anbuitachi

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I was talking to an ICU attending about a scheduled case for a young patient with mod-severe pulmonary HTN (RV pressure 1/2 to 2/3 systemic pressure), likely due to OSA currently on ventilator, paralyzed, on high FiO2, w some possible pulm infection (spiking fevers), going for a trach. I said it's a high risk procedure since it's a trach, meaning periods of lower fio2/apnea, causing pHTN to worsen. He told me to give lots of bicarb to make the patient alkalotic. Why would the answer be bicarb in this scenario? Am i dumb or did the attending not know what hes talking about

Also how would you guys manage this case?
 
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This is a planned procedure. Any base deficit should be corrected / optimized as much as possible while in ICU prior to surgery. Trach is a short 10-15 min procedure, and you wouldn't necessary want to bolus tons of bicarb intraop with period of apnea. Bicarb gets converted to CO2, so unless you compensate with increase minute ventilation, this increased in PaCO2 could be detrimental in pHTN. How does the RV function look? If RV function is moderate/severely decreased, you might want to consider Epi or Milrinone+vasopressin drips... obviously a preop A line or intraop TEE could be helpful if you're really worried. Flolan could be helpful too if available. Hyperventilate (decrease PaCO2), don't volume overload, maintain adequate diastolic BP, and limit periods of apnea as much as possible - you need a good surgeon who doesn't mess around. It's a short procedure so maybe small boluses of Epi is all you need to get through trouble.
On the other hand, it's an elective procedure. If his FiO2 requirement is high, you need to consider the risk/benefits of whether his RV could tolerate several minutes of FiO2 <40% for airway fire precaution. We have surgeon who wouldn't trach someone w/ FiO2 requirement >40%; this is debatable. Just my 2 cents.
 
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anbuitachi

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This is a planned procedure. Any base deficit should be corrected / optimized as much as possible while in ICU prior to surgery. Trach is a short 10-15 min procedure, and you wouldn't necessary want to bolus tons of bicarb intraop with period of apnea. Bicarb gets converted to CO2, so unless you compensate with increase minute ventilation, this increased in PaCO2 could be detrimental in pHTN. How does the RV function look? If RV function is moderate/severely decreased, you might want to consider Epi or Milrinone+vasopressin drips... obviously a preop A line or intraop TEE could be helpful if you're really worried. Flolan could be helpful too if available. Hyperventilate (decrease PaCO2), don't volume overload, maintain adequate diastolic BP, and limit periods of apnea as much as possible - you need a good surgeon who doesn't mess around. It's a short procedure so maybe small boluses of Epi is all you need to get through trouble.
On the other hand, it's an elective procedure. If his FiO2 requirement is high, you need to consider the risk/benefits of whether his RV could tolerate several minutes of FiO2 <40% for airway fire precaution. We have surgeon who wouldn't trach someone w/ FiO2 requirement >40%; this is debatable. Just my 2 cents.
Yea thats what i thought. wans't sure why i would bolus bicarb intraop (it seems like he was talking about bicarb for acidemia in situations of apnea..), but bicarb gets rapidly converted to CO2, which doesn't help in apneic patients.. Patient is already on a milrinone infusion. ive actually never used flolan in the OR before. Doesn't the infusion take some time to work? on the echo it says septum bowing to LV , RV significantly dilated mildly depressed, which is probably why it's handling a RV pressure of 100
The ICU attending claims the FIO2 is not going to improve so the case needs to go.
 

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@eggscal99 pretty much hit the nail on the head. Not much to add. need to figure out underlying cause of pHTN. Any underlying pulm path other than this acute infection that may be contributing (WHO class II?). Need to figure out underlying cause of pulm htn and possibly get RHC since echo can gross overestimate pressures and due vasoreactivity challenge as well. If there is an obvious cause of the pulm htn the answer is always treat the underlying cause.
 
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anbuitachi

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@eggscal99 pretty much hit the nail on the head. Not much to add. need to figure out underlying cause of pHTN. Any underlying pulm path other than this acute infection that may be contributing (WHO class II?). Need to figure out underlying cause of pulm htn and possibly get RHC since echo can gross overestimate pressures and due vasoreactivity challenge as well. If there is an obvious cause of the pulm htn the answer is always treat the underlying cause.
The presumed cause is chronic hypoventilation possibly due to OSA. Patient had a RHC which ruled out cardiac cause
 

Hamhock

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? add inhaled flolan
? percutaneous trach in the OR (no electrocautery needed)

HH
 
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nimbus

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This is a planned procedure. Any base deficit should be corrected / optimized as much as possible while in ICU prior to surgery. Trach is a short 10-15 min procedure, and you wouldn't necessary want to bolus tons of bicarb intraop with period of apnea. Bicarb gets converted to CO2, so unless you compensate with increase minute ventilation, this increased in PaCO2 could be detrimental in pHTN. How does the RV function look? If RV function is moderate/severely decreased, you might want to consider Epi or Milrinone+vasopressin drips... obviously a preop A line or intraop TEE could be helpful if you're really worried. Flolan could be helpful too if available. Hyperventilate (decrease PaCO2), don't volume overload, maintain adequate diastolic BP, and limit periods of apnea as much as possible - you need a good surgeon who doesn't mess around. It's a short procedure so maybe small boluses of Epi is all you need to get through trouble.
On the other hand, it's an elective procedure. If his FiO2 requirement is high, you need to consider the risk/benefits of whether his RV could tolerate several minutes of FiO2 <40% for airway fire precaution. We have surgeon who wouldn't trach someone w/ FiO2 requirement >40%; this is debatable. Just my 2 cents.

As a dinosaur who still uses PA catheters, the level of pHtn(1/2-2/3 systemic) described is generally well tolerated under GA. In fact the PA pressure will probably decline significantly with induction of GA. Don't think he'll need all that. Preinduction A-line is a good idea though.
 
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As a dinosaur who still uses PA catheters, the level of pHtn(1/2-2/3 systemic) described is generally well tolerated under GA. In fact the PA pressure will probably decline significantly with induction of GA. Don't think he'll need all that. Preinduction A-line is a good idea though.
Probably not. He is young and RV is only mildly decreased work in his favor. Maybe at least a stick of 10mcg Epi on hand to ward off evil spirits.
 
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BigRedBeta

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Pulmonary hypertension is always a fine line to walk. My fellowship teaching (PICU - sorry if I'm repeating things you already know) was that pulmonary vasoconstriction was a pH driven process. In a pulmonary hypertensive crisis, your pulmonary blood flow is limited, altering your ability to clear CO2, leading to the expected acidosis. Management should include trying to reverse the acidosis in the acute phase, in addition to O2, volume, Nitric, and other pulmonary vasodilators.

The bicarb though is at best a temporary solution as you've noted. It's these types of patients that make me miss THAM a lot.
Y'all know better than I do about the effects on pulmonary vasculature with GA, though I imagine it's of benefit.
Milrinone is not a great pulmonary vasodilator. The cardiac effects are probably a contributor to any improvement seen.

Can you put him on iNO for the case? Most patients generally have a 3-4 hour window of improvement in saturations even if later on they seem to be non-responders. That could help you get to a lower FiO2 long enough to do the case safely.
 
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anbuitachi

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Pulmonary hypertension is always a fine line to walk. My fellowship teaching (PICU - sorry if I'm repeating things you already know) was that pulmonary vasoconstriction was a pH driven process. In a pulmonary hypertensive crisis, your pulmonary blood flow is limited, altering your ability to clear CO2, leading to the expected acidosis. Management should include trying to reverse the acidosis in the acute phase, in addition to O2, volume, Nitric, and other pulmonary vasodilators.

The bicarb though is at best a temporary solution as you've noted. It's these types of patients that make me miss THAM a lot.
Y'all know better than I do about the effects on pulmonary vasculature with GA, though I imagine it's of benefit.
Milrinone is not a great pulmonary vasodilator. The cardiac effects are probably a contributor to any improvement seen.

Can you put him on iNO for the case? Most patients generally have a 3-4 hour window of improvement in saturations even if later on they seem to be non-responders. That could help you get to a lower FiO2 long enough to do the case safely.
So basically CO2 worsens pHTN because it reduces pH. So a pH of 7.2 caused by CO2 equally worsens pHTN vs a pH of 7.2 caused by metabolic acidosis?
 

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It's probably more complex than that. but fixing the pH will do more for your pulmonary pressures than normalizing the PCO2.
 

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@eggscal99 pretty much hit the nail on the head. Not much to add. need to figure out underlying cause of pHTN. Any underlying pulm path other than this acute infection that may be contributing (WHO class II?). Need to figure out underlying cause of pulm htn and possibly get RHC since echo can gross overestimate pressures and due vasoreactivity challenge as well. If there is an obvious cause of the pulm htn the answer is always treat the underlying cause.
Why would we need to figure out the cause of pHTN? Either it's acute or chronic. That's all we need to know for a 15-30min case.
 

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Just do the case and get on with the day. Avoid the usual causes of increased pulm resistance. This pt needs a Trach.

I don't know what the ICU doc was talking about and I would ignore his recommendation.
 
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@Noyac, its good to know what your getting into and i agree with OP in his attempts to figure out whats going on before taking a complicated patient in for procedure. I agree 15 minute procedure, in and out usually. The only concern is if something goes wrong and you have knowledge as to underlying cause who classification/chronicity it at least gives you a plan if something goes wrong. You wouldnt treat a chronic phtn case secondary to osa the same as someone with acute rv strain from pe.....that was my whole point. Do your research and avoid unnecessary risks if you don't have too.
 
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I'm not sure this guys WHO class means anything to me for a 15min trach. Would I like to know he has demonstrated vasodilatory response in the past? Sure, but this dude is likely chronic from his OSA. Meaning he likely lives with a compensated respiratory acidosis and you're not likely to see the textbook reduction in PVR just by getting his PaCO2 to 30, that doesn't mean let it get to 70 though. So avoid all the normal things that you know increase PAPs and focus on the RV as that's what gets you in trouble.

I'm not sure you'll see the response you want from iNO, flolan, or milrinone on the PVR, especially in a 15min case so don't put your eggs in that basket thinking you have a trump card. Support your RV with inotrope and maintain PaO2 and DBP and this shouldn't be a big deal.
 

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Also, let's not forget that an "academic" trach takes an hour, not 15 minutes, so all concerns are valid.
 
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Beyond FiO2 of 1.0 and optimizing ventilation, alkalinization with sodium bicarbonate is the best acute treatment for pulmonary hypertensive crisis. I wouldn't make a big deal of this case--the only clinically significant finding that you're likely to see is faster desaturation w/ apnea. Baseline systemic or suprasystemic pulmonary hypertension, on the other hand, requires more delicate management for cases like this.
 

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@Noyac, its good to know what your getting into and i agree with OP in his attempts to figure out whats going on before taking a complicated patient in for procedure. I agree 15 minute procedure, in and out usually. The only concern is if something goes wrong and you have knowledge as to underlying cause who classification/chronicity it at least gives you a plan if something goes wrong. You wouldnt treat a chronic phtn case secondary to osa the same as someone with acute rv strain from pe.....that was my whole point. Do your research and avoid unnecessary risks if you don't have too.
very good. So then maybe you would like to tell us how you would treat them differently. In my opinion you treat them the same. You don't let the Pulm pressure rise at all. I understand that the acute pHTN will lead to RV FAILURE more easily but I'm not planning on letting the pressure increase in any case.

I'm assuming this case is of the acute (or acute on chronic even more likely) version since this pt is on milrinone. But maybe not.
 
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My personal preference for drips is epi + milrinone due to the synergy. Vasopressin I don't believe is as effective in this case. But I haven't tried it either so correct me if I am wrong here.
 

Noyac

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@Noyac, its good to know what your getting into and i agree with OP in his attempts to figure out whats going on before taking a complicated patient in for procedure. I agree 15 minute procedure, in and out usually. The only concern is if something goes wrong and you have knowledge as to underlying cause who classification/chronicity it at least gives you a plan if something goes wrong. You wouldnt treat a chronic phtn case secondary to osa the same as someone with acute rv strain from pe.....that was my whole point. Do your research and avoid unnecessary risks if you don't have too.
Also, could you explain the pulm docs biCarb recommendation?
 
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My personal preference for drips is epi + milrinone due to the synergy. Vasopressin I don't believe is as effective in this case. But I haven't tried it either so correct me if I am wrong here.
Vasopressin sometimes can be used to offset the vasodilatory effect of milrinone, such as to maintain adequate DBP in a struggling RV. Vasopressin doesn't increased PVR as much as epi or norepi in the situation when pHTN is already significant. So epi + milrinone +/- vasopressin.
 
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anbuitachi

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Beyond FiO2 of 1.0 and optimizing ventilation, alkalinization with sodium bicarbonate is the best acute treatment for pulmonary hypertensive crisis. I wouldn't make a big deal of this case--the only clinically significant finding that you're likely to see is faster desaturation w/ apnea. Baseline systemic or suprasystemic pulmonary hypertension, on the other hand, requires more delicate management for cases like this.
so basically its the pH that vasoconstricts the pulmonary vasculature , not CO2.
 

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If all of this isn't just mental masturbation and there is a sincere concern for intraoperative RV failure 2/2 an acute rise in an already elevated PAP, then it's inhaled NO/some iteration of Flolan, a PAC/intra-op TEE and move forward. If not, put up or shut up. I'm with Noyac (I'm sure he's relieved). It is either very complicated or it isn't. Not trying to be glib, but things get stupid very quickly when we tread out into the tall weeds unnecessarily.
 
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Hoya11

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I was talking to an ICU attending about a scheduled case for a young patient with mod-severe pulmonary HTN (RV pressure 1/2 to 2/3 systemic pressure), likely due to OSA currently on ventilator, paralyzed, on high FiO2, w some possible pulm infection (spiking fevers), going for a trach. I said it's a high risk procedure since it's a trach, meaning periods of lower fio2/apnea, causing pHTN to worsen. He told me to give lots of bicarb to make the patient alkalotic. Why would the answer be bicarb in this scenario? Am i dumb or did the attending not know what hes talking about

Also how would you guys manage this case?

The conversation with the ICU doc should teach you that our field is unique and most everyone outside of it has no idea what is going on. Scary actually...

Think about this case: The guy is already stable on a ventilator, despite having pHTN. Take the guy and his vent settings and move them into the OR. Add 1% of sevo and Roc. 100% fio2 when possible and reduce for fire risk if needed. Transport back.

If I HAD to I would run nitroglycerine or Milrinone and cover the drop in BP with epi
 

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Vasopressin sometimes can be used to offset the vasodilatory effect of milrinone, such as to maintain adequate DBP in a struggling RV. Vasopressin doesn't increased PVR as much as epi or norepi in the situation when pHTN is already significant. So epi + milrinone +/- vasopressin.
What?
Epi is the go to drug for severe asthmatic attacks. Think Beta 2.
 
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What?
Epi is the go to drug for severe asthmatic attacks. Think Beta 2.
yes, at lower dose B2 predominates, but at higher dose alpha 1 kicks in. Any increase in PVR with Epi is mild, more significant with NE, and the effect is less when PV tone is already increased. Vasopressin, on the other hand, supposedly doesn't increase PVR. I rarely use it. Only in the situation when RV is dying, Epi is maxed out, Milrinone is going up but also dropping BP, and you need something else to maintain DBP while Milrinone is getting maxed out... as a last ditch effort prior to RVAD.
 

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fine call it mental masturbation but op had a question and I feel all posts have valid points to consider. If something happens at least all this "walking through tall weeds" maybe will lead to a good outcome. Being right or wrong personally doesn't matter, only thing matters to me is a good outcome for a patient. Not trying to ruffle feathers...but if you look at @Noyac recommendations to basically "ignore" what I said which was agreeing that @eggscal99 had some valid points. Everyone here has made solid sound points to think about. That's the purpose of this forum..... questions hopefully getting answered and being able to come to an open forum to learn and grow. Different vantage points whether that be from anesthesia, pulm/cc, cardiology etc are valid. that's my spiel, im out.
 
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hudsontc

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so basically its the pH that vasoconstricts the pulmonary vasculature , not CO2.
The distinction must be made between the elevation of EtCO2 as a result of sodium bicarbonate administration and elevation of CO2 from non-optimal ventilation. The former is a consequence of alkalinization and will be associated with a concomitant increase in pH and lowered pulmonary artery pressures. The latter is obviously the opposite.

To think that the increase in EtCO2 seen with bicarb. administration makes it an undesirable drug in the setting of pulmonary hypertension is exactly incorrect because the actual PaCO2 does not necessarily increase and pH certainly does...assuming ventilation is maintained.

Pulmonary vascular resistance in infants after cardiac surgery: role of carbon dioxide and hydrogen ion. - PubMed - NCBI

The other week I found myself helping with a coding chronic lung disease infant in the PICU with known suprasystemic pulmonary hypertension. He had been given 3 rounds of epinephrine and when I showed up, I asked if any bicarbonate had been given. The looks I got made me realize they thought it an 'out there', 'outdated, 'not in the PALS algorithm' idea. 4mEq/kg bolus resulted in almost immediate return of heart rate, oxygenation and blood pressure. I haven't been in practice that long but I have dealt with my fair share of pulmonary hypertension in the peds cath lab and the cardiac ORs and it works well for rescue or even pushing patients back from the ledge.
 
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The distinction must be made between the elevation of EtCO2 as a result of sodium bicarbonate administration and elevation of CO2 from non-optimal ventilation. The former is a consequence of alkalinization and will be associated with a concomitant increase in pH and lowered pulmonary artery pressures. The later is obviously the opposite.

To think that the increase in EtCO2 seen with bicarb. administration makes it an undesirable drug in the setting of pulmonary hypertension is exactly incorrect because the actual PaCO2 does not necessarily increase and pH certainly does...assuming ventilation is maintained.

Pulmonary vascular resistance in infants after cardiac surgery: role of carbon dioxide and hydrogen ion. - PubMed - NCBI

The other week I found myself helping with a coding chronic lung disease infant in the PICU with known suprasystemic pulmonary hypertension. He had been given 3 rounds of epinephrine and when I showed up, I asked if any bicarbonate had been given. The looks I got made me realize they thought it an 'out there', 'outdated, 'not in the PALS algorithm' idea. 4mEq/kg bolus resulted in almost immediate return of heart rate, oxygenation and blood pressure. I haven't been in practice that long but I have dealt with my fair share of pulmonary hypertension in the peds cath lab and the cardiac ORs and it works well for rescue or even pushing patients back from the ledge.
This is interesting, given the fact that it's well-known that bicarb produces intracellular acidosis, with or without good ventilation. It's probably the extracellular/intravascular alkalosis that matters here (for vasodilatory purposes).
 
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The conversation with the ICU doc should teach you that our field is unique and most everyone outside of it has no idea what is going on. Scary actually...

Think about this case: The guy is already stable on a ventilator, despite having pHTN. Take the guy and his vent settings and move them into the OR. Add 1% of sevo and Roc. 100% fio2 when possible and reduce for fire risk if needed. Transport back.

If I HAD to I would run nitroglycerine or Milrinone and cover the drop in BP with epi
Respectfully, our field is not unique. It's an extension of critical care. We may see more acute situations than intensivists, due to general anesthesia and concomitant surgical insult, but the fields overlap a lot (and that's the reason they are one big specialty in most countries).
 
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this patient does not seem like he is ready for a trach (paralyzed, 100% fio2). I would hope that he has some reversible cause of hypoxia if there is a chance of survival. If the icu team is insisting on a trach they should do it at bedside...takes 5 minutes. Regarding planning for this "case" they are already sedated and paralyzed so give 150 of fentanyl and call it a day.
 
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anbuitachi

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The distinction must be made between the elevation of EtCO2 as a result of sodium bicarbonate administration and elevation of CO2 from non-optimal ventilation. The former is a consequence of alkalinization and will be associated with a concomitant increase in pH and lowered pulmonary artery pressures. The later is obviously the opposite.

To think that the increase in EtCO2 seen with bicarb. administration makes it an undesirable drug in the setting of pulmonary hypertension is exactly incorrect because the actual PaCO2 does not necessarily increase and pH certainly does...assuming ventilation is maintained.

Pulmonary vascular resistance in infants after cardiac surgery: role of carbon dioxide and hydrogen ion. - PubMed - NCBI

The other week I found myself helping with a coding chronic lung disease infant in the PICU with known suprasystemic pulmonary hypertension. He had been given 3 rounds of epinephrine and when I showed up, I asked if any bicarbonate had been given. The looks I got made me realize they thought it an 'out there', 'outdated, 'not in the PALS algorithm' idea. 4mEq/kg bolus resulted in almost immediate return of heart rate, oxygenation and blood pressure. I haven't been in practice that long but I have dealt with my fair share of pulmonary hypertension in the peds cath lab and the cardiac ORs and it works well for rescue or even pushing patients back from the ledge.
Im guessing the kid was being well ventilated when you pushed the bicarb since it was an arrest.
 
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anbuitachi

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This is interesting, given the fact that it's well-known that bicarb produces intracellular acidosis, with or without good ventilation. It's probably the extracellular/intravascular alkalosis that matters here (for vasodilatory purposes).
what is the mechanism of this?
 

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what is the mechanism of this?
AFAIK, the hypothesis is that the CO2 generated in the blood also diffuses into the cells, where it lowers the pH.
 

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The distinction must be made between the elevation of EtCO2 as a result of sodium bicarbonate administration and elevation of CO2 from non-optimal ventilation. The former is a consequence of alkalinization and will be associated with a concomitant increase in pH and lowered pulmonary artery pressures. The later is obviously the opposite.

To think that the increase in EtCO2 seen with bicarb. administration makes it an undesirable drug in the setting of pulmonary hypertension is exactly incorrect because the actual PaCO2 does not necessarily increase and pH certainly does...assuming ventilation is maintained.

Pulmonary vascular resistance in infants after cardiac surgery: role of carbon dioxide and hydrogen ion. - PubMed - NCBI

The other week I found myself helping with a coding chronic lung disease infant in the PICU with known suprasystemic pulmonary hypertension. He had been given 3 rounds of epinephrine and when I showed up, I asked if any bicarbonate had been given. The looks I got made me realize they thought it an 'out there', 'outdated, 'not in the PALS algorithm' idea. 4mEq/kg bolus resulted in almost immediate return of heart rate, oxygenation and blood pressure. I haven't been in practice that long but I have dealt with my fair share of pulmonary hypertension in the peds cath lab and the cardiac ORs and it works well for rescue or even pushing patients back from the ledge.
I have just remembered that bicarb improves blood pressure and circulation through its osmotic load, an effect that used to be mistaken as improving sensitivity to pressors in acidosis. Which makes me wonder: have you ever witnessed PAP improvement from a bicarb bolus in a pHTN patient who actually had a Swan, or is it a different mechanism again?
 
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What's the rationale for the trache at all? At best no evidence of benefit, possible evidence of harm. Trachman and a few others

If this is all from osa then his et tube is already fixing that. If its due to infection then he needs that fixed first...

The bicarb physiology q is interesting
 

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Im guessing the kid was being well ventilated when you pushed the bicarb since it was an arrest.
Intubated and yes, probably overventilated for his CO.
 

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I have just remembered that bicarb improves blood pressure and circulation through its osmotic load, an effect that used to be mistaken as improving sensitivity to pressors in acidosis. Which makes me wonder: have you ever witnessed PAP improvement from a bicarb bolus in a pHTN patient who actually had a Swan, or is it a different mechanism again?
Usually not a swan but a PA cath in cardiac cath lab.

Oddly, I did have a patient awaiting lung transplantation who needed dental extractions and came to me with a Swan. His PA pressures were systemic at baseline and didn't change appreciably with a ketamine induction. A small bolus of bicarbonate did transiently reduce his PA pressures by ~20%. That said, I typically work with cardiac kids...so take that for what it is.
 
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