Delayed Intubation in Metabolic Acidosis

[Tony Held]

Patients experiencing severe metabolic acidosis primarily compensate with hyperventilation (respiratory alkalosis).  This results in low EtCO2 readings and low pH readings which would normally be counterintuitive.

It makes sense when you consider that their metabolic state is creating the acidosis.  The only way the body has to compensate is by offloading as much CO2 as it possibly can.  So their pH may be 7.1 with an EtCO2 of 10 and a respiratory rate of 30.

Why is this important?

If we make the decision to intubate these patients, we are inducing an episode of apnea.  While their oxygen saturation may be just fine during that episode of apnea, their CO2 will sharply rise.  Hypercapnia is normally well tolerated if rapidly reversed post-intubation, but the metabolic acidosis population is different than the respiratory acidosis population.  Their CO2 being low is the compensatory mechanism to their metabolic acidosis, meaning that any rise in CO2 will sharply drop their pH.  It is commonly accepted that pH < 6.8 will most often result in lethal dysrhythmia and pH's < 7.0 are associated with increased mortality.  As an aside, I found no pubmed info proving those numbers and even found an argument against those numbers here

Take care in inducing apnea for any purpose in patients exhibiting respiratory alkalosis.  Investigate the cause and treat accordingly.  Check here for a fun mnemonic:  MUDPILES.  If you're going down the intubation route, be very careful and explore some alternative airway techniques like awake intubation, Ketamine Supported Intubation, or non-invasive positive pressure support (NIPPV).

The ninja-level provider in you might be thinking:  "What if I temporize the situation with a little Sodium Bicarbonate?"  Well it's good you asked, because you're thinking of alternative therapies to this terrible scenario.  The problem with Sodium Bicarbonate is it needs the pulmonary circuit to be working well in order to perform the chemical reaction.  Inducing apnea will still result in a sharp drop in their pH from a different starting point.  You may make your numbers better, but there are a whole slew of consequences that come with it, not to mention it's never been proven to be beneficial.  Check out Chris Nickson's article on this very item here.


References:

Severe acidosis does not predict fatal outcomes in intensive care unit patients: a retrospective analysis.
Paz Y, Zegerman A, Sorkine P, Matot I.
J Crit Care. 2014 Apr;29(2):210-3. doi: 10.1016/j.jcrc.2013.11.007
www.ncbi.nlm.nih.gov/pubmed/24360596

Acid Base Online Tutorial
University of Connecticut
Faculty Advisor:  Dr. Steven Angus
fitsweb.uchc.edu/student/selectives/TimurGraham/Anion_Gap.html

When RSI isn’t the Right SI
April 22nd, 2014
by reuben in airway
emupdates.com/2014/04/22/when-rsi-isnt-the-right-si/

Sodium Bicarbonate and Diabetic Ketoacidosis
Chris Nickson
lifeinthefastlane.com/ccc/sodium-bicarbonate-and-diabetic-ketoacidosis/

[Kris Thompson]

Tony, this is great information. We often do our patients a disservice by or during intubation and we have to be careful with this tool. I have two things to add to this discussion. 

If you do decide to intubate, always consider that the patient's ventilatory status (tachypnea) was likely compensatory for some level of acidosis. You should consider continuing to ventilate them with the same minute volume that they had prior to induction if you think they might be acidotic. We often see patients who get (more) critically ill after intubation due to setting the ventilator to a standard rate of 12-14 bpm when the patient has been breathing at 30 bpm just to stay alive.

Secondly, note that EtCO2 readings can be falsely low (in comparison to the paCO2) due to V/Q mismatch. In the healthy person, this difference is usually 2-5 mmHg. However, we rarely intubate healthy people in emergency settings. Most of our patients are critically ill and have some sort of V/Q mismatch. In particular, dead space due to low perfusion can often cause low EtCO2 even when the blood concentration of CO2 is very high. Dead space is caused by poor perfusion to the alveolar capillaries and may be present in any sort of shock or low output state. Low EtCO2 could also be technically caused by shunt (poor aeration of the capillaries), but this is much more unlikely as the body will compensate by increasing perfusion and ventilation to perform more gas exchange in the working aveoli.

In practice: You are called for a middle-aged male medical patient in obvious distress. HR is 102, BP is 92/68, and RR is 28. You RSI and intubate him. Being a smart paramedic and recognizing likely acidosis, you set the ventilator rate to match his (28 bpm) and set goal tidal volume based on his height and predicted ideal body weight. You record an EtCO2 of 22. This could easily trick the best of us into turning down the rate or volume on the ventilator in order to decrease minute volume and let his EtCO2 normalize. Don't do it! If he has a metabolic acidosis (perhaps DKA or aspirin overdose?), the hypocarbia is compensatory and keeping his pH somewhat safe. Even without metabolic acidosis, if he is in a shock state with poor perfusion, you could actually have a paCO2 that's very high despite low EtCO2 readings! In one of my most memorable patients in shock, we recorded EtCO2's of 20's with a measured paCO2 of 80 on ABG. Scary stuff!

[silvia]

Thank God for EPOC! Great points, thanks for the review!

[Deleted]

Gang, thanks for the input here on this subject. This scenario in the field scares me, because currently, we don't have all the tools to get an accurate and complete look at our patients' function. We can't accurately compare EtCO2 with their PCO2 without ABG gear, not to mention checking an accurate pH, and I haven't found anything yet to ballpark those kinds of measures. It seems like the best way, with our current load-out, is to use CPAP, because we're not messing with their body's compensatory mechanism, right? And even then, using minimal sedation to lessen anxiety can buy us the time needed to get them in the hands of more definitive care. That seems to be the best way to improvise, adapt and overcome. If you have any other tips, I'm all ears.

[Kris Thompson]

This plan of "DSI" (delayed sequence intubation) with CPAP and slight sedation is really good, because these patients will often be hard to pre-oxygenate and do a good nitrogen washout. Especially with short transport times, this seems reasonable to me. Get them to the ER in a better condition, ready to be tubed.

If you do intubate these patients (maybe you have longer transport times, their GCS is low, or they otherwise aren't protecting their airway), realize that they are (hopefully) compensating pretty well before you tube them. So if you start with a RR of 26 and EtCO2 of 15, aim to keep those both right there. Personally, I would set the vent to their pre-RSI respiratory rate (or maybe just a couple bpm slower) with a reasonable tidal volume based on their ideal weight, and then aim to keep the EtCO2 the same as pre-intubation until I know their blood gas results. If it's appropriate and you have access to it, use ketamine for sedation so it doesn't depress their respiratory drive as much. I would be very careful with longer-acting paralytics or respiratory-depressant sedatives in these patients, as they won't trigger the vent on their own and you can quickly get into trouble when they lose this compensatory mechanism.

Feb 4, 2017 12:52:51 GMT -6 @cannoni said:

Gang, thanks for the input here on this subject. This scenario in the field scares me, because currently, we don't have all the tools to get an accurate and complete look at our patients' function. We can't accurately compare EtCO2 with their PCO2 without ABG gear, not to mention checking an accurate pH, and I haven't found anything yet to ballpark those kinds of measures. It seems like the best way, with our current load-out, is to use CPAP, because we're not messing with their body's compensatory mechanism, right? And even then, using minimal sedation to lessen anxiety can buy us the time needed to get them in the hands of more definitive care. That seems to be the best way to improvise, adapt and overcome. If you have any other tips, I'm all ears.