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88 Cards in this Set
- Front
- Back
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All patients who have received a NDMR must have what?
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Neuromuscular function assessed prior to reversal and extubation
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NM function is assessed prior to reversal/extubation...but when else is it appropriate to check?
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AFTER giving a DMR to check for return of function prior to giving a NDMR
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To assess NM function, one must apply what?
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Apply patterns of electrical stimulation to a muscle group
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The greater the NM blockade, the....
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Weaker the response to stimulation
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The _____ the NM blockade, the _____ the response to stimulation
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Weaker the blockade
Stronger the response to stimulation |
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What and how long is stimuli delivered in TOF?
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FOUR successive stimuli of equal duration and intensity over 2 seconds
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What do you see when assessing TOF after a NDMR has been administered?
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FOUR twitches that FADE in intensity
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TOF ratio:
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Response to 1st vs. 4th stimulus
This is a sensitive indicator of NDMR paralysis |
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TOF twitches
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1 twitch visible= more dense (more receptors blocked)
4 twitches visible= less dense (fewer rec bocked) |
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TOF response with a phase I block:
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Response is constant but DIMINISHED in amplitude
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TOF response in a Phase II block (or OD of DMR):
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Twitches progressively decrease in amplitude= fadeeeeeee
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Remember: there is NO phase I block for ______
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NDMRs
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What is the TOF "Watch"
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Device placed on ulnar side of hand, measures strength of ms contraction to TOF stimulus
More sensitive than simply observing twitches |
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How do we test Tetany?
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Sustained stimulus for 5 seconds of 50-100 Hz
Sensitive test of function |
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What is the DMR response to tetany?
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Constant but diminished (phase I block)
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NDMR response to tentany?
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Fade
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Sustained contraction w/tetany =
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adequate (not necessarily complete) return of function
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Is tetany painful?
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You betcha!
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Double Burst Stimulation is a variation of what other test? Is it more or less painful?
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Variation of tetany
Less painful |
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Phase I vs Phase II block response w/double burst stim?
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Phase I: Constant but diminished
Phase II: Fade |
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What is one way to determine if SOME NM function has returned? Why?
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Tetany.
By delivering tetanic stimulus, the NMJ is flooded w/any ACh able to bind to unoccupied receptor site causing transient inc in ACh available to bind |
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Application of ______ ______ increases the response to subsequent twitch stimulation
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tetanic stimulus
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Where are the two places you can use a peripheral nerve stimulator?
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Ulnar and Facial Nerve
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Ulnar nerve stimulates what muscle? What will you see when it is stimulated?
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Adductor pollicis muscle
See contraction of ulnar (pinky) side of hand |
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Ulnar nerver recovers _______ diaphragm, larynx and abd ms. Why do we care?
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Recovers AFTER
If you DON'T see ms contraction here, know that diaphragm may have function becomes it recovers BEFORE |
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Facial nerve testing stimulates what muscle?
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Stimulates orbicularis oculi muscle
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Does facial nerver recover before or after adductor pollicis?
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Recovers BEFORE adductor pollicis
*making it ideal place to test TOF |
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HUUUUGGGEEE POINT:
A patient can have 4 twitches and still have.... |
...70% of their ACh receptors BLOCKED!!
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T/F:
Recovery of orbicularis oculi and adductor pollicis do not exactly reflect recovery of respiratory and airway muscles |
True
Diff muscles respond differently. Remember: a pt can have 4 twitches and still have 70% of their ACh receptors blocked! |
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What are 3 other indicators of recovery from NMB (besides TOF, tetany, double-burst)
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1. Sustained head lift > 5 seconds
2. Forceful, purposeful hand grip 3. NIF at least -25cm H2O |
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"Cholinergic" =
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Acetycholine
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What is the neurotransmitter (nt) for the entire PNS?
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ACh
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What is the nt for the adrenal medulla, sympathetic ganglions and sweat glands?
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ACh
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Muscarinic Cholinergic rec act in what 3 places?
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Bronchial smooth muscle
Salivary glands SA node *see bronchoconstriction, inc salivation, bradycardia, inc GI motility and meiosis (pinpoint pupils) |
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Muscarinic receptors are blocked by what? Ex?
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Anticholinergic drugs
ex: Atropine |
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Nicotnic receptors act at what 2 places?
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Autonomic ganglia
Skeletal muscle |
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Do muscle relaxants block nicotinic or muscarinic receptors?
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Nicotinic
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Normal NM transmission relies on ACh to bind to what kind of receptor? Where?
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ACh binds to nicotonic cholinergic receptors on the motor end plate to create an action potential-->muscle contraction
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NDMRs block NM trnasmission by acting as _____ and bindnig to the ____ receptors and not letting _____ to bind
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Antagonists...bidn to ACh receptors and not allowing ACh to bind
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Spontaneous reversal of NDMR block depends on what 2 things?
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Diffusion
Metabolism of AChE |
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Pharmacologic reversal of NDMRs is acheieved by the admin of what?
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Acetylcholinesterase Inhibitors
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Cholinesterase inhibitors work by inhibiting the enzyme ____
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AChE
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Cholinesterase inhibitors ______ bind AChE
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Reversibly
Some bind more strongly than others depending on electrostatic or covalent bond |
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Cholinesterase inhibitors reversibly bind AChE, indirectly increasing what?
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Increasing the amount of ACh at the NMJ
*ACh competes w/NDMR for ACh binding sites-->return of normal NM transmission |
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cholinesterase inhibitors increase circulating ACh and stimulate _____ _____ receptors in the body
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muscarinic cholinergic
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Muscarinic cholinergic receptors cause what changes in the body?
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Heart: bradycardia
Lungs: bronchoconstriction Brain: EEG excitation GUT: increased GI motility, inc salivation |
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Muscarinic S/E are UNWANTED. How do we minimize them?
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Effects minimized/atenuated by concomitant administration of Anticholinergic drugs
Ex: Atropine and Glycopyrolate |
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What do anticholinergics do to muscarinic receptors? Nicotonic receptors?
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Muscarinic: BLOCK ACh from binding
Nicotinic: NOT blocked |
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What are some effects of anticholinergics (atropine/glyco)
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Potent CV effects: inc HR
Resp: bronchial secretions, dec airway resistance CNS: minimally crosses BBB GI: MARKED dec in salivary secretions Eyes: mydraisis (pupil dilation) GU: dec bladder tone: urinary retention |
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Dose of Atropine:
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0.01-0.02 mg/kg = 0.4-0.6mg
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Dose of Atropine w/Cholinesterase inhibitor:
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0.014 or 0.01 per 1mg of anti-cholinesterase administered
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Duration of atropine:
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30 min
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Caution w/use of Atropine in what 2 instances?
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Glaucoma
CAD |
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Dose of Gylco:
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0.005-0.01 mg/kg= 0.2-0.3mg
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Dose of Glyco w/cholinesterase inhibitor:
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0.05 mg/kg
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Duration of glyco:
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2-4 hours
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Muscarinic effects w/glyco
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Can't cross BBB so no CNS activity
Inc in HR POTENT dec in oral secretions |
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Because glyco causes such potent dec in secretions its used in what instances?
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With Ketamine administration
Fiber-optic Intubations Airway cases Prone cases |
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How are cholinesterase inhibitors metabolized? Excreted?
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Hepatic metabolism
Renal excretion |
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How do you know what dose of cholinesterase inhibitor to give?
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Depends upon degree of NMB that needs to be reversed
Estimated by response to peripheral nerve stimulation |
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The time required to fully reverse NDMR block depnds on what 3 things?
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1. Choice of cholinesterase inhibitor
2. Muscle relaxant being antagonized 3. Extent of blockade before reversal (TOF, tetany, etc) |
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Reversal agents should be routinely be given to...
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...any pt that has received an NDMR
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Rule of thumb as a student regarding NMB reversal:
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If pt got an NDMR, they get a FULL weight based dose of reversal
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What two times would you possibly not reverse an NMB?
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1. If FULL recovery can be demonstrated
2. If post-op plan is for pt to remain intubated |
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Neostigmine forms a ______ bond to AChE
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Covalent (strong)
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Dose, max dose, onset and duration of Neostigmine
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Dose: 0.05 mg/kg
Max Dose: 5mg Onset: 5-10 min Duration: 1hr |
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What is the dose of glyco when administerd concomitantly w/neostigmine
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Glyco 0.2 mg PER 1mg Neostigmine
Ex: 5mg Neostig/1mg Glyco |
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Neostig is mixed with, or given concomitantly w/_____
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Glycopyrolate
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Why is Neostig given w/glyco?
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The onset of these two drugs is similar
So, when neostig takes effect (5-10 min) it is at the same time that Glyco is blocking the muscarinic effects |
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Why isnt neostig given w/atropine?
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Because atropine onset is faster, so antimuscarinic s/e such as tachycardia, would be present long before the effects of Neostig
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Edrophonium forms a _______ bond to AChE.
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Non-covalent (weak) bond
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Edrophonium:
Dose, Onset, Duration |
Dose: 0.5-1mg/kg
Onset: 1-2min, *most rapid of all AChE inhibitors Duration: short (30-45 min) |
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Because of Edrophonium's short DOA, what are we worried about?
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May wear off before effect of NDMR= re-paralyzed pt!
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Dose of Edrophonium w/concomitant anticohlinergic:
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Atropine 0.014 mg/1mg edrophonium
Ex: 35 mg Edrophon/0.49 mg Atropine |
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Edrophonium is mixed with, or given concomitantly w/_____
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Atropine
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Why is Edrophonium given w/Atropine?
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Onset of the two drugs is similar
Both have onset of about 1 minute |
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Pyridostigmine is similar to what other drug? Forms _____ bond to AChE
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Similar in structure to Neostig
Forms covalent bond to AChE |
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Pyridostigmine:
Dose Max Dose Onset Duration |
Dose: 0.4mg/kg
Max: 20 mg Onset: 10-15 min (SLOWEST) Duration: >2hrs |
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Pyridostig is given concomitantly w/what anticholinergic:
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Glyco perferred d/t slower onset than atropine
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Other name for Pyridostigmine
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Mestinon
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Other name for Edrophnium
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Enlon
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Diazinon is an _______ and forms ______ bonds w/AChE
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Organophophate
Covalent bond with AChE |
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Organophosphates are primarly used for what? Secondary use?
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Primarly used as pesticides
Secondary use: in eye surgery d/t inc ACh in eye (Ex: Glaucoma) |
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Physostigmine is used when?
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NOT used as NDMR reversal agent
Useful for treatment of central cholinergic toxicity caused by atropine or scopolamine OD |
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What is used in an Atropine OD?
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Physostigmine
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Physostigmine is _____ soluble, and can cross the BBB
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Lipid
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Physostigmine is metabolized how?
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Metab by plasma esterases and is nearly complete
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3 S/E of Physostigmine admin?
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Salivation
Vomiting Seizures |
