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733 > Neuromuscular Blocking > Flashcards

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
Q

Time required to recover from intermediate NMBD from PTC-1 to TOFC-1

A

20-30 minutes

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26
Q

Problems with clinical testing of RNB

A

The best test cannot be performed while intubated!

Removal of tongue blade from clenched teeth

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27
Q

Why do we use the APM?

A

It is the sole hand uncle on the radial side that is innervated by the ulnar nerve

This decreases chance of direct muscle stimulation

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28
Q

Electromyography

A

Monitors action potential generated by nerve stimulation

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29
Q

Mechanomyography

A

Records the force of muscle contraction- clunky

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30
Q

Acceleromyography

A

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

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31
Q

BIS in paralysis

A

BIS is sensitive to changes in EMG

Controversial: but BIS values in awake paralyzed volunteered decreased to levels associated with general anesthesia

32
Q

Why do cholinesterase inhibitors have a ceiling effect?

A

Once 100% inhibition is reached the addition of more inhibitor may actually block the ACh receptors leading to neuromuscular weakness

33
Q

Considerations with Sugammadex

A

Oral contraceptives may be impacted for up to a week

Hypersensitivity reactions

34
Q

MG considerations

A

More sensitive to non-dep NMBDs
Generally resistant to Succ

Typically deep inhalational anesthetic with regional

35
Q

Issues with laparoscopic abdominal surgeries

A

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
Q

New cool Sugammadex

A

Calabadion-2

Higher affinity for roc with similar affinity for Cisatracurium

37
Q

Cause of myasthenia gravis

A

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
Q

MG patients with bulbar involvement are at risk for what?

A

-also respiratory muscle involvement

Pulmonary aspiration and pneumonia

39
Q

Impact of myasthenia gravis on NMBDs

A

Exquisitely sensitive*

IgG antibodies

40
Q

Lambert-Eaton and NMBDs

A

Very sensitive to depolarizing AND non depolarizing

41
Q

Why are muscular dystrophy patients at risk for pulmonary infections?

A

Ineffective cough

42
Q

What population are we avoiding succinylcholine?

A

Muscular dystrophy!!!

43
Q

Goal of anesthetic management in periodic paralysis

A

Prevent attacks

Frequent potassium checks
Careful ecg monitoring

44
Q

Response to NMBDs in periodic paralysis

A

Unpredictable

In hypokalemia they are very sensitive to non-depolarizing

45
Q

What does muscle relaxation not do?

A

Produce:
Amnesia
Analgesia
Unconsciousness

46
Q

Metabolism of depolarizing muscle relaxants

A

Diffusion away from NMJ and hydrolyzed in plasma by pseudocholinesterase/plasma cholinesterase

47
Q

What happens in atypical pseudocholinesterase?

A

Prolonged Succinylcholine

48
Q

Kidney failure will prolong which NMBDs?

A

Vecuronium and Pancuronium

49
Q

Metabolism of benzlysoquinoliniums….

A

Hoffman!! At physiologic pH and temperature

50
Q

Impact of neostigmine on succinylcholine block

A

Can prolong, they increase the amount of ACh in the cleft and inhibit the breachdown of SCh via pseudocholinesterase

51
Q

Tetany

A

Sustained stimulus of 50-100 Hz

52
Q

Single twitch (ST)

A

Single pulse of 0.2 ms in duration

53
Q

Cormack Lehane grade IIA

A

Partial view of vocal cords

(Posterior vocal cord view)

54
Q

C&L Grade IIB

A

Arytenoids and epiglottis only

55
Q

C&L grade II

A

Only the posterior portion of the glottic opening can be visualized, anterior commissure not seen

56
Q

How wide is the synaptic cleft?

A

50-70 nm

57
Q

Subunit replaced in nAChr

A

Y gamma-replaced

By

E Epsilon-adult

58
Q

Ach molecules in a quanta and number of quanta needed

A

5-10k

200-400 quanta

59
Q

NMJ stimulation increases in what conditions?

A

Burns
Immmobilization
Infection/sepsis
CVAs

60
Q

What does an increase in NMJ stimulation cause? -burns

A

Up-regulation of immature nAChrs

61
Q

All the names in succinylcholine metabolism

A

Pseudocholinesterase
Plasma cholinesterase
Butyrylcholinesterase

62
Q

Malignant hyperthermia- causes

A

Deficient gene in ryanodine receptor RYR1

Unable to properly regulate calcium release in skeletal muscle SR

63
Q

What does MH lead to?

A

Build up of Lactic ACID
Heat
Increased metabolism=increased CO2

64
Q

Warning signs in MH

A

Increased ETCO2
Slowly increasing body temp
Muscles spasms
Rapid heart rate
Sweating
Mottled skin

65
Q

If MH goes unchecked:

A

DIC/ excessive bleeding -use up all of your clotting factors

Multisystem organ failure

66
Q

What to do in MH

A

Notify surgeon
Get help
Call MHAUS
100% O2
Convert to TIVA-flush system
Cool
Document

67
Q

Order IA will potentiate NMB

A

Desflurane
Sevoflurane
Isoflurane
Halothane
Nitrous

68
Q

Facial nerve positioning and response and nerves

A

White/Black- just anterior to Tragus

Red- lateral to outer canthus of eye

Orbicularis oculi and Corrugator supercilii

69
Q

Posterior tibial nerve monitoring

A

Nerve: flexor hallicus brevis

Black- posterior aspect of medial malleolus over posterior tibial artery

Red-2 cm proximal black

70
Q

Lambert Eaton etiology

A

Antibodies attack Presynaptic voltage gated Ca channels= decreased ACh release

Corticosteroids and immunosuppressive therapy

71
Q

Duration of block for patient heterozygous for atypical pseudocholinesterase

A

20 min

72
Q

Duration of block for patient homozygous for atypical pseudocholinesterase

A

60-180 min

73
Q

Metabolism of Cisatracurium

A

Hoffman
&
Ester hydrolysis

74
Q

Calculate PVR

A

((MPAP-PAWP)/CO) (80)= dyne-sec/cm^5

75
Q

SVR calculation

A

((MAP-CVP)/CO) (80)= dynes-sec/cm^5

733 (10 decks)

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