NM Blocking agents Flashcards
1. Describe the neuromuscular junction, the motor endplate, nicotinic acetylcholine receptors, and how non-depolarizing muscle blockers cause paralysis. 2. Distinguish the prototype non-depolarizing blocking drugs based upon the clinical pharmacology. 3. Describe the mechanism of action of succinylcholine, list its primary clinical uses, and its contraindications. 4. List the prototype agents used to reverse neuromuscular blockade and to describe the physical signs of inadequate and ina
primary NT at the NMJ
ACh
ACh must bind to _______ at the motor end plate to open the Na+ channel
BOTH a alpha subunits
size and ionization of NMBs
large molecules, highly ionized
effect of size of NMB molecules on CNS
large molecules cannot pass through BBB, therefore cannot act on CNS. Therefore can result in awake, paralyzed pt
onset of action of NMB
slow (2-5 minutes)
how to decrease onset time of NMBs
multiple ED95 dose
how to prolong the duration of NMB
multiple ED95 dose
can effect kinetics of NMBs
age, other drugs, hepatic/renal disease
prototype non-depolarizing locking drug (NDBD)
d-tubocurare (d-TC)
MOA of d-TC
reversible (competitive) binding to ACh receptor on a subunit (only needs to bind to 1)
prototype sterolidal NMB
vecuronium and rocuronium
advantages of sterodial NMB
stable hemodynamics, duration not affected by renal dysfunction
SE of vercuronium
associated with prolonged blockage in ICU pts
SE rocuronium
associated with occasional prolonged duration
longest acting, least expensive NMB
pancuronium
pancuronium shows prolonged action in ___ pts
renal
pancuronium has profound dependance on:
renal metabolism
NDBD that is sympathonimetic
pancuronium
prototype Benzylisoquinolinium (BQ) drugs
cis-atracurium, mivacurium
NDBD safe for renal/hepatic failure
BQ (cis-atracurium, mivacurium)
NMB that can be inactivated by high ambient temps
BQs
side effect of Mivacurium
can cause histamine release
NMB that may not require reversal
mivacurium
can cause prolonged blockade in mivacurium and/or Sch
plasma cholinesterase insufficiency
prototype depolarizing agent
Succinylcholine (Sch)
MOA of Sch
depolarizes membrane by opening Na+ channels by binding both a - subunits
drug that causes fasciculations
Sch
drug that causes flaccid paralysis
Sch
cause of Sch termination of action
redistribution away from motor end plate, and/or matabolized by plasma cholinesterase
NMD metabolized by plasma cholinesterases
Sch
effect of deficiency of plasma cholinesterases on Sch
prolonged blockade
advantages of Sch
rapid onset (30 seconds)
clincal use of Sch
rapid intubation/ intubation of trauma pts with full stomachs
NMD with shortest duration of action
Sch
NMD that causes hyperkalemia
Sch
drug that can cause post op myalgia, increased IOP/ICP/IGP
Sch
drug that can cause malignant hyperthermia
Sch
drug not reversiable with anticholesterase drugs
Sch
NMB drug that can cause cardiac arrythmias
Sch
how Sch can cause arrythmias
Sch mimics ACh at cardiac muscarinic receptors
why is NMB montoring essential?
clinical accumen not always accurate
method for monitoring NM blockade
evoked stimulatory response
areas for testing NM blockade stimulation
ulnar nerve, facial nerve, posterior tibial nerve
drug causing phase 1 blockade
Sch
drug(s) causing phase 2 blockade
all of them
phase of blockade with an antidote
phase 1
type of blockade in phase 1
prolonged blockade
type of blockade in phase 2
repolarized, but blocked
antidote for phase 2 blockade
cholinesterase inhibitors
ways to measure blockade
subjective/objective/ assement of evoked responses and clinical assesment of muscle strenght
signs of residual blockade/inadequate reversal
strong hand grip that weakens, and jerky movement
NMB only anethetic drugs that are:_____
routinely antagonized with pharmacologic reversal agents
common (3) NMB reversal agents
neostigmine, edrophonium, pyridostigmine
MOA of blockade reversal agents
inhibition of ACh-esterase, increases synaptic ACh concentrations
short onset blocking reversal agent
edrophonium
longest onset blocking reversal agents
pyridostigmine
side effects of NMB reversal agents
bradycardia, icnreased secretions, post-op N/V
drug given with NMB reversal agents to attenuate side effects
atrooine (edro) or glycopyrrolate (___stigmines)
when are anticholinesterase drugs contraindicated
absence of measurable responses to muscle stimulation
inadequate reversal can lead to:
residual neuromuscular blockade (RNMB)
signs of RNMB
ventilatory insufficiency, insufficient airway protection, visual disturbances, inability to sit without assistance, facial weakness, systemic fatigue
inappropriate reversal of NMB results in
postop N/V, tachycardia or bradycardia, bronchial/nasal secretions, excess sweating (can mimic MI diaphoresis)
NDBD antagonist drug
sugammadex
MOA of sugammadex
binds rocuroum or vecurinium with high affinity in bloodstream
signs of malignant hyperthermia
rapid onset of tachycardia, hypercarbia, hypertension, rigidity, hyperthermia, acidosis
results of malignant hyperthmia if untreated
rhabdo, organ failure, death
triggers of malignant hyperthermia
inhaled anesthetics and Sch
pathophys of malignant hyperthermia
hypermetabolism due to exagerated release of Ca++ from sarcoplasmic reticulum
only drug treatment for malignant hyperthermia
dantrolene
MOA of dantrolene
binds ryanodine receptor, inhibiting release of Ca++ from SR