Sodium Bicard admin post arrest

[rhan101277]

I had a cardiac arrest patient the other day. He was attended to by firefighters almost immediately after collapse. When we arrived FD reports their AED shocked once. Initial rhythm is asystole, then PEA for two rounds of CPR then I get vfib and shock at 360 and get a pulse back. All this takes 15 minutes, I administer sodium bicarb in route thinking about acidosis and down time. I then realize there is not protocol for doing so and that bicarb admin should be led by ABG's, which I already knew.

He had a ETCo2 of 98 which was a reason I pushed it, I did realize it was that high due to all of the downtime. He got more bicarb after ABG showed his pH was 6.9. Bicarb is converted to CO2 and must be blown off and since the patient is only being ventilated 8-10 a minute it could cause worsening acidosis, though it is unlikely as long as patient is being ventilated.

My FTO talked to me about to get my reasoning, he said he has never seen it done that way before. In hindsight I should have called med control. I didn't get into any trouble but I wanted to see what others thoughts were.

 

[Smash]

I'm not sure I understand the rationale for giving the sodium bicarb. If the EtCO2 is high (which is not unexpected) it is safe to assume that the PaCO2 is high, although we don't know what the gradient is without an ABG. However, the way to fix that would be to increase your minute volume, not give another drug which is a CO2 donor.

 

[NomadicMedic]

Did he have an ETCO2 of 98 just after ROSC? What was his ETCO2 during the arrest portion?

 

[MSDeltaFlt]

I had a cardiac arrest patient the other day. He was attended to by firefighters almost immediately after collapse. When we arrived FD reports their AED shocked once. Initial rhythm is asystole, then PEA for two rounds of CPR then I get vfib and shock at 360 and get a pulse back. All this takes 15 minutes, I administer sodium bicarb in route thinking about acidosis and down time. I then realize there is not protocol for doing so and that bicarb admin should be led by ABG's, which I already knew.

He had a ETCo2 of 98 which was a reason I pushed it, I did realize it was that high due to all of the downtime. He got more bicarb after ABG showed his pH was 6.9. Bicarb is converted to CO2 and must be blown off and since the patient is only being ventilated 8-10 a minute it could cause worsening acidosis, though it is unlikely as long as patient is being ventilated.

My FTO talked to me about to get my reasoning, he said he has never seen it done that way before. In hindsight I should have called med control. I didn't get into any trouble but I wanted to see what others thoughts were.

Rhan,

If your protocols are anything like mine then you'll notice it says in the back in the formulary for sodium bicarbonate that you give it if pulseless for 10 min or more. Does not say call Med Control, though the protocol doesn't even mention it at all. But of a loop hole for you.

However, with your EtCO2 being 98, your problem was more respiratory than metabolic. I would have bagged faster first. Then if meds weren't working (because nothing works in an acid medium), I'd give NaHCO3.

FYI & IMHO.

 

[rhan101277]

Yeah it says give it if they are still is asystole or PEA, but the patient had a perfusing rhythm when I gave it. He went 15 minutes with CPR which at best gives 2L circulation, average heart pumps 5L.

So my line of thought was that he would be acidotic because of the down time. It doesn't seem like there would have been much difference if I gave it and he got ROSC right after or if I gave it after ROSC as long as I had good ventilations.

We only hyperventilate possible herniations over here, we can't hyperventilate someone based on ETCO2 readings.

 

[usalsfyre]

We only hyperventilate possible herniations over here, we can't hyperventilate someone based on ETCO2 readings.

Are they really going to gig you for doing what an intuitive clinician would?

 

[NomadicMedic]

We only hyperventilate possible herniations over here, we can't hyperventilate someone based on ETCO2 readings.

You don't adjust ventilations to maintain an appropriate end tidal? Then why do you use caponography? Just to verify a tube? It's so much more than that. In my opinion, caponography paints the absolute best prehospital picture of ventilation status, and if you're not adjusting your treatment after seeing numbers like an end tidal of 98, you're doing a huge disservice to your patients. Don't be a cookbook medic. Do what's right for your patients and have the knowledge and wherewithal to stand up for yourself and be a patient advocate.

 

[rhan101277]

Are they really going to gig you for doing what an intuitive clinician would?

No, I am not in any trouble for it. I just thought I would share the story. My FTO just wanted to make sure I had a good reason and that the treatment made since.

 

[usalsfyre]

No, I am not in any trouble for it. I just thought I would share the story. My FTO just wanted to make sure I had a good reason and that the treatment made since.

I was saying adjusting your ventilatory rate based on ETCO2. Not doing that would be like knowing a set of directions was wrong but following them anyway because thats what's written down.

 

[rhan101277]

You don't adjust ventilations to maintain an appropriate end tidal? Then why do you use caponography? Just to verify a tube? It's so much more than that. In my opinion, caponography paints the absolute best prehospital picture of ventilation status, and if you're not adjusting your treatment after seeing numbers like an end tidal of 98, you're doing a huge disservice to your patients. Don't be a cookbook medic. Do what's right for your patients and have the knowledge and wherewithal to stand up for yourself and be a patient advocate.

Think about what you posted, there are many things that cause high ETCo2 values such as low cardiac output, poor gas exchange, anxiety, COPD patients etc.

If you adjust ventilations just because you see a high ETCo2 number, you are doing a disservice to your patients.

I am definitely not a cookbook medic.

 

[Handsome Robb]

If you adjust ventilations just because you see a high ETCo2 number, you are doing a disservice to your patients.

True, you should be looking at the whole picture. Personally in this situation I'd say an ETCo2 of 98 after ROSC with a 15 minute downtime would indicate a tid bit of increase in ventilation rate, but that's just me.

I don't think anyone was calling you a cookbook medic...more of a statement than anything.

 

[Smash]

Think about what you posted, there are many things that cause high ETCo2 values such as low cardiac output, poor gas exchange, anxiety, COPD patients etc.

If you adjust ventilations just because you see a high ETCo2 number, you are doing a disservice to your patients.

I am definitely not a cookbook medic.

I think you might need to revisit the concept of EtCO2 and how it relates to PaCO2 and in turn, perfusion, ventilation, acid-base and so on.

If we go back to your original patient:

You have a patient who has arrested. In the process of going from flow to low-flow to no flow, acidosis will of course occur. When we get things going again, that acidosis persists as we reverse the no-flow to flow state, and metabolism starts up again, producing even more acid.
Therefore we have a lot of CO2 floating around: CO2 = acid.

Now, we don't want an acidotic state persisting, it is not good for all the enzymes and proteins and so on that need a very tight range of pH to function properly. As the patient is not breathing on his own, he cannot use the respiratory system to blow off all that acid. We have to do it for him. There is no reason for that EtCO2 to stay that high if you ventilate adequately. Assuming you are optimising perfusion with fluids and pressors/inotropes and ventilating adequately, that EtCO2 should come down nice and quickly to normo-capnic levels.

Personally, I aim for an EtCO2 of 30-40mmHg. In healthy person the EtCO2aCO2 gradient is usually 5mmHg, so this would give a PaCO2 of 35-45mmHg, i.e. normal. Of course this person isn't healthy so the gradient may be quite different, but in the absence of an ABG that assumption is the best I can do. If I were lucky enough (or smart enough) to work on one of our choppers, I would use the iStat to correlate the numbers and readjust the ventilator from there.

So your patient has high EtCO2. In the context of what has happened, this should mean 1) he has good perfusion (you need perfusion to create CO2) and 2) he has poor ventilation (you need ventilation to get rid of CO2)

So this patient, who is ventilating poorly, is then given a drug that, in the absence of good ventilation, causes increased acidosis by donating CO2, thereby increasing acidosis. Probably not what they need right now.

In some settings (such as the intubated asthmatic) we allow permissive hypercapnia, because the risks of trying to hyperventilate that patient outweighs the risk of allowing the CO2 to remain high for a time(we still bring it down, just not as fast). However, not adjusting ventilation in light of EtCO2 is a very, very bad idea.

 

[rhan101277]

I think you might need to revisit the concept of EtCO2 and how it relates to PaCO2 and in turn, perfusion, ventilation, acid-base and so on.

If we go back to your original patient:

You have a patient who has arrested. In the process of going from flow to low-flow to no flow, acidosis will of course occur. When we get things going again, that acidosis persists as we reverse the no-flow to flow state, and metabolism starts up again, producing even more acid.
Therefore we have a lot of CO2 floating around: CO2 = acid.

Now, we don't want an acidotic state persisting, it is not good for all the enzymes and proteins and so on that need a very tight range of pH to function properly. As the patient is not breathing on his own, he cannot use the respiratory system to blow off all that acid. We have to do it for him. There is no reason for that EtCO2 to stay that high if you ventilate adequately. Assuming you are optimising perfusion with fluids and pressors/inotropes and ventilating adequately, that EtCO2 should come down nice and quickly to normo-capnic levels.

Personally, I aim for an EtCO2 of 30-40mmHg. In healthy person the EtCO2aCO2 gradient is usually 5mmHg, so this would give a PaCO2 of 35-45mmHg, i.e. normal. Of course this person isn't healthy so the gradient may be quite different, but in the absence of an ABG that assumption is the best I can do. If I were lucky enough (or smart enough) to work on one of our choppers, I would use the iStat to correlate the numbers and readjust the ventilator from there.

So your patient has high EtCO2. In the context of what has happened, this should mean 1) he has good perfusion (you need perfusion to create CO2) and 2) he has poor ventilation (you need ventilation to get rid of CO2)

So this patient, who is ventilating poorly, is then given a drug that, in the absence of good ventilation, causes increased acidosis by donating CO2, thereby increasing acidosis. Probably not what they need right now.

In some settings (such as the intubated asthmatic) we allow permissive hypercapnia, because the risks of trying to hyperventilate that patient outweighs the risk of allowing the CO2 to remain high for a time(we still bring it down, just not as fast). However, not adjusting ventilation in light of EtCO2 is a very, very bad idea.

He isn't ventilating poorly, in fact after sodium bicarb admin and standard respiration rates of 10 his CO2 was down to 44 upon arrival at ED. That is ventilating at 10/minute.

 

[MSDeltaFlt]

He isn't ventilating poorly, in fact after sodium bicarb admin and standard respiration rates of 10 his CO2 was down to 44 upon arrival at ED. That is ventilating at 10/minute.

Now we have the bigger picture. Thank you for the information at the end of the call. You did fine. Good job. Consider yourself vindicated.

 

[NYMedic828]

Just as a side note for my own learning,

Excess CO2 is converted into Bi-Carb in the bloodstream, and vice-versa so technically giving NaBi-Carb to a patient with Respiratory Acidosis = More CO2 and more Acidosis?

Shouldn't the cure to respiratory acidosis be respiratory and the cure for metabolic be circulatory? (ventilation/drugs)

I always had trouble fathoming the acid-base balances and buffer systems around them. Some of you guys are so ridiculously knowledgeable :/ (granted I have 3 months as a medic )

Anyone have any good links explaining it in-depth?

 

[jwk]

He isn't ventilating poorly, in fact after sodium bicarb admin and standard respiration rates of 10 his CO2 was down to 44 upon arrival at ED. That is ventilating at 10/minute.

That's actually a pretty slow respiratory rate given the high EtCO2. There's a reason it's called "hyperventilation".

I'm from the age where every arrest got 2 amps of bicarb before anything else. Now we don't even give bicarb in the OR without ABG guidance, and even then, a lot of times we'll hyperventilate instead of pushing bicarb because of all the potential evils involved.

 

[MSDeltaFlt]

Just as a side note for my own learning,

Excess CO2 is converted into Bi-Carb in the bloodstream, and vice-versa so technically giving NaBi-Carb to a patient with Respiratory Acidosis = More CO2 and more Acidosis?

Shouldn't the cure to respiratory acidosis be respiratory and the cure for metabolic be circulatory? (ventilation/drugs)

I always had trouble fathoming the acid-base balances and buffer systems around them. Some of you guys are so ridiculously knowledgeable :/ (granted I have 3 months as a medic )

Anyone have any good links explaining it in-depth?

True. Think of it this way. And this is straight forward and as simple as I can make it.

(Bare in mind that unless you have the luxury of temperature corrected ABG's in hand, you have no other choice but to go with this process)

The goal is to keep the pH balanced. Period. We do this by controlling PaCO2 through EtCO2. If EtCO2 > 45, breathe faster. If EtCO2 <35, breathe slower.

EtCO2 has a margin of error, generally, of + or - 4-5pts. And that depends on your pt's cardiac output and temperature (>101°/<96°).

 

[NomadicMedic]

Think about what you posted, there are many things that cause high ETCo2 values such as low cardiac output, poor gas exchange, anxiety, COPD patients etc.

If you adjust ventilations just because you see a high ETCo2 number, you are doing a disservice to your patients.

I am definitely not a cookbook medic.

In a patient that had ROSC after an arrest I'm CERTAINLY going to adjust ventilations to help archive an acceptable end tidal reading. And I'm not going to push bicarb on a now perfusing patient, to "correct" an acidosis that should be fixed through ventilation. Think about it. Maybe that's why bicarb isn't in your standing orders.

 

[Veneficus]

surgical resuscitation (c)

In a patient that had ROSC after an arrest I'm CERTAINLY going to adjust ventilations to help archive an acceptable end tidal reading. And I'm not going to push bicarb on a now perfusing patient, to "correct" an acidosis that should be fixed through ventilation. Think about it. Maybe that's why bicarb isn't in your standing orders.

So what of the patient arrested secondary to DKA?

At that point, ventilation will not work as the patient has probably already hyperventilated for days if not weeks.

But the point of me illustrating this is not to split hairs, it's to point out that when resuscitating patients, when you can identify the specific pathology and treat accordingly, it doesn't make it the wrong choice if it's not directly on the protocol.

I agree though, giving bicarb to "normalize" a post arrest patient that did not need bicarb for resuscitation while not particularly harmful may not be optimal.

Ventilation is probably the optimal choice.

I know in every text book a big deal is made about PH, but if I could, I would just like to clarify those great minds.

Acidosis results either from a metabolic pathology (like DKA) or as a symptom of a pathology causing cells to convert to anaerobic respiration. Since that is usually caused by oxygen deficency, let's just assume that example.

During normal function, about 30% of oxygen delivered to tissue is used. Moving up to as high as 60% during extreme circumstances. When even this is not sufficent, usually because of a delivery problem, (do2) cells convert to anaerobic metabolism usually to maintain minimal life/function.

As acid increases PH decreases, and all the wonderful things that come with that. But, before we get to the point of systemic effects, cells of the initial insult are usually in a much worse position.

When you add the bicarb, it doesn't stop anaerobic metabolism. It only masks it. Which means you have to wait even longer to figure out if your therapies are working. If the patient is not so acute that later isn't coming.

Even small values of acidosis may point out there is still something that needs attention or intervention.

A true reading is also more useful when correlating other values in trying to get an accurate idea of what is going on.

Anyway, the take home point is, acidosisi is usually a symptom of pathology, not often the root cause. I liken empirically treating suspected acidosis to putting skin lotion on a dehydrated person. It may seem like it is helping, but it is not what the patient needs.

 

[NomadicMedic]

Point taken, but note I specifically said a patient with a high end-tidal following ROSC would be treated with ventilation. The patient that arrested secondary to DKA is a whole 'nother ball of wax, not particularly germane to this discussion.