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Posted

You arrive on the scene of a 60yo male who is unconscious and unresponsive GCS 3 with an unknown etiology. You are unable to obtain any patent history. The patients skin is warm pink and dry he is normotensive with good cap refill and he is breathing 30 breaths per minute his 02 saturation is 100% and he has an end tidal CO2 of 25mm/hg, you, for what ever reason decide to intubate and protect airway. ( the discussion here is not weather or not to intubate). After RSI you have knocked out the respiratory drive and know you must ventilate the patient. You have only a BVM , Oxygen, Capnography and Pulsoximetry, how would you properly ventilate this patient and what values would you seek?

Posted (edited)

I'm assuming that I've (for whatever reason) decided to completely take over his breathing because he's hyperventilating with the potential to aspirate. So, I'd be dropping his breathing rate to 10-12 breaths per minute with an anticipated ETCO2 in the 35 area. BVM w/ O2.

Is this the answer you are seeking?

Edited by tcripp
Posted

Thank you "tcripp". what if your patient was unc and unr from any number of conditions that cause a metabolic acidosis and has a low pH. Currently he is breathing on his own at 30 with an ETCO2 of 25 clearly hyperventilating. However, this hyperventilation is a compensatory mechanism due to his acidosis and is blowing off CO2 in an effort to raise the pH. If we take away his ability to breath and slow his respiration to 10-12 with an ETCO2 of 35 as the AHA suggests we will in fact be lowering his pH even more making the situation worse. Would it not be better to use the information we have regarding respiratory rate ETCO2 and Pulsox and maintain those numbers in route to the hospital were definitive blood work can be done?

This is a common situation of which I think the term "Rescue Breathing" and the AHA guidelines DO NOT APPLY. I think, in this scenario we are are mechanically protecting the airway and should just maintain its intrinsic respiratory rate, ETCO2 and Pulsox. I don't feel we have enough information in the field to determine the cause or to alter the bodies natural response. Remember the patient was not apnec pre-intubation and if he was then certainly i would agree 10-12 breaths with an ETCO2 of 35-45 and pulsox of greater than 95% is appropriate.

Posted

Causes of metabolic acidosis include DKA and renal failure. Pretty much might not figure out the renal failure other than maybe my patient is in dialysis and I would have seen the shunts. Where was my "scene"? Did we do a d-stick? Did we look for a medic alert bracelet? You see, I took what you gave and made my decision from exactly just that (kind of what I thought you were asking). In reality, I would have done a more thorough exam to make my decisions.

So, my questions to you:

  1. Are you inferring, then, that this patient is in DKA which I might have seen had we done a d-stick...or possibly would have determined with some type of medic alert bracelet indicating a diabetic patient?
  2. Are you trying to "pick a fight" with AHA on their suggestion for rescue breathing which is for the average patient?

One thing I have learned is that medicine (including para-medicine) is not black or white. It's an art and many shades of grays.

Frankly, depending on transport times / transport options (air vs. ground), it's possible I would not have RSI'd this patient but rather provided assistance. But, I think your point is on the rate and not the mechanism so I'll move on.

Additionally, my training included that you did adjust the patient's breathing even if in DKA with kusmaul breathing. Now, maybe I slept and just totally missed out on that lecture so I plan to do a little extra reading on that one, but I simply do not remember being told to maintain a breathing rate of 30...

Posted

Off topic, but some perspective. Often, people with compensatory respiratory patterns who require intubation require full support modes of ventilation such as assist control to ensure they can maintain respiratory compensation. I've seen a few poorly managed DKA patients where flight crews intubated and ventilated with "normal" rates and "normal" PeCo2's. Clearly, these patients had significantly deteriorated metabolic and acid/base wise from their initial presentation.

  • Like 1
Posted (edited)

Tcripp, why would you use O2 on this patient at this point in the scenario?

Also, something that I've been curious about for ages. After intubation, in this patient, why a BVM. I think we had this debate once that, as no collar without a longboard, no tube without a BVM. How come?

Overseas it wasn't common, but not uncommon to be delivered patients that had been intubated for a while without ever coming into contact with a BVM. When they were quiet and breathing quietly/sufficiently I simply left them as they were. I don't see the need to assist vents in a patient that is doing perfectly well on their own. (Making the assumption that his respiration, though rapid, are also exhibiting adequate tidal volume, and pt appears physically capable of maintaining this state.)

Now, having said that, I've never intubated a patient that I didn't bag, but sometimes only because I had no idea how I would explain not doing so to the hospital when I rolled in.

Yeah, I know, probably an idiotic question...Just add it to my already long list of idiotic questions..

But with an inline ETCO2, though I may want to protect his airway, I can't see why I would want/need to assist vents at this point. Again, assuming that we're not dealing with other pulmonary pathologies not mentioned up to this point.

Dwayne

Edited for spelling...

Edited by DwayneEMTP
Posted

All good input. and your right "tcripp" you never learned to maintain a respiratory rate of 30 nor did I, however every day I learn how much more I don't know.While I am not trying to pick a fight with the AHA I think they have pounded into our heads that "Rescue Breathing" is the panacea! Conversely we as Paramedics are told we must "think first" and not just "blindly do"? The thinking part here should tell us that essentially this patient is not in respiratory distress and does not have a problem with his airway as he is obviously moving air in quantity and able to exchange gas efficiently in the lungs as evident by the ETCO2 and Pulsox. Our intent behind intubation here is not to improve gas exchange or ventilation but merely to protect the airway in route to the hospital this, I feel is not "Rescue Breathing" the patient was breathing just fine before I intubated.

As I said this is not a discussion on why intubate! We have to accept the fact that we do not know! Primarily, why this patient is hyperventilating. if one did not intubate this patient would you use the BVM to retard his intrinsic respiratory rate to the standard 10-12 breaths per min? Just because we put a plastic tube into the trachea to prevent aspiration doesn't mean we are rescuing a patient in respiratory distress! Remembering this, if in the process if I temporarily inhibit his respiratory effort it is incumbent on me to restore or maintain it until the intrinsic drive is restored.

This problem is well documented http://www.anaesthesiamcq.com/AcidBaseBook/ab5_5.php As Paramedics we have to make a distinction between "Rescue Breathing" and maintaining the pt own breathing while we are just protecting his airway.

Posted

Tcripp, why would you use O2 on this patient at this point in the scenario?

Also, something that I've been curious about for ages. After intubation, in this patient, why a BVM. I think we had this debate once that, as no collar without a longboard, no tube without a BVM. How come?

Overseas it wasn't common, but not uncommon to be delivered patients that had been intubated for a while without ever coming into contact with a BVM. When they were quiet and breathing quietly/sufficiently I simply left them as they were. I don't see the need to assist vents in a patient that is doing perfectly well on their own. (Making the assumption that his respiration, though rapid, are also exhibiting adequate tidal volume, and pt appears physically capable of maintaining this state.)

Now, having said that, I've never intubated a patient that I didn't bag, but sometimes only because I had no idea how I would explain not doing so to the hospital when I rolled in.

Yeah, I know, probably an idiotic question...Just add it to my already long list of idiotic questions..

But with an inline ETCO2, though I may want to protect his airway, I can't see why I would want/need to assist vents at this point. Again, assuming that we're not dealing with other pulmonary pathologies not mentioned up to this point.

Dwayne

Edited for spelling...

Dwayne, from a respiratory point of view, intubation will significantly increase airway resistance. Add this onto a patient who may already be fatigued from working so hard to compensate along with the underlying electrolyte derangements, and this patient will likely require some type of support. Clearly, the scenario does not call for a ventilator, but this patient will need ventilatory support. Often, when we are forced to intubate DKA patients, they are fatigued to the point of exhaustion and a full support mode may be required while we fix the metabolic and underlying electrolyte derangements.

At a later time we can place the patient into a "spontaneous" mode for liberation and a spontaneous breathing trial when we have re-established homeostasis; however, spontaneous modes still provide support in the form of CPAP and PS.

T

  • Like 1
Posted

I'm with chbare. By intubating this patient, who is presumably demonstrating a compensatory respiratory alkalosis to deal with severe metabolic acidosis (like a DKA or salicylate toxicity) we have increased their work of breathing significantly. So in someone who is presumably already acidotic, we are then adding to that by working their respiratory muscles even harder, producing more lactate and fatiguing them to the point of failure.

I will generally try to ventilate at 6-8ml/kg, with 5cmH2O PEEP as a starting point, and maintain the EtCO2 where I found it before intubation, as a "normal" number will kill them. If I have a decent ventilator I'll use A/C to take the bulk of the work of breathing off the patient; if I'm using a BVM I'll consider paralysis to achieve the same ends as I find it tricky to synchronise my bagging with their breathing at the higher rates.

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