Neuromuscular blocking drugs Flashcards
What are the three components of the neuromuscular junction?
Presynaptic nerve terminal, synaptic cleft, postsynaptic muscle membrane
What does acetyhlocholinesterase do?
located at the NMJ it hydrolyzes acetylcholine
What is butyrylcholinesterase?
“plasma cholinesterase” or “pseudocholinesterase” synthesized in the liver and hydrolyzes succinylcholine in the plasma
What are reasons we would need to paralyze a patient for?
surgeries that compromise the chest or abdominal cavity or if the patient is fighting ventilation
Monitoring of the thumb
contraction of the adductor muscle or ulnar nerve is the preferred method
Monitoring of the face
facial nerve monitoring involves stimulation of the orbicularis oculi muscle (facial nerve)
When would you assess the ulnar nerve and when would you assess the face?
always assess the ulnar nerve unless arm is tucked and then we have to assess the facial nerve
What is the onset of relaxation with NMBD?
Eye muscles–> extremities–> trunk–>abdominal muscles–> diaphragm
Where is most of the drug distributed?
Blood flow is greatest to the head, neck and diaphragm so more drug distributed here
What are the five clinical tests of neuromuscular function?
Single twitch Train of Four Double-burst suppression Tetanus Post-tetanic count
Describe how the train of four works.
Gives four separate stimuli every 0.5 seconds at 2 Hz
comparison is made between the four twitches T1-t4
Describe what train of four will look like in non-depolarizing agent.
There is a successive decrease in twitch response between T1-T4 (fade)
Describe how much is blocked with 0-4 twitches.
zero twitches-100%
T2-T4 (1-2 twitches): 90-95%
T3-T4: 80-85%
T4: 75-80%
If a patient has 4 twitches, will we still reverse them?
It might depend because we know that even with 4 twitches they can still be 60% blocked. with sugammedex we reverse everyone
What is tetany monitoring?
continuous electrical stimulation for 5 seconds at 50-100 Hz
reliable for detecting fade
sustained contraction w/o fade; significant
paralysis unlikely
What is posttetanic count?
Tetany followed in 3 seconds by single twitch stimulations
the higher the count (>8) the less intense the block
What is single twitch?
Single twitch at 0.1-1 Hz for 0.1-0.2 milliseconds
only tells us whether we’re 100% paralyzed or not
What is double burst suppression?
improves the ability to detect residual paralysis
evaluating 2 rather than 4 twitches facilitates
detection
What are tests that are unreliable for extubation?
5-second head left (TOF ratio <0.6)
generate peak negative inspiratory pressure 20-30 cmH20
What is significant about the NMB structure?
All neuromuscular blockers are quaternary ammoniums meaning they have a charge so they won’t cross the BBB
low Vd
What will you see on the TOF monitor with a non-depolarizing blockade?
Decrease in twitch tension
fade during repetitive stimulation
post-tetanic potentiation acetylcholine
Why do we get a twitch depression?
d/t block of postsynaptic nicotinic acetylcholine receptors
Why do we get post-tetanic or TOF fade?
results from blocking presynaptic nicotinic acetylcholine receptors
amount of released ACh does not match the
demand
A depolarizing block is characterized by:
Decrease in twitch tension
no fade during repetitive stimulation
no postetanic potentiation
A phase 1 block is often preceded by
muscle fasiculation
With a depolarzing blockade, a phase 2 block is seen
in repeated or long-term administration
Doses >6 mg/kg
inhibit pre-synaptic AChR
it act like a non-depolarizer creating a higher concentration in the body
When would we re-dose succinylcholine?
we wouldn’t unless it’s an emergency
What kind of drug is succinylcholine?
only depolarizing muscular blockade
What is the dosage of succinylcholine?
1.0 mg/kg
How quickly does succinylcholine create intubating conditions?
60 seconds
What is the recovery from succinylcholine?
90% muscle strength in 9 to 13 minutes
How is succinylcholine metabolized?
short acting due to rapid hydrolysis by butrylcholinesterase
dissociates into succinylmonocholine and further into succinic acid and choline (whole process is done in minutes)
How do we get recovery from succinylcholine?
drifts away from the NMJ down its concentration gradient and out into plasma
Where is butrylcholinesterase metabolized and found?
metabolized in the liver and found in the plasma
What is butrylcholinesterase responsible for metabolizing?
Succinylcholine, mivacurium, procaine, chloroprocaine, tetracaine, cocaine, and heroin
What are factors that decrease PChE activity?
advanced liver disease, age, malnutrition, pregnancy, burns, oral contraceptives, MAOIs, echothiphate, cytotoxic drugs, neoplastic disease, and anticholinesterase drugs
Beta blockers also cause mild prolongation of succinylcholine but not long enough to notice in surgical cases
What is a dibucaine number?
A dibucaine number reflects the quality of cholinesterase not quantity (Dibucaine of 80 infers 80% of enzyme inhibited)
normal genotype= >70
heterogenous for atypical gene= dibucaine 40-60 (prolongs block for 1.5-2 x longer)
Homogenous for atypical gene= dibucaine <30 (prolongs block for 4-8 hours)
What are the cardiac side effects of succinylcholine?
Bradycardia, junctional rhythm or sinus arrest
acts on cardiac muscarinic receptors
symptoms more likely to occur in second dose given within 5 minutes of 1st dose or in pediatric patients
Stimulation of the autonomic ganglia may cause:
ventricular dysrhythmias, tachycardias, and increased blood pressure
How does succinylcholine affect potassium?
Hyperkalemia- 0.5 mEq/dL increase in plasma concentration in healthy individuals
may be severe in: burn patients, abdominal infections, metabolic acidosis, closed head injury and conditions associated with upregulation of nAChR (paraplegia, muscular dystrophy, Guillian-Barre)
avoid in children except for emergency intubation
What specific pediatric patient population do we avoid administration of succinylcholine and why?
in children’s with duchenne’s muscular dystrophy because succ can cause myoglobinuria which is damage to skeletal muscle
What type of surgery would we avoid succinylcholine administration in?
not widely accepted in open eye surgery because of increased intraocular pressure (peaks at 2-4 minutes and pressure returns to normal by 6 minutes)
What CNS effects does succinylcholine cause?
Increased intracranial pressure- can be attenuated with pretreatment of non-depolarizing drug
What GI effects does succinylcholine cause?
Increased intragastric and lower esophageal pressures
related to intensity of fasiculations of abdominal
muscles
prevented by prior administration of non-
depolarizing drug
does not increase risk of regurgitation
What patients are at risk of myalgias due to succinylcholine?
young, female, ambulatory patients