Term
| Predominant use for neuromuscular blockers |
|
Definition
| Paralyze skeletal muscle during surgical and orthopedic procedures |
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Term
|
Definition
| Depolarizing competitive AChR agonist. Phase I: fasiculations; Phase II: desensitization. |
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|
Term
| Succinylcholine adverse reactions |
|
Definition
| Side effects include: apnea, risk of hyperkalemia (in burn/trauma pts where receptors are upregulated), malignant hyperthermia is rare, prolonged action in pts with plasmaChE mutations or liver damage (plasmaChE comes from liver). Stimulates cardiac mAChR: bradycardia, slight release of histamine. |
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|
Term
| Nondepolarizing neuromuscular blockers: general characteristics () |
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Definition
| All delivered IV. Those metabolized by the kidney will have long half-lives while those metabolized by the liver have shorter half-lives; damage to respective organ can prolong action. Those metabolized by plasmaChE have the shortest half-life. |
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Term
|
Definition
(5-15 mins with rapid onset):
Succinylcholine
Mivacurium |
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|
Term
| Intermediate-acting NM blockers |
|
Definition
(20-60 mins):
Vecuronium
Atracurium
Cisatracurium
Rocuronium |
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|
Term
|
Definition
(1-2 hours):
Tubocurarine
Metocurine
Pancuronium
Pipecuronium
Doxacurium |
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|
Term
|
Definition
Short-acting, rapid-onset.
Autonomic ganglia: No effect
Histamine release: Low
Cardiac mAChR: None
Metabolism: plasmaChE |
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|
Term
|
Definition
Medium-acting, rapid-onset.
Autonomic ganglia: no effect
Histamine release: none
Cardiac mAChR: slight
Metabolism: Liver |
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|
Term
|
Definition
Medium-acting, slow-onset.
Autonomic ganglia: no effect
Histamine release: none
Cardiac mAChR: none
Metabolism: Liver (and kidney) deacetylation |
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|
Term
|
Definition
Medium-acting, slow-onset.
Autonomic ganglia: no effect
Histamine release: low
Cardiac mAChR: none
Metabolism: spontaneous hydrolysis |
|
|
Term
|
Definition
Medium-acting, slow-onset.
Autonomic ganglia: no effect
Histamine release: slight
Cardiac mAChR: none
Metabolism: Spontaneous hydrolysis
Concern for hypotension and bronchoconstriction. |
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|
Term
|
Definition
Long-acting, slow-onset.
Autonomic ganglia: blockade
Histamine release: high
Cardiac mAChR: none
Metabolism: Kidney excretion |
|
|
Term
|
Definition
Long-acting, slow-onset.
Autonomic ganglia: blockade
Histamine release: moderate
Cardiac mAChR: none
Metabolism: Kidney excretion |
|
|
Term
|
Definition
Long-acting, slow-onset.
Autonomic ganglia: no effect
Histamine release: none
Cardiac mAChR: moderate block (also called 'vagolytic effect': tachycardia)
Metabolism: Kidney deacetylation |
|
|
Term
|
Definition
Long-acting, slow-onset.
Autonomic ganglia: no effect
Histamine release: none
Cardiac mAChR: none
Metabolism: Kidney deacetylation |
|
|
Term
|
Definition
Long-acting, slow-onset.
Autonomic ganglia: no effect
Histamine release: none
Cardiac mAChR: no effect
Metabolism: Kidney excretion |
|
|
Term
|
Definition
| Peripheral nerve stimulation, either 'train-of-four' or tetany will display "fade" (response gradually decreases). |
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|
Term
|
Definition
| For blockers other than succinylcholine (and mivacurium) reversal can be accelerated by AChE-I such as neostigmine, with atropine or glycopyrrolate to prevent muscarinic effects. |
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|
Term
| Typical course of NMJ blockers |
|
Definition
| Succinylcholine and mivacurium will be given first for rapid-onset of paralysis followed by use of a long-acting blocker to maintain. Thus, succinylcholine is usually eliminated before reversal with neostigmine (as it would interfere otherwise). |
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