Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Sp: Pharm 1 > 2. Sedative, Hypnotics, IV Anesthetics > Flashcards

2. Sedative, Hypnotics, IV Anesthetics Flashcards

1
Q

sedation

A

calming and drowsiness
decreases activity
moderates excitement
calms pt

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

hypnosis

A

produces drowsiness
facilitates the onset/mx of sleep

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

anesthesia

A

global but reversible CNS depression results in loss of response to and perception of external stimuli
“deafferentation”

changes in behavior and perception

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

anesthetic effects

A

amnesia
decreased/diminished pain response
immobility to noxious stimuli
analgesia
unconsciousness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

anesthetic drugs can

A

enhance inhibitory synaptic activity
(GABA/Glycine)

or

diminish excitatory activity
(Glutamate)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

glutamate anatomy

A

relay neurons all levels and some interneurons

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

glutamate receptors

A

NMDA
AMPA
Kainate
metabotropic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

NMDA (gultamate)

A

excitatory
increase cation conductance
(esp Ca++)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

AMPA (glutamate)

A

excitatory
increase cation conductance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Kainate (glutamate)

A

excitatory
increase cation conductance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

metabotropic (glutamate)

A

inhibitory (presynaptic)
- decrease Ca conductance
- decrease cAMP

excitatory
- decrease K+ conductance
- increase IP3
- increase DAG

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

glycine anatomy

A

spinal interneurons and some brainstem interneurons

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

glycine receptors

A

glycine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

glycine receptor MOA

A

inhibitory
increase Cl conductance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

GABA anatomy

A

spuraspinal and spinal interneurons

pre and postsynaptic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

GABA receptors

A

GABAa
GABAb

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

GABAa

A

inhibitory
increase Cl conductance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

GABAb

A

inhibitory

presynaptic:
- decrease Ca conductance
postsynaptic:
- increase K conductance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

drug catetogies

A

sedatives
hypnotics
anesthetics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

potential drug effects

A

amnesia
analgesia
anticonvulsant
muscle relaxation
respiratory
depression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

drug classes

A

benzodiazepines
non-bz sedative hypnotics (Z drugs)
barbituates
melatonin congeners
IV anesthetics
inhaled anesthetics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

balanced anesthesia

A

combination of agents to limit dose and toxicity of each agent

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

triad of general anesthesia

A

unconsciousness
analgesia
muscle relaxation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

IV agent uses:

A
  • sedation-based
  • monitored anesthesia care
  • regional anesthesia
  • conscious sedation
  • deep sedation
  • light general anesthesia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

monitored anesthesia care (MAC)

A

regional or local anesthesia delivered with supplemental sedation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

conscious sedation

A

small doses
pt mxs airway
pt responds to commands
ICU for prolonged mechanical ventil

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

light state of general anesthesia

A

loss of protective reflexes
inability to mx airway
lack responsiveness to sx stimuli

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

IV induction side effects
(non-anesthetic)

A

CV (?)
pain at injection site
movement
hiccups
apnea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

IV recovery side effects
(non-anesthetic)

A

restlessness
nausea
vomiting

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

GABA type

A

inhibitory CNS neurotransmitter

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

GABAa receptor

A

pentameric structure
- subunits: aby
major isoform has
- 2 alpha 1
- 2 beta 2
- 1 gamma 2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

GABA binding site (GABAa)

A

2 sites (one on each lobe)
located between a1 and b2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

BZ binding site (GABAa)

A

between a1 and y2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

BZ binding is

A

allosteric modulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

BZ effects GABAa by

A

attracting more GABA to the receptor to bind

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

barbituates effect GABAa by

A

increasing the duration the channel is open

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

allosteric agonist

A

different binding site
enhance effect

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

allosteric antagnoist

A

different binding site
inhibit effect

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

onset time

A

how quickly the drug takes to get from blood to tgt organ
(brain/viscera)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

continuous infusion half life

A

pt may take longer to recover from a continuous infusion compared to a single dose due to a prolonged half life

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

barbiturates

A

methohexital (Brevital)
thiopental (Pentothal)
thiamylal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

barbituates MOA

A

-allosteric modulation
-enhance Cl conductance
-increased duration of GABA-gated Cl channel opening

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

barbituates structure

A

derived from barbituric acid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

methohexital will elicit

A

epilectiform activity

used in electroconvulsive therapy or surgeries where seizures are desired

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

barbituates admin

A
  • IV
  • rectally (peds)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

barbituates lipid solubility

A

high

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

barbituates distribution

A

plasma:brain equilibrium rapidly
- onset within 30 sec
rapid diffusion to other tissues
- limited duration of induction
(20 min)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

barbituates and elderly

A

reduce induction dose
slower redistribution
longer duration of action

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

barbituates repeated doses
(or continuous infusion)

A

saturates peripheral compartments
minimize redistribution effect
increases duration of action

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

barbituates metabolism

A

metabolized by CYP enzymes
no active metabolites

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

barbituates elimination

A

some renal elim of metabolites
some excretion in feces
methohexital cleared rapidly by liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

barbituates formulations

A

alkaline solution for solubility

will precipitate when mixed w/weak bases
- roc, lidocane, labetalol, morphine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

barbituates site of action

A

CNS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

barbituates CNS onset

A

10-20 sec
bolus lasts 8-20 min
half life: 3-12 hrs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

barbituates CNS impacts

A

constrict cerebral vasculature
-decrease BF/ICP
-decrease cerebral O2 consumption
anticonvulsant (except methohexital)
-decreases EEG
decrease pain threshold
involuntary muscle movements
-hiccups, myoclonus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

barbituates cardiovascular impacts

A

peripheral vasodilation: BP decreas
neg ionotropic effects (CO decrease) venous vasodilation
- (decrease BP/CO)
vagolytic compensatory responses
- HR and contractility

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

barbituates contraindications

A

Pt w/o adequate baroreceptor response
- hypovolemia
- beta blocker therapy
- congestive heart failure

asthma pt (histamine response)

acute intermittent porphyria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

barbituates respiratory impacts

A

dose related respiratory depression
incomplete suppress of airway reflex
apnea
bronchospasm
hiccup
laryngospasm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

barbituates histamine release

A

may cause hypotension/tachycardia
rare allergic reactions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

barbituates pharmacodynamics

A

no muscle relaxation
injection pain
no analgesia
no renal/hepatic toxicity
induce ALA-S (may trigger porphyrins)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

acute intermittent porphyria

A

neurological disease cause by inadequate porphyrin metabolism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

porphyrins

A

highly reactive oxudants
cause toxic neurological seueqlae

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

porphyrias symptoms

A

nausea
vomiting
abdominal pain
psychosis
lower motor neuron palsies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

barbituates status

A

being replaced by propofol
methohexital used for ECT
thiopental not used in US

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

barbituates interactions req dose reduction

A

opioid
alpha 2 adrenergic agonist
benzodiazepine
acute ethanol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

barbituate dose reduction for pts w/

A

anemia
low protein
decreased cardiac output
shock
elderly

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

benzodiazepines (BZ)

A

diazepam
lorazepam
midazolam

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

BZ mechanism of action

A

potentiate GABA inhibition
increase efficiency of GABA
increase freq of Cl channel openings
GABA must be present
binds to BZ receptor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

flumazenil

A

BZ receptor antagonist

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

BZ structure

A

3 ring structure
water soluble
- affects parenteral prep

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

BZ lipid solubility

A

high
speeds up CNS onset

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

diazepam absorption/admin

A

oral
- 1-2 hr onset
IM
- painful/erratic absorption

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

lorazepam absoprtion/admin

A

oral
- 1-2 hr onset
IM
- well absorbed
- 90 min peak

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

midazolam absorption/admin

A

oral
IM
- well absorbed
- 30 min peak
IV
- short onset (minutes)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

BZ lipid solubility

A

M>D>L

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

BZ distibution to brain

A

time to onset:
M<D<L

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

BZ redistribution

A

rapid
3-10 min
short duration of effect

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

BZ protein bound

A

high
>= 90%

79
Q

BZ metabolism

A

hepatic
phase 1 oxidation
active metabolites (D/M)
Phase 2 rxns = metabolite
conjugation for elimination

80
Q

BZ half life

A

D>L>M

81
Q

BZ excretion

A

renal
enterohepatic recirculation
- Diazepam

82
Q

enterohepatic recirculation

A

the process by which biliary excreted drug is reabsorbed in the intestine instead of being removed from the body

83
Q

high dose midazolam accumulation

A

accumulation of active metabolite in pts w/kidney failure

84
Q

high lipid solubility =

A

high volume of distribution

85
Q

volume of distribution

A

the theoretical volume that would be necessary to contain the total amount of an administered drug at the same concentration that it is observed in the blood plasma

86
Q

BZ Vd

A

L<D<M

87
Q

BZ hepatic extraction

A

Low: D/L
High: M

88
Q

BZ CNS effects

A

sedation
hypnosis
anesthesia
amnesia
anticonvulsant
muscle relaxation (not paralysis)
tolerance
dependence
decreased CBF/O2 consumpt/ICP
muscle relaxation at spinal cord
anterograde amnesia
antianxiety
stupor/unconsciousness (induction)
control seizure activity
no analgesia

89
Q

BZ cardiovascular impacts

A

minimal
lg doses may decrease BP
w/opioids may decrease BP
possible increase HR

90
Q

BZ respiratory impacts

A

minimal respiratory depression
decrease ventilatory resp to CO2
induction apnea
thrombophlebitis
(D>M»L)

91
Q

BZ drug interaction

A

drugs that induce/inhibit CYP P450
opioids - decrease SVR = hypotension
decrease MAC (incr potency of IA)
additive effects w/sedative/resp dep.B

92
Q

BZ status

A

perioperative period
sedation-hypnosis
procedure not req analgesia/full anes
seizure control
ICU sedation

93
Q

BZ receptor antagonist

A

flumazenil
reversal agent for midazolam
competitive antagonist
no impact to BZ elimination/conc
half-life: 54 min
duration of action: 20 min
re-sedation may occur

94
Q

Ketamine MOA

A

inhibit NMDA receptor complex

95
Q

NMDA complex

A

glutamate receptor
affects CNS/spinal cord
dissocaitive anesthesia
- dissociates thalmus to limbic
appears awake but unable to respond to stimuli
no global CNS depression (some stimulation)

96
Q

Ketamine potency

A

0.1
some psychotomimetic effects

97
Q

Ketamine isomers

A

S+: potent anesthetic w/o psychotomimetic effects
- greater affinity for NMDA = greater potency

98
Q

Ketamine absorption

A

IV

or

IM

99
Q

Ketamine distribution

A

lipophilic
fast onset
short duration (10-15min)

100
Q

Ketamine metabolism

A

induction of CYP enzymes
extensive hepatic extraction (oral)

101
Q

Ketamine active metabolite

A

Norketamine
(less potent)

102
Q

Ketamine excretion

A

renal elimination of metabolites
(aka renal elimination of norketamine)

103
Q

Ketamine analgesic

A

excellent analgesic at subanesthetic doses (2.5-15 mcg/kg/min)

104
Q

Which drug can be a complete anesthetic?

A

ketamine

analgesia
amnesia
unconsciousness

105
Q

“complete” anesthetic

A

analgesia
amnesia
unconcsciousness

106
Q

Ketamine CNS effects

A

cerebral vasodilator
- increase blood flow
- increase ICP
does not lower seizure threshold
anticonvulsant alt for status epilepticus

107
Q

Ketamine onset

A

15-30s

108
Q

Ketamine duration

A

10-15 min

109
Q

analgesia/amnesia onset/duration

A

immediate onset
duration: 40 min

110
Q

Ketamine emergenc reactions

A

occur in 10-30% of adults

  • delirium, excitement, confusion, euphoria, fear, vivid dreaming, hallucinations
  • 1st hour of emergence
  • lower rate in peds
111
Q

how to minimize ketamine emergence reactions

A

benzodiazepine

112
Q

Ketamine cardiovascular reactions

A

central sympathetic stimulation
- inhibits NE
- increase NE in synaptic cleft
- increase HR, BP, CO

113
Q

Ketamine contraindications

A

coronary artery disease
uncontrolled hypertension
congestive heart failure
arterial aneurysms

114
Q

Ketamine CV exceptions

A

may see direct myocardial depression in pts w/ depleted catecholamines/spinal cord transection

w/ very lg doses
(Ca++ channel blocker)

115
Q

Ketamine respiratory effects

A

minimal effect on RR
minimal effect on ventilatory drive (CO2)
bronchodilator (racemic)
increase salivary/trachiobronchial secretions

116
Q

Ketamine muscular effects

A

myoclonic activity (uncontrollable twitching)
stimulates uterine muscle contract
no risk for malignant hyperthermia

117
Q

Ketamine drug interactions

A

a/b adrenergic receptor antagonists
- block ketamine sympa effects
- direct myocardial depress. effects

118
Q

Ketamine drug additives

A

inhaled anesthetics
propofol
BZ
GABA acting agents

119
Q

Ketamine status

A

used w/BZ in emergent/trauma situations
severe depression

120
Q

Propofol MOA

A

interacts w/GABAa receptor
- binds to beta subunit
allosterically increases binding
affinity of GABA for GABAa receptor
- hyperpolarization of membrane
binds to multiple ion channels
- glutamate related

121
Q

Propofol formulation

A

Not water soluble
1% solution oil/water emulsion
lipophilic (10% fat emulsion)

122
Q

Propofol absorptions

A

IV only

123
Q

Propofol distribution

A

rapid onset
short duration

124
Q

Propofol initial distribution half life

A

2-8 min

125
Q

Propofol metabolism

A

hepatic &
extra hepatic clearance

hepatic conjugation to inactive metabolites –> renal clearance

126
Q

Propofol Cerebral/CNS effects

A

decrease cerebral BF, BV, ICP
antiemetic
antipruritic
no analgesic effects

127
Q

Propofol contraindications

A

pts w/elevated ICP
- can cause critical reduction in ICP unless steps are taken to support BP

pts w/porphyrias

128
Q

Propofol CNS effects

A

dystonic movements
- excitatory mvmt w/induct/emerg
seizures
- some anticonvulsant properties
- epileptogenic in pts w/seizure diag

129
Q

Propofol tolerance

A

does not occur w/repeated doses

130
Q

Propofol addiction

A

not common

131
Q

Propofol cardiovascular effects

A

decrease BP by 15-40%
- decreased SVR/cardiac filling
- effects contractility
- inhibits baroreceptor response
(HR unchanged w/BP decrease)

132
Q

Propofol BP impacts are greater in

A

pts w/
hypovolemia
elderly
LV dysfunction
beta blockers

133
Q

Propofol respiratory effects

A

respriatory depression
decreased CO2 response
30-60 sec apneic period post-induct
inhibits airway reflexes
minimal histamine release
lees impacts to asthmatics

134
Q

Propofol muscle effects

A

NO muscle relaxation

135
Q

Propofol pain w/injection

A

burning/stinging
can give lidocaine before/with
opioid before

136
Q

Propofol other effects

A

sedative/anxiolytic
antiemetic (subanesthetic doses)
antipruritic
OB/GYN safe

137
Q

Propofol porphyrinogenic

A

increases ALA reductase activity

138
Q

Hypertriglyceridemia

A

high blood lipids
can be caused by prolonged/continuous propofol
critical care/peds at higher risk

139
Q

Propofol infusion syndrome

A

metabolic acidosis
lipemic plasma
myocardial failure
hepatomegaly
rhabdomyolysis

140
Q

Propofol status

A

induction
anesthetic mx
ICU

141
Q

Propofol onset

A

10-20 seconds

142
Q

Propofol awakening

A

2-8 min

143
Q

Propofol induction

A

use w/midazolam
additive effect w/midazolam/opioids
- decrease propofol by 10%+

144
Q

Propofol TIVA

A

use w/remifentanil and ketamine

145
Q

Propofol and fentanyl

A

increase concentrations of fentanyl/alfentanil
may be able to decrease propofol dose

146
Q

Propofol dosing (elderly)

A

smaller induction dose

147
Q

Fospropofol formulation

A

water soluble prodrug
(no lipid emulsion)
sterile aqueous clear solution

148
Q

Fospropofol metabolism

A

metabolizes to:
- propofol
- phosphate
- formaldehyde

149
Q

Fospropofol onset/recovery

A

slower onset than propofol
longer duration than propofol

150
Q

Fospropofol uses

A

monitored anesthesia care
w/O2

151
Q

Etomidate MOA

A

enhances GABA
- binds to GABAa (increase affinity)
- increase Cl- conductance

152
Q

Etomidate absorption

A

IV only

153
Q

Etomidate distribution

A

high-protein binding
high lipid solubility
large non-ionized fraction

rapid onset

154
Q

Etomidate metabolism

A

metabolized by:
plasma esterases
hepatic CYP enzymes

155
Q

Etomidate clearance

A

renal clearance

156
Q

Etomidate CNS/Cerebral effects

A

potent
hypnotic
decrease cerebral metabolic rate
decrease CBF/ICP
well mx cerebral perfusion
EEG changes
- no seizures during ECT
- seizures in pts w/epilepsy
involuntary muscle movements

157
Q

Etomidate onset

A

20-30 sec

158
Q

Etomidate duration

A

5 min

159
Q

Etomidate cardiovascular effects

A

reduced sympa/barorecept response
decline in SVR
no histamine release
low rate incidence of hypersensitivity

160
Q

Etomidate indication

A

pts w/
impaired LV function
cardiac tamponade
hypovolemia
emergent tracheal intubation
high risk CV pts

161
Q

Etomidate respiratory effects

A

less depression
no apnea (unless +opioids)

162
Q

Etomidate endocrine effects

A

suppress adrenal cortical function
- inhibit 11-b-hydroxylase
(enzyme needed for steroid biosynt - cortisol
- body cant make cortisol 4-8 hrs post sedation

163
Q

Etomidate analgesia

A

None

164
Q

Etomidate contraindication

A

not used in ICU sedation
- cortisol not produced 4-8hrs post

165
Q

Etomidate status

A

typically used w/BZ for induction
- neurosurgical case
- CV risk pts

166
Q

Dexmedetomidine

A

Alpha 2 receptor agonist
greatest affinity for Alpha 2 in CNS

167
Q

Alpha 2 receptor

A

stops stimulating NE

168
Q

Dexmedetomidine FDA indications

A
  • sedation of intubated and ventilated pt in ICU
  • sedation prior to and/or during surgical procedures of non-intubated pts
169
Q

Dexmedetomidine MOA

A

selective alpha 2 adrenergic agonist
<24 hr sedation (prolonged use can cause withdrawl)

170
Q

Dexmedetomidine Uses

A
  • presedation
  • procedural sedation
  • GA supplementation
  • ICU sedation
  • withdrawl treatment/prevention
  • Epidural regional

** No amnesia

171
Q

Dexmedetomidine CV effects

A

hypotension (25-50% pts)
bradycardia (5-15% pts)
withdrawal effects > 24 hrs

nausea

172
Q

Dexmedetomidine withdrawal effects

A

BP
nervousness
agitation
headache

173
Q

Dexmedetomidine respiratory effects

A

little effect on ventilation

174
Q

Dexmedetomidine dosing

A

loading dose: 1 mcg/kg over 10 min
infusion: 0.2-0.7 mcg/kg/hr

175
Q

Dexmedetomidine onset/duration

A

rapid onset
half-life: 2 hrs

176
Q

Dexmedetomidine drug interaction

A

vasodilators
cardiac depressants
drugs that decrease HR
hypnotics

177
Q

Dexmedetomidine reduce dose for

A

combo w/hypnotics/volatile agents
- offsets hypotensive effects

renal/hepatic insufficiency

178
Q

Dexmedetomidine other uses

A

post-op shivering
premed for Ketamine/intubation

179
Q

Dexmedetomidine pt candidates

A

drug/alcohol withdrawal
chronic pain
unwilling/able to take opioids
hypertension
if you need hypotension for sx
ophthalmic surgery
ketamine anesthesia

180
Q

doxapam

A

respiratory/CNS stimulant
given for respiratory depression

181
Q

doxapam MOA

A

selective activation of carotid chemoreceptors by low doses

  • stimulates hypoxic drive (low PO2)
182
Q

doxapam adverse effects

A

seizures
muscle fasciculation
HA
dizzy
tachycardia
arrythmia
nausea/vomiting

183
Q

doxapam contraindictions

A

epilepsy
cerebrovascular and CAD
acute head injury
hypertension
asthma

184
Q

doxapam dosing

A

IV bolus
0.5-1 mg/kg

185
Q

doxapam onset

A

1 min

186
Q

doxapam duration

A

5-10 min

187
Q

doxapam continuous infusion

A

1-3 mg/min

Max: 4mg/kg

188
Q

malignant hyperthermia

A

rare (1:15000 peds, 1:40000 adults)
acute hypermetabolic state
mostly on induction

189
Q

malignant hyperthermia signs

A

profound MMR
tachycardia
hypercarbia
hyperthermia

190
Q

malignant hyperthermia MOA

A

uncontrolled release of intracellular Ca++ in skeletal muscle

VA or Succ bind to nAChR causing depolarization
depolarization is prolonged in MHR

191
Q

malignant hyperthermia treatment

A

stop VA/Succinycholine
hyperventilate
bicarbonate
dantrolene
cooling measures

192
Q

dantrolene MOA

A

binds to Ryr1 receptor of Ca channel
inhibits Ca release from SR

193
Q

dantrolene dosing

A

20 mg/60mL water

initial dose: 2.5mg/kg every 5 min until episode terminated

Max: up to 10 mg/kg

Sp: Pharm 1 (9 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions