used for induction

A

propofol IV

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7
Q

when are opioids administered during anesthesia (ie what stage)

A

maintenance

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8
Q

which opioid commonly administered during anesthesia

A

fentanyl

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9
Q

what route for maintenance of anesthesia

A

inhaled and IV

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10
Q

Excitatory ion channel targets for general anesthesia

A

ACh (nic and mus receptors), Glutamate, serotonin

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11
Q

what is lipid theory?

A

correlate anesthetic potency w/ lipid solubility

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12
Q

2 factors influencing inhaled anesthetics effiacy

A

concentration of agent in inspired gas and gas pressure, alveolar ventilation

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13
Q

time to onset and time to recovery relationhipo to solubility

A

inversely related ie lower solubility= faster onset and recovery

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14
Q

least soluble inhaled anesthetic

A

NO

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15
Q

Most soluble anesthetic

A

halothane

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16
Q

sevoflurane solubility range

A

low

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17
Q

isoflurane solubility range

A

mid range

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18
Q

alveolar-venous partial pressure pressure effect on anesthesia

A

larger the difference, the more anesthetic will be taken up by tissues and venous blood will have lower concentration than arterial blood which means that it will take to achieve equilibrium between general circulation and the brain

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19
Q

which inhaled anesthetics is metabolized the most by the liver

A

halothane

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20
Q

Minimal alveolar concentration (MAC) measures what?

A

potency

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21
Q

which inhaled anesthetic is more potent

A

halothane

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22
Q

which inhaled anesthetic is least potent

A

NO

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23
Q

rate anesthetics according to potency

A

Halothane 0.74%
isoflurane

sevoflurane
NO

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24
Q

what exactly does MAC measure

A

minimal alveolar concentration required to prevent responses to surgical incision in 50% of cases

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25
Q

Stage 1 of anesthesia

A

analgesia from conventional to drowsy, count to 10 if you can (propofol is so fast that ususally skip this phase now)

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26
Q

Stage 2 of anesthesia

A

excitement: delirium and possible combative behavior, increased irregular BP and respiration rate. Propofol reduces/eliminates this stage

27
Q

Stage 3

A

surgical anesthesia: loss of muscular tone and reflexes due to further CNS depression. breathing is regular and skeletal muscles relaxed. Need careful monitoring to ensure CNS is not depressed further

28
Q

Stage 4

A

death if no support

29
Q

inhaled anesthetics effect on brain

A

balance b/w decreased metabolic activityand the fact that Volatile anesthetics also cause cerebral vasodilation

30
Q

inhaled anesthetics effect on heart

A

halogenated= decreased contractility and MAP

31
Q

which anesthetics maintain CO as well as reduce preload and afterload?

A

isoflurane, desflurane, and sevoflurane

32
Q

inhaled anesthetics effect on lungs

A

rapid shallow breathing and respiratory depressants

33
Q

inhaled anesthetics effect uterus

A

halogenated= potent uterine muscle relaxants

34
Q

What are 3 compartments

A

blood, brain and viscera, and muscle/fat

35
Q

bevocaine and cocaine is what class and subclass

A

local anesthetic, ester, surface action

36
Q

procaine is what class and subclass

A

ester, short acting,

37
Q

tetracaine is what class and subclass

A

ester , long acting

38
Q

lidocaine is what class and subclass

A

amide, medium acting

39
Q

bupivocaine is what class and subclass

A

amide , long acting

40
Q

local anesthetics are weak acids/ bases

A

weak bases

41
Q

increased K levels increase/decrease efficacy of local anesthetics

A

increase

42
Q

increased Ca levels increase/decrease efficacy of local anesthetics

A

decrease

43
Q

how are esterLA metabolized

A

pseudocholinesterases

44
Q

how are amide LA metabolzed

A

liver, p450

45
Q

procaine half lfie

A

1-2 mintues

46
Q

lidocain half life

A

1.5 hours

47
Q

LA mechanism

A

block voltage dependent Na channels

48
Q

is ionized/ non-ionized form better at interactin w/ receptor

A

non ionized

49
Q

LA work better on narrower or thickier nerve fibers?

A

narrower

50
Q

LA work better on heavily myelinated fibers or non/lighlty myelinated

A

heavily

51
Q

LA work better on rapidly or slow firing nerves

A

rapid

52
Q

LA work better on peripheral nerves or nerve bundle

A

peripheral

53
Q

toxicity of LA

A
  • CNS tox can cause convulsion which are treated w/ BZDs or barbs
  • Cardiovascular depression which are treated w/ lipid rescue therapy
54
Q

Isoflurane mechanism

A

potentites GABA and opens k channels

55
Q

Isoflurane blood: gas partition coefficient

A

1.4

56
Q

isoflurane MaC

A

1.4%

57
Q

sevoflurane blood:gas partition coeffiecit

A

0.69

58
Q

sevoflurane MAC

A

2%

59
Q

NO blood:gas partition coefficient

A

0.47

60
Q

Ketolorac only used less than 5 days because..

A

GI toxicity

61
Q

propofol mechanism

A

potentiates GABAa receptor activity

62
Q

major propofol inteteraction

A

allergies- eggs

63
Q

Etomidate pahrm calss

A

IV general anesthetic and adjunct to general; hypnotic w/ no analgesic

64
Q

Bupivacaine interactions

A

MAO-Is, ergot alkaloids w/ epinephrine

Neuro Path (2nd Year) (6 decks)

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