Volatile Anesthetic Agents Flashcards
(47 cards)
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
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
3
Q
Protein centered theory
A
- signaling proteins (channels/receptors) are molecular site of action
- bind directly to amphiphilic cavity in proteins
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
5
Q
molecular target- VG ion channel
A
Na+, Ca++, K+ channels
6
Q
molecular target- intracellular signaling mechanisms
A
- G-protein coupled receptors
- protein phosphorylation
- gene expression
7
Q
neuronal excitability
A
- IA hyperpolarize neurons
- determined by resting membrane potential, threshold potential, input resistance
8
Q
presynaptic effects
A
-IA alter transmitter release
9
Q
postsynaptic effects
A
-IA alter NT responses
10
Q
Immobilizing site of action
A
spinal cord
11
Q
sedation, hypnosis, & amnesia site of action
A
supra-spinal mechanisms
12
Q
Immobility
A
SC NMDA receptors requires high (2.5-4x MAC) to achieve
13
Q
unconscious
A
- hyperpolarization of thalamic sites via “dimmer switch” effect
- interrupts synchronicity b/t neural networks
14
Q
Desired effects of IA
A
- immobility
- unconsciousness
- learning/memory
- sedation
- neuroprotection
- CV/respiratory
15
Q
learning/memory
A
hippocampus/amygdala dependent
0.3-0.4 MAC amnesia
16
Q
sedation
A
potent VA- stimulate GABA
N2O- antagonize NMDA
17
Q
neuroprotection
A
- prevents apoptosis
- decrease CMRO2 via increase inhibitory & decrease excitatory transmission
18
Q
neurotoxicity
A
irreversible cell damage by N2O??
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
- reduce toxicity d/t metabolism
- eliminate flammability
- 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
pulmonary effects- PVR
- resistance is lowest at lung vol equivalent to FRC
| - increase PVR -> increase PAP -> interstitial fluid transudation
26
increase PVR
- PEEP
- alveolar hypoxia
- alveolar hypercapnia
- critical closing pressure
27
hypoxic pulmonary vasoconstriction
- altered with VA
- all VA vasodilate the pulmonary vascular bed
- all VA cause a dose dependent myocardial depression
28
central control of respiration
- located near ventrolateral medulla/brainstem
- respond to changes in [H+] in CSF
- affected by resp alterations in arterial CO2 tension
29
peripheral control of respiration
- located in carotid bodies
| - responds to changes in arterial CO2 tension, pH, and arterial O2 tension
30
post-op effects on breathing
-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
CV effects- contractility
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
CV effects- SBP
dose dependent decrease SBP
33
CV effects- SVR
dose dependent decrease in SVR
34
CV effects- chronotropic
negative chronotropic effects d/t SA node depression and blunt baroreceptor reflex -> bradycardia, AV conduction abnormalities
35
CV effects- coronary
vitro- vasodilation
| vivo- vasoconstriction- reduce MVO2 via decrease HR, preload, afterload, inotropic state
36
neuro effects- CBF
increase CBF d/t decrease cerebrovascular resistance -> increase ICP
37
neuro effects- CMRO2
decrease CMRO2- neuro protective
38
neuro effects- SSEP/MEPs
depress SSEP/MEP monitoring
39
NM effects
centrally mediated muscle relaxant properties- synergistic effects with IV muscle relaxants
40
hepatic effects
liver receives blood from hepatic artery & portal vein
| decrease hepatic blood flow
41
hepatic metabolism
phase 1 rxn (CYP450_
phase 2 rxn (uridine 5' diphosphate transferase enzymes)
-affected by age, gender, disease, genetics
42
hepatic metabolite
trifluoroacetylated protein -> liver injury in "susceptible" patients
43
renal effects
decrease blood flow, GFR, and UOP
44
OB effects
decrease uterine blood flow and uterine contractility
45
N2O concentration effect
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
N2O second gas effect
second gas (VA) rises to a higher concentration more quickly d/t N2O concentration effect
47
N2O diffusion hypoxia
N2O washes out of tissues fast -> as N2O rushes into lungs it drags other gases with it -> displaces O2
