High bicarb CRRT for respiratory acidosis

[Crash44]

Hello everyone, first time on this subforum.
Have an attending who uses a high bicarb bath (up to 45 meq/l) to help respiratory acidosis. Anyone else encounter this or have evidence for it?


Thanks

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[deleted547339]

No. That’s dumb.

 

[inspirationmd]

No. That’s dumb.

Agree

 

[deleted171991]

All that bicarb will generate CO2, which will have to eliminated by the lungs (hence worsening the respiratory acidosis - just watch the EtCO2 after a bicarb bolus), or otherwise get trapped into the cells (hence worsening the intracellular acidosis - the one that really matters). I would be very suspicious of that attending's knowledge of modern critical care; intracellular acidosis is a well-known complication of bicarb administration (except for urinary/GI losses of bicarb).

People have survived even pCO2 of 250 mmHg for hours, without measurable health consequences. It's not the CO2 that kills.

Great acute critical care is experimental medicine, I get it. But, with interventions like this, if one doesn't see a significant change in the patient's clinical status within hours, one should stop using the patient as a guinea pig. Statistically, physician interventions have a higher chance of doing harm than good.

Don't just do something, stand there! The best intensivists do nothing, much more frequently than the average ones. It's called "watchful waiting", the opposite of "fools rush in".

tl;dr: Decompensated respiratory acidosis should be fixed with ventilatory support, not bicarb, until proven otherwise.

 

[Radetzky]

All that bicarb will generate CO2, which will have to eliminated by the lungs (hence worsening the respiratory acidosis - just watch the EtCO2 after a bicarb bolus), or otherwise get trapped into the cells (hence worsening the intracellular acidosis - the one that really matters). I would be very suspicious of that attending's knowledge of modern critical care.

People have survived even pCO2 of 250 mmHg for hours, without measurable health consequences. It's not the CO2 that kills.

Great acute critical care is experimental medicine, I get it. But, with interventions like this, if one doesn't see a significant change in the patient's clinical status within hours, one should stop using the patient as a guinea pig. Statistically, physician interventions have a higher chance of doing harm than good.

Don't just do something, stand there! The best intensivists do nothing, much more frequently than the average ones. It's called "watchful waiting", the opposite of "fools rush in".

tl;dr: Decompensated respiratory acidosis should be fixed with ventilatory support, not bicarb.

Agree with everything else but have to pick you up on a point here... bicarb worsens the CO2 but it doesn’t worsen the respiratory acidosis, assuming minute ventilation stays the same.

 

[deleted171991]

Agree with everything else but have to pick you up on a point here... bicarb worsens the CO2 but it doesn’t worsen the respiratory acidosis, assuming minute ventilation stays the same.

So the patient has a steady-state pCO2 of X. I give bicarb, which produces extra CO2. Would you be so kind to explain how the respiratory acidosis wouldn't worsen, IF the minute ventilation stayed the same (hence the extra CO2 cannot get eliminated)?

Also, a lot of that CO2 that doesn't get eliminated (and doesn't replenish the body's depleted bicarb buffers, as in NAGMA) will enter the cells, and produce clinically unmeasurable (but experimentally proven) intracellular acidosis.

 

[Radetzky]

So the patient has a steady-state pCO2 of X. I give bicarb, which produces extra CO2. Would you be so kind to explain how the respiratory acidosis wouldn't worsen, IF the minute ventilation stayed the same?

yes, CO2 goes up, H+ goes down. You’ve generated a new equilibrium which operates at a higher HCO3, a higher CO2, and a higher ph

this seems to be a common misunderstanding. People think that the extra CO2 somehow then goes backwards in the equation to regenerate H+. That’s not how an equilibrium works.

 

[deleted171991]

yes, CO2 goes up, H+ goes down. You’ve generated a new equilibrium which operates at a higher HCO3, a higher CO2, and a higher ph

this seems to be a common misunderstanding. People think that the extra CO2 somehow then goes backwards in the equation to regenerate H+. That’s not how an equilibrium works.

It does go backwards, inside the cells. That's how it gets trapped. CO2 can enter/leave the cells, H+ can't.

 

[Radetzky]

It does go backwards, inside the cells. That's how it gets trapped. CO2 can enter/leave the cells, H+ can't.

The intracellular acidosis theory certainly sounds appealing, however the scientific evidence behind it is flimsy. The initial studies used buffering solutions that were not comparable to plasma. Newer studies mostly show increases of intracellular pH following bicarb. Bicarb eventually makes it across the cell membrane.

 

[deleted171991]

The intracellular acidosis theory certainly sounds appealing, however the scientific evidence behind it is flimsy. The initial studies used buffering solutions that were not comparable to plasma. Newer studies mostly show increases of intracellular pH following bicarb. Bicarb eventually makes it across the cell membrane.

Then the OP attending is right, and you shouldn't agree to any part of my initial post.

 

[Radetzky]

Then the OP attending is right, and you shouldn't agree to any part of my initial post.

But I do haha. Ventilate the patient, treat the underlying condition, mild to moderate respiratory acidosis is well tolerated, treating the number is just a magic trick.

 

[Crash44]

All that bicarb will generate CO2, which will have to eliminated by the lungs (hence worsening the respiratory acidosis - just watch the EtCO2 after a bicarb bolus), or otherwise get trapped into the cells (hence worsening the intracellular acidosis - the one that really matters). I would be very suspicious of that attending's knowledge of modern critical care; intracellular acidosis is a well-known complication of bicarb administration (except for urinary/GI losses of bicarb).

People have survived even pCO2 of 250 mmHg for hours, without measurable health consequences. It's not the CO2 that kills.

Great acute critical care is experimental medicine, I get it. But, with interventions like this, if one doesn't see a significant change in the patient's clinical status within hours, one should stop using the patient as a guinea pig. Statistically, physician interventions have a higher chance of doing harm than good.

Don't just do something, stand there! The best intensivists do nothing, much more frequently than the average ones. It's called "watchful waiting", the opposite of "fools rush in".

tl;dr: Decompensated respiratory acidosis should be fixed with ventilatory support, not bicarb, until proven otherwise.

I dropped the baths the second he left service, but has been micromanaging from home and pressured nephrology into changing it back (took 2 days before they caved).

 

[Crash44]

yes, CO2 goes up, H+ goes down. You’ve generated a new equilibrium which operates at a higher HCO3, a higher CO2, and a higher ph

this seems to be a common misunderstanding. People think that the extra CO2 somehow then goes backwards in the equation to regenerate H+. That’s not how an equilibrium works.

This seems to be whats happening. Its what he is doing for his COVID ARDS ECMO patients as well in an attempt to minimize sweep....

Thank you everyone for your replies!

 

[Siggy]

Isn't the standard recommendation in ARDS with unacceptable pH due to respiratory acidosis with low tidal volumes a bicarb infusion pending development of compensation over the next 24-48 hours?

I agree with the general premise that the solution to respiratory acidosis is increasing minute ventilation, but there are exceptions.

 

[Siggy]

This seems to be whats happening. Its what he is doing for his COVID ARDS ECMO patients as well in an attempt to minimize sweep....

Thank you everyone for your replies!

I have extremely limited experience with ECMO, but what is the issue with increased sweep?

 

[aafisahar]

I have extremely limited experience with ECMO, but what is the issue with increased sweep?

Increases the removal of CO2 through gas exchange

 

[Siggy]

Increases the removal of CO2 through gas exchange

Isn't that the goal though? Why would someone want to minimize sweep in a hypercapnic patient. Wouldn't increasing sweep be preferred over bicarb?

 

[SurfingDoctor]

Giving NaHCO3 to reduce the sweep gas?

 

[deleted171991]

But I do haha. Ventilate the patient, treat the underlying condition, mild to moderate respiratory acidosis is well tolerated, treating the number is just a magic trick.

Obviously, this case wasn't about a mild-moderate acidosis. Of course, it's no big deal if one can blow the CO2 away. The problem is when there is profound acidosis already.

 

[Crash44]

Isn't that the goal though? Why would someone want to minimize sweep in a hypercapnic patient. Wouldn't increasing sweep be preferred over bicarb?

His thought process use ecmo as little as possible, create the higher equilibrium with the high bicarb, come off ecmo with high CO2 and normal pH allowing the lung to do minimal work.
I didnt see how well it worked during the first wave or other causes of ARDS he had previously, but the current patient who has been on for a month, is awake and gets tachypnic to the 50s with decreasing the sweep lower than 3.

A non ecmo COVID ARDS one with a 45 meq/l bicarb solution on CRRT just takes 800-1000cc TVs 16-20 times a minute (spontaneous mode, with us decreasing pressure support) to blow off his CO2.

I am guessing this would be more of a CO2 response curve problem and I don’t know how long that would take to right shift in the setting of hypercapnia.

 

[deleted547339]

His thought process use ecmo as little as possible, create the higher equilibrium with the high bicarb, come off ecmo with high CO2 and normal pH allowing the lung to do minimal work.
I didnt see how well it worked during the first wave or other causes of ARDS he had previously, but the current patient who has been on for a month, is awake and gets tachypnic to the 50s with decreasing the sweep lower than 3.

A non ecmo COVID ARDS one with a 45 meq/l bicarb solution on CRRT just takes 800-1000cc TVs 16-20 times a minute (spontaneous mode, with us decreasing pressure support) to blow off his CO2.

I am guessing this would be more of a CO2 response curve problem and I don’t know how long that would take to right shift in the setting of hypercapnia.

As a general rule, ecmo is an evidence-free zone. A lot of people like to pretend that the insertion of a pump changes the rules or medicine and physiology, when, in fact, it does not. Ecmo isn’t as complicated as people make it out to be. I spent a whole lot more time in a CTICU in fellowship than I needed to. The biggest “ah ha” moment for me wasn’t when all the physiology clicked, it was when I started to recognize the hand-waving.

 

[chessknt]

As a general rule, ecmo is an evidence-free zone. A lot of people like to pretend that the insertion of a pump changes the rules or medicine and physiology, when, in fact, it does not. Ecmo isn’t as complicated as people make it out to be. I spent a whole lot more time in a CTICU in fellowship than I needed to. The biggest “ah ha” moment for me wasn’t when all the physiology clicked, it was when I started to recognize the hand-waving.

This is just completely false. There is great evidence that ecmo can make you live forever according to my ct surgeons (or at least for their post-op disasters). Why rbg wasn't put on ecmo until January is the biggest conspiracy noone is talking about.

 

[jthedestroyr]

All that bicarb will generate CO2, which will have to eliminated by the lungs (hence worsening the respiratory acidosis - just watch the EtCO2 after a bicarb bolus), or otherwise get trapped into the cells (hence worsening the intracellular acidosis - the one that really matters). I would be very suspicious of that attending's knowledge of modern critical care; intracellular acidosis is a well-known complication of bicarb administration (except for urinary/GI losses of bicarb).

People have survived even pCO2 of 250 mmHg for hours, without measurable health consequences. It's not the CO2 that kills.

Great acute critical care is experimental medicine, I get it. But, with interventions like this, if one doesn't see a significant change in the patient's clinical status within hours, one should stop using the patient as a guinea pig. Statistically, physician interventions have a higher chance of doing harm than good.

Don't just do something, stand there! The best intensivists do nothing, much more frequently than the average ones. It's called "watchful waiting", the opposite of "fools rush in".

tl;dr: Decompensated respiratory acidosis should be fixed with ventilatory support, not bicarb, until proven otherwise.

That's because you're formally trained. Let me tell you, I know a few people that "dabble" and use bicarb for EVERYTHING when they're in acidosis, despite me explaining how it's converted into C02. You're anesthesia, you know this point is always lost in the OR with a certain cohort.

 

[deleted547339]

This is just completely false. There is great evidence that ecmo can make you live forever according to my ct surgeons (or at least for their post-op disasters). Why rbg wasn't put on ecmo until January is the biggest conspiracy noone is talking about.

B.S. Ecmo can only keep you alive exactly 30 days post-op, then it stops working. Or did I hear that they changed the post-op complication reporting to 90 days?

 

[deleted171991]

That's because you're formally trained. Let me tell you, I know a few people that "dabble" and use bicarb for EVERYTHING when they're in acidosis, despite me explaining how it's converted into C02. You're anesthesia, you know this point is always lost in the OR with a certain cohort.

Practicing critical care without subspecialty board certification is like practicing EM without it. It was OK 50 years ago, when FPs used to do surgeries; it should be unacceptable today, except maybe in BFE. There is way too much to know, and one wrong move can kill a patient.

My first rule is that I don't take advice about critical care from non-intensivist surgeons. I read more critical care than they do, I have forgotten more critical care than they know, and frankly I am way more passionate about healing and not harming their patients.

 

[jthedestroyr]

Practicing critical care without subspecialty board certification is like practicing EM without it. It was OK 50 years ago, when FPs used to do surgeries; it should be unacceptable today, except maybe in BFE. There is way too much to know, and one wrong move can kill a patient.

My first rule is that I don't take advice about critical care from non-intensivist surgeons. I read more critical care than they do, I forgot more critical care than they know, and frankly I am way more passionate about healing and not harming their patients.

Yes, I learned this the hard way my first job aka current as the only icu trained guy that joined 2 none intensivist. Its been, ya not fun.