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Pharm Test 3 > NMB Reversal and Monitoring > Flashcards

NMB Reversal and Monitoring Flashcards

1
Q

Some reasons why we need muscle relaxation?

A
  • Ideal intubating conditions
    • reduce chance of vocal cord injury or post op hoarseness
  • Optimize surgical exposure
    • NOT always required for adequate surgical conditions
  • ICU: Resp failure, prevent shivering, reduce oxygen consumption, help to contorl ICP
  • NOT a substitute for adequate anesthesia
    • movement can still occur with deep NMB (1or 2 twitches) due to pateitn inter-variability
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2
Q

TOF monitor in OR is _____

A

qualitative

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3
Q

What are the goals of NMB reversal?

A
  • Adequate postoperative ventilation
  • paryngeal patency
  • adequate swallowing
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4
Q

Who do we need to reverse?

A
  • Residual NMB can go undetected with qualitative TOF monitoring
  • Must have at least one twitch available to reverse (most sources say 2)
  • Consider timing of last dose of NDNMB
  • Consider need for post-operative intubation/ICU
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5
Q

A TOFR < ____ can still have altered upper airway closing pressure.

A

<0.9

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6
Q

If you only have one twitch, and try to reverse, how long will it take before reversal works?

A

At least 30 minutes

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7
Q

What are types of nerve stimulation?

A
  • Single twitch
  • TOF stimulation
  • tetanic stimulus
  • post-tetanic count
  • double burst stimulation
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8
Q

What method of nerve stimulator will be the easiest way to see reduction in contraction

A

Double burst stimulation

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9
Q

What response do you get from nerve stimulation during profound muscular blockade?

A

Nothing

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10
Q

What response do we get from nerve stimulator with deep block

A

>1 post tetanic count ONLY

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11
Q

What type of response happens from nerve stimulator with moderate block

A

1-3 TOF count

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12
Q

What type of response do you have with nerve stimulator with light (shallow) block?

A

4 TOF count with fade

TOF ratio is 0.1-0.4

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13
Q

What response form nerve stimulator with minimal blcok (near full recover)

A

4 TOF, No fade

TOF ratio >0.4 but <0.9

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14
Q

What response do we get from nerve stimulator with full recover (normal function)

A

4 TOF count with no fade

Measure TOF ratio >0.9-1

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15
Q

What are the characteristics of non-depolarizing block?

A
  • Decrease in twitch tension
  • Fade during repetitive stimulation (TOF or tetanic)
  • Posttetanic potentiation
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16
Q

Why does post tetatnic stimulation happen with non-depolarizing blocks?

A

Non-depolarizing is a competitive antaganoist. With stimulation of the nerve, increases release ACh at junction, and that means you have more ACh available to compete with the non-depolarizing blocks

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17
Q

What causes twitch depression in non-depolarizing block?

A

Block of postsynaptic nicotinic ACh receptors

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18
Q

What causes TOF fade in non-depolarizing block?

A

Block of preseynaptic nicotinic acetylcholine receptors vs solely postjunctional response (debatable, most say it’s combo of both)

  • prevents Ach from being made available from presynaptic nerve terminal to sustain muscle contraction
  • Released ACh does not match demand and this is why we see fade
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19
Q

What are characteristics of depolarizing block (Sch)?

A

MOST COMMONLY seen is Phase I block:

  • Decrease in twitch tension
  • no fade during repritive stimulation (Tetanic or TOF)
  • No post tetanic potentiation

Phase II block:

  • Seen with large single dose, repeated doses, continuous infusion
  • features of NDNMB block (fade with tetany and TOF stimulation; post tetanic potentiation)
    • think this is because of prejunctional effects with large/repeated dosing
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20
Q

What are the monitoring phases of neuromuscular blockers?

A
  • Baseline- no NMB
    • check funcitoning of neuromuscular monitor
    • choose appropriate nerve-muscle to be monitored
    • monitoring should be ideally started before administration of NMB but after induction of anesthesia
      • O’guinn mentioned she had mixed feelings because you don’t want to be fumbling with TOF monitor while you have an apneic patient.
  • Intubation- intubating dose of NMB
    • select appropriate method of stimulation
  • Maintenance- Redosing
    • observation and interpretation of evoked response
  • Emergence- reversal
    • observation and interpretation of evoked response
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21
Q

Why do we check NMB frequently?

A
  • Wide inter-patient variability in dose requirements
  • facilitate timing of intubation
  • allows careful titration to effect
  • allows assessment of readiness for reversal
  • allows assessment of adequacy of reversal
  • differentiates type of block
  • facilitates early recognition of psuedocholinesterase deficiency
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22
Q

What is order of relative sensitivities of muscle groups to nondepolarizing muscle relaxants from most resistant to most sensitiive?

A
  • Vocal cord<—- most resistant
  • diaphragm
  • orbiucularis oculi
  • abdominal rectus
  • adductor pollicis
  • masseter
  • pharyngeal
  • extraocular<—- most sensitive (pt can still have diplopia/objective difficulty swalling/breahing even with “full” NMB reversal)
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23
Q

What is the site of stimulation and movement observed for ulnar nerve?

A

SIte of stimulation: wrist of elbos

Movement observed:

  • thumb adduction
  • flexion of fourth and fifth fingers
  • abduction of fifth finger
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24
Q

Posterior tibial, site of monitoring, movement observed

A

Site of stimulation: posterior to medial malleolus

Movement observed: plantarflexion of big toe

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25
Q

What is site of stimulation and movement observed of peroneal nerve monitoring?

A

Site of stimulation: lateral to neck of the fublar

Movement observed: Dorsiflexion of foot

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26
Q

What is site of stimulation and movement observed for facial nerve monitoring?

A

Site of stimulation: near the tragus where nerve emerges from stylomastoid foramen, 2-3 cm posterior to the orbit

Movement observed: contraction of obicularis oculi, orbiuclaris oris, or corrugator supercilli

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27
Q

What is site of stimulation and movement observed for reucrrent larngeal nerve monitoring?

A

Site of stimulation: notch of thyroid cartilage

Movement observed: vocal cord adduction

28
Q

What is site of stimulation and movement observed for phrenic nerve monitoring?

A

Site of stimulation: inferoposterior border of SCM muscle

Movement observed: hemidiaphragm

29
Q

Disadvantage of adductor pollicis monitoring?

A
  • Possibility of movement of the diaphragm even with total elimination of response to TOF or single twitch
    • adductor pollicis is more sensitive to NMB and twitch will be lost first, even though diaphragm is not yet paralyzed.
30
Q

What is the advantage to adductor pollicis monitoring?

A
  • No residual blockade exits in diaphragm if adductor pollicis recovered from relaxation
31
Q

What is best nerve monitoring for intubation?

A

Obicularis oculi

32
Q

What is best nerve moniotring for recovery?

A

Adductor pollicis

33
Q

How many twitches on TOF do you need to give reversal of anticholinesterase?

A

1 (most sources say 2)

34
Q

Can you assume full recovery of muscle block with 4 twitches?

A

No

35
Q

What type of nerve stimulation allows for most accurate assessment of fade?

A

Double burst suppression

36
Q

What type of nerve stimulation is most accurate?

A

Quantitative assessment (with acceleromyography, kinemyogrpahy, phonomyogrpahy) this gives you a TOF ratio

37
Q

What TOF ratio shows adequate recovery of neuromuscular function

A

anything <0.9 can have residual effects

38
Q

There can be residual paralysis with TOF R as high as ___

A

0.8-0.9

39
Q

What does inadequate recovery from neuromuscular blockade predispose the patient to?

A

Regurgitation

aspiration

postop pulmonary complications

40
Q

What is TOF stimulation?

A
  • 4 single pulses of equal intensity delivered at intervals of 2/sec (one every 0.5 sec) to frequency of 2Hz
  • Each stimulus causes muscle to contract and “fade”
  • Dividing amplitude of 4th twitch by amplitude of 1st twitch- TOF ratio
    • useful for determining degree of NDMR block
  • Qualitative unless accelerometer or alternative ratio technology used
41
Q

What is % of receptors block and clinical relevance with no response from TOF?

A

100% receptors blocked

Sufficient for ETT

42
Q

% receptors blocked and clinical relevance for 1-2 twitches with TOF?

A

one= 90% block

2= 80-90% blocked

Sufficient for surgery<– where we live in OR

43
Q

% blockade and clinical relevance for 3 TOF twitches?

A

75-80% blockade

Needs reversal

44
Q

% blockade and clinical relevance for 4 twitches

A

up to 75%

Recovery phase

still take into account post tetanic, double burst, clinical indicators to make sure you don’t need reversal.

45
Q

What is post tetanic count?

A
  • after injection on non-depolarizer, there will be no response twitch
  • Quantifying intensity of blockade can be done by tetanic stimulation when TOF is 0/4
  • Stimuli given at 50 Hz x 5 seconds and observing response to twitch given at 1 hz 3 seconds after end of tetanic stimulation
    • # post tetanic twitches is counted
  • During intense blockade, no response to EITHER tetanic or post tetanic stimulation will be seen
  • before first TOF response returns, post tetanic twitches will be seen
    • means that it won’t be long until TOF is present
46
Q

What is double burst stimulation?

A
  • TOF less than 0.3 is difficult to detect
  • Evaluation of DBS response is superior to tactile evaluation of TOF response
  • Easier to feel fade in DBS response when compared to fade from TOF
  • Two impulses at 50 Hz separated by 750 ms
  • evaluate the ratio of second to first response
  • in non paralyzed muscle, response to double burst stimuli is two short contractions of equal strength (likely TOF ratio >0.7)
  • in paralyzed muscle, the second response is weaker than the first (fade)
47
Q

What are quantitative monitors for nerve monitoring?

A
  • Stimulation of peripheral nerve and quantificiation and recording of evoked response to nerve stimulation
    • provides nmerical ratio (>0.9= recovery)
    • requires a baseline
48
Q

What is acceleromyography?

A
  • Most accurate way to assess TOF ratio
  • quantitative
  • NEEDS BASELINE
  • Reduces risk of residual NMB in PACU
    • Decreases adverse respiratory events and symptoms of muscle weakness associated with incomplete NM recovery
49
Q

What are clinical signs of reversal?

A
  • Sustained head life (5 sec)
  • Spontaneous ventilation
  • eye opening
  • tongue protrusion
  • hand grip
  • leg raising
  • coughing
  • swallowing
  • reaching toward endotracheal tube

Non of these clnical signs can gurantee 100% recovery of neuromuscular function

50
Q

Of the clinical tests, which are unreliable test for neuromuscular recovery?

A
  • Sustained eye opening
  • protrusion of tongue
  • arm lift to opposite shoulder
  • normal tidal volume
  • normal or nearly normal vital capacity
  • maximum inspiratory pressure less than 40-50
51
Q

What clinical tests are more reliable test for neuromuscular recovery (but still not perfect)?

A
  • Sustained head lift for 5 sec
  • sustained leg lift 5 sec
  • sustained handgrip 5 s
  • sustained “tongue depressor test” (biting on tongue depressor)
  • maximum inspiratory pressure
52
Q

What residual NM blockade symptoms can you have with TOF ratio 0.7-0.75

A
  • Diplopia and visual disturbance
  • decreased handgrip strength
  • inability to maintain opposition of incisor teeth
  • “tongue depressor test” negative
  • inability to sit up without assistance
  • severe facial weakness
  • speaking a major effort
  • overall weakness and tiredness
53
Q

TOF ratio 0.8-0.9 will still have residual symptoms of ….

A

Diplopia and visual distrubances

Generalized fatigue

54
Q

What are acetylcholinesterase inhibitors?

A
  • Quarternary ammonium compounds
  • allow increase in ACh at NMJ to decrease competitive effect of remaining NDNMB
    • Drug inhibits acetylcholinesterase (which breaks down ACh), so more ACh is available at junction and it can increase concentration
  • ALWAYS given with anticholinergic
    • not specific where the AChE inhibitor happens
  • UNABLE TO REVERSE PROFOUND BLOCKADE
    • ceiling effect
  • Dose depends on level of neuromuscular blockade
55
Q

What is sugammadex?

A

Cyclodextrin

  • Forms a complex with non-depolarizing NMBA rocuronium and vecuronium
    • ​sugammedex and roc bond is stronger
  • can be used even with deep blockate (1-2 PTC)
56
Q

What are the factors that influence effectiveness of acetylcholinesterase inhibiotrs in reversing NMB?

A
  1. Depth of blockade when reversal attempted
  2. anticholinesterase chosen
  3. dose administered
  4. rate of spontaneous clear of neuromuscular blocker from plasma
  5. choice and depth of anesthetic agent administered
57
Q

What are some effects of increased ACh with administration of AChE inhibitor and how can we counteract them?

A
  • CV: bradycardia/vagal stimulation
  • Pulmonary: bronchospasm
  • GI: Increased peristalsis and secretions, N/V, fecal incontinence
  • Cerebral: physostimgmine cross BBB

Muscarinic effects minimized with co administration of anticholinergic

58
Q

Neostigmine dose, onset peak? What is it typically administered with?

A

Not reliable in profound block (100%), reliable in deep block (90%)

  • Dose 0.07 mg/kg
  • onset = 3 min
  • Peak 7-10 min

Given with glycopyrrolate

59
Q

What is glycopyrrolate? Dosing, onset, peak, metabolized by? Excretion?

A
  • Dose: 0.05-0.07 mg/kg neostigmine AND 0.01-0.02 mg/kg glyco (robinol)
  • Onet= 3-5 min
  • Peak 7-10
  • Metabolized by cholinesterase in NMJ and liver
  • Principle route of excretion is the kidney
60
Q

What is endrophonium? Dose, peak, excretion, administered with?

A
  • Not effective for deep block (need TOF 4/4 twitches before it will work)
  • Faster onset than neostigmine, less effective than neostigmine
  • Dose: 0.5 mg/kg-0.75 mg/kg with atropine 0.007-0.014 mg/kg
    • given with atropine due to fast onset
  • Peak 1-2 min
  • Excretion: renal (67%)
61
Q

What is pyridostigmine?

Dose, peak, excretion

A
  • Dose: 0.14-0.25 mg/kg
  • peak effect 12 min (can be as long as 15-20 min)
    • slower onset
    • co-administered with glyco
  • Excretion: dependent on renal clearance (75%)
  • 20% as potent as neostigmine (Very weak)
  • 40% longer duration
  • Given with myasthetnia gravis
62
Q

What is physostigmine?

A
  • Anticholinesterase drug but not given as reversal
  • given with people experiencing neurological side effects from scopolamine
    • used for reversal of confusion/disorientation following atropine and scopolamine (central anticholinergic syndrome)
  • 15-60 mcg/kg
63
Q

What is echothiophate?

A
  • Only organophosphate anticholinesterase drug used clinicaly
  • long acting miotic that lower IOP
    • useful in Rx glaucome
  • May prolong duration of succinylcholine after 1 month Rx as plasma psuedocholinesterase may decrease to <5% of normal
64
Q

Onset of anticholinergics?

A
  • Atropine: onset 1 min, Duration 30-60 min
  • Glycopyrrolate- onset 2-3 min/duration 2-4 hours
65
Q

What is sugammadex?

A
  • Dose dependent on level of blackade
  • Cannot be used for nonsteroidal NMB agents (ONLY ROC OR VEC)
  • Most recent article says sugammedex for age 2-17 is ok, <2 unsure
  • Not recommended for use in renal failure or dialysis patient
  • Marked bradycardia, some of which has resulted in cardiac arrest
  • Recurrence of NMB may occur d/t displacement of roc/vec from bridion by other drugs
66
Q

Dose of sugammades?

A
  • Dose dependent of level of blockade
  • 4mg/kg recommended if spontaneous recovery of twitch response has reached 1-2 pot-tetanic counts (PTC) and no twitches with TOF
  • 2mg/kg recommended if spontaneous recovery has reached the reappearance of second twitch in response to TOF sitmulation

ROC only: 16 mg/kg if clinical need to reverse NM blockade soon (approximately 3 min) after admin of single dose of 1.2 mg/kg of ROC

Pharm Test 3 (5 decks)

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