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Neuromuscular Blocking Flashcards

1
Q

Supramaximal current

A

Maximal- an increase in current no longer increases muscle response

-20% above maximal to ensure all fibers in innervated nerve will depolarize

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2
Q

Threshold current

A

Current threshold to evoke muscle contraction

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3
Q

Incidence of residual paralysis with qualitative monitoring

A

30-40%

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4
Q

When is subjective detection of fade unreliable?

A

Between 40-90%!!!!

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5
Q

Monitoring of facial vs adductor pollicis

A

Facial leads to over estimation of neuromuscular function

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6
Q

When do upper airway muscles recover?

A

Even at TOF 0.90 there can be an inability to protect the airway

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7
Q

Muscle innervation ratios

A

Fine control (eyes): 1 nerve innervating 2 fibers

Large muscles (thigh): 1:2,000

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8
Q

What electrolyte imbalances antagonize ACh release??

A

Hypocalcemia: think release from pre synapse

Hypermagnesemia-competes with Ca in Presynaptic channels

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9
Q

Post synaptic binding of ACh

A

Binds alpha subunit of nAChRs

Na influx
K efflux

Resulting in membrane depolarization

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10
Q

Explain Nicotinic receptor upregulation

A

Decreased NMJ stimulation

Causes increase in immature nAChRs
these have increased sensitivity to agonists (succinylcholine)
And decreased sensitivity to nondepolarizing NMBAs

Can lead to systemic lethal doses of intracellular K

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11
Q

Down regulation of nAChRs

A

Results from sustained agonism

Think chronic pyridostigmine in MG

Resistance to SCh and extreme sensitivity to non-depolarizing agents

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12
Q

Most effective prophylaxis of myalgia with SCh

A

NSAIDs

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13
Q

Explain SCh and regurg

A

Increases intragastric pressure
But lower esophageal sphincter tone is also increased such that the gradient remains the same and there is no increase in aspiration risk

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14
Q

NMBAs and potency

A

We use more of lower potency agents so they have a faster onset time

Vec vs roc

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15
Q

Intubation vs re-dosing for deeper block

A

2-3xED95 for intubation

Only 10% of ED 95 is necessary to reestablish deeper level of block

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16
Q

What occurs with defasiculating dose

A

Mutual antagonism between depolarizing and non depolarizing

Result: increased SCh dose

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17
Q

Acute vs chronic anticonvulsants with NMBDs

A

Acute- block is potentiated

Chronic- significantly decreases duration of action with amino steroids, little impact on Cisatracurium

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18
Q

Acidosis and NMBDs

A

Interferes with anticholinesterases when reversing block

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19
Q

Supramaximal current

A

20% above baseline

Ensures all fibers depolarize despite changes in resistance over time

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20
Q

Nerve stimulator orientation

A

Red to head

2cm above the wrist crease

Several centimeters apart on ulnar nerve (pinky side)

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21
Q

Double burst stimulation

A

Mini-tetanic burst of three stimuli at 50Hz seperated by 750msec

Two bursts of three*

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22
Q

TOF

A

Four stimuli at 2 Hz

no control needed

Able to differentiate between depolarizing and non-depolarizing

Useless above 0.40
Less painful than tetany

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23
Q

Post tetanic count

A

Allows assessment of profound block
(Redosing guide)

TET at 50 Hz for 5 sec followed 3 seconds later by ST at 1 Hz

More PTC responses=less block

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24
Q

Why does post tetanic count work??

A

The high frequency tetanic stimulation temporarily increases the amount of ACh released

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25
Time required to recover from intermediate NMBD from PTC-1 to TOFC-1
20-30 minutes
26
Problems with clinical testing of RNB
The best test cannot be performed while intubated! Removal of tongue blade from clenched teeth
27
Why do we use the APM?
It is the sole hand uncle on the radial side that is innervated by the ulnar nerve This decreases chance of direct muscle stimulation
28
Electromyography
Monitors action potential generated by nerve stimulation
29
Mechanomyography
Records the force of muscle contraction- clunky
30
Acceleromyography
Most common Measures acceleration of the muscle it is mounted to…acceleration is proportional to force Limitations: Time consuming Free thumb during surgery Need to be recalibrated Cannot be used when arms are tucked
31
BIS in paralysis
BIS is sensitive to changes in EMG Controversial: but BIS values in awake paralyzed volunteered decreased to levels associated with general anesthesia
32
Why do cholinesterase inhibitors have a ceiling effect?
Once 100% inhibition is reached the addition of more inhibitor may actually block the ACh receptors leading to neuromuscular weakness
33
Considerations with Sugammadex
Oral contraceptives may be impacted for up to a week Hypersensitivity reactions
34
MG considerations
More sensitive to non-dep NMBDs Generally resistant to Succ Typically deep inhalational anesthetic with regional
35
Issues with laparoscopic abdominal surgeries
Insufflation of the abdomen leading to high pneumoperitoneum pressures improve surgical exposure But this causes hemodynamic instability and requires deep neuromuscular block up until the end of the case (recovery takes about 60min and cannot be reversed by neo) Rec: rocuronium and Sugammadex
36
New cool Sugammadex
Calabadion-2 Higher affinity for roc with similar affinity for Cisatracurium
37
Cause of myasthenia gravis
autoimmune destruction or inactivation of postsynaptic acetylcholine receptors at the neuromuscular junction, leading to reduced numbers of receptors and degradation of their function and to complement-mediated damage to the postsynaptic membrane.
38
MG patients with bulbar involvement are at risk for what?
-also respiratory muscle involvement Pulmonary aspiration and pneumonia
39
Impact of myasthenia gravis on NMBDs
Exquisitely sensitive* IgG antibodies
40
Lambert-Eaton and NMBDs
Very sensitive to depolarizing AND non depolarizing
41
Why are muscular dystrophy patients at risk for pulmonary infections?
Ineffective cough
42
What population are we avoiding succinylcholine?
Muscular dystrophy!!!
43
Goal of anesthetic management in periodic paralysis
Prevent attacks Frequent potassium checks Careful ecg monitoring
44
Response to NMBDs in periodic paralysis
Unpredictable In hypokalemia they are very sensitive to non-depolarizing
45
What does muscle relaxation not do?
Produce: Amnesia Analgesia Unconsciousness
46
Metabolism of depolarizing muscle relaxants
Diffusion away from NMJ and hydrolyzed in plasma by pseudocholinesterase/plasma cholinesterase
47
What happens in atypical pseudocholinesterase?
Prolonged Succinylcholine
48
Kidney failure will prolong which NMBDs?
Vecuronium and Pancuronium
49
Metabolism of benzlysoquinoliniums….
Hoffman!! At physiologic pH and temperature
50
Impact of neostigmine on succinylcholine block
Can prolong, they increase the amount of ACh in the cleft and inhibit the breachdown of SCh via pseudocholinesterase
51
Tetany
Sustained stimulus of 50-100 Hz
52
Single twitch (ST)
Single pulse of 0.2 ms in duration
53
Cormack Lehane grade IIA
Partial view of vocal cords (Posterior vocal cord view)
54
C&L Grade IIB
Arytenoids and epiglottis only
55
C&L grade II
Only the posterior portion of the glottic opening can be visualized, anterior commissure not seen
56
How wide is the synaptic cleft?
50-70 nm
57
Subunit replaced in nAChr
Y gamma-replaced By E Epsilon-adult
58
Ach molecules in a quanta and number of quanta needed
5-10k 200-400 quanta
59
NMJ stimulation increases in what conditions?
Burns Immmobilization Infection/sepsis CVAs
60
What does an increase in NMJ stimulation cause? -burns
Up-regulation of immature nAChrs
61
All the names in succinylcholine metabolism
Pseudocholinesterase Plasma cholinesterase Butyrylcholinesterase
62
Malignant hyperthermia- causes
Deficient gene in ryanodine receptor RYR1 Unable to properly regulate calcium release in skeletal muscle SR
63
What does MH lead to?
Build up of Lactic ACID Heat Increased metabolism=increased CO2
64
Warning signs in MH
Increased ETCO2 Slowly increasing body temp Muscles spasms Rapid heart rate Sweating Mottled skin
65
If MH goes unchecked:
DIC/ excessive bleeding -use up all of your clotting factors Multisystem organ failure
66
What to do in MH
Notify surgeon Get help Call MHAUS 100% O2 Convert to TIVA-flush system Cool Document
67
Order IA will potentiate NMB
Desflurane Sevoflurane Isoflurane Halothane Nitrous
68
Facial nerve positioning and response and nerves
White/Black- just anterior to Tragus Red- lateral to outer canthus of eye Orbicularis oculi and Corrugator supercilii
69
Posterior tibial nerve monitoring
Nerve: flexor hallicus brevis Black- posterior aspect of medial malleolus over posterior tibial artery Red-2 cm proximal black
70
Lambert Eaton etiology
Antibodies attack Presynaptic voltage gated Ca channels= decreased ACh release Corticosteroids and immunosuppressive therapy
71
Duration of block for patient heterozygous for atypical pseudocholinesterase
20 min
72
Duration of block for patient homozygous for atypical pseudocholinesterase
60-180 min
73
Metabolism of Cisatracurium
Hoffman & Ester hydrolysis
74
Calculate PVR
((MPAP-PAWP)/CO) (80)= dyne-sec/cm^5
75
SVR calculation
((MAP-CVP)/CO) (80)= dynes-sec/cm^5

733 (10 decks)

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