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Ch. 16 - Neuromuscular Blocking Agents
Terms in this set (88)
They work on Nicotinic M receptors by blocking the effects of acetylcholine to cause muscle relaxation
*So they prevent acetylcholine from activating Nicotinic M receptors
What receptors do NBA work on and what do they do?
these drugs cause paralysis, which is?
NBA are used for muscle relaxation during what procedures?
nope, no oral forms.
Are there oral forms of neuromuscular blocking agents?
1. compeititve / nondepolarizing agents
2. depolarizing agents
Based on mechanism of action, neuromuscular blocking agents are split into 2 categories:
muscle contraction and neuromuscular blocking agents
The concepts of polarization, depolarization, and repolarization are important in understanding...
NO. So they have no impact on the CNS - they give paralysis NOT sedation
-in the placenta there are minimal effects on the fetus
can neuromuscular blocking agents cross the BBB?
polarization is resting muscle
The resting muscle is said to be ____ bc positive charges cover the outer surface of the membrane, and negative charges cover the inner surface - this is an uneven distribution of charges
positive charges move from OUT to INside
when the membrane depolarizes what happens to charges?
Repolarization ... depolarization of the muscle membrane is followed almost immediately by repolarization - which restores the original resting (polarized) state of the muscle membrane
this is when positive charged ions are pumped out of the cell so that the original resting membrane is restored
this is the #1 reason for increased Calcium levels
-with the arrival of an action potential at the terminal of a motor neuron - this causes the RELEASE OF ACETYLCHOLINE into the subneural space.
Steps in muscle contraction; the process of muscle contraction begins by what happening 1st?
Acetylcholine then binds reversibly to nicotinic M recptors on the motor end-plate (place that contains the receptors for acetylcholine) and causes this end plate to depolarize - when positive charges from from out to in
process of muscle contraction begins with the release of acetylcholine into the subneural space.
What does acetylcholine then have to do?
process of muscle contraction
-Acetylcholine is released
-Acetylcholine binds reversibly to nicotinic M receptors and causes the motor end plate to depolarize (moving charges from out to in)
-The depolarization initiates a muscle action potential (muscle membrane is no longer in a resting state)
-This wave of depolarization spreads rapidly over the entire muscle membrane and....
-this triggers the release of CALCIUM from the sarcoplasmic reticulum of the muscle
-CALCIUM permits the interaction of actin and myosin - thereby causing muscle contraction
-acetylcholine then disassociates , muscle membrane repolarizes back to its original resting state, and calcium is taken back up into the SR
-because Calcium is restored and taken back up, there is no longer available calcium to support the interaction of actin and myosin, so the muscles relax
starts with: A.N.C.
Acetylcholine released --> binds to nicotinic M receptors -->causes depolarization to trigger calcium release --> calcium supports interaction of actin and myosin causing muscle contraction -->acetylcholine leaves, repolarizes membrane, calcium taken back up-->muscle relaxation
In brief state what happens in the process of muscle contraction
we need this for muscle contraction more than anything
COMPETITIVE / nondepolarizing agents
these types of neuromuscular blocking agents compete with acetylcholine for binding to Nicotinic M receptors
This drug is used for intubation reasons
-Succinylcholin - a depolarizing neuromuscular blocking agent
-check K (potassium) levels. Too high --> death
This drug can cause Hyperkalemia. What is a nursing implication for this pt?
competitive neuromuscular blockers I: Tubocurarine - NO LONGER USED.
This is the oldest competitive neuromuscular blocker, but it is no longer used in the U.S. and is replaced by newer agents
-put a sign on the door that states this so in case they are to be intubated the RRT will know
If patient has a poor/bad airway, what should be on their hospital door?
B/c all drugs in this class contain at least 1 quaternary nitrogen atom - meaning these drugs will always carry a positive charge therefore they cannot cross membranes
Why can't any neuromuscular blocking agents cross membranes and effect the CNS?
1. They cannot be absorbed from the GI tract
2. they cannot be given orally
3. they must all be given thru parenteral IV route
*Since they cannot cross BBB, they have no effect on CNS
*they cannot readily cross the placenta - little or no effects on the fetus.
B/c NBAs cannot readily cross membranes, this characteristic leaves them with 3 clinical consequences when used...
What drugs contain a quartenary nitrogen atom disallowing them from readily crossing membranes or the CNS
-these drugs COMPETE with acetylcholine for receptor binding to nicotinic M receptors on the motor end-plate
-TheyDO NOT cause receptor activation when they bind with these receptors, though...
-Instead they block receptor activation by acetylcholine by causing the muscle to relax.
describe the mechanism of action of competitive NBA:
Muscle function can be restored by eliminating the drug from the body
-Or by increasing the amount of acetylcholine at the neuromuscular junction
When a pt is given a competitive NBA to relax their muscles, how do we reverse this and restore their muscle function???
primary effect: relaxation of the skeletal muscle - causing a state of flaccid paralysis
*although these drugs can paralyze muscles, not all muscles are paralyzed at once
Pharmacologic effects of Competitive Neuromuscular blocking agents:
what is the primary effect?
With competitive neuromuscular blocking agents, not all muscles become paralyzed at once.
cancer - causes hypercalcemia and risk for fractures
this is the number one reason why a person would have increased Ca levels
competitive / nondepolarizing neuromuscular blocking agents - these have a nitrogen atom
these drugs compete with acetylcholine for Nicitinic M receptors; they block receptor activation of acetylcholine
-muscle relaxation - flaccid paralysis* primary effect - these drugs can paralyze all muscles, but paralysis does not happen all at once. (diaphragm muscles are the last to be paralyzed. eyelids first)
-hypotension - histamine is released which lowers BP by causing vasodilation.
-CNS - has no effect on this bc drug cannot cross the BBB; even when they put a pt in complete paralysis, drugs cannot diminish consciousness or perception of pain which is why we need pain meds and a sedative when we give a NBA
3 main pharmacologic effects that competitive neuromuscular blocking agents are meant to cause:
-provide muscle relaxation during surgery, mechanical ventilation, and endotracheal intubation
list the therapeutic uses for competitive neuromuscular blocking agents:
competitive neuromuscular blocking agents
these drugs have a rapid onset of paralysis, peak in 20 - 45 mins, complete recovery is in 1 hour depending on patients liver
1. Respiratory arrest - due to the paralysis of resp. muscles
*when u give this drug, mechanical ventilation must be immediately available. - patients must be monitored closely and continuously.
2. cardiovascular effects: Hypotension - because the drug releases histamine which causes vasodilation. ALSO BRADYCARDIA.
2 main adverse effects of competitive neuromuscular blocking agents
pharm effects: used for muscle relaxation, flaccid paralysis and hypotension
-use saline to BP up, use 2 large bore IVs, use vasopressure?
competitive neuromuscular blocking agent
adverse effects of it include hypotension & resp. arrest & bradycardia
*How do you get the BP up?
BE CAREFUL IN PATEINTS WITH
-Myastehnia Gravis - bc the cause of muscle weakness Is reduction in the number of nicotinic M receptors - bc this receptor number is reduced, neuromuscular blockade occurs quickly. Dosing done with great caution.
-Electrolyte disturbances - responses to neuromuscular blockers can bealtered by electrolyte abnormalties.
ex: low K levels can enhance paralysis
-high K levels can reduce paralysis -maintain normal electrolyte balance
Contraindications for Competitive NM blocking agent: Pancuronium are??
a competitive neuromuscular blocking agent
what kind of drug is Pancuronium ?
-it's a competitive neuromuscular blocking agent
-approved for muscle relaxation during general anesthesia, surgery, intubation, mechanical ventilation
-DOES NOT cause histamine release - so it does NOT dilate vessels and does NOT cause hypotension.
-effects MAY CAUSE TACHYCARDIA.
-excreted thru the urine
what is Pancuronium used for?
-What adverse effects does It cause?
cautious of patients with liver disease, Myasthenia gravis, and those with electrolyte imbalance
*WE WORRY ABOUT LIVER DISEASE WITH THESE PATIENTS
with what patient should you be cautious for when giving Pancuronium
keep them in rehab for weeks to rebuild strength
For a patient in ICU post paralytic drugs, we need to keep them where?
what is the depolarizing neuromuscular blocking agent called that we need to know?
this is ultra-short acting and is the ONLY depolarizing neuromuscular blocking agent in use
-produces a state of depolarizing neuromuscular blockade
-succinylcholine binds to nicotinic M receptors and causes depolarization. - which produces transient (short) muscle contractions (fasiculations)
-prevents repolarization,and keeps muscles in a depolarized state --> keeps the muscles in paralysis since they cannot undergo polarization and depolarization cycle.
-paralysis occurs after brief period of contractions - stays paralyzed until plasma levels of succinylcholine decline
describe the mechanism of action of succinylcholine.
1. muscle relaxation - state of flaccid paralysis. DIFFERENCE: this paralysis begins as transient contractions. Paraylsis of this drug fades faster than with nondepolarizing drugs
2. No effects on the CNS - does not decrease consciousness or pain
Pharmacologic effects of Succinylcholine:
primarily used for muscle relaxation during endotracheal intubation - bc its such a fast acting drug.
also used for electroconvulsive therapy.
bc of its short duration, its not used during surgeries like Pancuronium would be.
what are the therapeutic uses for Succinylcholine?
-Prolonged apnea in patients with low pseudocholinesterase activity -paralysis can last them for hours instead of minutes
-Malignant Hypertermia - extremely high fatal temp
-Postoperative muscle pain - in neck, shoulders and back
Name the adverse effects of Succinylcholine:
provides muscle relaxtion ofr intubation and electroconvulisive therapy. wears off quickly.
-Sleep apnea / Patients with low pseudocholinesterase activity - bc they are unable to degrade succinylcholine rapidly; paralysis can persist for these ppl for hours rather than just a few minutes.
Succinylcholine is contraindicated for what patients?
This is a rare and fatal condition that can be triggered by Succinylcholine
Succinylcholine causes malignant hyperthermia
muscle rigidity associated with a profound elevation of body temperature - 43 Celcius. Temp rises due to uncontrolled metabolic scitivty in the muscle, and release of Ca from the SR.
manifestations: cardiac dysrhythmias, unstable BP,electrolyte derangements, metabolic acidosis.
left untreated: can be fatal.
-family history of this reaction should NOT receive what drug???
-discontinue med !!
-cool the patient off with ice packs and IV infusion of cold saline
-give IV dantrolene -reduces sketetal muscle metabolic acitivty to reduce heat production
what is treatment for succinylcholine-induced malignant hyperthermia?
-Drug causes the release of potassium from tissues. sufficient enough to cause hyperkalemia.
-death can result from cardiac arrest
-be careful of: burn patients, multiple trauma, upper motor neuron injuries., denervation of sketetal muscles.
With what drug is an adverse affect hyperkalemia? why does this occur
-Help reverse adverse effects of Pancronium - a competitive nondepolarizing NB agent
-Intensify effects of Succinylcholin - depolarizing NMB agent.
AVOID CHOLINESTERASE INHIBITORS WHILE ON SUCCINCYLCHOLINE
cholinesterase inhibtiors help reverse respiratory depression for which drug?
and for which do they intensify the effects of?
Antibiotics will both increase the effects
what drugs intensify the effects of Succinylcholine and interaction should be avoided?
can cause prolonged apnea- there is NO specific antidote to this poisoning.
What happens when there is an overdose/ toxic levels of Succinylcholine in a patient?
when toxic BOTH drugs cause prolonged apnea!!! - hard to breathe!
competitive; ex Pancronium - treatment is resp. mechanical ventilation to give reps. support and a cholinesterase inhibitor to reverse that
-depolarizing - theres no antidote. management is purely supportive. using a cholinesterase inhibitor for this would not help, but it would intensify the toxic effect of apnea
poisoning of each:
-a competitive non-depolarizing blocking agent? (IV)
-a depolarizing neuromuscular blocking agent (IM or IV)
Cholinesterase inhibitors can help speed up this recovery process
recovery from the effects of Pancronium can be accelerated with what?
Succinylcholine - it would relax the gag reflex msucles sothe tube can go into the trachea
this drug is the preferred choice for intubation bc of its short duration
neuromuscular blockers interfere with this receptor activation and thereby cause muscle relaxation
NO! No effects on the CNS
do neuromuscular blocking agents reduce pain or consciousness?
respiratory depression -think of paralysis on the diapgrham
what is the major adverse effect of all neuromuscular blocking agents?
- reverse the effects, speed up recovery, reverse resp. depression
-intensify the effects of succinylcholine
What do cholinesterase inhibitors do to:
-Competitive NM blocking agents
-Depolarizing NM blocking agents
-pt gets veryyyy hot and hightemp
-cool them off with ice packs, give them cold saline IV infusions
-discontinue succinylcholine immediately
-GIVE ANTIDOTE: dantrolene
***THIS EFFECT COMES FROM THE BRAIN
what is the most serious effect that Succinylcholine can cause. What do we do if this happens?
-those with a low plasma cholinesterase activity
-patients with malignant hyperthermia in family history
-patients with BURNS, multiple trauma, nerve problems in skeletal muscles, upper motor neuron injury --- these can have problems with hyperkalemia
succinylcholine is contraindicated for what patients?
ALL NBA must be delivered by what route?
what is the antidote to reverse malignant hyperthermia
***body temp gets VERY high , even to 43 C
*NO ONE GETS A TEMP IN THE OR BC ITS KEPT FREEZING. first sign of fever - we act. and we assess if pt is on succinylcholine
name the signs that a pt is having malignant hyperthermia:
1. discontinue succinylcholine
2. cool patient with external ice packs and IV infusion of cold saline
3. give IV dantrolene - stops heat generation by acting directly on skeletal muscle to reduce their metabolic activity.
describe the steps of treatment for malignant hyperthermia
-if post op pain, check calcium levels !!
-Give Diazepam (Valium) for muscle spasms
Post op pain is an adverse effect of succinylcholine: pain is common in what areas?
-may arise at 12 to 24 hours post op
-what does the nurse do to help??
succinylcholine - bc it releases K from tissues.
can result in death from cardiac arrest
what drug can cause hyperkalemia
DO NOT give succinylcholine if K levels are above ___
bc they have problems with hyperkalemia already in their initial burn phase.
Why don't we give succinylcholine to burn victims?
do an EKG to check their heart***
If a patient has hyperkalemia - what does the nurse do as a priority?
cholinesterase inhibitors & antibitotics
these drugs will potentiate the effects of Succinylcholine
-overdose can cause prolonged apnea (same with all NBAs)
-n ospecific antidote to help
-management is just supportive
describe the steps of treatment for succinylcholine poisoning
-pt can hear
-pt is fully awake just paralyzed
-this is why we give analgesics and general anesthesia with NBAs
Using neuromuscular blocking agents: facilitation of mechanical ventilation is needed so NBAs wil...
-these will help by suppressing spontaneous resp. muscles
-redue pt resistance to ventilation
-nurse should make pt comfortable
-can the pt hear?/?
-is the pt awake?
depolzaring meurmusclar blocking agents - succinylcholine bc its short acting - works by preventing convulsions movements during electroshock therapy
also helps with endotracheal intubation: suppresses gag reflex
these drugs are used during electroconvulsive therapy (severe depression)
give them an opioid and an anti-analytic or anesthesia.
(ex: give them Ativan, Fetynal, morphine, diuladid)
most important thing to do for a patient before giving them a NBA is to do what
5 to 10 mins
how long will muscle paralysis last with succinylcholine
contraindications for a bladder scan?
do a bladder scan
what do you do if the pt has urinary retention after surgery
have 2 ppl there
when giving discharge instructions for an elderly patient, what is important?
ALL NBA drugs must be used with caution for patients with __
-Patients predisposed to hyperkalemia (burns, trauma, nerve problems, upper motor neuron injury)
-patients with history or fam history of malignant hyperthermia
-pts with low pesudocholinesterase activity
Succinylcholine is contraindicated for whom?
-give mechanical ventiliation
-monitor respiration constantly
when drug is stopped, take vitals frequently until full recovery. q15mins
-if blockade is caused by a competitive NMB, give a cholinesterase inhibitor to reverse blockade effects
Minimizing adverse effects of NBAs:
Apnea. All NBAs can cause respiratory depression.
what can we do to help?
give an antihistamine to counteract the histamine being released
With NBAs: hypotension can happen.
what can we do?
-assess family history of the reaction
-stop the drug, cool with ice packs, give cold saline IV, give IV danrolene to stop metabolic activity an cool body down
predisposition to malignant hyperthermia is __
they'll only help competitive NMB agents like Pancronium.
this drug is contraindicated for patients receiving succinylcholine
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