Volatile Anesthetic Agents Flashcards

1
Q

Meyer-Overton correlation theory

A
  • chemically different substances that are soluble in fat
  • potency of VA depends on affinity for water & fat
  • fat:water partition coefficient
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2
Q

The concept of MAC

A
  • analogous to plasma ED50
  • universal measure of potency
  • non-paralyzed pt do not respond to surg stimuli in 50% of pt
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3
Q

Protein centered theory

A
  • signaling proteins (channels/receptors) are molecular site of action
  • bind directly to amphiphilic cavity in proteins
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4
Q

molecular target- ligand gated ion channel

A
  • potentiates/enhance synaptic transmission of GABA/glycine
  • extrasynapically by enhancing GABA receptors/leak channels
  • presynaptically by enhancing basal GABA release
  • inhibits ACh/glutamate
  • presynaptically reduce glutamate release
  • postsynaptically by inhibiting glutamate receptors
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5
Q

molecular target- VG ion channel

A

Na+, Ca++, K+ channels

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6
Q

molecular target- intracellular signaling mechanisms

A
  • G-protein coupled receptors
  • protein phosphorylation
  • gene expression
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7
Q

neuronal excitability

A
  • IA hyperpolarize neurons

- determined by resting membrane potential, threshold potential, input resistance

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8
Q

presynaptic effects

A

-IA alter transmitter release

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9
Q

postsynaptic effects

A

-IA alter NT responses

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10
Q

Immobilizing site of action

A

spinal cord

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11
Q

sedation, hypnosis, & amnesia site of action

A

supra-spinal mechanisms

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12
Q

Immobility

A
SC NMDA receptors
requires high (2.5-4x MAC) to achieve
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13
Q

unconscious

A
  • hyperpolarization of thalamic sites via “dimmer switch” effect
  • interrupts synchronicity b/t neural networks
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14
Q

Desired effects of IA

A
  • immobility
  • unconsciousness
  • learning/memory
  • sedation
  • neuroprotection
  • CV/respiratory
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15
Q

learning/memory

A

hippocampus/amygdala dependent

0.3-0.4 MAC amnesia

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16
Q

sedation

A

potent VA- stimulate GABA

N2O- antagonize NMDA

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17
Q

neuroprotection

A
  • prevents apoptosis

- decrease CMRO2 via increase inhibitory & decrease excitatory transmission

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18
Q

neurotoxicity

A

irreversible cell damage by N2O??

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19
Q

CV/respiratory

A
  • dose dependent myocardial depression & hypotension d/t decrease Ca++ availability/sensitivity
  • respiration depression via central depression -> decrease Tv, increase RR, increase EtCO2
20
Q

VA fluorination

A
  1. reduce toxicity d/t metabolism
  2. eliminate flammability
  3. increase speed of induction/recovery
21
Q

pulmonary effects- TV

A

-decrease TV -> inadequate increase RR -> increase EtCO2

22
Q

pulmonary effects- irritant receptors

A
  • increase laryngeal irritant receptors

- decrease pulmonary irritant receptors

23
Q

pulmonary effects- FRC

A
  • loss of intercostals
  • altered resp pattern
  • cephalad movement of diaphragm
  • altered thoracic blood volume
24
Q

pulmonary effects- smooth muscle

A

bronchodilation via direct depression of sm. musc contractility

  • bronchial epithelium/sm musc cells
  • indirect inhibition of reflex neural pathways
25
Q

pulmonary effects- PVR

A
  • resistance is lowest at lung vol equivalent to FRC

- increase PVR -> increase PAP -> interstitial fluid transudation

26
Q

increase PVR

A
  • PEEP
  • alveolar hypoxia
  • alveolar hypercapnia
  • critical closing pressure
27
Q

hypoxic pulmonary vasoconstriction

A
  • altered with VA
  • all VA vasodilate the pulmonary vascular bed
  • all VA cause a dose dependent myocardial depression
28
Q

central control of respiration

A
  • located near ventrolateral medulla/brainstem
  • respond to changes in [H+] in CSF
  • affected by resp alterations in arterial CO2 tension
29
Q

peripheral control of respiration

A
  • located in carotid bodies

- responds to changes in arterial CO2 tension, pH, and arterial O2 tension

30
Q

post-op effects on breathing

A

-dose dependent depression of ventilatory response to hypercapnia
<0.2 MAC- depress peripheral chemoreflex loop and inhibit ventilatory response to hypercapnia
0.1 MAC attenuate ventilatory response to hypoxia in dose-dependent manner
-diffusion hypoxia

31
Q

CV effects- contractility

A

dose dependent depression of myocardial contractility d/t intracellular Ca++ homeostasis, inhibition of Na+Ca++ exchange, LB diastolic dysfunction, LV after load effects, LA myocardial depression

32
Q

CV effects- SBP

A

dose dependent decrease SBP

33
Q

CV effects- SVR

A

dose dependent decrease in SVR

34
Q

CV effects- chronotropic

A

negative chronotropic effects d/t SA node depression and blunt baroreceptor reflex -> bradycardia, AV conduction abnormalities

35
Q

CV effects- coronary

A

vitro- vasodilation

vivo- vasoconstriction- reduce MVO2 via decrease HR, preload, afterload, inotropic state

36
Q

neuro effects- CBF

A

increase CBF d/t decrease cerebrovascular resistance -> increase ICP

37
Q

neuro effects- CMRO2

A

decrease CMRO2- neuro protective

38
Q

neuro effects- SSEP/MEPs

A

depress SSEP/MEP monitoring

39
Q

NM effects

A

centrally mediated muscle relaxant properties- synergistic effects with IV muscle relaxants

40
Q

hepatic effects

A

liver receives blood from hepatic artery & portal vein

decrease hepatic blood flow

41
Q

hepatic metabolism

A

phase 1 rxn (CYP450_
phase 2 rxn (uridine 5’ diphosphate transferase enzymes)
-affected by age, gender, disease, genetics

42
Q

hepatic metabolite

A

trifluoroacetylated protein -> liver injury in “susceptible” patients

43
Q

renal effects

A

decrease blood flow, GFR, and UOP

44
Q

OB effects

A

decrease uterine blood flow and uterine contractility

45
Q

N2O concentration effect

A

N2O is taken up fast -> leaves space in FRC for fresh gas saturated with VA inflow to occur -> concentration of VA in FRC increases faster

46
Q

N2O second gas effect

A

second gas (VA) rises to a higher concentration more quickly d/t N2O concentration effect

47
Q

N2O diffusion hypoxia

A

N2O washes out of tissues fast -> as N2O rushes into lungs it drags other gases with it -> displaces O2