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BushyFromOz

When it sucks to use sux

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When Mark Fitzgerald and a Steve Bernard come in next week for the RSI lectures ill tell em you you dispute their expertise

Edited by BushyFromOz

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Just because Mark Fitzgerald et al say something doesn't make it right or applicable in every situation; personal opinion only but I don't really think IFS is appropriate. RSI or go home.

**sigh**

Is this going to be another one of those "lets measure our dick" things?

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Nah man it's all good.

If you can use your cellular telephone to video the lecture that'd be pretty badass.

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RSI or go home

And just what educational foundation do you formulate this 'opinion' from?

Or did you pull it from the years of experience as a primary field RSI practitioner?

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Basically its a 30 y/o M, heroine OD who has aspirated and been in a feotal posion up against a cupboard for several hours. HR170, B/P 60/40, GCS 5, Temp 37.9, RR 18 with fine exp. crackles, SP02 of 88% despite being oxygenated with 100% 02 and an ECG showing sinus tach with triplets of VEB's. You have not seen anything that indicates hyperkalaemia or rhabdomyolysis either ECG or physical finding but you lecturer is a sadist who likes to arm you with a bunch of readings about the association of drug overdose and rhabomyolysis to complicate your thinking before cooking up a scenario like this to test you out.
[my bolding in text].
I think chbare nailed this. There's a couple of things to think about here:
(1) Why are we intubating this person? Clearly, having aspirated, and with a GCS of 5, they're at risk for further aspiration. Although, to some extent, that ship has already sailed, we can still make things worse if we allow the patient to aspirate further. At this point, it's probably not for oxygenation. An SpO2 of 88% is compatible with ongoing life, especially when you consider this person's probably a little acidotic and right-shifted. PEEP would be a consideration for ongoing management, but not until we raise that MAP a little.
(2) How are their baseline hemodynamics, and how is RSI going to affect them? Right now, we have a SBP of 60 mmHg, with a HR of 170 bpm. Given the relation BP = CO x PVR; i.e. HR * SV * PVR ... [will return, have to run!]

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Sick, very sick. While at this point you can't really avoid intubation, you need to do it properly, and not rush.

That BP isn't sustainable; start a large fluid bolus, and preferably finish it before giving any meds.

Have epi drawn up in a "push dose" concentration; 10-20mcg/ml and be ready to use that to get over any changes in the BP, or even to quickly and temporarily increase the BP just prior to giving a paralytic or sedative.

Depending on why you think that BP is low (the results of your overall exam) it's worth considering starting a pressor infusion now.

As to what meds you will/won't give; there wasn't any mention that I saw of how awake the patient is. Any sedative you give needs to be given in very reduced dose (yes, even the vaunted ketamine) and still has a high potential for causing a further drop in pressure. If the patient is awake you can't avoid it, but just bear in mind that this person won't actually require much for sedation (cut by at least half if not more), and, in this situation if there is a bit of recall...that may just be what has to happen.

Sux versus roc...in all honesty I'm less concerned with the possibility of hyperk than I am with what else is wrong. Is it possible? Absolutely. Likely? Well...that's debatable. I'd be comfortable in using sux but there is nothing wrong with the more conservative route of going directly to a long acting paralytic either. If this is someone that you judge to be an easy intubation and will be able to mask-ventilate it's less concerning. And in all honesty, if you can mask ventilate them it would be ok to use a mainanence dose of roc (0.6mg/kg) instead of the starting dose (1.2mg/kg) if the prolonged paralysis really was concerning to you.

No matter how you choose to intubate, it's going to be a problem, both during the act, and after. The bigger concern here shouldn't be on what paralytic, if any, that is used, but on how you are going to sustain this patient, and correct what is causing his hypotension.


And just what educational foundation do you formulate this 'opinion' from?

Or did you pull it from the years of experience as a primary field RSI practitioner?

The same the freak has for everything; his ass, google and wikipedia. Honestly, I don't understand why admin still allows him to post.

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Thanks system for you interrupted post and triemal.

I have submitted the assessment an elected to forgo sux and go sedation only for intubation with doses adjusted accordingly accordingly. I wont go into our dosages etc for my service because its not that relevant to here but conceptually i have reduced the sedation dose. All this however comes after concerted efforts at perfusion management with fluid and adrenaline, and pretty much in the same vein that you guys have posted here so im happy with that, its nice to know your on the right track

Ive read enough literature this past 2 weeks to begin to understand a few things about where i practice, in that we have good practice as far as the procedure is concerned but not best practice in terms of pharmacology (even though the outcomes are still favorable), but Ketamine sounds awesome. It was also nice to read that the concerns about ketamine in TBI have been largely debunked so i look forward to a more simplified intubation procedure when i get to that stage

Cheers

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So, just to finish off a couple of thoughts:

* He probably needs to be intubated, but his primary issue right now is circulatory collapse, not oxygenation, assuming there's a reasonable pleth with that pulseox, and there's no (unlikely) causes of a false high reading.

* His HR of 170, producing a MAP of 50mmHg means he has no preload / stroke volume. If you switch him to positive pressure ventilation, you increase the pressure in his chest, compress the IVC/SVC/RA/RV, and risk turning that into 0/0.

* Any instrumentation risks vagal afferent discharge, which is going to drop that rate. Our current pressure is not compatible with sustained life at a HR of 170. If we vagal him down to 120, we risk landing on 0/0.

* His preintubation saturation places him right on the shoulder of the oxyhemoglobin dissociation curve. If you can bring his pressure up, you can probably use CPAP or BVM+PEEP to improve his oxygenation, giving you a longer safe apnea time. Paralysing at SpO2 89% is not impossible, but it would be nice to avoid. If we can improve oxygenation, we have a safer RSI.

So, given the primary issue at the current time is circulatory, we should optimise hemodynamics first. I think this would be a good time to ensure we've done all our basic airway management, give a couple of liters of fluid, prep our push pressors, or, better yet, as triemal suggested, have that levo up and ready to go. I don't think you'd be wrong to push the pressure a little high pre-intubation, knowing that it's going to come down once they're tubed.

This patient is very sick, and a cavalier and rushed approach to securing the airway is going to risk disaster.

I feel like I'm echoing everyone else's points. I think there's been a lot of well-reasoned responses in this thread already.


A couple more things to add:

A ketamine-alone approach avoids some of the dangers of paralysis, but also carries some risks. There's still a chance of causing apnea -- you have to appreciate that this patient is peripherally constricted, so your peak CNS concentrations are going to be higher vs. an equivalent dose in a less shocked patient. An overaggressive or too rapidly administered dose of ketamine can cause respiratory depression or outright apnea, without the benefit of muscle relaxation.

I wouldn't expect too much of a bump in pressure here with ket, as the patient's already tached out. If anything, I'd be prepared for the ket to drop his pressure. It's probably still the best agent here, although arguments can be made for etomidate, it pretty much mandates paralysis.

Ketamine-alone is not generally going to give you the same intubating conditions as paralysis. Generally it's going to be inferior. So you're hoping that your ketamine doesn't worsen the patient's condition, and accepting that the intubation itself may be more difficult. This is a balancing of risks. Your hoping that you preserve respiratory drive, which should be advantageous, but you're accepting less-optimal intubating conditions, and potentially a more prolonged or repeated procedure in the hope that your patient is less likely to deteriorate. This isn't a given.

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Thanks mate, very much appreciated.

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