Midterm Flashcards

1
Q

Dose of fentanyl

A

5-10 mcg/kg (50-100 mcg clinical)

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2
Q

Dose of propofol

A

1-2 mg/kg

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3
Q

Dose of etomidate

A

0.2-0.3 mg/kg

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4
Q

Dose of Versed

A

0.1-0.2 mg/kg (1-2 mg clinical)

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5
Q

ketamine dose

A

2-4 mg/kg (10-50 mg clinical)

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6
Q

What stage of awareness is a MAC case?

A

3- subconscious, implicit recall

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7
Q

What stage of awareness is a general anesthesia case?

A

4- no awareness or recall

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8
Q

MoA of inhalational agents

A

activate GABA and glycine, inhibit glutamate

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9
Q

What is MAC?

A

minimum alveolar concentration- concentration required to keep 50% of humans from moving in response to painful stim

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10
Q

VP of halothane

A

244

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11
Q

VP of isoflurane

A

240

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12
Q

VP of desflurane

A

669

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13
Q

VP of sevoflurane

A

170

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14
Q

BG coefficient of nitrous

A

0.46

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15
Q

BG coefficient of halothane

A

2.54

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16
Q

BG coefficient of isoflurane

A

1.46

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17
Q

BG coefficient of desflurane

A

0.42

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18
Q

BG coefficient of sevoflurane

A

0.69

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19
Q

MAC of nitrous oxide

A

104

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20
Q

MAC of halothane

A

0.75

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21
Q

MAC of isoflurane

A

1.2

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22
Q

MAC of desflurane

A

6

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23
Q

MAC of sevoflurane

A

2

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24
Q

OG coefficient of nitrous

A

1.4

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25
OG coefficient of halothane
224
26
OG coefficient of isoflurane
98
27
OG coefficient of desflurane
18.7
28
OG coefficient of sevoflurane
55
29
What conditions increase MAC?
youth, hyperthermia, hypernatremia, chronic ETOH, stimulants
30
What conditions decrease MAC?
age, hypothermia, pregnancy, acute ETOH intox, other anesthetics, drugs (benzos, opioids, alpha 2 agonists)
31
MAC awake
50% respond to verbal stim- 0.2-0.3
32
MAC bar
block autonomic reflex- 1.7-2x MAC
33
MAC intubation
2x MAC
34
ED95
level where 50% don't respond- 1.3x MAC
35
Fick's law of diffusion
rate of diffusion directly proportional to gradient, surface area, and diffusion coefficient, and inversely proportional to membrane thickness
36
Graham's law
rate of effusion inversely proportional to square root of molecular weight
37
Blood gas coefficient
indicates how fast drug gets to site of action
38
Oil gas coefficient
indicates potency
39
What does increased CO do to uptake?
uptake increases and induction is slower
40
What gas is metabolized the most?
halothane
41
Where is nitrous metabolized?
in the gut by aerobic bacteria
42
What two gases are structurally similar?
iso and des- differ only by Cl atom
43
Which gas metabolite is a concern for liver?
halothane- hepatitis
44
Which gases have the least effect on blunting autoregulation?
isoflurane or desflurane
45
Who do you avoid using halothane in?
cardiac defects (down's syndrome)
46
What gas can cause bradycardia and junctional rhythms at high MAC?
sevo
47
What gases at higher doses will exhibit sympathetic response?
desflurane and isoflurane
48
Which gases produce the most "coronary steal"?
iso and des (sevo the least- can use to precondition)
49
What condition should you avoid the use of nitrous oxide with?
pulmonary hypertension
50
Describe gas breathing
increased RR, decreased TV
51
What metabolite is toxic to kidneys?
Compound A from sevo (avoid in renal patients if you can)
52
How do you reduce production of compound A?
higher flows, keep soda lime fresh, use lower concentration
53
How do anesthetic gases decrease total hepatic blood flow?
decrease portal vein flow
54
Complication of N2O use?
reduced immune function- disrupts DNA synthesis by inactivating B12
55
Contraindication to nitrous?
air containing cavities (air embolus, closed pneumo, etc)
56
What is the mechanism of malignant hyperthermia?
activation of ryanodine receptors- increased release of calcium from SR--> sustained m. contraction--> increased metabolism= heat production
57
What are the signs and symptoms of MH?
tachycardia, hypercarbia, hyperthermia, masseter spasm, tachypnea, arrhythmias, metabolic acidosis, m. rigidity, myoglobinemia, hyperkalemia
58
Treatment for MH
dantrolene, stop agents, 100% O2 with charcoal filter, arterial access, cooling measures
59
What does dantrolene do and what are the considerations?
blocks coupled calcium entry- causes m. relaxation so may need respiratory support
60
Which opioid receptor has antishivering effects?
kappa
61
Order of opioid potency from least to greatest
demerol < morphine < dilaudid < alfentanil < fentanyl < remifentanil < sufentanil
62
Which opioids have the fastest onset?
fentanyl, sufentanil, remifentanil
63
Which opioid has the shortest duration of action?
sufentanil (and fentanyl)
64
What causes cardiovascular effects from opioids?
histamine release (naturally occurring opioids)- venodilation, bradycardia--> hypotension
65
What can occur with high doses of synthetic opioids?
muscle rigidity- decreased chest wall compliance
66
What is the longest acting opioid?
morphine
67
Where is morphine metabolized and what is it conjugated to?
liver- morphine 3 (inactive- seizures), morphine 6 (active- resp depression)
68
Is morphine more for dull or sharp pain?
dull
69
Describe codeine
natural occurring opioid, 10% breaks down to morphine, more used for anti-tussive properties than pain
70
Why would you use Dilaudid over morphine?
renal insufficiency- no active metabolites
71
Dose of Dilaudid
0.2-0.5 mg IV
72
What is demerol used for?
post-op shivering
73
When should you avoid demerol?
renal insufficiency (active metabolite buildup --> seizures), and concurrent use with MAOIs (serotonin syndrome)
74
Storage site of inactive fentanyl metabolites?
lungs- significant first pass pulmonary uptake
75
How is remifentanil metabolized?
esterases in blood (majority) and some by N-dealkylation
76
What can remifentanil boluses cause?
bradycardia unresponsive to vagolytics- may need epi
77
Rare effect of remifentanil?
hyperalgesia
78
What opioid is best for chronic pain?
methadone
79
Why is fentanyl preferred over alfentanil?
longer duration of action
80
What opioid is preferred for cardiac and airway cases?
sufentanil- significant analgesia
81
Considerations for using opioids in neuraxial analgesia
smaller doses, watch for respiratory depression, must be preservative free
82
What is the ceiling effect in regards to agonist-antagonists?
increased doses do not produce additional responses
83
How do you administer Narcan?
20-40 mcg IV carefully titrated to prevent rapid reversal (can cause sympathetic response, pulmonary edema, severe pain, arrhythmias)
84
Duration of Narcan?
1-4 hours
85
When should you avoid using toradol?
renal patients, asthma patients, and ortho (inhibits bone healing)
86
What stage is a patient at risk for laryngospasm?
stage 2
87
CV effects of propofol?
tachycardia on induction, decreased SVR, hypotension
88
Propofol Infusion Syndrome symptoms
acidosis, hypertriglyceridemia, renal failure, bradycardia, hypotension, rhabdo
89
What are some phenomena that may occur on induction with propofol?
twitching, opisthotonus
90
What is a common side effect of etomidate?
myoclonus
91
Does a standard induction dose of etomidate cause apnea?
no
92
What do you want to ensure before giving barbituates?
adequate volume status (can cause profound vasodilation)
93
What can barbituates trigger?
acute intermittent porphyria
94
How is ketamine different from other induction drugs?
sympathomimetic (increased HR, BP, CO), increases ICP, CMRO2; also a NMDA antagonist instead of acting on GABA
95
What population is ketamine good for?
severe asthmatics
96
What may ketamine cause?
increased salivation
97
List benzos in order of shortest to longest half life
versed (2 hours), Ativan (15 hours), valium (30 hours)
98
Schedule 1 drugs
heroin, LSD, marijuana, qualudes, ecstasy
99
Schedule 2 drugs
cocaine, meth, pentobarb, fentanyl, codeine
100
Schedule 3 drugs
barbituates, hydrocodone, ketamine
101
Schedule 4 drugs
phenobarb, valium, butorphanol
102
Schedule 5 drugs
buprenorphine, codeine cough syrup
103
What are the different "tropys"?
ino- force of contraction; chrono- rate; dromo- speed of electrical conduction; lusi- relaxation
104
How do beta blockers work?
slow phase 4 depolarization
105
What are the vascular effects of nitric oxide?
vasodilation, antithrombotic, anti-inflammatory, anti-proliferative
106
What are drugs that act on the nitric oxide pathway?
hydralazine (arterial), nitro (venous), nitroprusside (both)
107
What is a neuro consequence of using nitro or nitroprusside?
increases ICP
108
What is a possible complication of nitroprusside?
cyanide toxicity
109
What are the effects of CCBs?
varying degrees of myocardial depression, vasodilation, activation of ANS
110
What do ACEIs do?
reduce BP by blocking the conversion of angiotensin I to angiotensin II
111
What do ARBs do?
reduce BP by blocking angiotensin II receptors
112
What are some interactions of CCBs with anesthetics?
potentiate m. relaxants and local anesthetics
113
How do you treat refractory hypotension as a result fo ACEIs?
vasopressin or methylene blue
114
What are the 4 classes of antidysrythmics?
1- sodium blockers; 2- beta blockers; 3- K blockers; 4- Ca blockers
115
What is the effect of lidocaine on the heart?
blocks fast Na channels, decreases automaticity, accelerates repolarization
116
What kind of beta blockers do we prefer to use?
selective- like esmolol
117
What is amio?
K channel blocker- used for life threatening ventricular rhythms
118
What kind of CCB is good for neuro cases?
nimodopine (crosses BBB)