Neuromuscular Reversal Agents + Monitoring Flashcards
Acetylcholinesterase rapidly hydrolyzes
Ach
AchE inhibitors
antagonize the residual effects of NMBD
Accelerate recovery from non-depolarizing drugs
AchE drugs include
neostigime
edrophonium
pyridostigmine
What AchE has a ceiling effect?
neostigimine
AchE inhibitors cause a build up of Ach in
NMJ
Once you’ve hit ceiling effect
max block depth that can be antagonized corresponds to return of fourth twitch in TOF
Cannot antagonize profound or deep levels of blockade
Administering more inhibitor may be detrimental
Antagonism of NMBD depends on
depth of blockade when reversal is attempted inhibitor chosen dose rate of spontaneous clear of NMBD choice and depth of anesthesia
Max Effective DOse of Neostigmine
0.06-0.08mg/kg
Max effective Dose of Edrophonium
1.0-1.5 mg.kg
Cardiovascular Side effects of Ach Inhibitor
muscarinic effects must be blocked by anticholinergic
Dose of Glycopyrrolate
0.01-0.005 mcg/kg
Dose of Atropine
0.007-0.01mcg/kg
Pulmonary side effects of Ach Inhibitor
bronchoconstriction
increased airway secretions
increased salivation
GI side effects of Ach Inhibitor
Increased bowel motilite
No effect on incidence of PONV
Sugammadex
modified gamma-cyclogextrin
reversal of shallow and profound aminosteroid-induced blockade
Sugammadex is
selective relaxant-binding
no effect on acetylcholinesterase
Dosing of Sugammadex
TOF> 2: 2mg/kg
TOF 1-2 4 mg/kg
TOF 0: 8-16 mg/kg
Sugammadex doesnt work against
succinylcholine
benzlisoquinoliniums
Side effects of Sugammadex
possible allergic reactions and bleeding
Onset of relaxation
eye muscles > extremities> trunk> abdominal muscles> diaphragm
b/c blood flow is greatest to the head neck and diaphargm
TOF
four separate stimuli every 0.5 seconds at 2Hz
To ensure reversal of NMBD
TOF > 0.9
TOF less then 0.9 is associated with
difficulty speaking
difficulty swallowing
visual disturbances
aspiration risk
AchE inhibitor side-effects
bronchoconstriction (increased airway restriction, increased salivation)
increased bowel motility
muscarinic effects must be blocked by antocholinergic
Why do we monitor NMB?
proper administration of NMBD is essential to surgery (under or over dosing)
Contraction of adductor muscle of thumb is
preferred method of determining level of blockade
Facial nerve monitoring involves stimulation of
orbicularis oculi muscle (facial nerve)
Blood flow greatest to head and neck and diaphragm
onset measured in facial nerves
recovery best measured in the hand
Onset of paralysis in non-depolarizing agent there is a decrease in
in twitch response between T1-T4 (fade)
TOF can aid in determining degree of block
Most sensitive between 70-100% paralysis
T4
75-80%
T3
80-85%
T2-4
90-95%
Tetany
continous electrical stimulation for 5 seconds at 50-100Hz
reliable for detecting fade
sustained contraction w/o fade, significant paralysis unlikely
Posttetanic count-
tetany followed in 3 seconds by single twitch stimulations
higher the count (>8) the less intense the block
Single Twitch
single twitch at 0.1-1Hz for 0.1-0.2ms
determine whether 100% paralysis is present
Double Burst Suppression
Seems to improve ability to detect residual paralysis
evaluating 2 rather than 4 twitches facilitates detection
Not reliable indictor for endotracheal extubation
5 second head life
toF ratio <0.6
generate peak negative inspiratory pressure 20-30 cmH20
