Download Neuromuscular Blockade

yes no Was this document useful for you?
   Thank you for your participation!

* Your assessment is very important for improving the work of artificial intelligence, which forms the content of this project

Neuromuscular Blockade
I. Cholinergic receptors (AChR)
A. Nicotinic cholinergic receptors
1. Muscular – neuromuscular junction (NMJ)
2.. Neuronal – autonomic ganglia and CNS
B. Muscarinic – autonomic ganglia, end organ sites of parasympathetic innervation, and CNS
C. Review of NMJ physiology
II. Monitoring
A. Peripheral nerve stimulators
1. Ulnar nerve – adductor pollicis
2. Facial
3. Posterior tibial
4. Peroneal
B. Stimulation
1. Single twitch 0.1 Hz
a. 75% of receptors must
be blocked before twitch
height begins to decrease
b. 75% may still be blocked
when it returnes to control
2. Tetanus 50-200 Hz
3. Posttetanic single twitch
a. Posttetanic potentiation
4. Train of four 2 Hz q 10secs
a. TOF Ratios
5. Double burst stimulation
6. Posttetanic count
III. Neuromuscular Blocking Drugs (NMBD)
A. Antagonists to AchR
B. Different Characteristics: onset, duration, metabolism, side effects, interactions with other durgs.
C. Depolarizing
1. Mimics Ach causes persistent depolarization and leads to inexcitability of the perijunctional
muscle membrane and thus muscle relaxation
2. Succinylcholine
3. Characteristics of block
a. Fasciculation then relaxation
b. No fade with tetanus or train of four (TOF)
c. No posttetanic potentiation (PTP)
d. Potentiation of block of anticholinesterases
e. Antagonism by nondepolarizing relaxants
4. Block ends when SCh diffuses away and hydrolyzed by plasma cholinesterase
5. Side Effects
a. Myalgias
b. Arrhythmias – ganglionic stimulation
c. Hyperkalemia
d. Increase intraocular pressure
e. Increase intragastric pressure
f.. Increase intracranial pressure
g. Trigger Malignant Hyperthermia
h. Phase II block
j. Prolong blockade
D. Nondepolarizing
1. Reversible Competitive Antagonists of Ach for AchR
2. Aminosteroids – pancuronium, vecuronium, rocuronium
3. Benzylisoquinolines – d-tubocurarine, cisatracurium, mivacurium
4. Characteristics of block
a. No fasciculations
b. Fade with tetanus or TOF
c. PTP
d. Antagonism by anticholinesterases
e. Antagonism by depolarizing agents
5. Side Effects
a. Histamine release: d-tubocurarine, atracurium, mivacurium
b. Vagolytic Activity: gallamine, pancuronium
c. Sympathetic Stimulation: gallamine, pancuronium
IV. Reversal of neuromuscular blockade
A. Depolarizing blockade
1. Normally resolves within 10-15min
2. Phase II block:
a. Half of patients resolves 10-15 min
b. Other half of patients have prolonged responses.
B. Nondepolarizing blockade
1. Normally resolves when drugs diffuse away from Ach
2. Can be accelerated by acetyl cholinesterase inhibitors (anticholinesterases)
a. Edrophonium, Neostigmine Pyridostigmine
b. Increasing Ach and can have muscarinic and nicotinic effects
c. SE: bradycardia, bronchoconstriction, salivation, lacrimation, miosis
d. Minimize SE by administering antimuscarinics: atropine or glycopyrrolate
3. Prolonged blockade
a. hypothermia
b. antibiotics (aminoglycosides, clindamycin, uridopenicillins)
c. electrolytes (hypokalemia, hypocalcemia, hypermagnesmia)
d. acid base (alkalosis prolongs block, acidosis inhibits reversal)
C. Clinical Signs of recovery
1. TOF ratio more than 0.75 – 0.90
2. Adequate Ventialtion and Oxygenation
3. Sustained Grip Strength
4. Sustained Headlift
5. Coordinated muscle activity
6. Clenching teeth precluding removal of oral airway