RSI rapid sequence intubation question

[BFE/RN]

I have asked this question on another site and have had no real response. What do you use for rapid sequence intubation dosing references. I have seen a dosing card on the internet and I am looking for anyone that may have used it or has a good idea. I saw it when I googled RSI www.rapitube.com We are looking for something to put on our crash carts and on our airway box. Please help

[MedicRN111]

Even funnier when someone makes a statement like this, then promptly makes a number of mistakes in their recipie.

From an anesthesia perspective, there are a lot of ways to skin the cat. I have used each of the drugs listed in various RSI scenarios, depending on the variables that different patients will have, and none of the drugs are "wrong" per se. Since doses are available everywhere, just a few comments about the drugs.

Lidocaine: Given for two reasons. First, if using propofol, it may attenuate the burning vein sensation that can accompany this drug's administration. Second, given IV, it can help to anesthetize the airway, making the patient less likely to buck against the tube once the paralytic wears off. 300 mg of lidocaine is a HUGE dose, and can cause the patient to seize. It won't help with fasciculations anyway. Back off on that dose.

Fentanyl: 3 mg/kg? Wow. Never given that much to a patient in my life. It is a narcotic, and can be given to a patient either in pain or about to undergo a painful procedure. When called to the ER for RSI, I don't take fentanyl along. I don't need it.

Versed: Given IV, it has rapid onset, causing sedation and amnesia. USUALLY, it has little or no effect on respiratory effort. Often, when called to the ICU to intubate a patient, it is the only drug I give prior to intubation. I dose it to effect, then proceed with direct laryngoscopy. However, if doing an RSI fearing potential aspiration, I'll usually give one of the hypnotics and sux.

Etomidate: Not my favorite drug for induction of general anesthesia, but it does have a place. Propofol is faster acting, but if the patient has a significant cardiac history, I'll use etomidate. If they have a potential brain injury, I'll use sodium thiopental. And as I already said, often I don't give this class of drug at all for emergent intubations outside of the OR.

Succinylcholine: A rapid and short acting depolarizing paralytic. Give atropine with it when giving the drug to peds patients, as sux can cause profound bradycardia in kids. Also, it is a depolarizer, and will cause a rise in K+ levels, so don't give it to someone who already has a high potassium level. Fasciculations are the muscle twitches you see when the drug causes depolarization, resulting in tensing of the skeletal muscle. This can leave the patient with mild to moderate myalgia for a day or so after administration. Once you understand the drug, you understand that giving 10% of the calculated dose to prevent fasciculations (called a defasciculating dose) is a waste of time. Your initial dose will simply cause milder fasciculations that you may not be able to observe, but can still leave the patient with the myalgia you are trying to prevent.

There is an upside to fasciculation. Fasciculation can be a direct monitor to tell you exactly when a patient is ready for intubation. Give the sux, then watch the patient's eyelids. In a moment, the eyelid will flutter. When the fluttering stops, intubate the patient. Since you cannot bag ventilate a patient who needs an RSI, and we have all seen patients who, even after prolonged prebreathing of 100% O2, desaturate quickly, sometimes it is in the patient's best interest to trade a short time of mild muscle pain for a direct, easily observed monitor of when you can tube the patient. (By the way, this is not recommended for potential head injury patients, as the fasciculations caused can cause a transient increase in ICP. However, there has been some discussion in the literature lately suggesting that this transient increase may not be clinically significant.)

Non-depolarizing neuromuscular blockers: (i.e. vecuronium, etc) These are much longer acting paralytics, and take longer to take effect than sux. The only one considered acceptable for RSI is rocuronium, and if you are going to use it, you better be damn sure you will be able to intubate the patient. In small doses, i.e. 5 - 10% of a calculated intubation dose, these are the only drugs that will prevent the fasciculations caused by succinylcholine. Once the sux has worn off, these drugs may be given to provide longer paralysis to prevent patient movement.

RSI is done whenever you are intubating a patient with a known or potential full stomach (i.e. they have eaten in the last 8 hours) or someone with known GERD. To my way of thinking, this means all ER intubations are RSI. If you are doing an RSI, you also must also have someone doing cricoid pressure. Pressure is applied at the cricoid membrane, NOT THE thyroid cartilage. The textbook says you must apply about 44 Newtons of pressure. That's about 10 pounds. Do not release the pressure until tube position is confirmed by CO2 and ascultation of breath sounds. It is done to help prevent vomiting and aspiration.

We are talking about RSI here. Not Intubating someone in the OR, a controlled environment, where a trained monkey could Intubate. The only place in a OR for a RN is to be handing the instruments to the MD. I understand the whole CRNA thing, but having any form of RN maintaining a airway is not her place. Other than that I wont even comment on this long drawn out post. I dont even have time to start picking it apart, with its multiple errors.

I can picture it now:

Nurse. Yes Doctor? Sponge my forehead! Yes Doctor.

HAHA

[Rio, ASN, RN]

Original Poster,

I would discuss the topic with the medical director, pharmacy and clinical staff and come up with your own cheat sheet based on formalary availability. Do some research, trauma.org, emedicine.com etc... and develop your own algorhythm. Knowing drug dosages is not enough. There are other concerns that must be addressed as the resuscitation team is just that: a team.

How do you handle difficult airway ? Sellicks maneuver, BURP or what works nicely is for the intubator to reach around with the right hand and manipulate the cricoid cart so that the cords come into view. Then the person assisting places there hand over that area and applys pressure. Please note that this is not typically done in the OR. If you are hospital based and have a fiber-optic scope, great. Bougies are handy devices that also double as a tube changer. What is your backup airway device ? LMA, combi-tube, surg cric ?

Recommend etCo2 monitoring, it's not just for placement. Anticipate the difficult airway: malampati class, thyomental distance. if the patient has trismus how would you asses the airway ?

[ginger58, ASN, RN]

Time to start posting myself. I always get a laugh when people who dont order the meds nor have any clue on how they work, start to offer their advice.

You can LOL as much as you want but I find your remarks offensive, egotistical and inflammatory.

[ginger58, ASN, RN]

We are talking about RSI here. Not Intubating someone in the OR, a controlled environment, where a trained monkey could Intubate. The only place in a OR for a RN is to be handing the instruments to the MD. I understand the whole CRNA thing, but having any form of RN maintaining a airway is not her place.

I have to ask you if you feel better degrading nursing. You obviously don't understand "the whole CRNA thing" and no, I'm not a CRNA. I'm a human being that is troubled that you have a license.:angryfire

[cardiacRN2006, ADN, RN]

We are talking about RSI here. Not Intubating someone in the OR, a controlled environment, where a trained monkey could Intubate. The only place in a OR for a RN is to be handing the instruments to the MD. I understand the whole CRNA thing, but having any form of RN maintaining a airway is not her place. Other than that I wont even comment on this long drawn out post. I dont even have time to start picking it apart, with its multiple errors.

I can picture it now:

Nurse. Yes Doctor? Sponge my forehead! Yes Doctor.

HAHA

So, basically you are saying that you cannot read an appropriate response because it is too wordy. So instead of educating yourself, you will just blow it off with some ignorant response?

Thanks for letting us know your maturity level.

[mced]

We are talking about RSI here. Not Intubating someone in the OR, a controlled environment, where a trained monkey could Intubate. The only place in a OR for a RN is to be handing the instruments to the MD. I understand the whole CRNA thing, but having any form of RN maintaining a airway is not her place. Other than that I wont even comment on this long drawn out post. I dont even have time to start picking it apart, with its multiple errors.

I can picture it now:

Nurse. Yes Doctor? Sponge my forehead! Yes Doctor.

HAHA

I find it interesting that you say an RN has no place in maintaining an airway. In the trauma center where I am currently training as an SRNA, the CRNAs are the ones the paramedic students come to when learning how to intubate. This is because the CRNAs are the anesthetists responisble for providing the majority of all anesthetics given at this facility. Sometimes it can be quite amusing observing these guys, kind of like watching a monkey bang a football. I believe you were right, you really can train a monkey to intubate!

[skipaway]

We are talking about RSI here. Not Intubating someone in the OR, a controlled environment, where a trained monkey could Intubate. The only place in a OR for a RN is to be handing the instruments to the MD. I understand the whole CRNA thing, but having any form of RN maintaining a airway is not her place. Other than that I wont even comment on this long drawn out post. I dont even have time to start picking it apart, with its multiple errors.

I can picture it now:

Nurse. Yes Doctor? Sponge my forehead! Yes Doctor.

HAHA

It's a shame you so underestimate your fellow RNs. You, being an RN, have slammed only yourself. Are you just an RN who sponges a Doctor's brow? I'd guess not. Why don't you try to shadow a CRNA and see what we do everyday. It may change your perspective.

[SaderNurse05, BSN, RN]

By chance is the argumentative poster a troll? One of my favorite things about this website is how nice everyone usually is and how they share information without trying to make other people feel stupid. Thanks to all who respond with class.

[ERnurse1139]

I have sat back and read these posts long enough. Time to start posting myself. I always get a laugh when people who dont order the meds nor have any clue on how they work, start to offer their advice. Here is correct and recommended doses for RSI, from someone who does it every day. In Order:

Lidocaine is given for Poss. Head Inj. not difisiculation

1 mg/kg

Atropine (Peds Only) Anyone know why??

0.01-0.02 mg/kg

Fentanyl

3 mg/kg

Etomadate for sedation

0.3 mg/kg

Succinylcholine for paralytic

Give 10% of your calculated dose before anything (difisiculating dose)

1-1.5 mg/kg max dose of 150mg

2 mg/kg for Peds Max dose 200mg Can anyone tell me why????

Vercuronium Long-term paralytic

0.1 mg/kg

Versed Long term sedative

2-5 mg PRN or Versed drip

:lol2: :lol2: :lol2: :lol2:

I don't want to sound dumb, so don't judge or attack me, I'm only asking so I can learn: What is this about giving a defasciculating dose? I've worked in a small ED for 2 years and we don't do RSI very often, patients who need it are usually intubated by medics prior to arrival, and I've only had the chance to participate a couple of times. I've seen patients fasciculate (short term muscle tremors after giving sedation drugs, right?) and was told this was normal.

First, if fasciculations only cause myalgia, and possibly slight/insignificant rise in ICP, and we are in an emergent situation, is it necessary or even advisable to delay intubation in order to prevent this? I can understand why this would be done in the OR, in a routine surgical anesthesia-administration, to decrease post-op pain/discomfort and increase patient satisfaction. But the nature of emergencies doesn't allow us to be that "nice" and probably the patient will have more to worry about when he wakes up than sore muscles anyway.

Secondly, even if it doesn't apply to the ED, which I don't think it does, I am curious, now, to know the process of giving a defasciculating dose, just so I know what it is, next time it comes up in conversation or something.

My understanding for the reason to give atropine to peds is that it dries up secretions, reducing the need to suction? Correct me (respectfully, please) if I'm wrong.

Finally, I have to agree with Larry77 about the attitude and patronizing and with everyone else who objected to your rude comments. This should be a place where we can relax, enjoy each other's company, and learn from each other. We deal with enough mean, hostile people in our jobs without having to do it here too! Disagree with posts, if you must, but do it respectfully please! I was taught to never assume you know everything, no matter how much education or experience you have. Doing so makes you a danger to your patients and alienates you from your colleagues. (Are you feeling that?)

[skipaway]

Succinylcholine: A rapid and short acting depolarizing paralytic. Give atropine with it when giving the drug to peds patients, as sux can cause profound bradycardia in kids. Also, it is a depolarizer, and will cause a rise in K+ levels, so don't give it to someone who already has a high potassium level. Fasciculations are the muscle twitches you see when the drug causes depolarization, resulting in tensing of the skeletal muscle. This can leave the patient with mild to moderate myalgia for a day or so after administration. Once you understand the drug, you understand that giving 10% of the calculated dose to prevent fasciculations (called a defasciculating dose) is a waste of time. Your initial dose will simply cause milder fasciculations that you may not be able to observe, but can still leave the patient with the myalgia you are trying to prevent.

There is an upside to fasciculation. Fasciculation can be a direct monitor to tell you exactly when a patient is ready for intubation. Give the sux, then watch the patient's eyelids. In a moment, the eyelid will flutter. When the fluttering stops, intubate the patient. Since you cannot bag ventilate a patient who needs an RSI, and we have all seen patients who, even after prolonged prebreathing of 100% O2, desaturate quickly, sometimes it is in the patient's best interest to trade a short time of mild muscle pain for a direct, easily observed monitor of when you can tube the patient. (By the way, this is not recommended for potential head injury patients, as the fasciculations caused can cause a transient increase in ICP. However, there has been some discussion in the literature lately suggesting that this transient increase may not be clinically significant.)

ERnurse1139

This was posted on page 2 and is an excellent answer to your question on the reason for a defasciculating dose. And no question is dumb.

[ERnurse1139]

Thanks very much for the helpful info! I appreciate learning from you!:)

[passgasser]

ERNurse1139

Please forgive me, some of the tone of my original post was directed elsewhere. It was not meant for those with genuine questions. (I am Passgasser, not MedicRN111.) In answer to your questions:

Sometimes, we (anesthesia) choose to give a small dose of a non-depolarizing neuromuscular blocker (NDMB) as our first drug in a sequence of drugs to induce general anesthesia. In my case, that is usually about five mg of rocuronium. The dose is small enough that it will not cause the patient to become completely paralyzed, but is large enough to prevent fasciculation. (This works because NDMB’s work at a different end of the neuromuscular chain than does succinylcholine.) In order to be effective, the NDMB must be given a long enough time to attach to the appropriate receptors before administration of sux. Whenever I do this, as I am giving the drug I warn the patient they may start to feel a bit weak, and their vision may blur. However, you are exactly correct that in emergent cases, such administration can often be a luxury, one for which you do not have time. The fact of the matter is that not all patients given sux without a defasciculating dose of another medication have myalgia, and for most who do, the myalgia is mild. If you have a patient in the ER in need of emergent intubation, you must assume that they have a full stomach, and you must do a rapid sequence induction. You will often need to know to the second when it is safe and possible to proceed with intubation, and in such cases, fasciculation can help. When the fasciculation ends, tube the patient.

The only drug that causes true fasciculation in use in the US (that I know of) is succinylcholine. It causes these fasciculations by causing the neurons of motor muscle to fire (depolarization), but for several minutes will not allow them to reset themselves to be able to fire again (repolarization). Hence, you have a brief period of skeletal muscle contraction (fasciculation), followed by several minutes of paralysis, until the drug is cleared from the neuronal junctions, allowing repolarization. (By the way, MedicRN111, would you care to enlighten the audience as to why this works on skeletal muscle, but does not cause what in effect would be a cardiac seizure? After all, isn't the heart just another muscle?)

So, in emergent situations, giving anything as a defasciculating medication serves only to prolong the time it takes before intubation, and take away the one monitor you have that tells you immediately when it is OK to proceed with intubation. No matter the dose, succinylcholine is always going to work at the same place in skeletal muscle neurons, therefore, giving 10% of the calculated dose up front won’t prevent fasciculation. By giving a sub-clinical dose, you will still cause depolarization of some of the neurons, and the rest will depolarize when you give the intubating dose. Now, I can think of at least one instance where giving the dose suggested by MedicRN111 could really bite you on the backside. We know that sux can cause profound bradycardia in pediatric patients. In fact, it will often do so when giving additional doses of the drug. So, without an anticholinergic, if you give 10% of your intubation dose, then give other drugs, then give the intubating dose of sux, you may find yourself in a far worse situation that where you started.

As to giving anticholinergics, yes, they can dry secretions. However, if that were the only reason they were given, in a situation requiring RSI, they would not have adequate time to do so prior to laryngoscopy. All the secretions in the mouth at the time you start administering drugs will still be there 30 to 45 seconds later when you try to intubate the patient. The primary reason atropine is given with succinylcholine in pediatric patients is to prevent profound bradycardia. To dry secretions, there are better choices than atropine anyway. Robinul is another anticholinergic drug that works very well to dry secretions, and does so with less tachycardia than atropine. In order to do so, it must be given several minutes before induction and intubation. My personal preference is that it not be given, because I have had patients whose mouths were so dry that insertion of the laryngoscope was tougher than usual.

To MedicRN111, if my last post contained so many errors, would you please be kind enough to show me where? All of us in anesthesia are waiting for you to show us the error of our ways. And if a "trained monkey" could intubate any patient in the OR, perhaps you would care to accompany this trained monkey and show me your skill and proficiency at bronchoscopic intubation of the patient whose epiglottis, much less airway, cannot be visualized with a laryngoscope? Or perhaps you would care to show me your skill at intubation where the patient has a trauma that is filling the oropharynx with blood. You can't suction it out fast enough to tube the patient, what do you do now?