Succinylcholine Chloride

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Succinylcholine (also known as suxamethonium and abbreviated as SCh) was first synthesized in 1906 and clinically introduced in the early 1950's after its neuromuscular blocking properties were discovered in 1949. It usually has chloride as its halogen ion in solutions, although bromide and iodide forms also exist. It is both the quickest acting and shortest duration neuromuscular blocker currently clinically used. It goes mainly by the trade names Anectine and Quelicin in the US, but it has also been called Scoline, Lysthenon, Celocurine, Midarine, Ectinex, Ethicholine, Mioflex, Myotenlis, Myoplegine, Myorelaxin, Uxicolin, Pantolax, Succicuran, Lycitrope, Fosfitone, Sucostrin, and Curacit, as well as the chemical names succinyldicholine and diacetylcholine.

It's pronounced "SUK-sin-il-KOH-leen." It's almost like "success" except it ends in "inylcholine." Some people call it "succs" or "sux". Other people think it sucks, mainly because of the risks associated with it being a depolarizing agent such as hyperkalemia and malignant hyperthermia.

It's officially classified as a rapid onset short duration depolarizing neuromuscular blocking agent. It has an onset of about 30 seconds to 1 minute and a duration of about 5-8 minutes. (Unless you have a pseudocholinesterase deficiency. Then, try 8 HOURS. Wikipedia says it's 2 hours, but I've heard of it lasting up to 8 hours from other sites if you have the worst type and are homozygous dominant for the pseudocholinesterase deficiency gene.)

As a depolarizing agent, succinylcholine first activates acetylcholine receptors causing initial fasciculations before relaxation occurs. Here is a very nice video showing fasciculations of the eyelids caused by succinylcholine.

Succinylcholine can cause malignant hyperthermia. Beware. Being prone to malignant hyperthermia is genetic. In hospitals, they sometimes keep a list of families with the malignant hyperthermia gene. The medication to treat malignant hyperthermia is dantrolene.

DO NOT USE NEOSTIGMINE (or any cholinergic agent) TO REVERSE DEPOLARIZING BLOCK. It will make it worse, one, since adding acetylcholine will only help contribute to depolarization, and two, because neostigmine also binds to and blocks the action of pseudocholinesterase, which is needed to break down SCh. If you gave the right dose and the patient doesn't have any unknown medical conditions to prolong the action of SCh, it'll wear off in about 5 minutes. Just give some artificial respiration and wait for it to wear off. With an unexpected pseudocholinesterase deficiency or prolonged effect, intubate and put the patient on a ventilator until it wears off. Time is the only truly safe reversal agent for succinylcholine.

On a syringe, succinylcholine gets its very own special label color. Like nondepolarizing agents, it's fluorescent red 805, but there is a black upper half of the label and "succinylcholine" is printed in fluorescent red against the black. Only depolarizing agents get this color combination. And succinylcholine is the only depolarizing agent currently used in medicine.

The ED95 of succinylcholine is about 0.3 mg/kg; I've seen other sites that say 0.5. The dose for intubation is from 1-2 mg/kg. Occasionally in the ER, they'll call for 200 mg of it, which is just an entire 10cc syringe or an entire 10 mL vial, since succinylcholine is usually at a concentration of 20 mg/mL.




Succinylcholine is comprised of two molecules of acetylcholine joined together at their acetyl groups. It is named because when two acetic acid molecules, which are part of ACETYLcholine, are joined together, they form succinic acid. Succinic acid + choline = succinylcholine. To be more accurate, the molecule commonly refered to as succinylcholine is succinyldicholine, and pseudocholinesterase actually breaks it down into succinylmonocholine, which has much weaker neuromuscular blocking properties, and then into succinic acid.


Succinic acid

Succinic Acid

Succinylcholine is also called suxamethonium, which is similar in name to decamethonium, another depolarizing agent structurally similar to succinylcholine but without the oxygen atoms. Decamethonium is made up of 2 quaternary ammoniums (N+ with methyl groups) and a 10 carbon chain in between the two ammonium cations.

Succinylcholine has the molecular formula C14H30N2O4.

Here is a nice 3d model of succinylcholine.

Mechanism of ActionEdit

Succinylcholine is what is known as a depolarizing agent. It works by binding to acetylcholine receptors in the neuromuscular junction at the sites where acetylcholine would normally bind to. Unlike with non-depolarizing agents, the acetylcholine receptors treat a molecule of succinylcholine as if it were a molecule of acetylcholine and open their channels. Since succinylcholine is simply 2 molecules of acetylcholine bound together, it is able to mimic acetylcholine very effectively. When succinylcholine binds to the acetylcholine receptors, the acetylcholine receptors open as if acetylcholine had bound to them, allowing sodium ions to rush into the muscle cells and potassium to rush out. The action of these positively charged sodium ions rushing in changes the voltage level in the muscle cells, causing depolarization and causing the action potential to travel into the muscle cells, where it causes an initial muscle contration (called a fasciculation). However, unlike acetylcholine, which is rapidly broken down by the enzyme acetylcholinesterase, succinylcholine is broken down much more slowly by plasma pseudocholinesterase. Since it is not broken down as quickly as acetylcholine, succinylcholine will simply stay in the acetylcholine receptors and prop them open so that sodium and potassium flow freely instead of being pumped back to their original concentrations by sodium-potassium pumps. Because of this, a concentration gradient between sodium and potassium cannot form, and the muscle cell cannot repolarize, and it instead remains depolarized, where the voltage is unable to change. Therefore, an action potential, which relies on the change of voltage to occur, cannot be generated. No action potential = no neuromuscular transmission = no movement. This phase where the ACh receptors are open and the muscle cells are depolarized is called Phase I block.

Phase II block occurs when there's a whole ton of succinylcholine, like when it's been given for a long period of time or you have a super overdose. Basically what is believed to happen is, eventually, your acetylcholine receptors figure out that there's something's up, they've been open for way too long, and so there must be way too much acetylcholine. Therefore, they become desensitized and close again. They stay closed regardless of if ACh or SCh binds to them, in order to compensate for the supposed extra amount of acetylcholine (even though it's actually SCh) in the neuromuscular junction, and repolarization can occur again. Because the acetylcholine receptors are closed and the muscle repolarizes during this phase, phase II block is similar to a non-depolarizing block.

ALSO, IF YOU KNOW, PLEASE ADD - can phase II block be reversed by cholinergic agents such as neostigmine? I have looked over many websites, many say it can, some others say it can't, and I don't have access to succinylcholine or neostigmine to test it out (I'm 17 years old, college freshman, not yet a doctor or researcher, so no access). People say it can be reversed because it's similar to a non-depolarizing block, which usually can be reversed (especially if it's not a complete block), but it's also possible that it can't be reversed because since phase II block occurs due to desensitization to acetylcholine, increasing the amount of acetylcholine may not have a significant effect and could possibly still make it worse. Neostigmine also binds to and blocks pseudocholinesterase, so it would also slow the breakdown of SCh regardless of what phase of depolarizing block is occuring.

Side EffectsEdit

Succinylcholine can cause many side effects. The two most serious side effects associated with succinylcholine are malignant hyperthermia and hyperkalemia. I still don't know the exact mechanism by which SCh causes malignant hyperthermia other than it has something to do with calcium and a defective gene. Feel free to explain if you know. But trust me, malignant hyperthermia is VERY BAD. You can die from it very quickly, and if not treated, the mortality rate is around 80%.

Hyperkalemia occurs because when succinylcholine activates the acetylcholine receptors, not only does sodium flow into the muscle through the channel, but potassium also rushes out of the channels into the extracellular space where it can go right into your bloodstream. In normal people, the increase in potassium is relatively small. However, when somebody has severe burns that have burnt away the nerve or upper motor neuron injuries, the amount of muscle contraction and often the amount of acetylcholine actually getting to those muscles whose movements are affected by the injury decrease greatly. To compensate for the decreased amount of muscle contraction, the muscles produce more acetylcholine receptors and begin to use different previously unused receptors, hoping that by doing this, any acetylcholine released by the nerve will be more likely to bind to a receptor and cause muscle contraction. Therefore, there are many more channels for potassium to rush through when they are opened by succinylcholine. Because of this, there is a much greater increase in serum potassium levels in people with nerve damage, leading to hyperkalemia, which can subsequently cause irregular heart rhythms and cardiac arrest.

Some other side effects include myalgia (muscle pain, and with SCh, it's worse in females)[1] rhabdomyolysis (breakdown of damaged muscle tissue)[2][3], increased intraocular pressure[4], and changes in heart rate and blood pressure, which can either increase or decrease depending on the activity of the patient's autonomic nervous system before administration of the drug [5]


There are several reasons not to give succinylcholine to a patient, primarily due to the effects caused by depolarization. In general, a good rule to follow is, if succinylcholine can cause any sort of symptom or condition to happen to the body, don't give it to a patient who already has that symptom or condition beforehand.

Causes hyperkalemia:

  • Muscular dystrophy, severe muscle injuries, rhabdomyolysis, burns, drowning, upper motor neuron injuries such as a spinal cord injury, Guillain-Barré syndrome, multiple sclerosis (MS), amyotrophic lateral sclerosis (ALS), stroke

Causes damage to bodily tissue

  • Glaucoma, especially open-angle glaucoma. Glaucoma itself is caused by increased intraocular pressure, and succinylcholine could further increase that pressure and damage the retina.

Malignant Hyperthermia

  • Malignant hyperthermia or a family history of the disease
  • Myotonia (associated with both hyperkalemia and malignant hyperthermia)

Inability to break down the drug

  • Known pseudocholinesterase deficiency
  • Severe liver disease (pseudocholinesterase is made there)


  • If you're not able to provide artificial respiration and you don't want to be charged for murder or malpractice

(list may be incomplete, but the ones above are the main ones),

Other/Uncategorized informationEdit

This will be categorized at some point. But for now, I don't have a spot for all these random other facts and links, so it's going here. This is where random fun facts and clips from movies and TV shows will go.

SUX RACING! (don't try this at home, or anywhere for that matter.) Sux racing takes place in the novel, Final Destination: End of the Line. The link leads to my own little guide, but seriously, just read it for fun, please don't actually do it.

"First, I'll inject some succinylcholine. I want you to watch her chest gauge because she'll stop breathing." (from the 1978 movie, Coma)

Some killers who used SCh as a murder weapon include Efren Saldivar, Arnfinn Nesset, Michael Swango, Carl Coppolino, Richard Angelo, Chaz Higgs, Stephan Letter (you won't find him searching for "succinylcholine," but he used "lysthenon," which is a name for it in Europe), William Sybers, Kim Hricko, and Genene Jones.

Succinylcholine is featured on several episodes of medical E.R. shows. All you have to do is watch an episode and watch for if they're going to have to intubate someone. If you're lucky, someone will call for succinylcholine or "sux". It might take a few episodes before they call for it, but it's worth it. While we're on the topic of NMBs on TV, cisatracurium tends to be seen on TV too, but not as often as SCh. Wait for someone to get a really bad head injury or be in a coma where they'll have to be in the ICU. If you're lucky, you'll hear someone talk about using Nimbex, which is cisatracurium. I've seen vecuronium a few times on TV too, but strangely enough, rocuronium doesn't seem to get much airtime, even though in real life, it's used all the time. But anyways, succinylcholine plays a good role in a few episode of Untold Stories of the E.R. On the episode "Deadly Diagnosis," with the girl with the fork stuck in her throat, they give her succinylcholine and there's a brief segment where they talk about it and the dangers of giving her a NMB. On the episode "A Day from Hell" of the same show, it's not mentioned directly in the episode, but the combative patient who overdosed on drugs was also most likely given succinylcholine as well. (That dude could be the sux racing world champion).

A funny video on a "sux" shortage. Click here. :P

Aaaand it's gone

Succinylcholine, 1949