Neuromuscular blocking agents: Difference between revisions
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*'''Depolarizing blocking agents''': These agents act by [[Depolarization|depolarizing]] the [[sarcolemma]] of the skeletal [[muscle fiber]]. This persistent depolarization makes the muscle fiber resistant to further stimulation by ACh. | *'''Depolarizing blocking agents''': These agents act by [[Depolarization|depolarizing]] the [[sarcolemma]] of the skeletal [[muscle fiber]]. This persistent depolarization makes the muscle fiber resistant to further stimulation by ACh. | ||
==Types== | |||
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|+Neuromuscular Blocking Agents | |+Neuromuscular Blocking Agents | ||
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|[[Atracurium]] (Tracrium) | |[[Atracurium]] (Tracrium) | ||
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|[[Cisatracurium]] (Nimbex) | |[[Cisatracurium]] (Nimbex) | ||
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* Non-depolarizing blockers are reversed by [[acetylcholinesterase inhibitor]] drugs since they are competitive antagonists at the ACh receptor so can be reversed by increases in ACh. | * Non-depolarizing blockers are reversed by [[acetylcholinesterase inhibitor]] drugs since they are competitive antagonists at the ACh receptor so can be reversed by increases in ACh. | ||
* The depolarizing blockers already have ACh-like actions, so these agents have prolonged effect under the influence of acetylcholinesterase inhibitors. Administration of depolarizing blockers initially produces ''fasciculations'' (a sudden twitch just before paralysis occurs). This is due to depolarization of the muscle. Also, post-operative pain is associated with depolarizing blockers. | * The depolarizing blockers already have ACh-like actions, so these agents have prolonged effect under the influence of acetylcholinesterase inhibitors. Administration of depolarizing blockers initially produces ''fasciculations'' (a sudden twitch just before paralysis occurs). This is due to depolarization of the muscle. Also, post-operative pain is associated with depolarizing blockers. | ||
==Sources== | |||
<references/> | |||
Revision as of 03:22, 24 February 2015
Background
These drugs fall into two groups:
- Non-depolarizing blocking agents: These agents constitute the majority of the clinically relevant neuromuscular blockers. They act by competitively blocking the binding of ACh to its receptors, and in some cases, they also directly block the ionotropic activity of the ACh receptors.[1]
- Depolarizing blocking agents: These agents act by depolarizing the sarcolemma of the skeletal muscle fiber. This persistent depolarization makes the muscle fiber resistant to further stimulation by ACh.
Types
| Agent | Time to onset (seconds) |
Duration (minutes) |
Side effects | Clinical use | Storage |
|---|---|---|---|---|---|
| Succinylcholine | |||||
| Atracurium (Tracrium) | 90 | 30 min or less[2] |
|
widely[2] | refrigerated |
| Cisatracurium (Nimbex) | 90 | 60–80 | does not cause release of histamine | refrigerated | |
| Vecuronium (Norcuron) | 60 | 30–40[2] | Few,[2] may cause prolonged paralysis[2] and promote muscarinic block | widely[2] | non-refrigerated |
| Rocuronium (Zemuron) | 75 | 45–70[citation needed] | may promote muscarinic block | non-refrigerated | |
| Pancuronium (Pavulon) | 90 | 180 or more[citation needed] |
(no hypotension)[2] |
widely[2] | non-refrigerated |
Comparison of Drugs
The main difference is in the reversal of these two types of neuromuscular-blocking drugs.
- Non-depolarizing blockers are reversed by acetylcholinesterase inhibitor drugs since they are competitive antagonists at the ACh receptor so can be reversed by increases in ACh.
- The depolarizing blockers already have ACh-like actions, so these agents have prolonged effect under the influence of acetylcholinesterase inhibitors. Administration of depolarizing blockers initially produces fasciculations (a sudden twitch just before paralysis occurs). This is due to depolarization of the muscle. Also, post-operative pain is associated with depolarizing blockers.