Neuromuscular blocking drugs

Question 1

How they work?

Answer 1

Muscle paralysis in surgery or mechanical ventilation. Selective for N
• nicotinic receptors at
neuromuscular junction but not autonomic , receptors.

Question 2

Depolarizing neuromuscular blocking drugs

Answer 2

Succinylcholine-strong N
nicotinic receptor agonist; produces sustained depolarization and
prevents muscle contraction.
Reversal of blockade:
• Phase I (prolonged depolarization) - no antidote. Block potentiated by cholinesterase inhibitors.
• Phase II (repolarized but blocked; N nicotinic receptors are available, but desensitized) — may be reversed with cholinesterase inhibitors.
Complications include hypercalcemia, hyperkalemia, malignant hyperthermia. † risk of prolonged muscle paralysis in patients with pseudocholinesterase deficiency

Question 3

Nondepolarizing neuromuscular blocking drugs
Atracurium, cisatracurium, pancuronium, rocuronium, vecuronium —

Answer 3

competitive N nicotinic receptor antagonist.
Reversal of blockade-sugammadex or cholinesterase inhibitors (eg, neostigmine). Anticholinergics (eg, atropine, glycopyrrolate) are given with cholinesterase inhibitors to prevent muscarinic effects (eg, bradycardia

Question 4

Malignant hyperthermia

Answer 4

Rare, life-threatening, hypermetabolic condition caused by the administration of potent inhaled anesthetics (sevoflurane, desflurane, isoflurane) or succinylcholine in susceptible individuals.
Susceptibility to malignant hyperthermia is caused by de novo or inherited (autosomal dominant) mutations to ryanodine (RYRI) or dihydropyridine receptors (DHPR).
t 1 Ca* release from sarcoplasmic reticulum - sustained muscle contraction - hypercapnia, tachycardia, masseter/generalized muscle rigidity, rhabdomyolysis, hyperthermia.
Treatment: dantrolene (ryanodine receptor antagonist).