IV induction/Neuro monitoring/Inhalation hx/volatiles Flashcards
(507 cards)
1
Q
what are examples of adjunct medications to primary anesthetics
A
antihistamines
antipsychotics
benzodiazipines
opioids
2
Q
what is balanced anesthesia
A
premedication
light sedation
regional anesthesia
3
Q
what is general anesthesia
A
balance of unconsciousness, analgesia, amnesia, suppression of stress response, immobility
-unarousable complete loss of consciousness
-inability to maintain airway control
-loss of eyelid reflex
4
Q
what pathway do the majority of IV inductions agents on on
A
excitement of inhibitory signals through the gamma-aminobutyric acid type A (GABA) receptors
5
Q
what are MOA theories
A
-membrane protein binding sites
-alter signaling between neurons (charges)
-GABA: ligand gated ion channels
6
Q
what receptors does ketamine work on
A
NMDA
7
Q
receptors contain multiple
A
subunits
8
Q
what is the primary binding site on GABA, what is the effect
A
GABA 2, hyper polarization
9
Q
GABA is an ______ neurotransmitter
A
inhibitory
10
Q
what are examples of excitatory neurotransmitters
A
acetylcholine
glutamate
11
Q
what are examples of secondary IV induction agents
A
Antihistamines
antipsychotics
benzodiazepines
opioids
12
Q
what is general anesthesia
A
A balance of unconsciousness, analgesia, amnesia, suppression of the stress
response, and sufficient immobility
13
Q
T/F general anesthesia results in an unarousable state and complete loss of consciousness
A
True
14
Q
T/F general anesthesia results in an inability to maintain airway or controll reflexes
A
true
15
Q
T/F general anesthesia results in the loss of eyelid reflexes
A
true
16
Q
what are the MOA theories for IV induction agents
A
-membrane protein binding sites
-altering signaling between neurons by altering ion channels
-GABA receptors
17
Q
where do the majority of IV induction agents act (receptor)
A
enhancement of inhibitory signals through the gamma-aminobutyric
acid type A (GABA) receptors
18
Q
what system do most IV induction agents have their action on
A
reticular activating system in brainstem
19
Q
what does the reticular activating system control
A
consciousness
20
Q
what controls the signals coming into the reticular activating system? where does it send the message
A
thalamus
cerebral cortex
21
Q
what neurotransmitter does the reticular activating system use
A
acetycholine
22
Q
what kind of feedback mechanism does the reticular activating system use
A
positive feedback
23
Q
what are examples of excitatory neurotransmitters
A
acetylcholine
dopamine
norepinephrine
glutamate
24
Q
what are examples of inhibitory neurotransmitters
A
Gamma-aminobutyric acid (GABA)
25
what is the most abundant inhibitory neurotransmitter in the brain
GABA
26
what does GABAa regulate
neuronal excitability
27
what does GABAa mediate
unconsciousness, amnesia, suppression of spinal reflexes
28
what channels does GABA work on
Ligand-gated ion cys-loop channels
29
how many protein subunits make up a GABA receptor
5
30
what channel does the GABA receptor control? what is the affect of its activation?
Cl-
hyperpolarization
31
what controls the release of GABA
Ca++
32
what happens when GABA is activated
-increases Cl- conductance
-cell membrane hyperpolarization
-decreased neuronal excitability
33
where on GABA receptor does the GABAa endogenous enzyme bind
alpha and beta subunit
34
where on GABAa receptor do Benzodiazepines bind
alpha and gamma subunits
35
where on GABAa receptor does propofol, etomidate, and barbituates bind
within or proximal to beta subunits
36
suppression of NMDA receptors leads to
depression of neuronal activity
37
Where are NMDA receptors found
pre, post, and extra synaptically
38
how many subunits are in an NMDA receptor
4 around a central ion channel pore
39
what types of subunits are NMDA receptors made from
-an NR1 receptor
-4 types of NR2 subunits (A-d)
-NR3
40
what effects the onset of an NMDA receptor
presynaptic glutamate
voltage of membrane
41
what blocks the channel pore of an NMDA receptor if agonist is present
Mg++
42
NMDA receptors play a significant role in CNS functions that require activity-dependent changes in cellular physiology such as
learning and processing of sensory information
43
what is an example of an NMDA antagonist
ketamine
44
IV induction agents that work on NMDA are
antagonists
45
IV induction agents that work on GABA receptors are
agonists
46
does ketamine competitively or non-competitively bind to NMDA receptrs
non-competitive
47
Ketamine can only bind to NMDA receptors that are in the _________ position
open
48
what are examples of barbituate IV induction agents
thiopental,
Methohexital (brevital),
Pentobarbitol
49
T/F brevital changes the seizure threshold
False
50
what receptors do barbituates work on
GABA
block action of Glutamate at AMPA and Kainate
inhibits neuronal nicotinic receptors
51
how do barbiturates affects GABAa receptor
Enhances GABAa receptor function and decreases the rate of disassociation of GABA
52
T/F barbituates block glutamate at NMDA receptors
false
53
how do high doses of barbiturates affect GABA receptors
directly activate GABA receptors (even in absence of GABA)
54
T/F barbiturates cause EEG changes
T, cause low to high frequency patterns on EEG
55
the CNS depression caused by barbiturates is ________ dependent
dose
56
barbiturates ________ cerebral metabolic rate for O2 (CMRO2) by _____ %
decrease
55%
57
which barbiturates have anticonvulsant properties
Thiopental
pentobarbital
58
barbiturates cause veno____________
dilation
59
barbiturates (increase/decrease) preload and CO
decrease
60
what conditions do you avoid barbiturates in and why
aortic stenosis/tamponade
decreased preload and CO
61
do you mix barbiturates with ROC
no
62
do you mix barbiturates with saline?
why?
no
will precipitate
63
what order of kinetics do barbiturates go thorugh
first order unless there is a high concentration
64
barbiturates are weak (acids/bases)
acids
65
barbiturates require a pH>_____ to remain aquas
10
66
what happens if you mix barbiturates in non-base solutions like N.S and L.R.
precipitate
67
barbiturates become ________philic in plasma
lipophilic
68
what is the onset of barbiturates? why?
30-60 seconds
readily pronate in plasma and become lipophilic
69
60% of barbiturates are __________ (ionized/non-ionized) at body pH due to pKa being higher.
this results in (easy/difficult) passage through lipid membranes
non-ionized
easy
70
what terminates the initial dose of barbiturates
redistribution
71
Vd of barbiturates is related to perfusion of what
vessel rich organs
72
muscles results in a _______ reservoir
large
73
fat results in a ______ reservoir
smaller, slow distribution
74
Barbiturates are (high/low) protein bound
highly 75-90
75
if a patient has liver disease how does this effect your barbiturate dose
decrease it
76
how are barbiturates metabolized
liver
77
T/F barbiturates cause histamine release
true
78
what are s/s histamine release
uticarial rash
anaphylaxis
Hives
Edema
Bronchospasm
Shock
79
which barbiturate causes pain on injection
methohexital
80
what happens with IV infiltration of barbiturates
severe tissue necrosis
81
what can happen with intra-arterial injection of barbiturates
chemical endarteritis
destroys tissue
intense vasospasm
excruciating pain
necrosis/gangrene
permanent nerve damage
82
what are signs of the intense vasospasm caused by intra-arterial injection of barbiturates
blanching of skin with disappearance of pulses
83
what is the induction dose of methohexital
1 mg/kg
84
what is the sedation dose of methohexital
0.2-0.4 mg/kg
85
what is the duration of induction dose of methohexital
5-10 min
86
what is the 1/2 life methohexital
3.9 hrs
87
what is the pediatric rectal dose of methohexital
25 mg/kg
88
what conditions is etomidate useful for
cardiac (aortic stenosis, tamponade, sepsis)
89
what IV induction agent has the greatest selectivity for GABAa
Etomidate
90
how many enantiomer are in etomidate? why?
1
R(+) isomer having the greatest hypnotic effects
91
T/F Etomidate is hydrophilic
F, it is lipophilic
92
T/F Etomidate is highly protein bound
true
93
how long does it take Etomidate to reach peak brain levels
2 min
94
how is Etomidate metabolized
liver
Plasma esterases
95
how is the end product of etomidate metabolism excreted
renal
96
what can Etomidate inhibit
11b-hydroxylase in the adrenal cortex, causes adrenal corticol suppression
97
what is the induction dose of Etomidate
0.2-0.4 mg/kg
98
what is the T1/2 of Etomidate
2.9 hrs
99
what is the onset/peak/DOA of Etomidate
30s/1 min/3-10 min
100
what is the Vd of Etomidate
2-4.5 L/kg
101
what is the CL of Etomidate
10-20 mL/kg/min
102
how does etomidate affect EEG
EEG slows to burst suppression
103
how does etomidate affect CMRO2
decreases
104
how does etomidate affecrt resp
resp depression
105
which causes more resp depression prop or etomidate
propofol
106
how does etomidate affect muscles, how do you mitigate this
myoclonus, inject slowly
107
how does etomidate affect injection site
pain on injection
thrombophlebitis
108
how does etomidate affect venous system
minimal vasodilation
109
in what conditions can etomidate still cause significant vasodilation
sepsis,
shock,
SVR <2500,
aortic stenosis
110
how does etomidate affect cardiac
minimal cardiac depression
111
how does etomidate affect GI
n/v
112
T/F etomidate is an anticonvulsant
true
113
what is 2,6 diisopropylphenol
propofol
114
What is MOA of propofol
-Potentiates GABA-mediated responses
-directly activates GABAA receptor
115
What GABA subunits does etomidate bind to?
likely b
116
T/F propofol is a weak base
false
its a weak acid
117
T/F propofol is lipophilic
true
118
T/F propofol is a chiral molecule
F, it is achiral
119
propofol is formulated in a lipid emulsion to mitigate its
hydrophobia
120
what is the lipid emulsion of propofol formulated from
soybean oil,
glycerol,
purified egg phospholipid (lecithin)
121
T/F egg allergy crossover is common in propfol
f its rare
122
how long can an open vial or syringe of prop be open before disposal
12 hrs
123
how long can propofol be in a syringe before it is thrown away
1-2 hrs
124
what is in prop to stop bacterial growth
an antimicrobial
125
what are examples of antimicrobials in propofol
ethylenediaminetetraacetic acid or sodium metabisulfite
126
what causes the pain in propofol injection
its free aqueous concentration
127
how can you mitigate pain of propofol injection
use AC vein
coadmin with lidocaine
128
what causes propofols rapid onset
lipid solubility
129
young people require (more/less) propofol
more
130
how is propofol metabolized
liver
131
how is propofol excreted
renal
132
what is CL of propofol
25 ml/kg/min
133
T/F moderate hepatic or renal impairment has a large effect on DOA of propofol
F, it is little effect
134
what causes the short DOA of propofol
rapid redistribution
135
what is the induction dose of propofol
2-2.5 mg/kg
136
what is the induction dose of propofol for >65 yo
1-1.5 mg/kg
137
what is the onset/peak/doa of propofol
60 s, 1 min, 5-10 min
138
what is the elimination 1/2 life of propofol
0.5-1.5 hrs
139
what is the Vd of propofol
2-10 L/kg
140
do you use propofol in sepsis
no
141
how much do you lower propofol dose by in sever hypovolemia
80-90%
142
if you fluid resuscitate a hypovolemic patient patient how much do you decrease prop dose by
50%
143
how does propofol affect EEG
slows to burst suppression
144
how does propofol affect CMRO2
decreases
145
how does propofol affect airway muscles
decreases reflexes and tone
146
how does propofol affect heart
myocardial depression
147
how does propofol affect muscles
rhabdomyolysis with infusion syndrome (rare)
148
how does propofol affect liver
hypertriglyceridemia with prolonged infusions
149
how does propofol affect injection site
pain on injection
150
how does propofol affect venous system
decreased vascular resistance
151
how does propofol affect lungs
bronchodilation, resp depression
152
how does propofol affect GI
antiemesis
153
T/F propofol is an anticonvulsant
true
154
what is the only IV induction drug that decreases pain
ketamine
155
what kind of drug is Ketamine
NMDA receptor antagonist
156
what kind of mixture is ketamine
racemic mixture of R and S enantiomers
157
T/F ketamine is competitive binding
false
158
what other receptor does ketamine block
nicotinic
159
what gives ketamine its local anesthetic properties
Na+ channels and binds mu and k opioid receptors
160
what are common clinical uses of ketamine
OB/C section
161
T/F Ketamine depresses RAS
false
162
T/F ketamine dissociates thalamus from limbic cortex
true
163
how does ketamine affect CMRO2, CBF, and ICP
increases
164
T/F ketamine is a good drug for head trauma patients
F, it increases ICP
165
what are emergence reactions from ketamine
unpleasant hallucination,
vivid dreams,
delirium
166
how can you reduce the incidence of emergence reactions with ketamine
benzos
167
how does ketamine affect IOP
increases, dont give in glaucoma
168
do you use ketamine in open eye injuries
no, increases IOP
169
T/F nystagmus is common in ketamine
true
170
what is the induction dose of Ketamine
1-2mg/kg IV or
4-8 mg/kg IM
171
what is the onset/peak/doa of ketamine
30s/1min/5-15 min
172
what is the elimination 1/2 life of ketamine
2-3 hours
173
what is the Vd of Ketamine
2.5-3.5 L/kg
174
what is the CL of ketamine
17 ml/kg/min
175
how does ketamine affect venous system
increased vascular resistance
176
What are the CNS effects of ketamine?
dissociative sedation
possible emergence delirium
177
how doe ketamine affect eyes
nystagmus
178
how does ketamine affect mouth
increased salivation
179
what drugs can you used to decrease salivation
glyco
IV scoplamine
180
how does ketamine affect lungs
bronchodilation with preserved resp drive
181
how does ketamine affect heart
indirect myocardial stimulation
direct myocardial depression
182
what are the "good" effects of ketamine
maintains SVR
increased HR
bronchodilation
awake intubations
maintain resp drive
local mac on sick patient
183
what are the "Bad" effects of ketamine
dont use on head traumas
dont use on eye traumas
dont use in cardiac or aortic stenosis 2/2 tachycardia
184
what does too much muscle relaxant lead to
longer recovery phase
prolonged mechanical ventilation
increased expense to institution
185
what is the last muscle to be paralyzed and the first to wake up
diaphragm
186
can a muscle fiber partially contract?
no it is all or none
187
the response of the entire muscle depends on
the # of nerves activated
188
what is a supramaximal stimulus
>50 mA, +20-25% of necessary, so painful
189
when do we use supramaximal stimulus
when patient is asleep
190
when do we use submaximal stimulus
when patient is awake
191
what is the number of cycles/)second of electrical stimulation (how rapidly a stimulation occurs)
Hz (hertz)
192
what is 0.1 Hz
one stimuli every 10 seconds
193
what is 1.0 Hz
one stimuli every second
194
the electricity during PNA stimulation is _______
constant
195
what are the 2 variables of Peripheral nerve stimulator
Hz-how often stimuli is applied
mA- electrical output, how much electricity
196
what percent of patients experience residual paralysis
50%
197
what patients do not notice residual paralysis
young healthy
198
what patients suffer from residual paralysis
obese, emphysema
199
what do you give patients suffering from residual paralysis
reversal like sugammadex or neostig
200
where do we place the red electrode for monitoring
directly over nerve, toward head
201
where do we place the black electrode for monitoring
directly over nerve, distal
202
what does an electrical current cause to be released
an action potential releases ACh at the synaptic cleft
203
what are the different patterns of nerve stimulation
single twitch
TOF (train of four)
Tetanus
Post-tetanic count (PTC)
Double-burst stimulation (DBS)
204
how do you use TOF
compare T1 to T4 and make ratio/percentage
205
how do we use tetanus
constant shock, watch for fade
206
in a phase 2 block if you do 5 seconds of tetany and there is no fade what does this tell you
you are safe to extubate
207
what is benefit of DBS
more accurate supposedly
208
when single twitch stimulation results in no twitches what muscles have been relaxed
laryngeal and diaphragm
209
what do you have to do before using the single twitch stimulation method
require baseline stimulation prior to NMBA given
210
how long does a single twitch stimulation last
0.2 msec
211
how often does TOF give stimuli
every 0.5 seconds (2 Hz)
212
what is the frequency of TOF
2Hz
213
how is TOF evaluated
fade
214
how is TOF ratio determined
twitches/4
T4/T1
215
how do you determine TOF %
T4/T1
216
if there is NO neuromuscular blockade the 4th twitch will feel the same as the ______
1st
217
as neuromuscular blockade increases, 4th twitch__________ until it ________
decreases
disappears
218
after 4th twitch is lost what twitch is lost next
3rd then 2nd
219
what is the optimal # of twitches
1-2
220
with deep neuromuscular blockade how many twitches are present
none
221
when is TOF most sensitive
70-100% paralysis
222
the 4th twitch in TOF disappears at _________ blockade
75-80%
223
the 3rd twitch in TOF disappears at _________ blockade
80-85%
224
the 2nd twitch in TOF disappears at _________ blockade
90-95%
225
what is considered the ideal operative paralysis %
85-95% blockade, 1-2 twitches
226
how many twitches are present at 75-80% blockade
3
227
how many twitches are present at 80-85% blockade
2
228
how many twitches are present at 90-95% blockade
1
229
what percent block is this
<70%
230
what percent block is this
75%
231
what percent block is this
80
232
what percent block is this
90%
233
what percent block is this
100%
234
what are advantages of TOF
less painful
degree of block in nondepolarizing block can be evaluated
good for assessing surgical relaxation
235
what is a phase one block
depolarization
236
what is a depolarizing drug
Succinylcholine
237
what happens with a high dose of succs
phase 2 block
238
how does train of four appear in depolarizing blocks
all twitches are the same so all strong, all weak, or all gone
239
which block has muscle fasciculation
depolarizing/phase 1
240
which block has sustained response to tetanic stimulation
depolarizing/phase 1
241
which block has absence of posttetanic potentiation, stimulation, or facilitation
depolarizing/phase 1
242
which block has a lack of fade to tetanus, train of four, and double burst stimulation
depolarizing/phase 1
243
which block is antagonized by prior admin of nondeplarizer as pretreatment
depolarizing/phse 1
244
which block is potentiated by anticholinesterase drugs
depolarizing/phase 1
245
which block has an absence of muscle fasciculation
nondepolarizing/phase 2
246
which block has the appearance of tetanic fade and posttetanic potentiation, stimulation, or facilitation
nondepolarizing/phase 2
247
which block has TOF and double burst fade
nondepolarizing/phase 2
248
which block is reversible with anticholinesterase drugs
nondepolarizing/phase 2
249
which block can be produced by an overdose and desensitization with succs at doses greater than 6 mg/kg
nondeplarizing/phase 2
250
what does a TOF with succs look like
251
what order do twitches reappear in
same order the disappear
252
what is the TOF response of non-depolarizing block
253
what is TOF response of depolarizing block
254
what TOF indicates adequate recovery
0.7
255
what does a TOF ratio of 0.7 mean
4th twitch is 70% as strong as 1st twitch
256
at a TOF of 0.7 patients should be able to maintain ___________
airway
257
at TOF of 0.7 ther are enough unoccupied receptors to bind with
Ach
258
at what Hz does can tetanic stimulation deliver shock
30, 50, or 100
259
what is the most common shock for tetanic stimulation
50 Hz for 5 seconds or 100 Hz for 5 seconds
260
what are we observing for in tetanic stimulation
fade
261
what is the physiology behind fade
presynaptic event
at beginning of tetanus large Ach released from nerve terminal
as stores are depleted the rate of release of Ach is depleted
262
what does the degree of fade depend on
degree of neuromuscular blockade
frequency (Hz)
length (seconds)
how often tetanic stimulation is applied
263
what causes fade in tetany
receptors are still occupied by NDMR
264
what is the best shock indicator for extubation
5 second tetany, fade is easy to see
265
50 Hz is _________ shocks per second OR one shock every ___________
50
20 msec
266
100 Hz is _________ shocks per second OR one shock every ___________
100
10 msec
267
does fade occur in depolarizing muscle relaxant
no
268
if a patient is completely blocked with succs how will tetanus appear
no contraction
269
if patient is partially blocked with succs how will tetanus appear
weak contraction that does not get weaker
270
what do you do if you blocked a patient with an NDMR and you get no response to TOF
count post tetanic twitches
-shock 50 Hz for 5 sec then wait 3 seconds then do a single twitch stimuli at 1 Hz
271
post tetanic twitches will appear __________ the first twitch in TOF. This is called ________
before
post tetanic potentiation
272
what is the Hz and interval of Double burst stimulation
two bursts of 50 Hz separated by 750 msec
273
how does double burst stimulation appear in nonparalyzed muscle
2 equal contractions
274
how does double stimulation appear in partially paralyzed muscle
2nd response is weaker than first
275
how many receptors are occupied when a patient has a tidal volume of 5 ml/kg
80% (20% free)
276
how many receptors are occupied when a patient has no palpable fade to TOF stimulation
70-75% (25-30% free)
277
how many receptors are occupied with sustained tetanus at 50 Hz for 5 sec
70% (30% free)
278
how many receptors are occupied with vital capacity of 20 ml/kg
70% (30% free)
279
how many receptors are occupied when there is no palpable fade with double-burst stimulation
60-70% (30-40% free)
280
how many receptors are occupied when inspiratory force reaches -40 cm H2O
50% (50% free)
281
how many receptors are occupied when patient can lift head for 5 sec
50%
282
how many receptors are occupied with sustained hand grip
50%
283
how many receptors are occupied with sustained bite and jaw clench on tongue blade
50%
284
what peripheral nerves are used for stimulation
ulnar nerve
orbicularis oculi
corrugator supercilii
orbicularis oris
posterior tibial nerve
common peroneal nerve
median nerve
285
T/F ulnar nerve is well correlated with larynx and diaphragm
false
286
what response are you looking for when shocking ulnar nerve
thumb adduction
287
what response are you looking for when shocking facial nerves
eyelid and eyebrow movement
288
what is benefit of ulnar nerve site
easy access
289
what is benefit of facial nerve site
easily accessed when arm not available
best site to measure onset (paralyzed first)
290
which is more resistant to relaxants corrugator supercilli or orbicularis oculi
corrugator supercilii (eyebrow muscle)
291
the diaphragm requires ________ times the amount required to black the adductor pollicis muscle
1.4-2x
292
which recovers faster the diaphragm or adductor pllicis
diaphragm
293
a surgeon is complaining that the patient is pushing, so you check twitches on the adductor pollicis and the patient is blocked, what is happening
diaphragm takes more drug to paralyze and comes off faster
294
list muscles from the most to least sensitive to blockade
abd
orbicularis oculi
geniohyoid
masseter
upper airway muscles
peripheral limbs
laryngeal
diphragm
295
where should red electrode be placed on arm
ulnar groove
296
the inner eyebrow is _________ sensitive than the outer eyebrow
less
297
facial stimulation sites
298
when does intense blockade happen after giving an intubating dose of a NDMR
3-6min
299
do you reverse during total blockade?
no
300
what is another name for surgical blockade
moderate blockade
301
how many twitches are present during an intense blockade
none
302
when does moderate/surgical blockade begin
when 1st twitch of TOF returns
303
how many twitches are present during surgical blockade
1-2
304
T/F patients cannot cough or buck during surgical blockade
false
305
can you reverse during surgical/moderate blockade
yes
306
how many receptors are blocked with complete paralysis, 0/4 TOF
99-100
307
how many receptors are blocked when diaphragm moves 0/4 TOF
95
308
how many receptors are blocked with abdominal relaxation is adequate 1/4 TOF
90
309
how many receptors are blocked when TV and VC are normal and 4/4 TOF
75% (25% free)
310
how many receptors are blocked when patient can inspire -20 cm H2O and head lift is sustained
50%
311
how many receptors are blocked when hand grasp is sustained
30% (70% free)
312
sevoflurane belongs to which anesthetic drug class
ethers (C-O-C)
313
vapor pressure
the pressure exerted by a vapor in equilibrium with its liquid or solid phase inside of a closed container
directly proportional to temp
increased temp= increased vapor pressure
314
vapor pressure is _____(less than/greater than) atmospheric pressure
less than
315
what occurs when vapor pressure is equal to atmospheric pressure?
boiling
316
what can transform volatile anesthetics into toxic compounds?
CO2 absorbent and the liver
317
what is not stable in hydrated soda lime
sevo
produces compound A
318
what does des and iso make if they become unstable in desiccated soda lime
carbon monoxide (des>iso)
319
vapor pressure of sevo
160
320
vapor pressure of des
660
321
vapor pressure of iso
238
322
vapor pressure of N2O
38,770
323
boiling point of sevo
59*C
324
boiling point of des
22*c
325
boiling point of iso
49*C
326
boiling point of N2O
-88*c
327
what is the molecular weight of sevo
200g
328
molecular weight of des
168g
329
molecular weight of iso
184g
330
molecular weight of N2O
44g
331
what anesthetics are stable in hydrated CO2 absorber
des
iso
N2O
332
what anesthetics are stable in dehydrated CO2 absorber
N2O
333
what is the blood:gas partial coefficient of des
0.42
334
what is the blood:gas partial coefficient of N2O
0.47
335
what is the blood:gas partial coefficient of sevo
0.6
336
what is the blood:gas partial coefficient of iso
1.4
337
define the blood: gas coefficient
the ability of the anesthetic agent to dissolve into the blood and tissues;
the relative solubility of an inhalation anesthetic in the blood vs alveolar gas when partial pressures between the two compartments are equal
338
a polar solute will be more soluble in a ____
hydrophilic solvent
339
a non polar solute will be more soluble in a ______
lipophilic solvent
340
an anesthetic gas with low blood:gas solubility is _____ likely to be taken up in the blood
LESS
341
oil : gas sevo
50
342
oil : gas des
18.7
343
oil : gas iso
99
344
oil : gas N2O
1.4
345
what three factors determine anesthetic uptake into the blood
agent solubility
partial pressure difference between alveoli and the blood
cardiac output
346
low solubility = _____ equilibration of FA/FI
faster
this means faster onset
347
high solubility = _____equilibration of FA/FI
slower
means slower onset
348
FA is determined by what two factors
delivery from anesthesia machine to alveoli
rate of transfer from alveoli to the blood
349
what affects the delivery from anesthesia machine to alveoli
setting on the vaporizer
time constant of delivery system
anatomic dead space
alveolar ventilation
volume of the FRC
350
what affects the rate of transfer from alveoli to the blood
blood: gas solubility
cardiac output
351
what factors increase FA/FI
increase wash in:
-high FGF
-high alveolar ventilation
-low FRC
-low time constant
-low anatomic dead space
352
what factors decrease FA/FI
decrease uptake:
-low solubility
-low cardiac output
353
what are determinants of tissue distribution
tissue blood flow
solubility of anesthetic in tissue
arterial blood to tissue gradient
354
what does the VRG include
heart, brain, kidney, liver, and endocrine glands
represents 10% of body mass
receives 75% of cardiac output
1st group to saturate with anesthetic gas
355
what is responsible for the majority of anesthesia continued uptake after VRG is saturated?
the muscle group
then fat once muscle is saturated
356
what are the ways volatile agents are eliminated
1. ventilation
2. hepatic biotransformation
-des 0.02%
-iso 0.2%
-sevo 2-5%
357
define FI
concentration gradient that pushes anesthetic agent from the vaporizer towards the alveoli
358
define FA
The anesthetic washes into the alveoli and establishes a partial pressure
359
what is uptake
the buildup of anesthetic partial pressure inside the alveoli is being opposed by continuous uptake of the agent into the blood
360
FA/FI curve for inhaled anesthetics
361
what metabolites are produced from des halothane and iso
trifluoroacetic acid (TFA)
small risk of immune mediated hepatic dysfunction
362
what metabolites are produced from sevo
free fluoride ions
theoretical risk of high output kidney failure
363
what are signs of high output renal failure
polyuria
hypernatremia
hyperosmolarity
increased plasma creatinine
inability to concentrate urine
364
what accelerates the production of compound A
desiccated soda lime
365
that is the recommended gas flow for sevo
1L/min for up to 2 MAC hrs
2L/min after 2 MAC-hrs
<1L/min not recommended at anytime
366
what is a MAC-hr
one times the minimum alveolar concentration that prevents movement in response to a noxious stimulus in 50% of subjects (MAC) administered for 1 hour
367
which P450 enzyme is chiefly responsible for halogenated anesthetic metabolism in the liver
CYP2E1
368
what by product of halothan metabolism has been implicated in causing halothane hepatitis
TFA
trifluoroacetic acid
369
concentration effect
the higher the concentration of inhalation anesthetic delivered to the alveolus (FA) the faster its onset of action (aka overpressuring)
370
what are the two components of the concentration affect
concentrating affect
augmented gas inflow effect
371
what is the concentrating effect
alveolus shrinks reducing the alveolar volume and causes relative increase in FA
372
what is augmented gas inflow effect
the concentrating effect causes an increased inflow of tracheal gas containing the anesthetic agent to replace the lost alveolar volume
this increase in alveolar ventilation augments FA
alveolar volume is restore quickly, so very temporary phenomenon
373
how does the concentration effect affect the rate of rise on the FA/FI curve
the higher the concentration of inhalation anesthetic delivered to the alveolus, the faster its onset of action
374
which concept best explains why N2O has faster onset than desflurane
concentrating effect
375
what is the ventilation effect
changes in alveolar ventilation affect the rate of rise in FA/FI
376
what is second gas effect
describes the consequences of the concentration effect when a second gas is co-administered with N2O
377
does the second gas effect have a more meaningful impact on iso or sevo and why
it produces more meaningful benefit with agents of higher blood: gas solubility
iso>sevo>des
378
what is the best way to mitigate diffusion hypoxia after N2O is discontinued
increase the FiO2 for 3-5 min after d/c N2O
it does not have to be 100% FiO2
379
how does right to left shunt affect FA/FI
slower induction with volatile agent (less soluble agents are affected to a greater extent)
faster induction with an IV agent
380
how does left to right shunt affect FA/FI
no meaningful impact on induction with a volatile agent
slower induction with an IV agent
381
what is the MAC value for iso
1.15
382
what is the MAC value for sevo
2.10
383
what is the MAC value for des
7.25
384
what is the process of converting liquids/solids to vapor
vaporization
385
what is the temperature of a liquid at which point the majority will be converted to vapor
boiling point
386
what determines the rate of vaporization
temp
vapor pressure of liquid
partial pressure of the vapor above the evaporating liquid
387
what is gas molecules exerting kinetic energy as a pressure measured in mmHg
vapor pressure
388
vapor pressure is dependent only on
temp
389
as temp increased, vapor pressure
increases
390
what is the vapor pressure of isoflurane
238 mmHg
391
what is the vapor pressure of sevo
160 mmhg
392
what is the vapor pressure of des
660 mmhg
393
all liquids that exert high vapor pressure are known as a
volatile liquid
394
if des is placed in an iso vaporizer, concentration will be -________ than expected
higher
395
if iso is placed in a des vaporizer, the concentration will be _________ than expected
less
396
what is the MAC vol% of Iso
1.15
397
what is the MAC vol% of Sevo
2.10
398
what is the MAC vol % of Des
7.25
399
what is the Pmac1 of iso at atmosphere
8.7 mmHg
400
what is the partial pressure of sevo at atmosphere
16
401
what is the Pmac1 of Des at atmosphere
55
402
what is the constant in charles law
pressure
403
what are the variables in the charles law
temp
volume
404
according to charles law as temp increases, volume _______________
increases
405
what is henrys law
at a constant temperature, the amount of gas dissolved in a liquid is directly proportional to the partial pressure of that gas at equilibrium above the gas-liquid interfaces
406
what is the solubility constant for O2
0.003ml/100ml
407
what is the constant for CO2
0.067 ml/100ml
408
what is grahams law
the rate of effusion of a gas is inversely proportional to the square root of its molecular weight
(the bigger the molecule the slower)
409
what is 1 MAC
the amount of gas where 50% of patients do not move under surgical stimulation
410
what is MAC based on
sea level,
no other sedatives/narcotics,
40 yo male
411
what factors increase MAC (meaning you need more gas)
-hyperthermia (henrys law)
-alcohol abuse
-drug-induced central nervous system activity (MAOIs)
-Hypernatremia
-age <40
412
what factors decrease MAC (so you need less gas)
hypothermia
age over 40
A2 agonists
acute alcohol ingestion
sedatives narcotics
413
factors increase MAC
hyperthermia
drug induced increases in central nervous system activity
hypernatremia
chronic alcohol abuse
414
factors decrease MAC (from naglehaut)
-hypothermia
-increasing age
-preopsedatives
-drug-induced decreases in central nervous system activities
-alpha2 agonists
-acute alcohol ingestion
-pregnancy
-postpartum
-lithium
-lidocaine
-hypoxia
-hypotension
-cardiopulmonary bypass
-hyponatremia
415
what does blood gas partition coefficient tell us
speed of uptake and elimination
416
the lower the blood gas coefficient the ________ the onset/offset
faster
417
blood gas partition tells you how much gas in is _______ as compared to tissues
blood
418
the _______ the blood solubility the slower the uptake to the brain, so the slower the onset/elimination
higher
419
what is the BG coefficient of ISO
1.4
420
what is the BG coefficient of SEVO
0.6
421
what is the BG coefficient of DES
0.42
422
what is the BG coefficient of N2O
0.47
423
what is the fastest gas in practice
N2O
424
what does a BG coefficient of 1.4 mean
1.4x as much drug stay in blood rather than the tissue
425
blood gas partition coefficients
426
how does an MV affect onset/offset of gases
increased MV increases onset/offset
427
what order of tissues do inhaled gases enter
vessel rich to vessel poor
Muscle>Fat>cartilage>bone
428
what is the concentration affect
filling the breathing tube with gas to give a "loading dose" of gas
429
what type of gas works best with concentration effect
higher BG coefficients like iso
430
how does concentration effect affect onset
increase speed of onset
431
when do we usually use concentration effect
with kids (ear tubes, tonsillectomy)
432
what is the second gas effect
volatile + N2O speeds onset or emergence
N2O acts a a carrier
433
what happens with second gas effect and emergence
N2O brings gas back into lungs causing a dilutional hypoxia (decreased O2 in alveoli)
434
how does the addition of N20 affect the concentration of other gases
increases concentration
435
N20 is _____x more soluble than nitrogen
34
436
how do you correct dilutional hypoxia
give 100% O2
437
What does the oil:gas partition coefficient correlate with
potency
438
what agent was oil/gas coefficient tested in
olive oil
439
the higher the oil:gas coefficient, the ________ the potentency
higher
440
the higher the oil:gas coefficient the _________ agent able to penetrate the BBB
more
441
a gas with _______ MAC # has more potency
lower
442
oil: gas coefficiency is like
lipid solubility
443
the higher the oil:gas the _______- the MAC
lower
444
MAC/ BG/ OG coefficients
445
what is the MAC % of SEVO
2
446
what is the BGC of SEVO
0.6
447
what is the OGC of SEVO
50
448
what is the MAC % of ISO
1.15
449
what is the BGC of ISO
1.4
450
what is the OGC of ISO
99
451
what is the MAC% of N2O
105
452
what is the BGC of N2O
0.47
453
what is the OGC of N2O
1.4
454
what is the BGC of DES
0.42
455
what is the OGC of DES
18.7
456
what is stage one of anesthesia
analgesia
mild cortical center depression
loss of sensation to pain
skeletal muscle movement intact
457
T/F we often see stage 1 anesthesia
F, usually skip straight to 3
458
what is stage two of anesthesia
excitement
central depression of motor centers, involuntary system is dominant
urinary incontinence
tachy
htn
tachypnea
eyes divergent
459
T/F we extubate in stage 2
false
460
T/F we should stimulate patients in stage 2
false
do not stimulate
461
what is stage 3 anesthesia
surgical anesthesia
462
what is stage 4 anesthesia
OD, dead, resp paralysis, severe CV/resp depression
463
what is stage 3 plane 1
loss of spinal reflexes (spontaneous breathing)
464
what is stage 3 plane 2
decreased muscle reflexes
465
what is stage 3 plane 3
paralysis of intercostal muscles (true deep sx anesthesia)
466
what is stage 3 plane 4
loss of muscle tone
decreased BP, dont want to be here
467
vaporizer delivery output calculation
468
what is the volume of breathing circuit
8L
469
what is Fa
alveolar gas concentration
470
what is an indicator of brain concentration
FA
471
what process allows gas to move from blood to tissues
simple diffusion
472
1 time constant is equal to what percentage
63%
473
2 time constants is equal to what percentage
86%
474
3 time constants is equal to what percentage
95%
475
4 time constants is equal to what percentage
98%
476
what is the formula for time constant
T= volume of circuit (8L) / fresh gas flow
477
if fresh gas flow is 2L/min what is your time constant
4 min
478
what is Fi
Concentration of anesthetic exiting the vaporizer
479
what factors affect Fa/Fi fraction
Fi
inspired concentration
fresh gas flow
circuit volume
dead space
mv
FRC
Fa
solubility
CO
partial pressures
480
what causes an increase in Fa/Fi
low solubility
low CO
high fresh gas flows
high MV
481
what causes a decreased Fa/Fi
high solubility
high CO
low fresh gas flows
low MV
482
What anesthetics are ethers
Des
Iso
Sevo
Enflurane
Methoxyflurane
Ether
483
What anesthetics are alkanes
Halothane
Chloroform
484
What anesthetics are gases
Nitrous oxide
Cyclopropane
Xenon
485
IUPAC name for desflurane
Difluoromethyl 1,2,2,2-tetrafluoroethyl ether
486
IUPAC name for sevo
Fluoromethyl 2,2,2-trifluoro-1-(trifluoromethyl) Ethyl ether
487
IUPAC name for iso
1-Chloro 2,2,2-trifluoroethyl difluoromethyl ether
488
IUPAC name for halothane
2-bromo-2-chloro-1,1,1-trifluoroethane
489
What’s another term for pseudocholinesterase
Butyrylcholinesterase
490
What are the steroidal NDNMB
Roc
Vec
Pancuronium
491
what is this
sevoflurane
492
what is this
desflurane
493
what is this
isoflurane
494
what is this
halothane
495
what is this
nitrous oxide
496
high vapor pressure agent in a low vapor pressure agent vaporizer would result in
higher concentration than desired
497
vapor pressure is solely dependent on
temp
498
standard conditions
760 atm
760 mmHg
29.92 inch pressure
499
Higher blood solubility =
Slower uptake to the brain
Slower onset and elimination
500
Blood: gas represents
Onset
501
Oil :gas represents
Potency
502
Thiopental induction dose
3-6 mg/kg
503
Thiopental sedation dose
0.5-1.5mg/kg
504
Thiopental DOA
5-8 min
505
Thiopental 1/2 life
11 hrs
506
Drug chloride is a weak
Base
507
Weak acid drugs have what in the name
Na Mg or Ca
