Test 2 Muscle Relaxants Flashcards
Pancuronium
Non-depolarizing neuromuscular agent. Competitive Nm receptor antagonist.
Used as an adjuvant to anesthesia, relaxation of chest during mechanical ventilation.
t1/2 = 75-107 min (slowest)
Renal elimination
Tox: Not an analgesic, apnea, muscarinic blockade (inc HR and CO)
Interactions: Enhance inhaled anesthetics and enhances antibiotics (esp. aminoglycosides).
Antidote: Increase Ach at synapse, so Neostigmine (Nm receptor agonist) w/ glycopyrrolate (Nm antagonist) to protect gut.
Tubocurarine
Non-depolarizing neuromuscular agent. Competitive Nm receptor antagonist.
Used as an adjuvant to anesthesia, relaxation of chest during mechanical ventilation.
t1/2 = 107-237 min (slowest, but not used anymore)
Renal/Hepatic elimination
Tox: Not an analgesic, apnea
Interactions: Enhance inhaled anesthetics and enhances antibiotics (esp. aminoglycosides).
Antidote: Increase Ach at synapse, so Neostigmine (Nm receptor agonist) w/ glycopyrrolate (Nm antagonist) to protect gut.
Vecuronium
Non-depolarizing neuromuscular agent. Competitive Nm receptor antagonist.
Used as an adjuvant to anesthesia, relaxation of chest during mechanical ventilation.
t1/2 = 61.1 min (middle)
Renal elimination
Tox: Not an analgesic, apnea
Interactions: Enhance inhaled anesthetics and enhances antibiotics (esp. aminoglycosides).
Antidote: Increase Ach at synapse, so Neostigmine (Nm receptor agonist) w/ glycopyrrolate (Nm antagonist) to protect gut.
Rocuronium
Non-depolarizing neuromuscular agent. Competitive Nm receptor antagonist.
Used as an adjuvant to anesthesia, relaxation of chest during mechanical ventilation, and larynx relaxation for endotracheal intubation.
t1/2 = 60 min (middle)
Hepatic elimination
Tox: Not an analgesic, apnea, muscarinic blockade (inc HR and CO)
Interactions: Enhance inhaled anesthetics and enhances antibiotics (esp. aminoglycosides).
Antidote: Increase Ach at synapse, so Neostigmine (Nm receptor agonist) w/ glycopyrrolate (Nm antagonist) to protect gut.
Mivacurium
Non-depolarizing neuromuscular agent. Competitive Nm receptor antagonist.
Used for larynx relaxation for endotracheal intubation.
t1/2 = 3-5min (fastest)
Metabolic elimination.
Tox: Not an analgesic, apnea, histamine release
Interactions: Enhance inhaled anesthetics and enhances antibiotics (esp. aminoglycosides).
Antidote: Increase Ach at synapse, so Neostigmine (Nm receptor agonist) w/ glycopyrrolate (Nm antagonist) to protect gut.
Succinylcholine
Depolarizing agent. Stimulates Nm receptors so they are unable to repolarize (one initial contraction followed by flaccid paralysis).
Phase I - initial block caused by depolarized neuron
Phase II - desensitization over time –> resembles non-polarizing blockade (paralysis persists after succinylcholine removal)
Use: Endotracheal intubation, suppression of muscle contractions during electroconvulsive shock therapy (ECST)
Tox: Not analgesic, apnea, muscle pain (from fasciculations), inraocular/intragastric pressure increase, stimulation of ganglionic nicotinic receptors (arrhythmia/hypertension), stimulation of muscarinic receptors/SA node (bradycardia), hyperkalemia (K+ release from motor endplate)
Drug interactions: Enhance local anesthetic. Cholinesterase inhibitors enhance phase I block
Antidotes: Phase I = time. Phase II = cholinesterase inh after succinylcholine is gone.
Contra: Family history of malignant hyperthermia (ryanodine receptor mutation –> Ca2+ release), immediately after burns, or 7-10 days post-crush injury.
Baclofen
GABAb (inhibits NT release) receptor agonist. Decreases Ca2+ influx at 1a afferent nerve terminals, decreases substance P release in the spinal cord.
Use: Spinal cord spasticity, MS
Tox: Drowsiness, mental disturbances (altered mental state)
Given orally or intrathecally (next to spinal cord) to decrease side effects
Diazepam
Increases allosteric modulation of GABAa receptor (opens Cl- channels) –> hyperpolarized membrane.
Use: Flexor/extensor spasm, spinal spasticity, and MS.
Tox: Drowsiness, sedation
Contra: Acute narrow-angle, or untreated open-angle glaucoma.
Tizanidine
α2-adrenergic agonist-mediated pre- (inhibits 1a) and post- (hyperpolarize) synaptic inhibition in spinal cord.
Use: Spinal cord spasticity, MS
Tox: Drowsiness (not as bad as the other spasmolytic drugs), hypotension (α2 mediated)
Dantrolene
Blocks sarcoplasmic reticulum Ca2+ release from skeletal muscle.
Use: Spasticity due to stroke, spinal cord injury, MS, or cerebral palsy. Malignant hyperthermia.
Tox: Muscle weakness, sedation, hepatitis (rare)
