skeletal muscle relaxers Flashcards
two groups of skeletal muscle relaxers
depolarizing and non-depolarizing
5 steps of normal neuromuscular function
- Axn potential arrives at nerve terminal
- influx of Ca++ and release of Ach
- Ach diffuses across synaptic cleft
- Nicotine receptors activated on nerve endplate
- Muscle contracts
what are the non-depolarizing (antagonist) agents ?
” - curiums” and “-roniums”
what is the depolarizing (agonist) agent ?
succinylcholine
MOA of neuromuscular blocking agents
Agents block cholinergic transmission between motor nerve ending and nicotinic receptors on skeletal muscle
uses for neuromuscular block?
Facilitate tracheal intubation
Provide complete muscle relaxation
adjunct to anesthesia (decreased anesthesia dose and faster recovery)
what are the two groups of non-depolarizing (antagonist) neuromusc. blocking agents?
short acting ( 30-60min) long acting( 60-120min)
what are the short-acting non-depolarizing NM blocking agents?
Atracurium
Cisatracurium
Rocuronium (VERY rapid onset, short DOA)
Vecuronium
what is the long-acting non-depolarizing NM blocking agent?
Pancuronium
MOA of non-depol. NM blockers
competitive antagonists - block Ach from binding to receptor and activating it
clinical effect of non-depol NM blockers
progression- muscle weakness then complete muscle paralysis
large or small muscles more resistant to NM blockade ? what does this mean?
large muscles, paralyzed last but recover first
all NM blocking agents (depol and nondepol) are polar or nonpolar, why is this significant?
polar: can’t get into CNS when given orally so NEED to be IV.
you can get an increase NM blockade when giving nondepol agents with _______
antibiotics (usually aminoglycosides- GNATS)
- the abx DECREASE the release of Ach which enhances the blockade but INCR. RESPIRATORY DEPRESSION
how can you reverse the effect of nondepol NM blockers?
they are competative antagonists, so you can FLOOD with an agonist (Ach)
- give acetylcholinesterase inhibitors (e.g. neostigmine) so you have more Ach
what is the MOA of succinylcholine?
this is our “agonist” depolarizing agent.
- mimics Ach to depolarize NM, stays attached and constantly is depolarizing… unable to depol again while this drug is present.
when are you using succinylcholine?
adjunct to general anesthesia
- help tracheal intubation, skeletal muscle relaxation during surgery or mechanical ventilation in adequately sedated patients
what is the metabolism of of succinylcholine (depol NM block) ?
Metabolized by plasma pseudocholinesterase
DOA: 4-30 minutes
-drug disappears rapidly after discontinuation
what is the “genetic variant” for succinylcholine?
some people (w/ this variant) have PROLONGED effects from the drug
4 ADRs of depolarizing NM blocker (succinycholine)?
- apnea
- hyperkalemia
- muscle pain
- malignant hyperthermia
how can succinycholine cause apnea?
Deficiency/atypical form of plasma cholinesterase leads to prolonged apnea from diaphragm paralysis
how can succinycholine cause hyperkalemia? why is this significant?
Succinylcholine increases K+ release from intracellular stores.
- Damaged tissue ( burns, nerve damage, trauma, etc) has rapid loss of K+
- can lead to cardiac arrest
what 4 things can cause malignant hyperthermia ?
inhaled anesthetics + succinylcholine OR
-Genetic excitation-contraction coupling defect, burn victims, muscular dystrophy
what is malignant hyperthermia? what can it ultimately lead to?
Uncontrolled increased in skeletal muscle metabolism with SUDDEN, PROLONGED RELEASE OF Ca++
(overwhelm’s body’s capacity to supply O2, remove CO2 and regulate temp)
-fast rise in BODY TEMP, SEVERE MUSCLE CONTRACTIONS
- circulatory collapse and death !!
