Paralytic Question

[Nurseboy1]

Just a quick question for some of you anesthesia providers. I am an ICU nurse, and when we have to page anesthesia for an RSI intubation they always ask two questions : what is going on and what is their latest potassium.

Why do they always want to know what the potassium is?

[NRSKarenRN, BSN, RN]

fda rejects schering-plough's anaesthetic drug sugammadex nda

[Happy Halothane]

I am no CRNA or MDA but are there are not reversal agents in the event as you put it "the laryngoscopist can't place the snorkel?"

There is no reversal for succinylcholine but time (plasma cholinesterase). The reason why it's used for RSI is because of its fast onset and short duration. If too much was given, and the block resembles a Phase2 block (TOF fade, post-tetanic stimulation) then Neostigmine could be given after observing spontaneous twitch recovery for 20-30 minutes. Giving an anticholinesterase before the appropriate time would actually limit the terminating enzyme, prolonging succinylcholine's block.

We do use reversal agents for non-depolarizing NMBAs (Roc), but you must have a spontaneous >1 twitch. A post-tetanic count can usually help determine the timing to give reversal. For a longer acting agent (atracurium/vec), the twitch may take 10 min after post-tetanic stimulus. Long acting agents (Pancuronium) may take 40 minutes after tetany to get the first spontaneous twitch TOF.

Giving the reversal too early or inappropriately could create a transient, misleading recovery, followed by return of paralysis/muscle weakness (bad).

The appealing theory behind Suggamadex was that it encapsulated Rocuronium specifically, inactivating it at any point during blockade. Being a cyclodextrin, I'm suprised that it had questionable allergic reactions. Even though it's been taken off the "fast-track", I believe more studies (along with Europe's clinical use) will hopefully put in the US market in the next 5-10 years.

[Qwiigley, BSN, MSN, DNP, RN, CRNA]

I don't use a paralytic when called for an emergency intubation in the ICU IF I can ventilate witha mask. If not, I have to find a way to ventilate and quick. If the pt is still breathing on his own, then again, no paralytic, as they are at least getting something in.

When possible, try putting your pts to sleep in a controlled situation (like the OR) , don't use a paralytic, and intubate. It is good practice for when you need to do this. PS In my experience, don't eveer let your ER team intubate. When they can't get it, they look at you. Then all you have is a bloody mess.

[traumaguy8]

The two paralytics of choice in my unit are vec and cisat. we don't use succ probly due to our pt population (trauma/burn). we generally use vec, but for renal compromised pt's we us cisat. I was taught that vec is harder on the kidneys, not necissarily that it causes an increase in serum K. I know this thread is dealing with succ but what is the more precise pathological reason behind not using vec on a renal compromised pt?

[wtbcrna, MSN, DNP, CRNA]

The two paralytics of choice in my unit are vec and cisat. we don't use succ probly due to our pt population (trauma/burn). we generally use vec, but for renal compromised pt's we us cisat. I was taught that vec is harder on the kidneys, not necissarily that it causes an increase in serum K. I know this thread is dealing with succ but what is the more precise pathological reason behind not using vec on a renal compromised pt?

Vec is excreted by the kidneys...so you can have a longer duration of action if the patient has kidney damage. Cisatrcurium is eliminated by hoffmann elimination in the patient so it is favored for patients with kidney damage.

[CerebralCRNA]

I don't use a paralytic when called for an emergency intubation

On the other hand, I use 20-40 of sux on the floor when necessary. It is much easier to intubate a "non-moving" target and the duration of action of that dose is extremely short.

It all depends on your comfort level and of course your assessment of the situation.

"Sometimes you feel like a "Sux", sometimes you don't..... :) )

[foraneman]

I don't use a paralytic when called for an emergency intubation in the ICU IF I can ventilate witha mask. If not, I have to find a way to ventilate and quick. If the pt is still breathing on his own, then again, no paralytic, as they are at least getting something in.

When possible, try putting your pts to sleep in a controlled situation (like the OR) , don't use a paralytic, and intubate. It is good practice for when you need to do this.

I must be missing something since this makes no sense to me. If I am called to the ICU for an emergency intubation (and they need it), and the patient has a gag reflex (whether they are breathing on their own or not), AND I am not placing a nasal ET tube, then 100% of the patients will be getting a paralytic as part of a rapid sequence induction (since all ICU patients are full stomach, sedation/general anesthesia without a muscle relaxant taunts and dares these patients to retch during laryngoscopy and begin vomiting...especially since many cannot tolerate large amounts of anesthesia) in the interest of securing an airway as rapidly and safely as possible.

So if you can mask the patient, then no paralytic, but you knock em out and then intubate (or attempt to)? What advantage is there in this technique? Even propofol will not wear off much sooner than sux. If you can't mask and have to 'find a way to ventilate and quick', then sux and an endotracheal tube cures that.

I assume that you were not suggesting that the iCU patient should be moved to the OR for their intubation, but mentioned it in the context of practice on other surgical patients.

[anesthesia_insomniac]

Succ is the only depolarizing muscle relaxant available. Here is the quick and dirty of why a potassium level is only pertinent in regards to succ. In skeletal muscle, muscles contract and relax by depolarization and repolarization. At the ion channels in skeletal muscle, succ causes these channels to open (depolarize), releasing potassium out and bring sodium into these channels. However succ does not allow it to close "repolarize" which then leads to paralysis. The subseqent release of potassium throughout these channels across the body can lead to an increase in K by around 0.5. In patients with renal failure or elevated K levels this can send that person into dangerous life-threatening levels from hyperkalemia. Non-depolarizing agents (Roc, vec etc) do not cause this because they keep these ion channels from opening (depolarizing) leading to paralysis without the electrolyte shifts.

The benefit to still using succ is that it does not need to be reversed like other agents might. It is fast acting and if only intubation is needed then it can be a good choice if the appropriate clinical data is available.

I'm only a relatively new SRNA so don't take this to gospel! But this is how I understand it.