End tidal CO2 questions

[ParamedicStudent]

I have a couple questions about EtCO2:

Let's talk about patients with COPD/Asthma. I know they retain CO2 due to physical damage to tissues, so that does that mean that their end tidal CO2 would be low on the monitor, because they're holding back CO2 and not all of it is being released out when they exhale? How about when they're having an exacerbation? Is it the same logic?

How about in the case of DKA? A diabetic patient with DKA has too much sugar in their bloodstream, and that causes them to have metabolic acidosis. They usually have Kussmaul's respirations. They're trying to change their metabolic acidosis to respiratory acidosis to try to blow off their CO2, but is that possible? Will their EtCO2 be higher because they're blowing off CO2? Or will it be lower because they are hyperventilating?

 

[VentMonkey]

I have a couple questions about EtCO2:

Let's talk about patients with COPD/Asthma. I know they retain CO2 due to physical damage to tissues, so that does that mean that their end tidal CO2 would be low on the monitor, because they're holding back CO2 and not all of it is being released out when they exhale? How about when they're having an exacerbation? Is it the same logic?

Their (COPD) ETCO2 would be higher because they're retaining carbon dioxide. These folks often live in 60's. As far as their exacerbation, I would think an increase in their ETCO2 coupled with increasing muscle fatigue, lethargy, and an increased PaCO2, and PaO2 (done via ABG at the hospital once they fail less invasive therapies) is highly indicative of respiratory failure.

How about in the case of DKA? A diabetic patient with DKA has too much sugar in their bloodstream, and that causes them to have metabolic acidosis. They usually have Kussmaul's respirations. They're trying to change their metabolic acidosis to respiratory acidosis to try to blow off their CO2, but is that possible? Will their EtCO2 be higher because they're blowing off CO2? Or will it be lower because they are hyperventilating?

It's not the sugar. The ketones being a cellular waste product of the hyperglycemia is what's creating this metabolic acidosis, and in turn, and elevated (Kussmaul's) respiratory pattern.

This is a protective mechanism to rid the body of this waste product. The causes a respiratory alkalosis as they're compensating, again, with an increased respiratory drive. If the problem is not corrected (hyperglycemia is the problem not the respiratory rate; they need tons of fluids and Insulin), then certainly they can stop breathing, or under breathe/ hypoventilate causing respiratory acidosis.

Op, it sounds to me like you're genuinely confused. Hopefully this helps a little. Here's a decent article that breaks it down better than me:

http://www.paramedicine.com/pmc/End_Tidal_CO2.html

 

[RRTMedic]

I know they retain CO2 due to physical damage to tissues, so that does that mean that their end tidal CO2 would be low on the monitor, because they're holding back CO2 and not all of it is being released out when they exhale?

So ETCO2 is a correlation to PaCO2, not necessarily an accurate picture of the partial arterial pressure of carbon dioxide. Actually, in normal lungs, ETCO2 reads approximately 5 mmHg lower that PaCO2. However, your question regards the retention of CO2... I'll see if I can give you an illustration for ETCO2 vs PaCO2.

Our lungs contain areas that do not ventilate well... whether this be a perfusion problem or a ventilation problem. Take for instance a patient having a pulmonary embolism; this patient is not moving blood well to the lungs for gas exchange, meaning that the CO2 would not be exhaled, meaning your ETCO2 would be.... LOW. Poor perfusion, right?

On the same token, lets say that same area of lungs that aren't performing gas exchange well has GREAT blood perfusion to the alveoli, but the alveoli are not being ventilated due to pulmonary edema or say pneumonia. Then gas exchange can't occur because there is a physical barrier there. The CO2 builds in the blood, but the ETCO2 would read LOW because that area of the lung isn't being ventilated.

Just remember, ETCO2 is a great tool, but you have to understand the physiological concepts. ETCO2 most closely matches PaCO2 in patients with NORMAL lungs, but not so much with patients who have chronic respiratory conditions (ie COPD). If you want a more in depth look at the physiology, check out the terms "Deadspace" and "Shunt" (or "V/Q Mismatch"). Little difficult to grasp at first, but will widen your perspective of pulmonary maladies.

How about in the case of DKA? A diabetic patient with DKA has too much sugar in their bloodstream, and that causes them to have metabolic acidosis. They usually have Kussmaul's respirations. They're trying to change their metabolic acidosis to respiratory acidosis to try to blow off their CO2, but is that possible? Will their EtCO2 be higher because they're blowing off CO2? Or will it be lower because they are hyperventilating?

So in the case of DKA, the body is most definitely in a metabolic acidosis because there is an excess of ketones from fat breakdown (for the sake of this discussion, ketones = acid). When ketones are present, what buffers them? That's right, sodium bicarbonate. The ketones combine with the sodium bicarb, effectively lowering the bicarbonate level, which will drop the blood pH. To compensate, the respiratory rate picks up to try and blow off CO2 (which also = acid) in a nature response to try and normalize pH (which rarely happens in a metabolic acidosis).

When considering ETCO2, it is likely that the ETCO2 will be lower due to hyperventilation. BUT, it's a cool and reliable way to trend your respiratory rate. Just remember, these patients may LOOK bad respiratory wise, but they DO NOT need ventilatory support unless failure is imminent. They are a NIGHTMARE to manage on a ventilator. Aggressive fluid resuscitation, insulin, and treatment of hyperkalemia goes a long way.

 

[VentMonkey]

When considering ETCO2, it is likely that the ETCO2 will be lower due to hyperventilation. BUT, it's a cool and reliable way to trend your respiratory rate. Just remember, these patients may LOOK bad respiratory wise, but they DO NOT need ventilatory support unless failure is imminent. They are a NIGHTMARE to manage on a ventilator. Aggressive fluid resuscitation, insulin, and treatment of hyperkalemia goes a long way.

Not sure where you were going with the rest of your post, but this is 100% on point. Also, understanding a simple tool like "Winter's Formula" may actually go a long way if you do find yourself having to manage their airway post haste. Meeting their metabolic demands, and understanding why these patients must stay acidotic isn't something most prehospital providers may (initially) understand, but at the very least understand at this stage in the game their current metabolic state must be matched for, well, lack of a better word, survival. Decent post overall, welcome to the forum @RRTMedic.

 

[RRTMedic]

Decent post overall, welcome to the forum

Thanks... I find myself at a remote/slow base staring at the wall haha. What better to do than put my thoughts on a forum?

 

[VentMonkey]

Thanks... I find myself at a remote/slow base staring at the wall haha. What better to do than put my thoughts on a forum?

NP, feel free to peruse the HEMS section, I'm always promoting that section of this forum, haha.

 

[Tigger]

http://www.medicscribe.com/capnography/

I still find myself confused and I find this to be a decent primer.

Had a DKA patient the other night, respiratory rate of 44 and EtCO2 of 6. Initially that didn't make sense to me, the patient is acidotic right? Metabolically yes, but your end tidal is reading the compensatory hypocapnia/alkalosis.

 

[RRTMedic]

Initially that didn't make sense to me, the patient is acidotic right? Metabolically yes, but your end tidal is reading the compensatory hypocapnia/alkalosis

You're absolutely right. These patients are acidotic. The low ETCO2 is most definitely due to the hyperventilatory compensation that is occurring.

An ABG may look something like this: pH 7.29 / PaCO2 25 / PaO2 89 / HCO3- 10

Just remember that the acidosis is due to the LOW bicarb... because the bicarb has essentially been "ate up" by the ketonic acids

 

[Tigger]

You're absolutely right. These patients are acidotic. The low ETCO2 is most definitely due to the hyperventilatory compensation that is occurring.

An ABG may look something like this: pH 7.29 / PaCO2 25 / PaO2 89 / HCO3- 10

Just remember that the acidosis is due to the LOW bicarb... because the bicarb has essentially been "ate up" by the ketonic acids

Incidentally the pH was 6.96...yikes.

 

[VentMonkey]

http://www.medicscribe.com/capnography/

I still find myself confused and I find this to be a decent primer.

Had a DKA patient the other night, respiratory rate of 44 and EtCO2 of 6. Initially that didn't make sense to me, the patient is acidotic right? Metabolically yes, but your end tidal is reading the compensatory hypocapnia/alkalosis.

http://fitsweb.uchc.edu/student/sel...ompensatory_responses_metabolic_acidosis.html

Here's a quick tutorial on Winter's Formula, but basically the thought process is to "match" their CO2 number to what their most recent ABG reflected if the patient's airway is being managed via mechanical ventilations. Bringing their ETCO2, and moreover, their PaCO2 within "normal" limits can be detrimental, as the primary cause for their drop in PaCO2 is metabolic in nature, hence the reason, aggressive IVF, and insulin is indicated until their pH can restored WNL, and extubated; make sense, I hope?...

 

[Tigger]

http://fitsweb.uchc.edu/student/sel...ompensatory_responses_metabolic_acidosis.html

Here's a quick tutorial on Winter's Formula, but basically the thought process is to "match" their CO2 number to what their most recent ABG reflected if the patient's airway is being managed via mechanical ventilations. Bringing their ETCO2, and moreover, their PaCO2 within "normal" limits can be detrimental, as the primary cause for their drop in PaCO2 is metabolic in nature, hence the reason, aggressive IVF, and insulin is indicated until their pH can restored WNL, and extubated; make sense, I hope?...

It does.

I was concerned that I was going to have to intubate this patient and that prospect did not excite me. He was exhausted (tachypneic for three days) and fairly altered. At one point his work of breathing increased significantly and he became significantly altered, fortunately some positioning and an NRB seemed to right the ship.

But having to ventilate him seemed awful...I need that compensation to stave off further metabolic issues and trying to match that with mechanical ventilation sounded...difficult.

 

[RRTMedic]

http://fitsweb.uchc.edu/student/sel...ompensatory_responses_metabolic_acidosis.html

Here's a quick tutorial on Winter's Formula, but basically the thought process is to "match" their CO2 number to what their most recent ABG reflected if the patient's airway is being managed via mechanical ventilations. Bringing their ETCO2, and moreover, their PaCO2 within "normal" limits can be detrimental, as the primary cause for their drop in PaCO2 is metabolic in nature, hence the reason, aggressive IVF, and insulin is indicated until their pH can restored WNL, and extubated; make sense, I hope?...

This is definitely off-topic to the original post... but I have found these patients (who are on mechanical ventilation) are usually best placed in a spontaneous, pressure supported mode (which may be PS/CPAP or just SIMV with an extremely low rate). It has been my experience that their respiratory drive is so strong that trying to use an Assist/control mode results in dyssynchrony and obvious discomfort. I may be wrong, but they sure do look much better when you just let them do their thing on their own.

I typically find this approach at 3 AM to be most useful to your TBI patient "neurostorming" as well

 

[VentMonkey]

It does.

I was concerned that I was going to have to intubate this patient and that prospect did not excite me. He was exhausted (tachypneic for three days) and fairly altered. At one point his work of breathing increased significantly and he became significantly altered, fortunately some positioning and an NRB seemed to right the ship.

But having to ventilate him seemed awful...I need that compensation to stave off further metabolic issues and trying to match that with mechanical ventilation sounded...difficult.

Yeah, IMO, unless they have to absolutely positively be intubated in the field, there's no reason to. If you do need to though, try and grab the most current set of ABG's, and/ or have respiratory draw a set, figure out the formula, and match the minute ventilation best you can to meet the ETCO2 closest to their most recent/ current PaCo2. This type of patient is the quintessential patient that displays the importance of prehospital ventilator management. They should not be BVM-d.

Side note: glad to see I have a fellow respiratory nerd in @RRTMedic.

 

[Tigger]

Yeah, IMO, unless they have to absolutely positively be intubated in the field, there's no reason to. If you do need to though, try and grab the most current set of ABG's, and/ or have respiratory draw a set, figure out the formula, and match the minute ventilation best you can to meet the ETCO2 closest to their most recent/ current PaCo2. This type of patient is the quintessential patient that displays the importance of prehospital ventilator management. They should not be BVM-d.

Side note: glad to see I have a fellow respiratory nerd in @RRTMedic.

This was a 911 call so if we ended up intubating I am not sure what we would have done. Certainly not shooting for the usual 35-45 range, but really it be anyone's guess.

We have an IStat but it's for the community paramedic program right now.

 

[VentMonkey]

This was a 911 call so if we ended up intubating I am not sure what we would have done. Certainly not shooting for the usual 35-45 range, but really it be anyone's guess.

We have an IStat but it's for the community paramedic program right now.

What kind of vents does your service carry? I always advocate learning that bad boy so when that "just in case" patient presents, it's use is not in question.

 

[Tigger]

What kind of vents does your service carry? I always advocate learning that bad boy so when that "just in case" patient presents, it's use is not in question.

PneuPac Parapac. Pretty limited options wise. We do have PEEP valves on the circuits in addition to the actual vent's settings.

 

[VentMonkey]

PneuPac Parapac. Pretty limited options wise. We do have PEEP valves on the circuits in addition to the actual vent's settings.

Right on, fair enough. If I am not mistaken that model is somewhere between an AutoVent, and an actual ventilator. Still, It's better than a BVM, which our ground/ 911 ops carry only.

 

[StCEMT]

PneuPac Parapac. Pretty limited options wise. We do have PEEP valves on the circuits in addition to the actual vent's settings.

I've got the same, I really wish we carried something a bit better. Like Vent said, better than a BVM, but it is a step down from what I was taught vent operations on.

 

[Tigger]

Right on, fair enough. If I am not mistaken that model is somewhere between an AutoVent, and an actual ventilator. Still, It's better than a BVM, which our ground/ 911 ops carry only.

Pretty much. Less mickey mouse than auto/surevent but not exactly customizable.

 

[RRTMedic]

Right on, fair enough. If I am not mistaken that model is somewhere between an AutoVent, and an actual ventilator. Still, It's better than a BVM, which our ground/ 911 ops carry only.

Here in NC we carry Newport HT70 for interfacility transports. Pretty bulky but does give more options that ATVs. I can do AC, SIMC, VC, PC, and PS...switch it to NIV and do CPAP/BiPAP. Can even do a descending ramp on my flow rate. Cool stuff... fairly cheap ~$9000