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Ah, but why?
A brief succinylcholine #tweetorial
#MedTwitter
https://twitter.com/absitesmackdown/status/1292159439382994945
A brief succinylcholine #tweetorial
#MedTwitter
https://twitter.com/absitesmackdown/status/1292159439382994945
Succinylcholine (sux) is a short-acting, depolarizing muscle relaxant used to help establish airways and for short procedures requiring muscle relaxation (e.g., ECT).
It’s two acetylcholine (ACh) molecules stuck together.
It’s two acetylcholine (ACh) molecules stuck together.
In the neuromuscular junction (NMJ), sux binds to the postsynaptic nicotinic ACh receptor, causing depolarization in skeletal muscle (why you see fasciculations). It then remains bound, preventing further ACh binding and muscle activity (generally for ~6-10 minutes).
There are two “phases” to the mechanism of action, depending on dosage. Phase I is desirable for surgery, as Phase II can last for hours (and prevents further pharmacological manipulation of the NMJ).
Sux diffuses out of the NMJ and is hydrolyed in the serum by circulating pseudocholinesterase (or butyrylcholinesterase).
(Patients with pseudocholinesterase deficiency remain paralyzed for longer depending on how many copies of the gene they inherited)
https://en.wikipedia.org/wiki/Pseudocholinesterase_deficiency?wprov=sfti1
(Patients with pseudocholinesterase deficiency remain paralyzed for longer depending on how many copies of the gene they inherited)
https://en.wikipedia.org/wiki/Pseudocholinesterase_deficiency?wprov=sfti1
An elevation of K+ (typically ~0.5 mmol/L) occurs transiently because the ACh receptor is propped open, allowing flow of K+ ions into the extracellular fluid.
Conditions such as burns (after the first 24 hours), denervation injury, prolonged immobilization, sepsis, and SIRS, cause upregulation of extrajunctional (“immature” or “fetal”) acetylcholine receptors outside the motor end plate, expressed anywhere in the muscle membrane.
Immature receptors have a γ-subunit that has yet to mature into an ε-subunit. This causes the ion channel to remain open 2-10 times longer than mature receptors.
So the combination of an increase in the number of receptors and receptors that stay open longer results in massive hyperkalemia in susceptible patients.
