EMCrit Podcast 3-Intubating the patient with Severe Metabolic Acidosis

This lecture is part of the Laryngoscope as a Murder Weapon Series:

Sorry about the voice–blame the swine flu.

Case

Thanks to Joe Chiang

Severe DKA; Obtunded with pH 6.65, PaCO2 18, Bicarb 5
Pt’s mental status is worsening
The decision is made to intubate

Should you give NaBicarb?

Probably won’t help as patient is already breathing at their maximum. Unless they blow off the Bicarb-generated CO2, they won’t increase their pH significantly.

What you need

Properly fitted NIV mask
Ventilator, not a NIV machine
Someone who knows how to work the vent
Normal intubation stuff
If available, Quantitative ETCO2

Procedure

  • Place pt on pseudo-NIV

Settings are
Mode Volume SIMV
Vt 550 ml
FiO2 100%
Flow Rate 30 lpm
PSV 5-10
PEEP 5
RR 0

  • Attach ETCO2 and observe value
  • Push the RSI Meds
  • Turn the Resp Rate to 12
  • Perform jaw thrust
  • Wait 45 seconds

This violates the tenets of RSI, but keeping the pt alive is probably more crucial right now.
Most experienced operator should intubate the patient

  • Attach the ventilator
  • Confirm tube placement by observing ETCO2
  • Immediately increase Respiratory Rate to 30
  • Change Vt to 8 cc/kg predicted IBW
  • Change Flow Rate to 60 lpm, this si the normal setting for intubated patients (forgot to mention this in the audio)

Why 30 BPM? Listen to the podcast.

  • Make sure ETCO2 is at least as low as it was when you started
  • Check ABG
  • Pat yourself on the back
Play

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Comments

  1. JamesD says:

    Thanks for the useful info. It’s so interesting

  2. It would be interesting to have this great approach modified if ED has no quantitative ETCO2. Thanks.

    • You can definitely manage without quantitative, in which case you just have to go by the 240 ml/kg/min, which translates to 30 breaths per minute if you set the tidal volume to 8 ml/kg. Just make sure to get the post-tube abg with alacrity.

  3. Great podcast, and I really like the idea of using a regular ventilator in a non-invasive way. Occasionally, I have two or more people requiring BiPap at the same time with only one BiPap machine available.

    What would the disadvantage of setting the initial respiratory rate to 12 breaths per minute using the NIV mask and using this to pre-oxygenate the patient? Certainly the SIMV mode would allow spontaneous breaths, and you wouldn’t have to remember to change the rate once you’ve paralyzed the patient.

    Also, do you generally leave the vent mode on SIMV once the patient is intubated, with the settings you mentioned above?

    Thanks!

    • Mike

      only disadvantage is the patient may not tolerate the machine breaths, otherwise no problem. i don’t generally use simv once the pt is intubated, my take on vent management is in two of the later podcasts. just search the site for “dominating the vent.”

      Scott

  4. Scott Weingart says:

    Scott-

    We discussed this recently and the question of why SIMV came up? Could you explain your take on SIMV vs. PRVC or even BVM in this situation?

    Thanks!

    • BVM is almost always a flail. BVM at high rates is just plain dangerous. PRVC would be fine but it is a more complex mode than straight SIMV, and I try to keep vent stuff as easy as possible. There will be no inherent advantage to PRVC.

      • Hey Scott,

        Very cool concept! One question ….any attempts in the past taking the rate beyond 12 during the “pseudo NIV” phase???

        thanks!!

        • You absolutely can, but you are balancing additional breath-induced gastric insufflation with the need to keep down CO2. You can make a determination on a per-patient basis.

  5. Charles Hoood says:

    I listened to this podcast months ago and actually got to apply it in an aeromedical transport. Severe metabolic acidosis with RR 40′s, awake nasal intubation done by CCU as we arrived. Problem was patient was fighting the vent and grabbing for the tube. I didn’t want to use paralytics but after exhausting our options it was decided that was the safest option. Prior to paralyzing I placed the patient on our monitors including capnography. ETCO2 19 with RR 24. ABG at same time with pCO2 23. pH 7.1 I set the vent with TV 500 AC, RR 23 and paralyzed the patient. Placed on vent and maintained the ETCO2 of what it was previous to paralytics by adjusting the rate. No ectopy during flight. Vitals stayed solid. Uneventful transport. I would not have thought of doing that if I didn’t listen to your podcast. Thank you.

  6. Thank you for the detailed podcast Dr. Wiengart. I’m giving a case conference on a similar patient in a few weeks. I haven’t found much in the literature in terms of airway management in severe metabolic acidosis with respiratory compensation. There is a Journal of Emergency Medicine article by Manthous from 2010 that provides a few suggestions but nothing as detailed as your podcast. Do you have any other suggested readings on the topic?
    Thanks Dan.

    • Lewis Nelson wrote something up on the intubation of ASA overdoses, that one and the one you mention are all I have seen.

      • frank hansen says:

        is it this one ? “Mechanical ventilation was associated with acidemia in a case series of salicylate-poisoned patients”Acad Emerg Med. 2008 Sep;15(9):866-9.

  7. DocXology says:

    I have also seen it played out this way;

    Patient moribund and hypotensive but still maintaining airway and spont venting. ICU started inotropes and placed the vascath in, dialysed to a more comfortable pH and then intubated a few hours later.

  8. Anand Senthi says:

    Hey Scott,
    great podcast, thanks
    2 questions:
    1. What do you think of using RSA as an adjunct to or instead of the NIV proposition in your podcast? i.e just pop your sedation/paralytics and place an LMA and bag to maintain an appropriate CO2, then intubate via the LMA. I know RSA has been suggested as a strategy for the hypoxic pt requiring intubation but I see no reason why it would not be a great strategy for the acidotic with critically important compensatory hyperventilation that must be maintained through the intubation process.

    2. In your suggested protocol, assuming you’ve timed your meds right, how much real apnoea time should you have before you start attempting to intubate? i.e what I’m asking is really how much time will the patient not be breathing while you have the vent turned on to RR on 12? And if you they are still breathing, will this be an issue?

    • The only time I use RSA is in the pt you describe. I don’t find an LMA to be a great preox device, but it is a fantastic ventilatory device. I mentioned RSA as the key to this situation in the intubation checklist podcast.

      45 sec for Sux, Roc is 60 sec.

      • Anand Senthi says:

        1. Interesting. Why don’t you find the LMA a great preox device? Surely you get the benefits of BVM +/- PEEP valve attached but with a more direct airway?

        2. what I mean re the timing is that after you push your paralytics there may be 45/60 seconds before you can intubate but for most of this time the patient is still breathing cause your sedatives haven’t taken full effect yet.
        Therefore is there great benefit in turning the rate up to 12?

        • It’s not that it is not a good preox device just an unnecessary one. Patients don’t need to be ventilated to maintain oxygenation.

          As to timing, not sure what drugs you are using but propofol, etomidate, and thiopental all lead to apnea within seconds. The paralytics at the does we use would lead to apnea on their own with 10-15 seconds.

          • Anand Senthi says:

            ok I see your point but what if the cause of their hypoxaemia is inadequate ventilation? eg the obtunded/resp fatigued patient who is failing to ventilate and who is not acidotic so you don’t care about a rise in C02 but you need to ventilate to pre-ox before intubation? RSA makes sense then surely.

            Anyway in this particular acidotic patient in your podcast, instead of pushing your drugs and turning the RR=12 for the apnoeic period, would it not be better to just RSA and flick the ventilator right up to RR = 30 (and increase your flow rate). Then you would achieve 2 things:
            - minimise risk of CO2 rise as you provide more ventilation
            - minimise risk of gastric insufflation.

            then intubate via the LMA

            Thoughts?

  9. Anand Senthi says:

    Is the point of that first period where you have them on pseudo-NIV and a RR =0 before pushing RSI drugs just so you get an idea of what their end tidal CO2 is pre intubation so that you know where you want to keep it during/post intubation?
    Is there any other purpose of this first period other than getting you prepared for the next period (where you can click them up to a RR 12 during apnoea)?

    • Anand, You are giving them PSV during that period sharply augmenting their own resp efforts in an attempt to blow off CO2 prior to the intubation.

      • Anand Senthi says:

        I see, thanks

      • Anand Senthi says:

        actually that then leads me to another question. If the RR=0 all they are getting is PSV for their spontaneous breaths. Is that right? If so, what is the purpose of having the tidal volume set to 550ml? Is that merely so you have set up the machine to be ready for the 2nd period when you crank up the RR to 12 during apnoea? Is there any other benefit of the TV=550ml in the first period before you push the RSI drugs?

  10. Anand Senthi says:

    Do you think using ketamine would be preferable to other agents like prop/thio in these acidotic patients because it would minimise the apnoeic period before paralysis occurs and thus reduce the rise in C02 during this?

    • Interesting. I think we would be talking about a difference of seconds as the onset of apnea occurs early after pushing the relaxants compared to the time for full small muscle relaxation in the pharynx.

      • Anand Senthi says:

        I see. I thought the early apnoea occurred primarily due to the effect of sedative agents such as propofol/thio. Are you are suggesting that even in their absence the paralytic alone would cause apnoea not long after … and still a fair bit before the pharyngeal muscles paralyse?
        If so then yeah ketamine might not help that much.

        • Correct. Watch at what point the pt stops breathing on your next RSI. For me it is usually at the 10 sec mark.

          • Anand Senthi says:

            Yep, but that probably wouldn’t prove if it was the sedative or the paralytic causing the apnoea at the 10 second mark.

            I spose the only way to know is to watch when they stop breathing after a ketamine + paralytic RSI.
            Have you noticed apnoea starting much later than the 10 second mark in such situations?

            • Anand Senthi says:

              just read a section of Miller’s Anaesthesia suggesting that the diaphragm is the most resistant to paralytic agents and the pharyngeal muscles are more sensitive suggesting the latter would paralyses first.

              • The onset and intensity of blockade vary among muscle groups. This may be due to differences in blood flow, distance from the central circulation, or different fiber types. Furthermore, the relative sensitivity of a muscle group may depend on the choice of muscle relaxant. In general, the diaphragm, jaw, larynx, and facial muscles (orbicularis oculi) respond to and recover from muscle relaxation sooner than the thumb. Although they are a fortuitous safety feature, persistent diaphragmatic contractions can be disconcerting in the face of complete adductor pollicis paralysis. Glottic musculature is also quite resistant to blockade, as is often confirmed during laryngoscopy. The ED95 for laryngeal muscles is nearly two times that for the adductor pollicis muscle. Good intubating conditions are usually associated with visual loss of the orbicularis oculi twitch response.

                Diaphragm takes longer than larynx, less time than glottic structures, which is what I lazily referred to as small muscles of pharynx above. If this was different, we would be able to achieve ideal tube conditions while the pt was still breathing as opposed to waiting through 30 sec of apnea. Also diaphragm plays only a small role in maintaining resp. when you lose thoracic back-up/support muscles, a contraction of diaphragm alone ain’t doing much-hence need for tube in C6 spines.

                Anesth. speak about this stuff b/c of recovery. Diaphragm comes back before pharyng and pt may get neg pressure pulm edema as a result.

                This has

            • It is the ketamine RSIs I was thinking of, they still go apneic v. soon after push. May be even sooner as ketamine distributes muscle relaxants quicker than propofol. In ED, we rarely give enough induction agent to cause apnea.

  11. Anand,

    I was going to say that all of this needs to be taken into the context of the fact that I use at least double the dose of NMBs most anesthetists do.

  12. Anand Senthi says:

    I see, thanks

  13. Great. Loved it ! I was wondering why you choose flow @ 30 LPM first and then switched to 60 LPM later.Do we really need to set a flow rate for spontaneously breathing patient on PSV ? Why not just leave it at 60 LPM from beginning (normal setting of ventilators) ?

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