Other helpful links: Coming soon
Succinylcholine (UNDER CONSTRUCTION)
Introduction
Succinylcholine (also known as suxamethonium and abbreviated as SCh) was first synthesized in the early 1900's and clinically introduced in 1951 after its neuromuscular blocking properties were discovered in 1949. It was officially FDA approved on August 20, 1952. 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)
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, although I've seen other sites that say 0.5 mg/kg. Generally though, it ranges from about 0.3-1.1 mg/kg. 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.
Chemistry
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. 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 Action
Note: Succinylcholine's mechanism of action is still not well-known. This mechanism may change as more is understood about how it works.
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 neuromuscular junction and keep binding to and opening the receptors so that sodium and potassium can pretty much flow freely through them 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. Again, this mechanism is uncertain and may change as our understanding of succinylcholine improves.
Side Effects
Succinylcholine can cause many side effects. The two most serious side effects associated with succinylcholine are malignant hyperthermia and hyperkalemia, but there are a multitude of others.
Hyperkalemia
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. When this happens, the muscles produce more acetylcholine receptors and begin to use different previously unused receptors. These additional receptors are fetal receptors, have a half life of about 1 day, and can sometimes extend to covering the entire muscle, not just the motor end plate. 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.
Malignant hyperthermia
Malignant hyperthermia is a very rare and very dangerous condition that can occur after the administration of succinylcholine or volatile anesthetics. Note that it may not occur immediately after succinylcholine is given, and it may not even happen until after the surgery is over. This is just another reason that you must be ever-vigilant in monitoring your patients at all times.
I also have recently made a really awesome malignant hyperthermia site for a school project for my biochemistry class that explains the symptoms and mechanism in detail. Check it out here!
Other Side Effects
Contraindications
There are several reasons not to give succinylcholine to a patient, primarily due to the effects caused by it opening the nicotinic receptor. In general, a good rule of thumb 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.
Here is a more complete list of possible reasons that you would not want to give succinylcholine.
Can cause hyperkalemia:
Causes damage to bodily tissue
Malignant Hyperthermia
Inability to break down the drug
Other:
How long is it safe to give succinylcholine after a recent spinal injury or after a patient suffers burns?
Stuff to still add and figure out:
Why does succinylcholine cause MH but normal muscle contraction doesn't?
Also as to why volatile anesthetics cause MH, NOBODY KNOWS WHY! It's still unknown! (source)
Phase freaking II block. Or phase I block for that matter. It's a mysterious mechanism.
About pseudocholinesterase, dibucaine number, the different pseudocholinesterase genes and types, and mechanism of pseudocholinesterase breaking down succinylcholine, like I want to put the biochemistry step-by-step enzyme mechanism diagram in there. I'm hoping pseudocholinesterase just uses serine and works like AChE too. That would be nice and convenient, and logical. I know it does hydrolysis, but then again, it seems like they all do hydrolysis nowadays.
Succinylcholine has a half life of 47 seconds.
Other/Uncategorized information 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
Succinylcholine (also known as suxamethonium and abbreviated as SCh) was first synthesized in the early 1900's and clinically introduced in 1951 after its neuromuscular blocking properties were discovered in 1949. It was officially FDA approved on August 20, 1952. 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)
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, although I've seen other sites that say 0.5 mg/kg. Generally though, it ranges from about 0.3-1.1 mg/kg. 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.
Chemistry
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. 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 Action
Note: Succinylcholine's mechanism of action is still not well-known. This mechanism may change as more is understood about how it works.
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 neuromuscular junction and keep binding to and opening the receptors so that sodium and potassium can pretty much flow freely through them 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. Again, this mechanism is uncertain and may change as our understanding of succinylcholine improves.
Side Effects
Succinylcholine can cause many side effects. The two most serious side effects associated with succinylcholine are malignant hyperthermia and hyperkalemia, but there are a multitude of others.
Hyperkalemia
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. When this happens, the muscles produce more acetylcholine receptors and begin to use different previously unused receptors. These additional receptors are fetal receptors, have a half life of about 1 day, and can sometimes extend to covering the entire muscle, not just the motor end plate. 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.
Malignant hyperthermia
Malignant hyperthermia is a very rare and very dangerous condition that can occur after the administration of succinylcholine or volatile anesthetics. Note that it may not occur immediately after succinylcholine is given, and it may not even happen until after the surgery is over. This is just another reason that you must be ever-vigilant in monitoring your patients at all times.
I also have recently made a really awesome malignant hyperthermia site for a school project for my biochemistry class that explains the symptoms and mechanism in detail. Check it out here!
Other Side Effects
- Increase in serum potassium levels, about 0.5 mEq/L about 3-5 minutes after administration. [1]
- Myalgia (muscle pain, and with SCh, it's worse in females)[2]
- Rhabdomyolysis (breakdown of damaged muscle tissue)[3][4]
- Increased intraocular pressure (5-10 mmHg) [5]
- Increased intragastric pressure
- 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 [6]
- Bradycardia - May occur especially in infants and young children, and it is also more likely following a second dose of succinylcholine.
- Cardiac arrhythmias.
- Possibly increased intracranial pressure of about 5-10 mmHg. Unfortunately there are no large studies on this, and there are mixed results regarding whether or not it actually increases ICP, but it has happened, and when it did, pressure increased around 5-10 mmHg. This increased ICP seems to be preventable with a preliminary dose of a nondepolarizing NMB. The mechanism by which this ICP occurs is also not known for sure, but it is possibly due to muscle spindle activity that occurs when succinylcholine causes fasciculations. [7] [8]
Contraindications
There are several reasons not to give succinylcholine to a patient, primarily due to the effects caused by it opening the nicotinic receptor. In general, a good rule of thumb 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.
- Succinylcholine causes paralysis. Patient already paralyzed due to perhaps a spinal injury or GBS? DON'T GIVE SUCCINYLCHOLINE.
- Succinylcholine can cause malignant hyperthermia. Patient already has burns or can get MH? DON'T GIVE SUCCINYLCHOLINE.
- Succinylcholine causes increased intraocular pressure. Patient already has glaucoma due to increased intraocular pressure? DON'T GIVE SUCCINYLCHOLINE.
- Succinylcholine can cause rhabdomyolysis. Patient already has rhabdomyolysis? DON'T GIVE SUCCINYLCHOLINE.
Here is a more complete list of possible reasons that you would not want to give succinylcholine.
Can cause hyperkalemia:
- Muscular dystrophy (This is why you have to be careful giving SCh to children, especially young boys. If a child has undiagnosed MD, succinylcholine could cause hyperkalemia and subsequent cardiac arrest.)
- Severe muscle injuries
- Burns
- Drowning
- Upper motor neuron injuries such as a spinal cord injury or stroke
- Guillain-Barré syndrome
- Multiple sclerosis (MS)
- Amyotrophic lateral sclerosis (ALS)
- Pre-existing hyperkalemia (If someone has hyperkalemia already, giving something that increases potassium levels is generally a BAD idea)
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.
- Rhabdomyolysis
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)
Other:
- If you're not able to provide artificial respiration and you don't want to be charged for murder or malpractice, you should not give a person succinylcholine.
How long is it safe to give succinylcholine after a recent spinal injury or after a patient suffers burns?
- After a burn, it is only safe to give succinylcholine within the first 24 hours after the injury is sustained, and some believe that it should only be given if the injury was within <6 hours. In addition, just because a burn covers a small surface area DOES NOT mean it's safe. Hyperkalemia following succinylcholine administration in one case where only 8% of the body was burned. In another case, hyperkalemia occurred after administering SCh over a year after the burn first occurred. (source)
- After a spinal injury, you should only give succinylcholine in the first 48 hours after the injury. After 48 hours, the patient will have a risk of hyperkalemia after administration of succinylcholine.
Stuff to still add and figure out:
Why does succinylcholine cause MH but normal muscle contraction doesn't?
Also as to why volatile anesthetics cause MH, NOBODY KNOWS WHY! It's still unknown! (source)
Phase freaking II block. Or phase I block for that matter. It's a mysterious mechanism.
About pseudocholinesterase, dibucaine number, the different pseudocholinesterase genes and types, and mechanism of pseudocholinesterase breaking down succinylcholine, like I want to put the biochemistry step-by-step enzyme mechanism diagram in there. I'm hoping pseudocholinesterase just uses serine and works like AChE too. That would be nice and convenient, and logical. I know it does hydrolysis, but then again, it seems like they all do hydrolysis nowadays.
Succinylcholine has a half life of 47 seconds.
Other/Uncategorized information 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