NMB part two Flashcards
what dose for roc if you want it to work quick?
1-1.2 mg/kg
Out of vec, roc, and cis, which has the least cumulative effects?
cis
Supposedly, why does roc work faster?
“lack of potency”
since it is less potent than vec or cis, we inject 5x the dose / molecules (0.6-1.2 mg/kg) therefore more receptors are blocked faster due to greater number of roc molecules
tell me about a “priming dose”
give 10% of the ED95 about 4 minutes before the main dose to speed onset, the priming dose will occupy the spare receptors leaving the main dose to get right to work
not really applicable for roc
vec drug class, concentration, onset, duration
monoquaternary aminosteroid
0.1 mg/kg
3-5 minute onset
20-35 minute duration
“pancuronium minus the quaternary methyl group in the A-ring of the steroid nucleus”
vec metabolites and potency
3-desacetyl vec, 50% potent
3,17-desacetyl vec, less than 10% potent
since vec undergoes __ metabolism and __ excretion, if your patient doesn’t have those organs it’s probably not the best choice
hepatic metabolism
renal excretion
tell me about hypoventilation enhancing vec postop, or why you should always reverse your patients
let’s say you don’t reverse the vec, take the patient to the pacu where they get snowed with morphine and hypoventilate, become acidotic and re-paralyze
does vec has cardiovascular effects?
is vec a good choice for infusion?
no cv effects
not a good choice for infusion due to large Vd and cumulative effects
Can vec cross the placental barrier?
nope
should you dose vec on actual or ideal body weight?
ideal
does vec alter intraocular pressure or trigger MH?
no and no
what is roc’s drug class, dose, onset, and duration?
monoquaternary aminosteroid- basically vec with a hydroxyl group instead of an acetyl group on the A-ring of the steroid nucleus
0.6-1.2 mg/kg
1-2 minutes onset
20-35 minutes duration
what is the only non-depolarizer that serves as an alternative to succs for rapid sequence?
roc
roc metabolism and excretion
50% excreted unchanged in bile
hepatic metabolism and renal excretion, so duration prolonged with ESRD and lived dsfxn
Cis drug class, dose, onset, duration, concentration
benzylisoquinolinium 0.1 mg/kg onset 3-5 minutes duration 20-35 min 2mg/ml concentration
Is cis good for constant infusion?
yes, rate of recovery not influenced by prolonged infusion
How is cis metabolized? Metabolites?
(Cari) Hoffman elimination (77%)
laudanosine and a monoquaternary acrylate
Succs onset, duration, dose
30-60 seconds onset
3-5 minutes duration
1-1.5 mg/kg for intubation
is succs degraded by acetylcholinesterase like ACH or by pseudocholinesterase?
pseudocholinesterase- slower hydrolysis than ACH by acetylcholinesterase = prolonged depolarization
most succs is hydrolyzed before reaching junction, however because pseudo cholinesterase is not found in the junction, end of succs blockade is due to succs ___ away from the junction
diffusion
how much can succs raise your K+
average 0.5 mEq per liter, due to K+ leakage from sustained ion channel opening
succs doses >2mg/kg, repeated doses, or infusions may cause __ of response to succs, leading to a phase 2 block
inhibition/desensitization
metabolites and potency of metabolites of succs
hydrolyzed by plasma cholinesterase to succinylmonocholine then to succinic acid and choline, not active
succs dosing for infants and small children?
2mg/kg
may result in profound brady or asystole, pretreat with atropine
who is succs contraindicated for?
major burns multiple trauma extensive denervation of skeletal muscle upper motor neuron injury = severe hyperK = cardiac arrest
how does succs cause bradycardia / arrest?
ACH is the primary neurotransmitter of the parasympathetic nervous system, so give a big dose of a drug that mimics ACH (succs) and you will have a huge parasympathetic response (brady or arrest). Pretreat with vagolytic.
Let’s say your IV just died and your patient is suddenly having laryngospasm, what do you do?
IM succs 3-4 mg/kg, onset at laryngeal muscles will be faster than complete flaccidity which will take 2-3 minutes
How many days after a burn covering >30% of your patient’s body will their risk of hyperK be highest?
7-10 days
Will pretreatment with non-depolarizers prevent hyperK?
NO NO NO
succs adverse effects
dysrhythmias, hyperK, myalgia, myoglobinuria, increased intragastric pressure, increased ICP, increased IOP, sustained skeletal muscle contractions
can succs cause MH?
yes
if your patient is on digoxin and you don’t know their current dig level (they could be dig toxic) should you use succs?
best to avoid it
Two ways succs can alter your heart rhythm
- vagal stimulation (stimulation of cardiac muscarinic cholinergic receptors by mimic ACH) (most likely to occur with second dose, atropine will NOT prevent this brady)
- hyperK
how to treat a hyperK cardiac arrest
IV calcium
bicarb
glucose/insulin
hyperventilate
for PEDS, don’t use succs unless it is
an emergency intubation laryngospasm difficult airway full stomach IM use
“when seconds matter”
symptoms of histamine release following succs administration includes
flushing, hypotension, bronchoconstriction
your patient has an eye injury, should you use succs?
if you want their vitreous humor to squirt out of their eye
If your patient has a full stomach, why should you pretreat them with a non-depolarizer before giving succs?
Because succs can increase intragastric pressures greater than 20 cmH2O leading to reflux back through lower esophageal sphincter.
Will a phase 1 block exhibit post-tetanic potentiation?
NO
slide 87
A phase 2 block with succs looks __ like a non-depolarizer block
exactly
What is more sensitive, single twitch or fade on TOF/tetanus?
fade on TOF/tetanus
What is the % blockade and clinical significance of no twitches?
100% blocked, suitable for intubation
What is the % blockade and clinical significance of 1 twitch?
90%, suitable for mechanical ventilation
What is the % blockade and clinical significance of 2 twitches?
80-90% blocked, mech. ventilation some patients, short term relaxation
What is the % blockade and clinical significance of three twitches?
75-80%, maintenance doses needed.
What is the % blockade and clinical significance of 4 twitches?
0-75% blocked, suitable for reversal
Why should you check TOF after giving succs and before giving non-depolarizers?
To make sure you’re not in a phase 2 block, which is indistinguishable from a non-depolarizer block. The treatment is different for the two. Phase 2 block from succs = go sleep it off in the ICU for 12 hours. Non-depolarizer block = give anticholinesterase and anticholinergics.
How to reverse a phase 2 block.
Do not give anticholinesterases until 20 minutes of spontaneous recovery has passed and a plateau has been reached. Giving it before this time could lead to prolongation of a mis-diagnosed phase 1 block. Try edrophonium first to confirm phase 2, then if reversal occurs use a longer acting like neostigmine.
Obese patients have __ plasma cholinesterase activity and therefore may require __ amounts of succs.
increased plasma cholinesterase
increased succs
Dibucaine number of 80%? 60%? 20%?
80% normal
60% reduced quality, 30 minute paralysis
20% greatly reduced quality, prolonged paralysis
dibucaine number is indicative of the QUALITY, not the QUANTITY of plasma cholinesterase.
plasma cholinesterase activity is diminished with…
genetics pregnancy severe liver or kidney dz malignant tumor infection burns anemia decompensated heart dz
