Pharm Flashcards
1
Q
Halothane:
- B:g
- MAC
- MAC-awake
- SVP
A
- b:g - 2.4
- MAC - 0.76%
- MACawake - 55% of MAC
- SVP - 244
2
Q
Isoflurane:
- B:g
- MAC
- MAC-awake
- SVP
A
- B:g - 1.4
- MAC - 1.17%
- MAC-awake - 38% of MAC
- SVP - 240
3
Q
Desflurane
- B:g
- MAC
- MAC-awake
- SVP
A
- B:g - 0.42
- MAC - 6.6%
- MAC-awake - 34% of MAC
- SVP - 669
4
Q
boiling point of des
A
22.8 degrees C
5
Q
Sevoflurane:
- B:g
- MAC
- MAC-awake
- SVP
A
- B:g - 0.69
- MAC - 1.8%
- MAC-awake - 34% of MAC
- SVP - 170
6
Q
Nitrous Oxide:
- B:g
- MAC
- MAC-awake
- SVP
- critical temperature
A
- B:g - 0.46
- MAC - 104%
- MAC-awake - 64% of MAC
- SVP - 44,000
- critical temp - 35.5 degrees C
7
Q
halothane’s chemical name
A
2-bromo-2-chloro-1,1,1-trifluoroethane
8
Q
isoflurane chemical name
A
1-chloro-2,2,2-trifluoroethyl-difluoromethyl ethyl ether
9
Q
desflurane chemical name
A
1-fluoro-2,2,2-trifluoroethyl difluoromethyl ether
10
Q
sevoflurane chemical name
A
2,2,2-trifluoro-1-trifluoromethyl ethyl ether
11
Q
which volatile is not stable in moist soda lime
A
sevo
12
Q
main advantage of increased fluorination
A
decreased solubility
13
Q
factors that decrease MAC
A
- Age (decreases 6% per decade)
- decreased body temp
- pregnancy
- decreased CNS sodium
- depressant drugs (opioids, benzos, barbiturates, propofol, acute ETOH)
- IV lidocaine
- N2O
- clonidine & precedex
- some beta blockers & CCBs
- PaO2 < 38 mmHg
- BP < 40 mmHg
- bypass
- adenosine
14
Q
Decreased MAC:
infants > children > neonates > adults
A
:)
15
Q
for every 10 degree C decrease in temp, MAC of des decreases by:
A
almost ½
16
Q
why does pregnancy decrease MAC
when does it normalize?
A
increased progesterone
normalizes 12-72 hrs postpartum
17
Q
how do clonidine and precedex affect MAC?
A
decrease by decreasing CNS catecholamines & hyperpolarizing cell membranes in CNS
18
Q
factors that increase MAC
A
- red hair (excess pheomelanin)
- increased CNS catecholamines (cocaine, ketamine, amphetamine)
- hyperthermia
- hypernatremia
18
Q
factors that increase MAC
A
- red hair (excess pheomelanin)
- increased CNS catecholamines (cocaine, ketamine, amphetamine)
- hyperthermia
- hypernatremia
19
Q
things that do not alter MAC
A
- gender
- duration of anesthesia
- PaO2 > 50
- PaCO2 < 80
- Hct > 10%
- BP > 40 mmHg
20
Q
how is MAC-awake affected by age?
how is the ratio of MAC:MAC-awake affected?
A
MAC-awake decreases with age
ratio of MAC/MAC-awake is not affected by age as both decrease
21
Q
what does a high MAC-awake:MAC ratio indicate?
A
poor amnestic and fast recovery
22
Q
how do low-dose opioids affect MAC-awake and ratio of MAC-awake:MAC?
A
minimally affect MAC-awake
decreases MAC - increases MAC-awake: MAC and awakening should happen quicker
23
Q
what is MAC-TE?
A
MAC at which there’s no coughing/bucking during suctioning, no movement or coughing within 1 min of extubation, and no breath-holding or laryngospasm after extubation
“MAC-intubation”
24
what is MAC-bar?
MAC that **b**locks **a**utonomic **r**esponses to surgical stimulation
25
Meyer-Overton Hypothesis
* direct correlation between anesthetic potency and lipophilicity
* suggests inhaled agents site of action is lipid portion of membrane
26
according to the Meyer-Overton hypothesis, what's the relationship between MAC and oil:gas partition coefficient
indirect relationship
27
possible site of action for amnestic effect of inhaled agents
RAS
28
MAC assoc. with hyperalgesia
0.1
29
respirations in Guedel's Stage 2
irregular breathing, breath-holding
30
respirations in Guedel's stage 3 planes I-III
I: shallow
II: deep
III: shallow
31
signs of light anesthesia
what signs are the best indicators?
* lacrimation
* tachycardia, HTN
* sweating
* reactive, dilated pupils
* movement\*
* laryngospasm\*
\*best indicators
32
how do volatiles affect CMRO2/CBF coupling
* no uncoupling \< 1 MAC
* uncoupling \> 1 MAC = decreased CMRO2 at the same time CBF is increased
33
how do volatiles affect CBF
dose-dependent increase
iso = des \> sevo
34
how does MAP affect increase in CBF seen with volatiles?
doesn't - CBF increases within minutes independent of MAP
35
neuro effects of N2O
* significantly decreased cerebral vascular resistance
* increased CBF
* **increased** CMRO2
36
how do volatiles affect CMRO2
dose-dependent **decrease**
37
how do volatiles affect cerebral vascular reactivity to CO2
des, sevo, and iso maintain at \< 1 MAC
halothane eliminates autoregulation
at 1.5 MAC, sevo preserves autoregulation better than iso
38
intervention to counter increased ICP caused by volatiles
**hyperventilation to decrease PaCO2 to 30 mmHg**
* halothane: hyperventilate before agent
* others: hyperventilate with start of agent
39
iso, des, sevo, and N2O effects on CSF
* **iso**: increased reabsorption
* **des:** may increase or not change
* **sevo:** decreases production
* **N2O:** no change
40
how do volatiles affect EEG
* ~1 MAC = increased voltage, decreased frequency
* 1.5 MAC = burst suppression
* 2 MAC = isoelectric
41
volatile that has been associated with sz activity
what things might increase this risk?
sevoflurane
increased with sustained \> 2 MAC, hypocarbia (doubles), repeated auditory stimulation, preexisting sz disorder
42
how does MAC affect temperature regulation
dose-dependent impairment
threshold between shivering and vasoconstriction decreases as MAC increases
43
**dose-dependent** ventilatory effects of volatiles
* breathing pattern
* response to CO2
* airway resistance
44
alveolar ventilation and minute ventilation with volatiles
minute ventilation may not change
alveolar ventilation decreases with deadspace ventilation
45
how does substituting a portion of MAC with N2O affect PaCO2
substitution attenuates increase in PaCO2
46
how do volatiles affect PaCO2
increases proportionately with concentration of volatile
47
how do inhaled anesthetics affect response to hypoxemia
depressed response **when PaO2 \< 55mmHg**
**not** dose-dependent
48
what factors increase likelihood of airway irritability with des
\> 6% concentration
smoker
49
how to blunt airway irritability of des
* premed with 1.5 mcg/kg fentanyl or 0.1 mg/kg morphine
* increase slowly
* avoid inhalation induction
* humidify inspired gases
* add N2O
50
how do volatiles affect HPV?
concentrations used clinically do not prevent
51
how do volatiles affect MAP
all have dose-dependent decrease
halothane d/t decreased contractility
others d/t decreased SVR
52
how do volatiles affect CO, contractility, and O2 demand?
all cause dose-dependent myocardial depression
increased HR may offset decreased CO
decreased contractility = dose-dependent decrease in O2 demand
53
how does N2O affect CO
increased (mild sympathomimetic effects)
54
how do inhaled agents affect RAP
all increase except sevo (d/t decreased SV)
N2O increases d/t increased PVR
55
which volatile decreases SVR the most?
iso
56
how does N2O affect pulmonary vasculature
increases PVR - exaggerated in pts with preexising pHTN
57
how do volatiles affect HR
* sevo: increases only \> 1.5 MAC
* iso & des: increase at lower concentrations
* halothane: bradycardia
58
how do volatiles affect the baroreceptor reflex
dose-dependent depression (no reflex increased HR when BP decreases)
* des: attenuates response, doesn't abolish
* iso: maintained at 1 MAC, depressed at 2 MAC
* sevo: increasing to 4% (~2 MAC) decreases response
59
MAP that prevents coronary steal from happening
\> 60
60
risk factors for halothane hepatitis
* female
* middle age
* obese
* multiple halothane exposures
* potential genetic factor
61
metabolism of N2O
0.004% metabolized by normal flora in the gut (none by liver)
62
renal effects of volatiles & how to attenuate
* all cause dose-related decreased RBF
* decreased GFR & UOP
* attenuated by preop hydration
63
adverse effects of compound A
* high output renal failure
* inability to concentrate urine
* decreased response to vasopressin
64
how to decrease risk associated with compound A formation
* min. flows 2 L/min if case \> 2 hours, 1 L if \< 2 hours
* lower concentrations of sevo
* avoid KOH and NaOH in absorbent
* avoid increased temp in absorbent
65
how do volatiles affect skeletal muscles?
TOF?
dose-dependent skeletal muscle relaxation
the higher the MAC multiple, the greater the fade on tetanus
66
how do volatiles affect nondepolarizing NMBs
which has the biggest effect
enhanced neuromuscular blockade
des (specific study - effect on Roc)
des \> sevo \> iso \> TIVA
67
how do volatiles affect uterine smooth muscle & effects at different MACs
dose-dependent relaxation
0.5 MAC = modest relaxation
\> 1 MAC = significant
68
how does N2O affect uterine contractility
no effect
69
max. MAC to use in a pregnant mom having a non-labor procedure
why?
1.5
volatiles decrease uterine blood flow
70
what might trigger the antibody response that leads to halothane hepatitis?
TFA produced by degradation of halothane, iso, and des
71
immune effects of halothane
depresses defense against infection
oxidative burst response of neutrophils
72
how does iso affect CO?
preserved by increased HR (baroreceptor reflexes partially preserved)
73
which volatiles has mild beta adrenergic properties?
isoflurane
74
how does iso affect conduction?
slows rate of SA node discharge
increases refractoriness of accessory pathways & AV conduction system
prolongs QT in **healthy** pts
75
why is iso used for deliberate hypotension?
decreased O2 demand when used for deliberate hypotension
76
which volatile requires a preservative
halothane (thymol)
\*sevo has water added
77
adverse effect of rapidly increasing des concentration to \> 6%
SNS stimulation - increased BP/HR
can double HR and BP with change from 4 to 8% in \< 1 minute
(returns to normal within 5 minutes)
78
does N2O attenuate SNS stimulation that occurs with rapidly increasing des?
nope
but apparently does help blunt airway irritability
79
is coronary steal seen with CAD pts when des is used
nope
80
which volatile has less of an effect on hypoxic drive
desflurane
81
why is des used for deliberate hypotension
rapid titratability
reduced CMRO2 and CPP
82
at what MAC is autoregulation maintained with des
1
83
which volatile is the least metabolized
des (0.02%)
84
which volatile is assoc. with the greenhouse effect
des
85
how does sevo affect CO
decreased at 1-1.5 MAC, recovered at 2 MAC
86
how to treat bradycardia that occurs with sevo
decrease concentration
87
how does sevo affect conduction
may prolong QTc in pts with **preexisting** long QTc syndrome
88
change in SVR with iso vs. sevo
iso: dose-dependent, gradual reduction in arteriolar resistance
sevo: abruptly decreases resistance via aortic arch (at higher concentrations)
89
which volatile preserves the baroreceptor reflex to a greater extent than with other agents
sevo
90
which volatile has the least degree of airway irritation among available agents
sevo
91
volatiles assoc. with platelet aggregation
sevo, halothane
| (sevo more)
92
which volatile suppresses arachidonic acid
sevo
93
how much sevo is metabolized
what is the metabolite and is it significant
5-8% metabolized to inorganic fluorides
no evidence of clinically significant renal failure
94
is N2O organic or inorganic
inorganic
95
which inhalation agent supports combustion
N2O
96
CV effects of N2O & pts more prone to these changes
* direct myocardial depression
* SNS stimulation, increased SVR - more in young/healthy pts
* increased PVR - more in preexisting elevation
97
how does N2O affect NMBs
no effect on non-depolarizing
potentiates succs
98
which inhaled agent is assoc. with rigidity with opioids
N2O
99
why is N2O assoc. with analgesia
increased enkephalins
100
why does N2O cause polyneuropathy
oxidizing effect on cobalt atom of vitamin B12
101
which inhaled agent inhibits methionine synthetase & thymidylate synthetase?
what is the significance?
N2O
necessary for myelin and DNA - prolonged exposure can result in bone marrow suppression, pernicious anemia, and peripheral neuropathies
102
pts at increased risk for cobalamin deficiency with N2O
nutritional disorders: elderly, vegans, alcoholics
malabsorption: prolonged PPIs/H2 antagonists, pernicious anemia, atrophic gastritis, postgastrectomy, Whipple, ileal resection, Crohn's
infection, tapeworm
103
absolute contraindications to N2O
known deficiency of enzyme or substrate in methionine synthetase pathway
emphysema, PTX, middle ear surgery, pneumocephalus, air embolus, bowel obstruction
104
relative N2O contraindications
* increased ICP
* pHTN
* prolonged anesthesia (\>6 hrs)
* 1st trimester (teratogenic?)
* high risk PONV
105
how to avoid diffusion hypoxia assoc. with N2O
supplemental O2 for first 5-10 min after N2O discontinued
106
what is the second gas effect
theoretical - admin of high concentrations of N2O will cause increase in alveolar concentration of 2nd gas
107
where do SNS nerves arise
T1-L2
108
preganglionic vs. postganglionic fiber lengths
SNS: short preganglionic, long postganglionic
PNS: long preganglionic, short postganglionic
109
where do PNS nerves arise
CN III, Vi VII, IX, X from sacral spinal cord
110
neurotransmitter secreted by **all** preganglionic fibers
ACh
111
when do postganglionic fibers release ACh
all PNS postganglionic
some SNS (Sweat glands, some blood vessels)
112
what do most SNS postganglionic fibers release?
norepi
113
ANS fibers that go to adrenal medulla
**only** preganglionic
114
what is responsible for termination of action of norepi
reuptake
115
what metabolizes ACh
acetylcholinesterase (**not** pseudocholinesterase)
116
how does alpha 1 stimulation affect smooth muscles
vasoconstriction r/t increased intracellular calcium
117
how does alpha 1 stimulation affect insulin
inhibits secretion and lipolysis
118
how does alpha 2 stimulation affect norepi
inhibits release (negative feedback loop)
119
effects of postsynaptic alpha 2 receptors in CNS
hyperpolarization = sedation, decreased MAC, decreased SNS outflow
120
CV effects of beta 1 stimulation
inotropy, chronotropy, dromotropy
121
how does beta 2 stimulation affect muscle and vasculature
relaxation of respiratory, uterine, and vascular smooth muscles
vasodilation of skeletal muscle vasculature
122
effects of D1 receptor agonism
vasodilation of renal, mesenteric, coronary, and cerebral blood vessels
123
effects of D2 receptor agonism
presynaptic inhibition of NE release
N/V
124
where are nicotinic cholinergic receptors located
within ANS ganglion and at NMJ
125
how is the adrenal medulla mediated by the ANS?
innervated by preganglionic fibers directly from spinal cord
126
function of NE and epi once secreted from adrenal medulla
hormones, not neurotransmitters
127
does chronic treatment with albuterol cause upregulation or downregulation
downregulation
128
patients who may not have desired response with indirect acting sympathomimetics
denervation (heart transplant)
neurotransmitter depletion (sepsis)
129
receptors activated at \> 0.15 mcg/kg/min of epi
alpha1, beta1, beta2
130
effect of a beta blocker + epi
bronchoconstriction (especially with non-selective)
131
which catecholamine has the most significant metabolic effects
epi (increased blood sugar)
increased glycogenolysis and lipolysis
alpha 2 inhibits insulin release
131
receptors agonized by norepi
alpha1 = alpha2
beta1 \>\>\>\> beta2
132
how does high-dose norepi gtt affect HR
decreased d/t baroreceptor reflex (may be offset by beta1-mediated increased HR)
133
when should norepi gtt be avoided
cardiogenic shock/failing LV
134
how does dopamine have indirect sympathomimetic effects
increased NE release via beta 1 stimulation (but the ANS ppt says D2 inhibits NE release so idk)
135
how do dopamine vs dobutamine affect myocardial O2 supply and demand
dopamine: can make demand \> supply
dobutamine: less imbalance (coronary vasodilation increases supply & balances increased demand)
136
respiratory effects of dopamine
inhibits ventilatory response to arterial hypoxemia and hypercarbia
137
which catecholamine inhibits HPV
dobutamine
138
use of dobutamine
increase CO In CHF pts
139
most potent beta agonist
isoproterenol
140
good and bad uses of isoproterenol
**good**: increase HR in heart block or denervated heart, induce arrhythmias in cath lab, chemical pacemaker
**bad**: CAD
141
direct & indirect actions of ephedrine
direct: stimulates alpha and beta
indirect: stimulates NE release or prevents is reuptake
142
main effect of ephedrine
increased contractility (beta 1)
143
effect of ephedrine + beta blocker
resembles alpha agonist
144
how does ephedrine affect SVR
might not change d/t vasoconstriction (alpha1) **and** vasodilation (beta2)
144
how does ephedrine affect SVR
might not change d/t vasoconstriction (alpha1) **and** vasodilation (beta2)
145
DBP in epi vs. ephedrine
epi may decrease
ephedrine increases
146
how does ephedrine affect MAC
increases (CNS stimulation)
147
how does phenylephrine affect CO
decreased d/t decreased afterload or reflex bradycardia
148
drug of choice for treatment of hypotension in CAD
phenylephrine
149
phenylephrine preserves uterine blood flow
cool
150
MOA of clonidine & precedex
centrally acting alpha agonist (Alpha2 \> alpha 1 \>\>\>\> beta)
decreased SNS outflow from CNS
precedex is 7x more selective for alpha2
151
how does clonidine affect MAC
can decrease 50% d/t hyperpolarization of CNS cell membranes
152
CV effects of clonidine
dose-dependent decreased BP, HR, CO
rebound HTN if abruptly stopped
153
how to treat bradycardia with clonidine
decreased NE release (alpha 2) = decreased catecholamine levels = may require **anticholinergic** for decreased HR
154
use of clonidine in neuraxial techniques
inhibits spinal substance P release, blunts perception of noxious stimuli
prolongs effects
155
adverse effect of rapid precedex injection
HTN
156
how does precedex affect MAC
decreases \> 90%
157
conditions that are contraindications to digoxin
* WPW (30% develop Vfib)
* hypertrophic CM: increased contractility = increased obstruction
* acute MI: increased O2 demand
158
conditions that are contraindications to digoxin
* WPW (30% develop Vfib)
* hypertrophic CM: increased contractility = increased obstruction
* acute MI: increased O2 demand
159
MOA of digoxin
inhibits Na-K-ATPase which increases Na, affects Na-Ca exchange, and increases Ca inside the cell
= increased contractility
160
CV effects of digoxin
increased contractility
increased CO
161
EKG changes seen with digoxin
* prolonged PR
* short QTc
* ST depression
* small/inverted T wave
162
most common cause of digoxin toxicity
renal dysfunction
163
every 10 mmHg decrease in PaCO2 = serum K decreases by \_\_\_\_
0.5 mEq/L
164
correctable causes of digoxin toxicity
hypokalemia
hypomagnesemia
arterial hypoxemia
165
meds that cause dysrhythmias when given with digoxin
halothane, beta agonists, pancuronium, calcium
166
drugs that cause increased automaticity with digoxin
fentanyl
isoflurane
167
effect of increased cAMP in the myocardium vs vascular smooth muscle
what drug class does this
myocardium: increased intracellular Ca and increased contractility
muscle: decreased intracellular Ca, smooth muscle relaxation/vasodilation
PDE3 inhibitors
168
use of milrinone
what class is this?
PDE3 inhibitor
acute LV dysfunction after surgery, weaning from CBP
169
things that enhance and slow metabolism of theophylline
decreased/slowed: alcoholism, cimetidine, age extremes
enhanced: smoking
170
CV effects of alpha blockers
vasodilation
reflex tachycardia
orthostatic hypotension
hypoglycemia
171
uses of phentolamine
acute HTN emergencies, preop pheo
**PIV norepi infiltration** (should restore perfusion immediately)
172
how does phenoxybenzamine affect BP
increased CO despite decreased BP
## Footnote
**orthostatic hypotension with preexisting HTN or hypovolemia**
173
vasculature effects of beta blockers
blocking beta 2 = alpha 1 predominates = vasoconstriction
174
does prolonged use of beta blockers cause upregulation or downregulation
upregulation
175
which beta blockers are not recommended for diabetics? why?
nonselective (propranolol, timolol)
mask s/s hypoglycemia (HR), glycogen can't be broken down
176
contraindications to beta blockers
* AV heart block
* hypovolemia (eliminates compensatory tachycardia)
* COPD
* diabetic
* PVD, raynaud's
* alpha agonist use
177
treatment for beta blocker overdose
avoid epi and dopamine
1st: atropine, then glucagon
CaCl, isoproterenol (nonselective), dobutamine, pacemaker, iHD (minimally protein bound, renally excreted)
178
when can withdrawal be seen with beta blockers
within 24-48 hours (d/t upregulated beta receptors)
179
symptoms of beta blocker withdrawal
profound HTN
tachycardia
increased contractiltiy
180
which antagonist can dcrease its own metabolism
propranolol (via decreased hepatic blood flow)
181
how does propranolol affect myocardial O2 supply and demand
decreased o2 requirement \> coronary blood flow
182
how does propranolol affect fentanyl
decreases pulmonary uptake (more circulating)
183
when should metoprolol be held
HR \< 60 or SBP \< 100
184
most selective beta 1 blocker
atenolol
185
which antagonist provides better protection than fentanyl or lidocaine against tachycardia/HTN from DL
esmolol
186
MOA of labetolol
selective alpha 1 block, nonselective beta block
intrinsic beta 2 agonism
187
CV effects of labetolol
decreased SVR
unchanged CO
vasodilation (alpha 1 block, beta 2 agonism)
188
HR with labetolol
no reflex tachycardia - attenuated by beta 2 block
189
adverse effects of labetolol
orthostatic hypotension (most common)
bronchospasm (offset by alpha 1 block?)
CHF, bradycardia, heart block
190
MOA of carevedilol
alpha 1 + nonselective beta block
191
how do pts on antihypertensives respond to direct sympathomimetics
exaggerated response (no counter-balancing beta 2 activity)
192
how do ACE inhibitors affect aldosterone
decreased (decreased Na, H2O retention, increased K retentioN)
193
when are ACE inhibitors contraindicated
pts with renal artery stenosis
194
ideal HTN treatment in diabetics
ACE inhibitors (no metabolic effects)
195
how to treat angioedema from ACE inhibitors
IM epi
TXA
icatbiant
FFP
196
most common side effect of ACE inhibitors
cough
197
periop complication to expect if pt takes ACE inhibitor DOS
hypotension
198
how do calcium channel blockers affect vessels
arterial vasodilation
little effect on venous circulation
199
uses of CCBs
coronary artery spasm
unstable or chronic stable angina
essential HTN
200
how do CCBs affect NMBs
potentiate like mycin antibiotics
201
effect of verapamil + dantrolene
hyperkalemia, CV collapse
202
how does verapamil effect contractility, HR, and **conduction through AV node**
all decreased
203
effect of CCBs + volatiles
additive myocardial depression, especially if preexisting LV dysfunction
204
why shouldn't nifedipine be stopped abruptly
abrupt stop assoc. with coronary artery vasospasm
205
which CCB has the greatest vasodilating effects
nicardipine
| (especially coronaries)
206
when is nicardipine contraindicated
advanced aortic stenosis
207
which CCB is metabolized by esterases
clevidipine
208
use of nimodipine
treat vasospasms r/t SAH
209
which produces more NO - arteries or veins
arteries
210
how does NO affect smooth muscles
NO = increased cGMP = smooth muscle relaxation
211
NO has antithrombotic effects
kewl
212
how do NO synthase inhibitors affect MAC
dose-dependent reduction
213
MOA of Nipride
direct-acting arterial and venous vasodilation & smooth muscle relaxation
## Footnote
**reacts with hgb to form methemoglobin and releases cyanide & NO**
214
dose of nipride assoc. with cyanide toxicity
\> 2 mcg/kg/min
215
symptoms of cyanide toxicity with Nipride
tachyphylaxis
increased MvO2
metabolic acidosis
seizures
216
how to treat cyanide toxicity
stop gtt
100% O2
sodium bicarb
**sodium thiosulfate**
217
how does Nipride affect ICP?
increased d/t increased CBF & CBV
increase is **maximal if MAP decreases less than 30%**
\>30% decrease in MAP = ICP at awake levels
218
contraindications to Nipride
increased ICP and inadequate CBF
carotid artery stenosis
219
how does Nipride alter HPV
alters and causes shunting
more with healthy lungs
treat with PEEP
220
MOA of nitroglycerin
produces NO
venous dilation (arterial dilation at high doses)
221
how does nitroglycerin affect venous return
decreases
222
how does nitroglycerin affect CO in a normal heart vs. failing heart
normal: decreases CO
failing: increases, relieves pulmonary congestion
223
HR with nitroglycerin
baroreceptor-mediated reflex tachycardia
224
condition nitroglycerin is bad for
CAD
increases inotropy, which increases demand and decreases supply
225
nitroglycerin = better blood flow to ischemic areas
vs nipride which can cause coronary steal
226
MOA of hydralazine
interferes with calcium ion transport
direct systemic arterial vasodilator
227
how does hydralazine affect coronary perfusion
may decrease
| (Decreases DBP \> SBP)
228
how can hydralazine cause MI
baroreceptor-mediated direct increase in HR + increased SV & CO can affect supply/demand
229
which vasodilator is assoc. with a lupus-like syndrome
hydralazine
230
elimination ½ time of adenosine
0.6-1.5 seconds
231
BP goals in deliberate hypotension
SBP 80-90 mmHg
MAP 50-60 mmHg in normotensive pts
(best definition: 30% reduction)
232
contraindications to deliberate hypotension
severe anemia
untreated HTN
233
how to reduce rebound HTN with use of nipride gtt for deliberate hypotension
pretreat with propranolol or captopril
234
spinal blockade that prevents tachycardia
T1-T4
235
PaO2 and PaCO2 in deliberate hypotension
increased PaCO2 (increased dead space)
decreased PaO2 (increased shunt) - seen with Nipride not iso, in normal lungs not COPD lungs
236
at what MAP does CBF no longer respond to changes in PaCO2
\< 50 mmHg
237
MAP at which GFR is reduced
\< 75 mmHg
238
SBP guideline for deliberate hypotension
don't decrease to \< preop DBP
239
what determines FI (inspired gas concentration)
FGF
breathing circuit volume
circuit absorption
240
**vessel rich group:**
what's included?
body mass?
% CO?
brain, heart, liver, kidneys, endocrine
10% mass
75% CO
241
what determines FA (alveolar gas concentration)
* uptake
* alveolar ventilation
* concentration effect
* 2nd gas effect
242
**lean muscle group:**
what's included?
body mass?
% CO?
muscle, skin
50% body mass
18% CO
243
**fat group:**
what's included?
body mass?
% CO?
fat, duh
20% body mass
5% CO
244
**vessel poor group:**
what's included?
body mass?
% CO?
bone, ligament, cartilage
20% mass
2% CO
245
which of the 4 compartments in the 4 compartment model is slowest to equilibrate
vessel poor
246
Factors determining partial pressure gradient from machine to alveoli (input):
247
how does alveolar ventilation affect induction
increased alveolar ventilation = more rapid induction
more evident with more soluble anesthetics
248
how to prevent inhaled anesthetic overdose in inhaled induction
maintain spontaneous ventilation (potential for OD with controlled ventilation)
249
what is a time constant?
L / L/min
minutes required for 63% turnover of gas within a container
250
how many time constants until equilibrium is reached
4
251
Factors determining rate of transfer of agent from alveoli to arterial blood (Uptake)
* Solubility
* CO
* Alveolar to venous partial pressure gradient
252
Factors determining rate of transfer of agent from alveoli to arterial blood (Uptake)
* Solubility
* CO
* Alveolar to venous partial pressure gradient
253
how does b:g affect PA/PI
lower b:g = lower solubility = faster rate of rise
254
how does CO affect inhalation induction
increased CO = slowed induction (increased uptake, slower rise in alveolar partial pressure)
255
how does V/Q mismatch affect inhalation induction
slowed induction
poorly soluble more affected
(dilutional effect)
256
Factors determining the transfer of agent from arterial blood to brain (uptake)
* Brain:blood partition coefficient
* Cerebral blood flow
* Arterial-to-venous partial pressure difference
257
methods to increase elimination
* high FGF
* low anesthesia circuit volume
* low absorption by anesthesia circuit
* decrease solubility
* high cerebral blood flow
* increased alveolar ventilation
