final Flashcards
1
Q
enzyme that rapidly hydrolyzes Ach (<15 milliseconds) into acetic acid and choline
prevents the sustained depolarization of muscles!!
A
Acetylcholinesterase (AchE):
2
Q
Burns, muscular dystrophy, stroke, immobilization, paralysis, Guillian-Barre
Channels remain open 4x longer, major issue with hyperkalemia!
A
extra junctional receptors
3
Q
If you apply electrical activity directly to muscle, it will _____________ regardless of NMB (false positive)
A
retract
4
Q
what lead goes directly to the nerve
A
BLACK
5
Q
adductor pollicis brevis (thumb)
A
ulnar nerve
6
Q
PLANTAR flexion of big TOE
A
Posterior tibial nerve
7
Q
DORSIflexion of foot
(this is preferred for lower extremity)
A
Lateral popliteal/peroneal nerve
8
Q
Facial nerve=orbicularis oculi or frontalis
reflects onset of ____________
A
laryngeal muscle relaxation
9
Q
if using facial nerve, it is possible to _______dose the relaxant, _________estimate recovery, ______estimate blockade
A
it recovers first!
so you will overdose relaxant
overestimate the patient being recovered
and
understimate the blockade
10
Q
If looking for onset of NMB use:
A
orbicularis oculi or frontalis
11
Q
onset of NMB
A
small rapidly moving muscles, then
trunk, abd, then
diaphragm
12
Q
recovery of NMB
A
diaphragm, then
small rapidly moving muscles, then
trunk, abd
13
Q
what recovers first in NMB
A
diaphragm
14
Q
what is the issue with single twitch
A
there is no control
15
Q
Ideal for maintenance phase and helps decide whether you need to re-dose
A
TOF
16
Q
true or false
4 twitches back are NOT an indication of recovery
A
true
17
Q
2/4 means: ____ block
A
90% block
18
Q
3/4 means: ____ block
A
80% block
19
Q
4/4 means: ____ block
A
70-75% block still!!!
20
Q
is headlift an indication of recovery?
A
NO (50-60%)
21
Q
Easier to detect fade than TOF, still not great
A
double burst
22
Q
Best indication of recovery for NMB
A
tetanus (tetanic stimulation)
painful
WAIT at least 10 minutes between! To avoid false info (due to increased Ach)
23
Q
Post-tetanic twitches of ____ coincides with 1st twitch of TOF
A
10 PTT=1st twitch TOF
24
Q
Post-tetanic twitch of 1 means ___ minutes (intermediate) or ____ minutes (long acting) until TOF has its 1st twitch
A
8 min=intermed
30 min=long acting
25
what is the indication of recovery
sustained tetanus with no fade
26
Always assess baseline twitches after _____, and before NMB; there is potential issue with ____ and atypical plasma cholinesterase and you need to know the source of what is wrong
Sch
27
Guidelines for Reversal:
no twitches
do not attempt (can PROLONG it)
28
Guidelines for Reversal:
1 twitch
30 minutes
29
Guidelines for Reversal:
2-3 twitches
4-12 minutes
30
Guidelines for Reversal:
4 twitches
2 minutes (edrophonium)
5 minutes (neostigmine)
31
Binds to the alpha subunits of the postsynaptic nicotinic receptor and mimics Ach; causes the muscle cell membrane to depolarize
Sch (depolarizers)
32
side effects of Sch
bradycardia, tachycardia
increased BP
increased SVR
33
indications for Sch
difficult airway***
RSI
full stomach/aspiration risk
34
Blockade is ENHANCED/accentuated by anticholinesterase
phase I
35
* Fasciculations; rapid recovery, short duration of action
* Decreased single twitch
* Lack of fade of tetanus
* Minimal fade of train-of-four
* No post-tetanic twitch
phase I
36
* Fade of tetanus
* Fade in train-of-four
* Posttetanic twitch
* Prolonged duration in 50%
* Blockade is REVERSIBLE/attenuated by anticholinesterase!
phase II
37
which phase do you NOT use reversal
phase I
38
Metabolizes Sch
By the time it gets to the receptor, there is very little left
plasma/pseudo cholinesterase
39
Dibucaine 80
homozygous normal
5-10 minutes until recovery
40
Dibucaine 40-60
heterozygous atypical
30 minutes until recovery
41
Dibucaine 20
homozygous atypical
>3 hours
42
which drug do you dose for TOTAL body weight for obese patients
Sch
43
Anticholinesterase Drugs
(leading to PROLONGED Sch)
* Insecticides
* Myasthenia gravis medications
* Glaucoma medications
* Chemo drugs
* Alzheimer’s medications (not clinically significant)
44
Inhibitors of Plasma Cholinesterase
(leading to PROLONGED Sch)
reglan
45
Hyperkalemia (increase ___ to __ in labs)
.5 to 1
(Do NOT use Sch after 24 hours with burns)
46
Bad side effects of Sch
histamine
hyperkalemia
brady and tachy
increased IOP, ICP, IGP
myalgia
myoglob/rhabdo
MH
masseter spasm
skelatal muscle contraction
47
If you give the nondepolarizing DEFASCICULATING dose, then you need to ___________ the Sch dose*
INCREASE
48
what is NOT prevented with defasciculating dose for Sch
hyperkalemia
49
Competes with Ach to bind with the alpha subunits on the postjunctional AchR to prevent the ion channel from opening and preventing the muscle cell membrane from depolarizing
Nondepolarizing NMBs
50
________curonium:
steroidal
51
________curium:
Benzylisoquinoline
52
what are NMBs reversed by
ANTIcholinesterase
Anticholinesterases metabolize acetylcholinesterase, leading to increased Ach
53
Less potent the drug=the _________ the number of the ED95=the more rapid the onset
less potent=higher number=more rapid
54
fastest to slowest onset for NMBs
(SCh) > Rocuronium > Atracurium, Vecuronium, Mivacurium > Nimbex
55
potency NMBs
Roc/Sch 0.3
Atracurium 0.2
Vec/cisat 0.05
Pancuronium 0.07
Mivacurium 0.08
56
To facilitate MORE RAPID intubation, a small dose (1/10th the intubating dose) of the same NMB is given prior to the induction
priming dose
57
3 NMBs that cause histamine
atracurium
mivacurium
curare
58
NMB plasma cholinesterase elimination
mivacurium
59
NMB
Inhibiting histamine-N-methyl-transferase
(Like histamine)
vecuronium
60
Independent of organ function
Good for infusions
Indicated for pulm issues, organ dysfunction
hoffmann mainly
nimbex
61
Laudanosine*: metabolite that is a CNS stimulant (seizures in animals)
prolonged elim in renal failure
independent of organ function
atracurium
62
Anaphylactoid
(Like histamine)
good for RSI
NOT indicated for difficult airway
roc
63
NMB can cause release of norepi
pancuronium
64
Block is LESS dense; patient will recover FASTER; must give BIGGER dose to have similar effect
resistance
65
phenytoin would lead to increase in __________ to NMBs (leading to ___________ duration)
increased RESISTANCE
shorter duration
66
what are the drugs for NMBs that cause increase in RESISTANCE
phenytoin
CHRONIC corticosteroids
aminophylline/theophylline
LARGE lasix
67
chronic hyperkalemia
nondepolarizers=more resistant
depolarizers=sensitive
68
true or false
denser block= potentiated
true
69
volatile anesthetics = _________ anticholinesterases
RETARD
this leads to decrease in Ach, leading to more sensitivity to nondepolarizers
70
which type of abx cause increased sensitivity to NMBs
aminoglycosides
gentamicin, neomycin, streptomycin, kanamycin, amikacin, tobramycin
NOT erythromycin
71
if giving Sch first, give a _________ dose of NMB
SMALLER DOSE
72
elderly have ________ onset to drugs
slower onset
ALWAYS give smaller dose
73
reversals for NMBs
ANTIcholinesterases
edrophonium
neostigmine
pyridostigmine
physostigmine (ONLY lipid soluble/tertiary amine, cross BBB)
74
which drugs are irreversible anticholinesterases
o Insecticides (dog dipper)
o Echothiophate (eye drops)
o Nerve gases
75
Once acetylcholinesterase is maximally inhibited, giving more anticholinesterase will ____ reverse a block
NOT reverse it
you will just have to WAIT for block to end
(IF GIVING Sch AFTER LARYNGOSPASM and nondepolarizer, BLOCK WILL BE PROLONGED)
76
what is reversal of NMBs affected by
o Antibiotics
o Hypothermia
o Respiratory acidosis (PaCO2>50 mm Hg)
o Metabolic acidosis
o Hypokalemia
77
true or false
anticholinesterases are the OPPOSITE of anticholinergics
true
anticholinergics treat anticholinesterases
78
Anticholinesterase Overdose*
TOO much Ach! (think of PNS symptoms)
NMJ: weakness ranging to paralysis
Miosis (constriction)
inability to focus vision
copious salivation
bronchoconstriction
bradycardia
abdominal cramps
loss of control of bowel and bladder
Confusion
ataxia
seizures
coma
respiratory depression
TREATMENT: atropine or pralidoxime
79
what are the anticholinergics
robinul (secretions + HR)
atropine (HR + CNS)
scopolamine (N/V/CNS + secretions)
80
Central Anticholinergic Syndrome
too much SNS
restlessness, hallucinations, somnolence, unconsciousness
81
what type of NMBs does suggamedex work on
steroidal group
82
drug of choice for difficult airway
Sch
83
which drugs inhibit plasma cholinesterase
neostigmine
cyclophosphamide
reglan
84
true or false
do NOT use Sch for long cases
true
85
longest to shortest CSHT
FASR
fentanyl
alfentanil
sufentanil
remifentanil
86
what is CSHT
distribution, metabolism, duration, infusion
87
the DRUGs affect on the body
pharmacodynamics
(ED95, MOA, sensitivity/resistance, etc)
88
½ time between drug concentration in the blood and site of effect; accounts for the delay in effect
effect site equilibration
89
Vd is __________ related to protein binding
inverse
90
plasma level decreases to the point that drug diffuses away from site of effect and to peripheral groups or to elimination phase
redistribution
91
besides NMB,
can occur with gentamycin, quinidine, tricyclic antidepressants, naloxone, local anesthetics
channel blockade
92
treatment for central anticholinergic syndrome
physostigmine
93
sugga is incompatble with what drugs
verapamil, ondansetron, ranitidine
94
Neostigmine- paired with _______
Edrophonium- paired with ___________
Neostigmine- paired with glyco
Edrophonium- paired with atropine
95
Potency (most potent > least potent)
Sufentanil > Fentanyl > Alfentanil > Morphine > Tramadol > Demerol
96
Lipid Solubility (most lipid > least lipid)
Sufentanil > Fentanyl > Alfentanil > Demerol > Morphine
97
potency
Meperidine 1/10 as potent
Fentanyl 100 times more potent
Sufentanil is 10 times more potent than fent
Alfentanil 1/5 as potent as fent
Remi 5 times more potent than fent
98
o Closure of voltage-gated Ca2+ channels on PREsynaptic nerve terminals to cause a reduction of the release of neurotransmitters
o Opening of K+ channels to hyperpolarize the cell (conductance), thus causing inhibition of the POSTsynaptic neurons
opioids
99
Alpha blockade causing direct aortic dilation
sufentanil + alfentanil
100
treatment for sphincter of oddi
glucagon
101
moderate increase in ICP due to vasodilation when without hypercarbia
fentanyl
102
More intense, but LESS respiratory depression; can extubate sooner than fentanyl
sufentanil
103
good alternative to morphine if in renal failure
dilaudid
104
most reliable indication of respiratory depression is
decreased LOC
105
what is NOT dose dependent for neuraxials
urinary retention
106
glycine
Anxiolytic = ____________ (think STEM-SPINAL)
brainstem=anxiolytic
107
glycine
muscle relaxant= ____________(think STEM-SPINAL)
spinal cord
108
GABA
Anticonvulsant= _______________
(think C-C)
Anticonvulsant= brain motor circuits
109
GABA
Sedation = __________ (think C-C)
cortex=sedation
110
bind to benzodiazepine receptors (part of the GABA receptor), which ENHANCE the AFFINITY of binding of GABA to its receptor , opening of chloride channel, hyperpolarization of the neuron, inhibition of the neuron to excitation
benzos
111
Apnea with larger doses and exaggerated in patients with COPD
versed
112
Metabolite that prolongs sedative effect
best benzo hemodynamics
diazepam
113
most potent
Lasts up to 6 hours- vented patients
lorezepam
114
best to least for amnesia
lorezapam
115
CNS stimulant; stimulates hypoxic drive via the activation of chemoreceptors in the carotid bodies (PaO2 is 38 mmHg)
doxapram
116
doxapram does what to the lungs
increases Vt, with some RR increase
117
most lethal to least lethal dose
morphine, fentanyl, alfentanil, sufentanil, then remi
118
which drug causes weak alpha blockade
sufentanil
119
SA node depression, slowed conduction through AV node
bradycardia in opioids
120
decreased respiratory rate,
increased Vt
opioids
121
accentuated vent depression
Older age >60 years
Occurrence of natural sleep/sleep disorders
Male
Opioid naivety
Chronic heart failure
Intra-articular morphine
122
renarcotization (increase in resp depression)
1) Mobilization of opioids from other compartments (e.g., muscles, fat group)xcg rincreased blood flow, increased movement, warming
2) Reduction in stimulation post-extubation
123
opioids cause cerebral vaso_______________ for NORMAL paco2
vasoconstriction (good thing)
cerebral vasodilation for HYPERcarbic patients
124
MOA: direct stimulation of chemoreceptor trigger zone in floor of the fourth ventricle
opioids N/V
125
Low lipid solubility of morphine
slow onset and prolonged duration
126
o First-pass effect
Fentanyl and sufentanil
127
termination of action for opioids
Small/single opioid doses: redistribution
Large/massive/repeated opioid doses: Metabolism
128
opioid by plasma esterases
remi
129
byproduct that is a CNS stimulant that can cause seizures with renal failure
normeperidine
do NOT give with renal failure
130
An active metabolite that is toxic for renal failure patients, leads to prolonged duration
M6G
131
When used with propofol for TIVA (total intravenous anesthesia), propofol inhibits degradation of alfentanil and sufentanil by ___-___%!
50-60%
132
neuraxials ONSET
Morphine: ONSET 6-12 hrs until respiratory effects!
Sufentanil: 6 minutes
133
MOA: interacting with opioid receptors in the trigeminal nucleus
pruritus
134
treatment for pruritus
gabapentin
135
neuraxial side effect NOT related to dose size
urinary retention
136
Similar in chemical structure to atropine (antimuscarinic/anticholinergic)
Causes tachycardia! And increased bronchodilation
demerol
137
More intense analgesia, LESS respiratory depression, extubated sooner!
sufentanil
138
Single, brief stimulus
Laryngoscopy
Retrobulbar block (cataract)
alfentanil
139
Opioid-Induced-Hyperalgesia
+
neuro assessments
remi
140
o Great for patients with renal failure
o Similar metabolism to morphine
dilaudid
141
rarely dysphoria
stadol
142
antagonist agonist good for CV
nubain
143
not good for CV patients
talwin and stadol
144
narcan does not work
buprenex
145
good for hyperalgesia
suboxone
146
Hypovolemic patients (trauma, extreme dehydration): exaggerated MAJOR decrease in SVR and BP
versed
147
Decrease in Vt (tidal volume)!
benzos
148
Only slightly less potent than diazepam
Drowsiness returns after 6 hours
o Dezmethyldiazepam
149
o Competes with benzos and displaces them for the benzodiazepine receptor site on the GABA receptor
flumazenil
150
o Displaces the opioid from the receptor, binds to receptor, inactivates it
narcan
151
Acute pulmonary edema
Sympathetic stimulation due to rapid return of pain
Tachycardia
V fib
HTN
N/V
Return of airway reflexes (could lead to laryngospasm)
narcan
o Critically ill
o CAD, CHF, cardiac surgery
o Lung dx
o Opioid dependence
152
o Cerebrovascular disease
o Acute head injury
o CAD, HTN
o Asthma (reactive airways)
* Caution!
doxapram
153
o Primary mechanism for redistribution/termination is redistribution from VRG to lean muscle group
iv anesthetics
154
ideal IV anesthetic is ________soluble
water soluble
155
pH of 10.5 (alkaline); bacteriostasis
If mixed with acidic things (opioids, catecholamines, NMBs), will form precipitate
pentothal
156
the more drug bound, the _________ the diffusion
slower
157
MOA
Increases the DURATION of GABA
Directly MIMICS GABA at its receptor
Activates: glutamate, adenosine, nACh receptors
barbiturates
158
normovolemic barbiturates
Minimal decrease in BP
Reflexively increase in HR (due to carotid sinus baroreceptor)
Slowing the rate of administration (giving incrementally) does NOT change the decrease in BP or increase in HR
159
Decreased Vt and decreased RR
barbiturates
160
Cerebral protection= gold standard*
* Only for incomplete cerebral ischemia: cardiopulmonary bypass, hypotension, circulatory arrest
pentothal
161
which barb is an anticonvulsant
pentothal
(causes histamine)
162
Increased excitatory activity,
methohexital + etomidate
163
o Increases AFFINITY for GABA
o Mimics inhibitory effects of GABA
Depresses reticular activating system
etomidate
164
Decreased Vt; increased RR
etomidate
165
Adrenocortical suppression
etom
166
o Plasma esterases
etom
167
which drug for cardiac patients
etom
168
o Alpha2 adrenergic agonist (8x more selective than clonidine)
precedex
169
reduces emergence delirium
Titratable
o Easily arousable
o Antisialagogue (reduces secretions)
o Longer duration than propofol
o Decreased PONV
precedex
170
Hyperpolarization (cell becomes more negative) with efflux of K out of the cell
Decreased norepi release due to presynaptic receptors (results in vasodilation)
Inhibition of adenylyl cyclase decreased cAMP decreased calcium
precedex
171
Precedex given fast and bolus
HTN!!!
bradycardia
172
o “Some” analgesia (pain relief) for neuropathic, chronic pain only
propofol
173
GABA receptor agonist: leads to inhibition of GABA and hyperpolarization of cell membranes
propofol
174
Decreased HR, SVR, BP, CO
bronchoCONSTRICTION
Extreme issues with hypovolemia, LV dysfunction, elderly (lead to exaggerated BP decline)
propofol
175
best anti emetic
propofol
176
Decreased CMRO2, CBF, ICP, IOP
Helps support SSEPs and MEPs (evoke potentials)
propofol
177
* >75 mcg/kg/min for >24 hours in the ICU
* Initially tachycardia, then BRADYcardia (lethal in peds)
* Metabolic/lactic ACIDOSIS
Propofol Infusion Syndrome
178
Antagonist, non-competitively binds to NMDA receptors to block it
Inhibits glutamate (excitatory transmitter)
Interacts with all opioid receptors (mu, kappa, delta)
Anti-muscarinic (leads to bronchodilation, sympathomimetic)
Anti-nicotinic: analgesia
Na+ channels: local anesthetic
Ketamine
179
Lots of thick secretions (pretreat with antisialagogue: glycopyrrolate)
Emergence delirium occurs (midazolam)
ketamine
180
DO NOT GIVE WITH
CAD* + pulmonary HTN
LOW catecholamines (critically ill)
ketamine
181
causes bronchodilation (good for asthma)
ketamine
182
Cardiac (most safe to least safe)
Etomidate > methohexital > pentothal > ketamine > propofol
183
Emesis (greatest emesis to least)
Etomidate > ketamine > pentothal/methohexital > propofol
184
Lipid Solubility (most lipid to least lipid)
* Pentothal > methohexital
185
Potency (greatest to least)
* Methohexital > pentothal
186
COX-1; Non-Selectives (1 & 2)
NSAIDS
decreased platelet aggregation
o Decreased renal function
o Increased GI toxicity risk
187
NSAIDS
SMALL Vd
HIGH protein bound
malnourished, elderly will have GREATER effect
188
Allergic reaction with nasal polyps
Bronchoconstriction, rhinitis, urticaria, aseptic meningitis
Reye’s syndrome (peds)
nsaids
189
_______volemia (increases renal toxicity risk)
HYPO
190
delayed bone healing
do NOT use with hypovolemia
do not use with ulcerative patients
toradol
191
IRREVERSIBLY inactivates COX-1: leading to prolonged/inhibited platelet aggregation*
aspirin
(at least 7 days before using neuraxial)
192
true or false
o Give TIVA as an infusion rather than bolus
true
193
when is the largest thrombin produced
propagation phase (common pathway)
194
MOA
o Binds to antithrombin leads to enhanced binding with thrombin
heparin
195
Dosed based on circulating heparin (often over-dosed)
clearance is fast
anaphylaxis
protamine
196
Newer Oral Anticoagulants (NOACs)
and
Low Molecular Weight Heparin (LMWH)
no reversal
197
Vitamin K ____ days for reversal
2-3 days
198
elective procedures
Consider patient specific risks/benefits
199
effects of aspirin are around for the life of the __________*; other NSAIDS effects are for the life of the drug
platelet
200
Activates plasminogen into plasmin increased clot breakdown
thrombolytics
(tPA)
201
NOT a “procoagulant”
o Reduces risk of death due to bleeding, regardless of the cause*
Blocks conversion of plasminogen to plasmin decreased clot breakdown/lysis
Decreased blood loss, decreased blood products, no risk of thrombi
antifibrinolytics
(TXA), amicar, aprotinin
202
o Must give < 3 hours post-injury
antifibrinolytics
203
indications
o Hemophilia
o Life-threatening hemorrhage
o CV surgery
very expensive
novoseven
204
high risk for N/V
o Post-op opioids
o General anesthesia
o Volatile anesthetics, nitrous oxide
o Female
o History of PONV/motion sickness
o Non-smoker
o Younger age (<50)
o Surgery (ENT, strabismus, abdominal, gyn, laparoscopic)
205
o If prophylaxis fails: don’t give the same drug as before, use a different drug class*
If prophylaxis worked, then 6 hours later patient has PONV: give same drug
206
peds are ____x as likely to vomit as adults
2x
(age 3-13)
207
Dopamine
Serotonin 5HT3
Opioid receptors
Chemoreceptor Trigger Zone (CTZ)
208
Muscarinic (Ach)
Histamine (H1)
vestibular system
209
Irritation of the Pharynx (vagus nerve)
Gag and retch response
210
Vagal and Enteric Afferents
Mucousa of the GI tract
Stomach stretch*
Serotonin 5HT3
211
o GABA
o Acetylcholine = muscarinic
o Histamine = H1
o Serotonin 5HT3
o Dopamine
o Substance P
o Neurokinin 1
receptors
212
MOA
Anticholinergic (Ach/muscarinic) + antihistamine effect
antihistamines
213
contraindicated with parkinsons
PBR
phenothiazines (phenergan, compazine)
butyrophenones (droperidol, inapsine)
reglan
214
MOA
o Blocks transmission to the medulla of impulses from overstimulation of vestibular apparatus (motion sickness)
scopolamine
215
MOA
o Dopamine blockade (alpha blockade)
o Causes vasodilation due to peripheral alpha blockade (leading to decrease in BP)
butyrophenones (droperidol)
216
serontonin 5HT3 only has affect on
vomiting ONLY
217
increases CRMO2 and ICP
ketamine
