Depolarizing Neuromuscular Blockers

Succinylcholine reversibly binds to nicotinic receptors at the neuromuscular junction resulting in increased stimulation of the nicotinic receptors.  Succinylcholine is not able to be metabolized by acetylcholinesterase, so stimulation persists. The physiologic effects of the persistent succinylcholine stimulation occurs in two phases. Phase 1: Depolarization of receptor leads to fasciculations of muscles (stimulation). Phase 2: Receptor repolarizes but is desensitized to stimulus, leading to paralysis.

Class Drugs

• Succinylcholine

Class Mechanism of Action

Stimulates nicotinic receptor and depolarizes the neuromuscular junction.  Acetylcholinesterase does not metabolize succinylcholine, so the nicotinic receptor stimulation persists.  Succinylcholine is metabolized by plasma pseudocholinesterase.  The action of succinylcholine occurs in two phases:

• Phase 1: Depolarization of receptor leads to fasciculations of muscles (stimulation).

• Phase 2: Receptor repolarizes but is desensitized to stimulus, leading to paralysis.

Class Adverse Effects

Apnea

Malignant Hyperthermia

• Results from uncontrolled increase in skeletal muscle contraction resulting in overwhelming need for oxygen and removal of metabolites.

• Ultimately leads to circulatory collapse if not treated properly with Dantrolene and cooling measures  

• Susceptibility seems to be inherited in an autosomal dominant fashion.

Hyperkalemia

• Sudden rise in potassium levels may cause cardiac arrest when used in patients with hyperkalemia or upper motor neuron disease greater than 72 hours.

• Use caution in the following patients:

Burns >72 hours

• Stroke >72 hours

• Crush injury

• Renal failure (unless known potassium)

• Congenital myopathy

Drug Table

Drug Name	Application	Comments	Image
Succinylcholine	Facilitate Intubation; Relaxes skeletal muscle in surgery		"Furnace sucking in coal"