Volatile - Concepts Flashcards
(98 cards)
1
Q
Concentration that will produce absence of movement in 99% of people in response to a noxious stimulus
A
1.3 MAC
2
Q
B:G N2O
A
0.46
3
Q
B:G desflurane
A
0.42
4
Q
B:G sevoflurane
A
0.69
5
Q
B:G Isoflurane
A
1.4
6
Q
B:G enflurane
A
1.8
7
Q
B:G halothane
A
2.4
8
Q
B:G Diethyl ether
A
12
9
Q
lower hematocrit will alter
A
the B:G coefficient
10
Q
With a HCT of 21 (vs 43)
A
the B:G coefficient will be 20% less.
Effectively having a LOWER solubility and therefore increased induction
11
Q
the faster FA = FI
A
the faster the onset
12
Q
PAlveoli is used to estimate
A
aka Fa is used to estimate
depth of anesthesia
recovery from anesthesia
anesthesia potency or MAC
13
Q
PAlveoli is determined by (4)
A
- Pi
- Alveolar ventilation
- Breathing Circuit
- FRC
14
Q
The higher the alveolar ventilation
A
the faster the onset
15
Q
first knee of Fa/Fi =
A
saturation of vessel rich group
16
Q
second knee of Fa/Fi =
A
saturation of muscle group
17
Q
terminal climb after second knee of Fa/Fi =
A
progressing to saturation of vessel poor group, i.e. fat. Would take a very long amount of time
18
Q
terminal climb after second knee of Fa/Fi =
A
progressing to saturation of vessel poor group, i.e. fat. Would take a very long amount of time
19
Q
uptake of a volatile agent is determined by
A
- solubility of agent
- cardiac output
- A-v [alveolar to venous] pressure differences
20
Q
The higher the FRC
A
the SLOWER the induction
21
Q
induction is faster in
A
children , smaller FRC
22
Q
To achieve faster induction with agents that are more soluble
A
we over pressure.
high initial input (Fi) offsets impact (duration) of uptake
23
Q
Increased Cardiac output =
A
INCREASED uptake, effect of increasing solubility, net = slower induction
24
Q
Decreased CO =
A
decreased uptake, effect of decreasing solubility = faster induction
25
Pulmonary blood flow =
CO
26
Agents more affected by CO are
soluble agents
27
vessel rich group reach equilibrium within
5-15 minutes
28
after induction, the FI should be decreased as
the VRG equilibrates and again as the MRG equilibrates
29
For maintenance, due to decrease in uptake over time
the FI should be decreased otherwise overdose
30
increasing ventilation is a more effective strategy with
a more soluble agent , doesn't make much of a difference for lower solubility drugs
31
negative feedback in the spontaneously breathing ventilating patient
in spontaneously ventilating patient, as the % inspired increase, ventilation is depressed (r/t drug effect) and the Fa/Fi will decrease (r/t decrease in alveolar ventilation)
this is protective against overdose
32
if you keep someone spontaneously breathing on volatile agents, the risk for overdose is
low
33
larger circuit volume will decrease
FA/FI slope will decrease , overcome with higher flow rates
34
with conditions of higher metabolism, you may have
increased minute ventilation and also increased cardiac output . This results in net Fa/Fi increase but only slightly
35
right to left shunt is more consequential for
agents with LOW solubility
36
V/Q mismatches will
generally SLOW induction, more pronounced in less soluble agents
37
the concentration effect states that the higher the PI
the more quickly the PA will approach the PI
38
N2O to nitrogen
N2O is 34x more soluble
39
blood gas solubility of nitrogen
b:g 0.014
40
emergency and recovery depends on [4]
1. length of anesthesia
2. depth of anesthesia
3. solubility of the agent
4. MAC awake
41
sevoflurane's biotransformation does result in
inorganic fluoride ions. Theoretical risk for fluoride induced high output renal failure.
[[unresponsive to ADH]]
42
Soda lime + sevo =
compound A
accelerated when desiccated
43
N2O irreversibly binds to
B12, which inhibits methionine synthase and thymidylate synthesis
44
potential effects of prolonged exposure to N2O and B12
```
megaloblastic anemia [bone marrow suppression]
neuropathy
immunocompromise
impaired DNA synthesis
concern for teratogenicity?
possible spontaneous abortion
homocysteine accumulation
```
previous history of alcoholism, pernicious anemia, strict vegan diet make these more likely
45
amnesia and loss of consciousness occur at
LOWER MACs also these are SUPRASPINAL
46
MAC awake =
alveolar concentration at which a patient opens his or her eyes,
47
MAC bar =
alveolar concentration at which autonomic responses are blunted (1.5 MAC)
48
HYPONATREMIA and MAC
hyponatremia will decrease MAC
49
Older age and MAC
6% reduction in MAC for every decade after 40
50
Hyperkalemia and MAC
no effect on MAC -
hyperkalemia, hypokalemia
hypermagnesemia, hypomagnesemia
51
Hyperthermia and MAC
MAC will INCREASE.
52
Hypothermia and MAC
MAC will DECREASE
53
In red heads, MAC is generally
increased by 19%
"presumably due to mutations in the melanocyte stimulating hormone receptor and an increased production of pheomelanin"
54
Meyer-Overton Rule
Meyer-overton rule states that lipid solubility is directly proportional to the potency of an inhaled anesthetic .
or, the greater the lipid solubility the lower the MAC value. [the greater the potency]
Implies the depth of anesthesia is determined by the number of anesthetic molecules that are dissolved in the brain and not necessarily the particular anesthetic agent that is used.
55
unitary hypothesis
states that all anesthetics share a similar mechanism of action, but each may work at a different site.
56
General rule, volatile anesthetics have the following effects on their target receptors
stimulate inhibitory pathways [GABA, GLYCINE, K channels]
Inhibit stimulatory pathways [NMDA, Nicotinic, sodium, dendritic spine function and motility ]
57
In the brain, the most important site of volatile anesthetic action is the
GABA A receptor
spine -> glycine receptor
NMDA receptor
Na+ channel inhibition.
58
Immobility is not due to GABA a in the spinal cord
ventral horn of spinal cord, glycine
59
N2O + opioid =
can cause myocardial depression
60
current theory on anesthetics
current potential sites of actions are modulating proteins:
1. pre-synaptic voltaged gated sodium channels
2. 2-pore potassium channels [trek + task}
3. Inotropic and metabotropic receptors
either inhibit stimulatory or stimulate inhibitory
61
stage 1 of anesthesia
"analgesia or induction stage"
dizziness, a sense of unreality, and lessening sensitivity to touch and pain
Sense of hearing is INCREASED and responses to noises are INTENSIFIED
62
stage 2 of anesthesia
is the stage of excitement. Vital signs show evidence of physiological stimulation, pt may respond violently to very little stimulation, MOST susceptible to laryngospasm
63
stage 3 of anesthesia
Surgical anesthesia! Here we have 4 plans.
| Each successive plane is achieved by increasing the concentrations of the anesthetic agent
64
stage 4 of anesthesia
OVERDOSE! toxic or danger stage.
65
fourth plane of anesthesia
demonstrated by cardiovascular impairment that results fro diaphragmatic paralysis, if this plane is not corrected immediately, stage 4 quickly ensues
66
thymol is used in
Halothane as a preservative. Can cause sticky turnstiles or temperature compensating valves
67
risk factors for halothane hepatitis
obese, female, multiple exposures to halothane
68
classic presentation of halothane hepatitis
fever, anorexia, nausea, chills ,myalgia, rash, arthralgia, eosinophilia followed by jaundice 3-6 days later
69
volatile not recommended during cardiac ablation
ISOFLURANE
it increases the refractoriness of accessory pathways and AV conduction so can interfere with interpretation of electrophysiological studies
70
Isoflurane decrease in BP is because of
decrease in SVR
71
CO in isoflurane is
maintained by HR, because partial preservation of baroreceptors
72
tachypnea less pronounced at 1 MAC with
isoflurane
73
electrically silent EEG at 2MAC with
isoflurane
74
vasodilator of hepatic circulation
isoflurane
75
isoflurane C/i
MH or maybe* extremely low CO -> r/t decrease in SVR
76
Desflurane baroreceptors
INTACT
77
isoflurane baroreceptors
partial preservation
78
Decrease BP with desflurane is r/t
Decreased SVR
79
When you give a higher concentration of desflurane [overpressure]
you will have a sympathomimetic effect, rapid transient increase in transient HR, blood pressure, catecholamine levels,
80
desflurane C/I
malignant hyperthermia
| kind of asthmatics
81
CO not as well maintained with
sevoflurane
82
Only common agent that does not increase R atrial pressure / CVP
sevoflurane
83
best choice of a volatile for asthmatics is
sevoflurane because minimal airway irritation
84
hepatic blood flow with sevo
is maintained
85
sevoflurane C/I
MH and relative: renal impairment
86
enflurane and hypoxic drive
ABOLISHED. Marked respiratory depression at 1 MAC
87
Depresses mucociliary function
enflurance
88
Increased secretion of CSF but decreased outflow
Enflurane
89
EEG changes with enflurane are exacerbated by
high concentrations, hypocapnia, and repetitive auditory stim
90
Hyperventilation with enflurane
IS NOT RECOMMENDED, can exacerbate EEG changes and lead to seizures
91
enflurane C/I
avoid in patients with pre-existing kidney disease or impairment
avoid in patients with known or suspected seizure disorder
avoid in patients with increased ICP
MH
92
OSHA and waste gas
no worked should be exposed to more than
2 ppm halogenated agents in o2
0.55 halogenated if used with n2o
25 ppm n2O
93
no significant increase in MAC until
>1.5 MAC
94
increase risk of arrthymias with epi
Halothane
enflurane
N2O
95
aminophylline is linked to serious
ventricular dysrthymias when used with halothane
96
most potent MH trigger
halothane
97
things that increase MAC (6)
```
1. chronic ETOH
2 .Increased CNS neurotransmitters
3. HYPERnatremia
4. Increased in infants 1 -6 months
5. HYPERthermia
6. Red hair
```
98
factors that decrease MAC (16)
1. acute ETOH
2. IV anesthetics
3. N2O
4. Opioids
5. HYPONATREMIA
6. Older age
7. Prematurity
8. HYPOthermia
9. HYPOtensino
10. HYPOxia
11. Anemia
12. Cardipulmonary by pass
13. Metabolic Acidosis
14. HYPOosmolarity
15. Pregnancy through 72 hours post party
16. PaCO2 >95 mmHg
