Unit 4 - Inhaled Anesthetics Flashcards
1
Q
3 groups of inhaled anesthetics
A
ethers alkanes gases
2
Q
inhaled anesthetics - ethers
A
Desflurane
Isoflurane
Sevoflurane
Enflurane
Methoxyflurane
Ether
3
Q
inhaled anesthetics - alkanes
A
Halothane
Chloroform
4
Q
inhaled anesthetics - gases
A
Nitrous oxide
Cyclopropane
Xenon
5
Q
relationship between fluorination and potency
A
tends to reduce potency
6
Q
type & number of halogens in isoflurane
A
5 fluorine atoms
1 chlorine atom
7
Q
type & number of halogens in desflurane
A
6 fluorine atoms (fully fluorinated)
8
Q
type & number of halogens in sevoflurane
A
7 fluorine atoms
9
Q
inhaled anesthetics that have a chiral carbon
A
desflurane
isoflurane
10
Q
what is vapor pressure
A
pressure exerted by a vapor in equilibrium with its liquid or solid phase inside a closed container
11
Q
relationship between vapor pressure and temperature
A
directly proportional
12
Q
what is boiling point
A
vapor pressure = atmospheric pressure
13
Q
what is evaporation
A
process where compound transitions from liquid to gas at temp below its boiling point
vapor pressure < atmospheric pressure
14
Q
relationship between atmospheric pressure and boiling point
A
- ↑ atmospheric pressure = ↑ boiling point (ex. Hyperbaric O2 chamber)
- ↓ atmospheric pressure = ↓ boiling point (high altitude)
15
Q
what is partial pressure
A
fractional amount of pressure a single gas exerts within a gas mixture
16
Q
what is Dalton’s law of partial pressures
A
total gas pressure in a container is equal to the sum of the partial pressures exerted by each gas
17
Q
what determines the depth of anesthesia
A
partial pressure of anesthetic agent in the brain
NOT the volumes percent (set on vaporizer dial)
18
Q
partial pressure of 6% Desflurane at sea level vs. in Denver (1 mile above sea level)
A
sea level = 45.6 mmHg
Denver = 37.2 mmHg
19
Q
inhaled anesthetics that can become unstable in dessicated soda lime
what can they produce
A
desflurane
isoflurane
can produce carbon monoxide (des > iso)
20
Q
vapor pressure of sevo
A
157 mmHg
21
Q
vapor pressure of des
A
669 mmHg
22
Q
vapor pressure of iso
A
238 mmHg
23
Q
vapor pressure of N2O
A
38,770 mmHg
24
Q
boiling point of des
A
22 dec C
25
molecular weight of sevo
200 g
26
molecular weight of des
168 g
27
molecular weight of iso
184 g
28
molecular weight of N2O
44 g
29
inhaled anesthetic that is unstable in hydrated CO2 absorbent
sevo
30
inhaled anesthetic that is stable in dehydrated CO2 absorber
N2O
31
what is solubility of an anesthetic agent
ability of anesthetic agent to dissolve in blood & tissues
32
which is more soluble in a hydrophilic solvent - polar or nonpolar solute?
polar
33
what describes the relative solubility of a solute in 2 different solvents
partition coefficient
34
describes relative solubility of an inhalation anesthetic in blood vs. in alveolar gas when partial pressures between compartments are equal
blood:gas partition coefficient
35
how is b:g partition coefficient calculated
anesthetic dissolved in blood / anesthetic inside alveolus
36
anesthetic implications of a low b:g
faster onset, faster speed of emergence
37
anesthetic implications of a higher b:g
slower onset, slower speed of emergence,
38
b:g of sevo
0.65
39
b:g of des
0.42
40
b:g of iso
1.46
41
b:g of N2O
0.46
42
what is FA/FI
* Concentration of agent inside alveoli is proportional to concentration inside blood, which is proportional to anesthetic inside brain
* Alveolar partial pressure ~ blood partial pressure ~ brain partial pressure
43
what is FA?
partial pressure of anesthetic inside the alveoli (surrogate for measurement of anesthetic inside the brain)
Anesthetic washes into alveoli & establishes a partial pressure
44
what is FI
concentration of anesthetic exiting vaporizer
45
how are anesthesia gases transferred from machine to the patient's brain (4 steps)
1. machine to fresh gas
2. fresh gas to alveoli
3. alveoli to arterial blood
4. arterial blood to brain
46
what is speed of induction a function of?
solubility
47
opposes buildup of anesthetic partial pressure in alveoli
continuous uptake of agent into blood
48
3 factors that have the most significant impact on anesthetic uptake into the blood (determinants of removal from alveoli)
1. b:g
2. CO
3. partial pressure difference between alveolar gas and mixed venous gas
49
how does low solubilty affect speed of induction
↓ uptake into blood = ↑ rate of rise = faster equilibration of FA/FI = **faster onset**
50
how does high solubility affect speed of induction
↑ uptake in blood = ↓ rate of rise = slower equilibration of FA/FI = **slower onset**
51
what does the FA/FI curve show us?
the speed at which alveolar partial pressure equilibrates with partial pressure leaving the vaporizer
52
fastest to slowest rate of rise of FA/FI
N2O \> des \> sevo \> iso \> halothane
53
6 determinants of gas delivery to alveoli
1. setting on vaporizer
2. FGF
3. time constant of delivery system
4. anatomic dead space
5. alveolar ventilation
6. FRC
54
3 determinants of tissue uptake of gas
1. tissue:blood solubility
2. tissue blood flow
3. partial pressure difference between arterial blood and tissue
55
what must happen for FA/FI to increase
there must be greater wash in or reduced uptake
56
what must happen for FA/FI to decrease
there must be either a reduced wash in or an increased uptake
57
5 factors that increase wash in and therefore increase FA/FI
* high FGF
* high alveolar ventilation
* low FRC
* low time constant
* low anatomic dead space
58
3 factors that decrease uptake and therefore increase FA/FI
1. low solubility
2. low CO
3. low Pa-Pv difference
59
5 factors that decrease wash in and therefore decrease FA/FI
1. low FGF
2. low alveolar ventilation
3. high FRC
4. high time constant
5. high anatomic dead space
60
3 factors that increase uptake and therefore decrease FA/FI
1. high solubility
2. high CO
3. high Pa-Pv difference
61
body mass for VRG, muscle, fat, and vessel-poor groups
* VRG = 10%
* muscle = 50%
* fat = 20%
* vessel poor = 20%
62
CO received by VRG, muscle, fat, and vessel-poor groups
* VRG = 75% CO
* muscle = 20%
* fat = 5%
* vessel poor = \< 1%
63
organs in vessel rich group
* brain
* heart
* kidneys
* liver
* endocrine glands
64
what is contained in the muscle group
skeletal muscle & skin
65
contained in vessel-poor group
bone, tendon, cartilage
66
what 3 things is the rate of anesthetic uptake into tissues dependent on?
1. tissue blood flow
2. solubility coefficient
3. arterial blood:tissue partial pressure gradient
67
first to equilibrate with FA
VRG - These organs receive most of the anesthetic agent during induction,
68
uptake of N2O by different body compartments
uptake minimal in all groups; partitions the same to all compartments
69
3 ways inhaled anesthetics are eliminated
1. Elimination from alveoli (primary mechanism)
2. Hepatic biotransformation (secondary)
3. Percutaneous loss (minimal, not clinically significant)
70
hepatic biotransformation of inhaled anesthetics
* N2O = 0.004%
* des = 0.02
* iso = 0.2
* sevo = 2-5
* halothane = 20
71
why does desflurane undergo a greater degree of elimination from the lungs than other anesthetics
the greater the hepatic metabolism, the less is eliminated from the lungs
72
how are halogenated agents metabolized
**P450 system**
primarily **CYP2E1**
73
primary mechanism for immune-mediated hepatic dysfunction
**Trifluoroacetic acid** (TFA)
74
metabolites of des & iso
inorganic fluoride ions
TFA
75
what is concentration effect
the higher the concentration of inhalation anesthetic delivered to alveolus (FA), the faster its onset of action (**overpressurizing**)
76
concentration effect is probably only clinically relevant for what inhaled anesthetic
N2O
77
which is more affected by concentration effect - higher or lower solubility gases
higher
78
N2O is ____ x more soluble in the blood than nitrogen
~34
79
why does N2O acheive the fastest rate of rise of FA/FI even though des is less soluble?
concentration effect
* When N2O introduced in lung, volume of N2O going from alveolus to pulmonary blood is much higher than amount of Nitrogen moving in opposite direction - **alveolus** **shrinks** - reduction in alveolar volume causes relative increase in FA
80
what is the augmented gas inflow effect
* Concentrating effect temporarily reduces alveolar volume
* Subsequent breath - concentrating effect causes increased inflow of tracheal gas containing anesthetic agent to replace lost alveolar volume
* **Increases alveolar ventilation, augments FA**
81
what is ventilation effect
describes how changes in alveolar ventilation can affect rate of rise of FA/FI
## Footnote
Greater alveolar ventilation = greater rate of rise of FA/FI
82
how does ventilation effect minimize risk of anesthetic overdose
In spontaneously ventilating patient, as anesthetic deepens alveolar ventilation decreases - reduced anesthetic input to alveolus
83
what is the 2nd gas effect
consequences of concentration effect when a second gas is co-administered
* When N2O and the second gas are introduced into alveolus, rapid uptake of N2O causes alveolus to temporarily shrink
* Reduction in alveolar volume and augmented tracheal inflow = relative increase in concentration of 2nd gas
* Partial pressure of alveolar O2 also increases when alveolus shrinks (transient)
* **End result**: alveolar concentration of the other gases is higher vs. admin alone
* More meaningful benefit with agents of higher b:g (iso \> seo \> des)
84
how does R-L shunt affect FA/FI
* causes some deoxygenated blood leaving R heart to bypass lungs
* Results in **reduced PaO2**
* Results in **slower rate of rise, reduction in partial pressure of anesthetic** in arterial blood
85
examples of conditions that cause a R-L shunt
ToF, PFO, Eisenmenger’s syndrome, tricuspid atresia, Ebstein’s anomaly
86
are gases of high or low solubility more affected by R-L shunt
why
lower
## Footnote
Less soluble agents undergo very little uptake by blood (effect of dilution unchecked)
87
inhaled anesthetic FA/FI curves affected the most and least by R-L shunt
most = des (lowest b:g)
least = iso (highest b:g)
88
how is IV induction affected by R-L shunt
faster induction (blood bypasses lungs and travels to brain faster)
89
what is MAC
concentration that prevents nociceptive withdrawal reflex following painful stimulus in 50% of population
90
potency of inhaled anesthetics from most to least
isoflurane \> sevoflurane \> desflurane \> N2O
higher MAC = lower potency
91
what is MAC-awake
alveolar concentration where a pt opens eyes (**~0.4-0.5 during induction,** as low as **~0.15** **during recovery**)
92
what is MAC-bar
alveolar concentration required to block ANS response following painful stimulus (**~1.5 MAC**)
93
movement is prevented in 95% of the population at what MAC
~ 1.3
94
awareness and recall generally assumed to be prevented at what MAC
0.4-0.5
95
what is MAC-hour
one times the MAC that prevents movement in response to a noxious stimulus in 50% of subjects administered for 1 hour
96
what is the essential triad of anesthetic action
amnesia, loss of consciousness, immobility
97
drugs that increase MAC
* Chronic ETOH
* Acute amphetamine intox
* Acute cocaine intox
* MAOIs
* Ephedrine
* Levodopa
98
how does sodium level affect MAC
hypernatremia = increased MAC
hyponatremia = decreased mAC
99
how does age affect MAC
* increased in infants 1-6 (sevo is the same for infants & neonates)
* decreased in prematurity, older age
**MAC ↓ 6% per decade after 40 years**
100
how does core temp affect MAC
hyperthermia = increased MAC
hypothermia = decreased MAC
101
how does red hair affect MAC
why
~19% increase
presumably d/t mutations in menalocute-stimulating hormone receptor and ↑ pheomelanin
102
drugs that decrease MAC
* Acute ETOH intox
* IV anesthetics
* N2O
* Opioids (IV & neuraxial)
* Alpha-2 agonists
* Lithium
* Lidocaine
* Hydroxyzine
103
misc. things that decrease MAC
* MAP \< 50
* Hypoxemia
* Anemia (\< 4.3 mL O2/dL blood)
* CPB
* Metabolic acidosis
* Hypo-osmolarity
* 24-72 hrs postpartum
* PaCO2 \> 95
104
how does HTN affect MAC
no effect
105
how do electrolytes affect MAC
only Na affects
106
what is the Meyer-Overton rule & what does it imply
* states that **lipid solubility** is directly proportional to the **potency** of an inhaled anesthetic
* Implies that depth of anesthesia determined by # anesthetic molecules dissolved in brain, not necessarily particular agent used
107
what is the unitary hypothesis
Implies that depth of anesthesia determined by # anesthetic molecules dissolved in brain, not necessarily particular agent used
108
how is general anesthesia produced?
* produced by membrane-bound protein interactions in the brain & spinal cord
* Stereoselectivity of anesthetic potency suggests **chiral binding site**
* Probably affect specific areas of cell membrane
109
how do volatiles affect inhibitory and stimulatory receptors
**1)** stimulate inhibitory receptors
**2)** inhibit stimulatory receptors
110
inhibitory pathways stimulated by inhaled anesthetics
* GABA-A
* glycine channels
* K+ channels
111
stimulatory pathways inhibited by inhaled anesthetics
* NMDA receptors
* nicotinic receptors
* Na+ channels
* dendric spine function & motility
112
most important site of volatile action in the brain
GABA-A receptor (ligand-gated chloride channel)
likely increase duration chloride channel remains open
113
effect of GABA-A stimulation in the brain
increased chloride influx, hyperpolarized neurons
impairs ability of neurons to fire
114
how do volatiles produce immobility
ventral horn of spinal cord
important sites of action: glycine receptor stim, NMDA inhibition, Na+ inhibition
115
pathways affected by N2O & Xenon
NMDA antagonism
K+ 2-P channel stimulation
116
sites of anesthetic function responsible for amnesia
amygdala
hippocampus
117
sites of anesthetic function responsible for autonomic modulation
pons & medullla
118
sites of anesthetic function responsible for unconsciousness
cerebral cortex
thalamus
RAS
119
sites of anesthetic function responsible for analgesia
spinothalamic tract
120
function of the amygdala
emotion
response to pain
formation of stress response
121
function of hippocampus
memory formation
122
function of thalamus
relay station of sensory and motor input to cortex
123
function of RAS
influences consciousness & arousal
124
function of ventral horn of spinal cord
upper and lower motor neurons synapse
125
function of spinothalamic tract
inhibit nociceptive signals along ascending pain pathway
126
how do volatiles affect cardiac and vascular smooth muscle
**↓ Ca2+** influx in sarcolemma & ↓ Ca2+ release from sarcoplasmic reticulum
causes systemic vasodilation, decreased SVR/VR
127
primary mechanism of dose-dependent MAP decrease with volatiles
↓ intracellular Ca2+ in vascular smooth muscle = systemic vasodilation = decreased SVR & venous return
128
secondary mechanism of dose-dependent MAP decrease with volatiles
↓ intracellular Ca2+ in cardiac myocyte = myocardial depression = decreased inotropy
129
how do volatiles affect NO, ACh, and Na/Ca pump
modulate **NO** release, inhibit ACh-induced vasodilation, & impair **Na+/Ca+ pump** (↓ intracellular Ca2+ concentration)
130
how do volatiles affect HR
* **↓ SA node automaticity**
* ↓ Conduction velocity through AV node/His-Purkinje/ventricular conduction pathways
* ↑ Duration myocardial repolarization by impairing outward K+ current = increases AP duration (**prolongs QT** interval)
* Altered **baroreceptor** function
131
which 2 volatiles increase HR 5-10% above baseline
des and iso
132
how do volatiles affect contractility
small dose-dependent decrease in baseline
myocardium remains preload responsive
133
how do volatiles affect SVR
which affects it the least
↓ intracellular Ca2+ in vascular smooth muscle = systemic vasodilation = ↓ SVR
Of volatiles, sevoflurane decreases the least
134
how do volatiles affect coronary vascular resistance
* Volatiles **↑ coronary blood flow** in excess of myocardial O2 demand
* Preferentially **dilate** **small cardiac vessels** (20-50 micrometers diameter)
135
Potency of **coronary dilation**:
isoflurane \> desflurane \> sevoflurane
136
respiratory effects of volatiles
↑ apneic threshold
↓ vent. Response to CO2
Airway obstruction
Bronchodilation
↓ Vt
↑ RR
↓ FRC
137
physiologic control of PaCO2
central chemoreceptor in medulla
138
every 1 mmHg increase in PaCO2 above baseline will increase Vm by:
3 L/min
139
how do volatiles imapact central chemoreceptors and respiratory muscles
dose-dependent depression
140
3 mechanisms of volatiles that contribute to hypercarbia
1. altered resp pattern
2. impaired response to CO2
3. impaired motor neuron output & muscle tone to upper airway and thoracic muscles
141
how do volatiles affect Vt
decrease
142
how does the body try to compensate for reduced Vt from volatiles
* Body attempts to compensate with ↑ RR (not enough to prevent ↑ PaCO2)
* Smaller, faster breaths increase dead space to Vt ratio
143
what does the slope of the CO2 response curve represent
sensitivity to PaCO2
144
what happens to the CO2 response curve with decreased response to CO2
curve shifts down and to the right
145
what is the apneic threshold
PaCO2 at which a patient is stimulated to breathe
usually **3-5 mmHg** below PaCO2 maintained during spontaneous ventilation (if ventilation is assisted below threshold, pt won't breathe)
146
what does a right shift of the CO2 response curve imply
* Implies Vm is \< predicted for given PaCO2 - **respiratory acidosis**
* depressed ventilation
147
what can cause a right shift of the CO2 response curve
* GA
* opioids
* metabolic alkalosis
* denervation of peripheral chemoreceptors
148
what does left shift of CO2 response curve mean
implies Vm is \> predicted for given PaCo2 - **respiratory alkalosis**
stimulates ventilation
149
causes of CO2 response curve left shift
* anxiety
* surgical stimulation
* increased ICP
* salicylates
* aminophylline
* doxapram
150
how do volatiles depress ventilation
by inhibiting muscle function in upper airway, diaphragm, & intercostals
151
152
what PaO2 stimulates carotid bodies to increase Vm to restore arterial oxygenation
\< 60 mmHg
153
where do carotid bodies relay afferent input
respiratory center via CN 9
154
how do aortic bodies relay afferent traffic
via CN 10
155
what is the sensory arm of the hypoxic drive
glomus type 1 cells in carotid bodies
hypothesized that volatiles create **reactive O2 species** that impairs these cells
156
source of reactive O2 species that impair glomus cells
anesthetic metabolism
157
what determines how much a volatile inhibits hypoxic drive
agents that undergo the most **biotransformation** inhibit hypoxic drive the most (sevo \> iso \> des)
158
when does impaired response to acute hypoxia begin with volatiles
at 0.1 MAC
| (does not impair response to PaCO2)
159
what 2 things is CMRO2 dependent on
**1)** electrical activity & **2)** cellular homeostasis
160
what determines total brain O2 consumption
electrical activity is 60%
cellular homeostasis is 40%
161
MAC required to produce isoelectric state
1.5-2 MAC
162
how do volatiles affect CMRO2
↓ (only to the extent that they reduce electrical activity - can’t reduce any further once isoelectric)
163
volatile that can produce seizure activity in high concentrations (\> 2 MAC)
how can this effect be exacerbated
sevo
exacerbated by **hypocapnia** & more common with **inhalation induction**
164
how does the body adjust for increased CMRO2
vasodilation to ↓cerebrovascular resistance, ↑ CBF
165
how does the body adjust for decreased CMRO2
vasoconstriction to ↑ cerebrovascular resistance
166
how do volatiles affect CBF & CMRO2
cause uncoupling
concentrations \> 0.5 MAC increase CBF even though CMRO2 is decreased
167
downside of volatiles causing uncoupling of CBF and CRMO2
increases ICP
168
upside of volatiles causing uncoupling of CBF and CRMO2
favorable cerebral O2 supply-demand ratio
169
how can cerebral vasodilation from volatiles be partially offset
* mild hyperventilation (PaCO2 \< 35)
* propofol, opioids, barbiturates
170
sensitivity of evoked potentials to volatiles
VEP \> SSEPs ~ MEPs \> brainstem
171
how are SSEPs produced
* by applying current to a peripheral nerve
* Most commonly tibial or ulnar n.
172
what do SSEPs monitor
* integrity of **dorsal column** (medial lemniscus)
* **posterior spinal a.** perfusion
173
what do MEPs monitor
* integrity of corticospinal tract
* anterior spinal a. perfusion
174
what is amplitude of an evoked potential
strength of nerve response
175
what is latency of an evoked potential
speed of nerve conduction
176
when are there concerns for ischemia with evoked potentials
**amplitude ↓ \> 50%** or **latency ↑ \> 10%**
177
best anesthesia technique to preserve evoked potentials
TIVA without N2O
178
maximum MAC if volatiles used with evoked potentials
0.5
179
how does ketamine affect evoked potentials
enhanced signal
180
how do volatiles affect evoked potentials
Des, sevo, & iso = dose-dependent ↓ amplitude, ↑ latency (signal is not as strong & slower to conduct)
181
when does an evoked potential suggest ischemia
loss of signal
182
goals if evoked potential signal disappears or diminishes
improve neural tissue perfusion (↑ BP, volume expansion, transfusion if anemic)
183
how do hypoxia, hypercarbia, and hyperthermia affect evoked potentials
can affect amplitude
184
chemical name of desflurane
difluoromethyl 1,2,2,2-tetrafluoroethyl ether
185
which 2 volatiles are nearly identical
des & iso
des - chlorine atom replaced by fluorine (fully fluorinated)
186
effects of fluorination
* ↓ potency (↓ oil:gas solubility) = ↑ MAC
* ↑ vapor pressure (↓ intermolecular attraction)
* ↑ resistance to biotransformation (↓ metabolism) = ↓ trifluoroacetate makes an immune-mediated hepatitis extremely unlikely
187
methods to minimize tachycardia with rapid increase in des
opioids, alpha 2 agonists, beta 1 antagonists
188
volatile that can cause bronchoconstriction in asthmatics
desflurane
189
which anesthetic agent impairs hypoxic drive the **least**
des
190
how does des affect CSF
↑ or no change in CSF **production**
191
chemical name of sevoflurane
fluoromethyl 2,2,2-trifluoro-1-(trifluoromethyl) ethyl ether
192
why is sevo more potent than des with regards to fluorination
most likely d/t bulky propyl side chain
193
which volatile is unstable in hydrated soda lime
sevo
194
minimum FGF requirements for sevo
* **1 L/min** for up to 2-MAC hours
* **2 L/min** after 2-MAC hours
* \<1 L/min not recommended at any time
195
theoretical concern of sevo biotransformation
* Biotransformation results in liberation of inorganic fluoride ions
* Theoretical concerns of fluoride-induced **high output renal failure**
196
s/s high-output renal failure with sevo
* typically unresponsive to vasopressin
* polyuria
* hypernatremia
* hyperosmolarity
* ↑ plasma creatinine
* inability to concentrate urine
197
how does sevo affect CSF
decreased production
198
chemical name of isoflurane
1-chloro 2,2,2-trifluoroethyl difluoromethyl ether
199
why is iso more potent than sevo and desflurane
Addition of heavier chlorine atom
200
how does addition of chlorine atom affect isoflurane
* more potent than sevo (2x) and des (5x)
* increases blood and tissue solubility
201
volatile that is the most potent coronary vasodilator
iso
202
what is coronary steal
* **Thought** is that ↑ myocardial O2 demand = dilation of healthy vessels, heart increases its own flow to satisfy O2 requirement
* diseased vessels may not be able to dilate further
* coronary blood flow would be preferentially directed to healthy tissue
203
chemical name of halothane
**2-bromo-2-chloro-1,1,1-trifluoroethane**
204
which volatile has a bromine atom and no ether bridge
halothane
205
important metabolic byproduct of halothane metabolism
TFA
may cause halothane hepatitis
206
N2O is ___ times more soluble than nitrogen
34
207
Gas-containing areas of the body can absorb up to __ L N2O within first __ hours of admin.
30L
2 hours
208
how does N2O cause decreased stimulus to breathe
Can temporarily **dilute alveolar oxygen & CO2** = diffusion hypoxia & hypocarbia
209
b:g of nitrogen
0.014
210
rate of pressure change inside space with N2O
compliance of space, partial pressure of N2O, perfusion of surrounding tissue, and time
211
what happens in a compliant air space filled with N2O
volume ↑, pressure unchanged
212
what happens in a noncompliant air space filled with N2O
pressure ↑, volume unchanged
213
negative effect of discontinuing N2O in middle ear surgery
can quickly decrease middle ear pressure & lead to **serous otitis**
214
N2O use with SF6 bubble
d/c at least 15 min prior to placement
avoid for 7-10 days after
215
avoid N2O for how long with these ocular gas bubbles:
air bubble
perfluoropropane
silicone oil
air = 5 days
perf = 30 days
silicone = no contraindications
216
how does N2O affect vitamin B12
* irreversibly inhibits B12
* Inhibits **methionine synthesis** (required for folate metabolism, myelin)
217
side effects of vitamin B12 inhibition from N2O
* immune compromise
* homocysteine accumulation
* possible risk of spontaneous abortion
* megaloblastic anemia (bone marrow suppression)
* neuropathy
* ↓ DNA synthesis
218
increases risk of vitamin b12 inhibition with N2O
* prolonged exposure
* pre-existing B12 deficiency (alcoholism, pernicious anemia, strict vegan diet, recreational use)
219
complications of N2O vitamin B12 inhibition
* megaloblastic anemia (bone marrow suppression)
* immune compromise
* neuropathy
220
CV effects of N2O
* Increased HR
* BP increased/unchanged
* CO decreased
* SVR increased
* Doesn’t meaningfully ↓ contractility by itself; may ↓ combined with opioid
* May increase CVP & PAP
221
neuro effects of N2O
Increases CBF as a function of increased CMRO2
222
2 classes of ethers
1. methyl isopropyl ether (sevo)
2. methyl ethyl ether (des, iso)
223
best agent to use in a pt with hx of halothane hepatitis
sevoflurane
| (metabolism doesn't produce TFA)
