Depolarizing blockers like succinylcholine have a rapid onset, paralyzing arms, neck, legs and respiratory muscles within minutes of administration. Following intravenous injection, succinylcholine mimics the endogenous ligand acetylcholine and binds nicotinic receptors at the motor end plates of skeletal muscles. Although acetylcholinesterase readily hydrolyzes acetylcholine, succinylcholine is more resistant and is hydrolyzed slowly. So, it remains bound to receptors longer, prolonging membrane depolarization. However, succinylcholine has a very short duration of action of 5-10 minutes because it diffuses away into the plasma. There, it is readily metabolized by the plasma cholinesterase into succinylmonocholine, which is further hydrolyzed into choline and succinic acid and eliminated from the body. Such rapid hydrolysis allows only a tiny portion of the injected drug to remain available at the motor end plates. To calculate the dose of succinylcholine required to produce adequate paralysis, plasma levels of cholinesterase are estimated from a detailed patient assessment.