Neuromuscular Blocking Flashcards
Supramaximal current
Maximal- an increase in current no longer increases muscle response
-20% above maximal to ensure all fibers in innervated nerve will depolarize
Threshold current
Current threshold to evoke muscle contraction
Incidence of residual paralysis with qualitative monitoring
30-40%
When is subjective detection of fade unreliable?
Between 40-90%!!!!
Monitoring of facial vs adductor pollicis
Facial leads to over estimation of neuromuscular function
When do upper airway muscles recover?
Even at TOF 0.90 there can be an inability to protect the airway
Muscle innervation ratios
Fine control (eyes): 1 nerve innervating 2 fibers
Large muscles (thigh): 1:2,000
What electrolyte imbalances antagonize ACh release??
Hypocalcemia: think release from pre synapse
Hypermagnesemia-competes with Ca in Presynaptic channels
Post synaptic binding of ACh
Binds alpha subunit of nAChRs
Na influx
K efflux
Resulting in membrane depolarization
Explain Nicotinic receptor upregulation
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
Down regulation of nAChRs
Results from sustained agonism
Think chronic pyridostigmine in MG
Resistance to SCh and extreme sensitivity to non-depolarizing agents
Most effective prophylaxis of myalgia with SCh
NSAIDs
Explain SCh and regurg
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
NMBAs and potency
We use more of lower potency agents so they have a faster onset time
Vec vs roc
Intubation vs re-dosing for deeper block
2-3xED95 for intubation
Only 10% of ED 95 is necessary to reestablish deeper level of block
What occurs with defasiculating dose
Mutual antagonism between depolarizing and non depolarizing
Result: increased SCh dose
Acute vs chronic anticonvulsants with NMBDs
Acute- block is potentiated
Chronic- significantly decreases duration of action with amino steroids, little impact on Cisatracurium
Acidosis and NMBDs
Interferes with anticholinesterases when reversing block
Supramaximal current
20% above baseline
Ensures all fibers depolarize despite changes in resistance over time
Nerve stimulator orientation
Red to head
2cm above the wrist crease
Several centimeters apart on ulnar nerve (pinky side)
Double burst stimulation
Mini-tetanic burst of three stimuli at 50Hz seperated by 750msec
Two bursts of three*
TOF
Four stimuli at 2 Hz
no control needed
Able to differentiate between depolarizing and non-depolarizing
Useless above 0.40
Less painful than tetany
Post tetanic count
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
Why does post tetanic count work??
The high frequency tetanic stimulation temporarily increases the amount of ACh released
Time required to recover from intermediate NMBD from PTC-1 to TOFC-1
20-30 minutes
Problems with clinical testing of RNB
The best test cannot be performed while intubated!
Removal of tongue blade from clenched teeth
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
Electromyography
Monitors action potential generated by nerve stimulation
Mechanomyography
Records the force of muscle contraction- clunky
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
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
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
Considerations with Sugammadex
Oral contraceptives may be impacted for up to a week
Hypersensitivity reactions
MG considerations
More sensitive to non-dep NMBDs
Generally resistant to Succ
Typically deep inhalational anesthetic with regional
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
New cool Sugammadex
Calabadion-2
Higher affinity for roc with similar affinity for Cisatracurium
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.
MG patients with bulbar involvement are at risk for what?
-also respiratory muscle involvement
Pulmonary aspiration and pneumonia
Impact of myasthenia gravis on NMBDs
Exquisitely sensitive*
IgG antibodies
Lambert-Eaton and NMBDs
Very sensitive to depolarizing AND non depolarizing
Why are muscular dystrophy patients at risk for pulmonary infections?
Ineffective cough
What population are we avoiding succinylcholine?
Muscular dystrophy!!!
Goal of anesthetic management in periodic paralysis
Prevent attacks
Frequent potassium checks
Careful ecg monitoring
Response to NMBDs in periodic paralysis
Unpredictable
In hypokalemia they are very sensitive to non-depolarizing
What does muscle relaxation not do?
Produce:
Amnesia
Analgesia
Unconsciousness
Metabolism of depolarizing muscle relaxants
Diffusion away from NMJ and hydrolyzed in plasma by pseudocholinesterase/plasma cholinesterase
What happens in atypical pseudocholinesterase?
Prolonged Succinylcholine
Kidney failure will prolong which NMBDs?
Vecuronium and Pancuronium
Metabolism of benzlysoquinoliniums….
Hoffman!! At physiologic pH and temperature
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
Tetany
Sustained stimulus of 50-100 Hz
Single twitch (ST)
Single pulse of 0.2 ms in duration
Cormack Lehane grade IIA
Partial view of vocal cords
(Posterior vocal cord view)
C&L Grade IIB
Arytenoids and epiglottis only
C&L grade II
Only the posterior portion of the glottic opening can be visualized, anterior commissure not seen
How wide is the synaptic cleft?
50-70 nm
Subunit replaced in nAChr
Y gamma-replaced
By
E Epsilon-adult
Ach molecules in a quanta and number of quanta needed
5-10k
200-400 quanta
NMJ stimulation increases in what conditions?
Burns
Immmobilization
Infection/sepsis
CVAs
What does an increase in NMJ stimulation cause? -burns
Up-regulation of immature nAChrs
All the names in succinylcholine metabolism
Pseudocholinesterase
Plasma cholinesterase
Butyrylcholinesterase
Malignant hyperthermia- causes
Deficient gene in ryanodine receptor RYR1
Unable to properly regulate calcium release in skeletal muscle SR
What does MH lead to?
Build up of Lactic ACID
Heat
Increased metabolism=increased CO2
Warning signs in MH
Increased ETCO2
Slowly increasing body temp
Muscles spasms
Rapid heart rate
Sweating
Mottled skin
If MH goes unchecked:
DIC/ excessive bleeding -use up all of your clotting factors
Multisystem organ failure
What to do in MH
Notify surgeon
Get help
Call MHAUS
100% O2
Convert to TIVA-flush system
Cool
Document
Order IA will potentiate NMB
Desflurane
Sevoflurane
Isoflurane
Halothane
Nitrous
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
Posterior tibial nerve monitoring
Nerve: flexor hallicus brevis
Black- posterior aspect of medial malleolus over posterior tibial artery
Red-2 cm proximal black
Lambert Eaton etiology
Antibodies attack Presynaptic voltage gated Ca channels= decreased ACh release
Corticosteroids and immunosuppressive therapy
Duration of block for patient heterozygous for atypical pseudocholinesterase
20 min
Duration of block for patient homozygous for atypical pseudocholinesterase
60-180 min
Metabolism of Cisatracurium
Hoffman
&
Ester hydrolysis
Calculate PVR
((MPAP-PAWP)/CO) (80)= dyne-sec/cm^5
SVR calculation
((MAP-CVP)/CO) (80)= dynes-sec/cm^5
