What are some reasons a provider may choose rocuronium over
succinylcholine for a rapid sequence intubation (RSI)?
- Although succinylcholine has a more rapid onset of action, it carries the risk of hyperkalemia, malignant hyperthermia, and mylagia.
- Succinylcholine is not safe for patients with neuromuscular disorders, severe burns, trauma, or elevated K+.
- Rocuronium provides longer paralysis and is reversible with sugammadex.
What is the neuromuscular junction?
- NMJ is where the axon terminal meets the muscle fiber.
3 PARTS
1. Presynaptic membrane: Membraine of an axon terminal
2. Postynaptic membrane: Membrane of a skeletal muscle fiber i.e. myocyte (aka motor end plate)
3. Synpoatic cleft (Space bt 1 & 2)
Describe how muscle contraction is initiated.
- Action potential (AP) reaches axon terminal → depolarization occurs → Na+ influx into neuron
- Depolarization of the axon terminal turns on rvoltage-gated Ca channels in the presynaptic neuron.
- Ca2+ influx → Vesicles containing Ach fuse to cell membrane of axon terminal → Ach releases into synaptic cleft
- Ach binds to ligand-gated ion channels (aka nicotinic receptors) on myocyte (aka motor end plate)
- Ion channels open → Na+ & Ca2+ influx into skeletal muscle fiber → Some K+ exits cell + Overall increased positive charge inside skeletal muscle cell → Depolarization → Muscle contraction
What is the only depolarizing neuromuscular blocker (NMB)?
Succinylcholine
Name the 3 non-depolarizing neuromuscular blockers (NMB).
- Rocuronium
- Vecuronium
- Cistracurium
MOA: Depolarizing NMB - Succinylcholine
- Succinylcholine binds to post-junctional nicotinic receptors, mimicking Ach → Na+ channels open + motor end plate depolarized → muscle fasciculations
- Bc resistant to acetylcholinesterase (enzyme that breaks down Ach) → remains bound to receptor longer → Sustained depolarization prevents repolarization → flaccid paralysis
MOA: Non-depolarizing neuromuscular blockers (Roc, Vec, Nimbex)
- Occupy nicotinic receptors on motor end plate → Prevent Ach from binding and depolarizing motor end plate (This is known as competitive antagonism) → No muscle contraction
- Do not cause muscle fasciculations pre-paralysis
Succinylcholine
* Onset & Duration
* RSI dose
* Regular (non-intubation) dose
* Infusion dose
- Onset: 30-60s
- Duration: 5-12m
- RSI dose: 0.6-1.2 mg/kg
- Regular (non-intubation) dose: Same
- Infusion dose: None
Rocuronium
* Class
* Onset & Duration
* RSI dose
* Regular (non-intubation) dose
* Infusion dose
- Class: Aminosteroid
- Onset: 1.5-2.5 min
- Duration: 30-60m
- RSI dose: 1-1.2 mg/kig
- Regular (non-intubation) dose: 0.6-1.2 mg/kg
- Infusion dose: 5-12 mcg/kg/min
Vecuronium
* Class
* Onset & Duration
* RSI dose
* Regular (non-intubation) dose
* Infusion dose
- Class: Aminosteroid
- Onset: 2-3min
- Duration: 40-60min
- RSI dose: None
- Regular (non-intubation) dose: 0.1-0.2 mg/kg
- Infusion dose: 0.8-1.7 mcg/kg/min
Cistracurium (Nimbex)
* Class
* Onset & Duration
* RSI dose
* Regular (non-intubation) dose
* Infusion dose
- Class: Benzylisoquinolinium
- Onset: 3-6 min
- Duration: 40-55min
- RSI dose: None
- Regular (non-intubation) dose: 0.15-0.2 mg/kg
- Infusion dose: 1-3 mcg/kg/min
Succinylcholine
* Metabolism
* Elimination
- Metab: Via enzyme called pseudocholinesterase (aka plasma cholinesterase or butyrylcholinesterase)
- Elimination: Rapid metab via pseudocholinesterase in plasma (blood) → 2 main byproducts (succinylmonocholine + choline) may undergo renal excretion
Rocuronium
* Metabolism
* Elimination
- Metab: Hepatic
- Elimination: ~90% bile, ~10% kidneys
Vecuronium
* Metabolism
* Elimination
- Metab: 50% hepatic, 50% unchanged in urine
- Elimination: Cleared via bile & kidneys
Cistracurium
* Metabolism
* Elimination
- Metab: Hoffman Elimination = organ independent elimination in plasma & tissue, does not rely on heptic or renal metab
- Elimination: Hoffman Elimination converts 77% to inactive metabolite, laudanosine; Some excreted unchanged in urine
Succinylcholine
Special Considerations
- Can cause malignant hyperthermia
- Can raise K+ by 0.5 mEq/L so avoid in patients who are hyperkalemic
- Avoid in patients with burns, denervation injuries, upper motor lesions, Guillian-Barre, and prolonged immobility
Rocuronium
Special Considerations
- The most frequently used NMB in the U.S.
- For RSI, higher doses are used to achieve quicker onset
- Sometimes avoided in patients with hepatic disease due to hepatic metabolism
- Avoided in ESRD due to active metabolites
Vecuronium
Special Considerations
- Not used in RSI
- Also sometimes avoided in patients with hepatic disease due to hepatic metabolism
- Avoided in ESRD due to active metabolites
Cistracurium
Special Considerations
- Not used in RSI
- Often used in patients with severe liver or renal dysfunction
- Laudanosine, from Hoffman Elimination, can cause CNS toxicity and seizures
