ABG and bicarb

[Monty Python]

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Yesterday I was doing a 10 hour A+P spinal fusion with multi-level hardware.
Pt was a 40 y/o smoker, otherwise generally healthy (except for very impressive osteomyelytic lesions of the vertebral bodies on MRI).

About two hours into the case the crit has drifted down from 30 to 27, and the surgeon warned me he was about to get into more blood loss. I gave two units and ran an ABG for the heck of it. At this point all VS and other parameters were normal.

Came back 7.28 with base excess -10 and HCO3 at 18. My attending happened to pass by and I said I was about to give bicarb using the formula BE x KG x 0.3. She said to give absolutely no bicarb as she didn't want to make the pt hypernatremic.

Of course, a little while later her relief came by and went ballistic because I hadn't given any bicarb.

What would you have done?

 

[Noyac]

Yesterday I was doing a 10 hour A+P spinal fusion with multi-level hardware.
Pt was a 40 y/o smoker, otherwise generally healthy (except for very impressive osteomyelytic lesions of the vertebral bodies on MRI).

About two hours into the case the crit has drifted down from 30 to 27, and the surgeon warned me he was about to get into more blood loss. I gave two units and ran an ABG for the heck of it. At this point all VS and other parameters were normal.

Came back 7.28 with base excess -10 and HCO3 at 18. My attending happened to pass by and I said I was about to give bicarb using the formula BE x KG x 0.3. She said to give absolutely no bicarb as she didn't want to make the pt hypernatremic.

Of course, a little while later her relief came by and went ballistic because I hadn't given any bicarb.

What would you have done?

This happens all the time and the outcomes are usually similar. I'm on the no bicarb fence. Base deficit of -10 can be corrected with volume easily and the PRBC's will suffice. I reserve bicarb for cases were the pressors are not very effective b/c of the acidosis.

 

[Anesthesia1979]

My thoughts.. you probably got behind on your fluids.... time start squeezing in some blood and crystalloid. Check coags as well... FFP if oozing.


Was there a central line? CVP? Pt in Supine position?
EBL? Etc....

 

[urgewrx]

What was you PaCO2?
High PaCO2= ventilate more
Low PaCO2= check volume status, maybe some bicarb

A pH of 7.28 is not that bad. I'll probably not use it unless I was having problems with BP.

 

[proman]

Were you mixing it with 0.9% saline? Adding 2 amp (100 mEq) of sodium bicarb to NS would give an osmolarity of 508 and a huge sodium load. 8.4% sodium bicarb give 2 mmols/ml. That's why bicarb infusions are mixed with D5W or 0.45% saline. I made that mistake on a kidney transplant patient once (on the wards). Her sodium went from high 140s to high 150s in 6 hours, when the nephrologist corrected me.

 

[dhb]

recommended Na intake is < 2,4 gr/ day 1L of NS is 9gr of Na thus everything you give bar G5W is a huge sodium load...

7.28 is not nearly low enough to require treatment with Bicarb imho remember that pH is logarithmic: 7.4 is 40nmol of H+ 7.3 is 50nm and 7.1 80nmol

 

[Planktonmd]

one word: "Volume"

 

[VolatileAgent]

one word: "Volume"

yes. and LR for that volume. problem solved.

 

[militarymd]

recommended Na intake is < 2,4 gr/ day 1L of NS is 9gr of Na thus everything you give bar G5W is a huge sodium load...

7.28 is not nearly low enough to require treatment with Bicarb imho remember that pH is logarithmic: 7.4 is 40nmol of H+ 7.3 is 50nm and 7.1 80nmol

9 grams of Sodium Chloride.

Atomic weight of Na is about 23
Atomic weight of Chloride is about 35...

so only about 40% of the 9 grams is actual Sodium....3.5 grams.

 

[militarymd]

Yesterday I was doing a 10 hour A+P spinal fusion with multi-level hardware.
Pt was a 40 y/o smoker, otherwise generally healthy (except for very impressive osteomyelytic lesions of the vertebral bodies on MRI).

About two hours into the case the crit has drifted down from 30 to 27, and the surgeon warned me he was about to get into more blood loss. I gave two units and ran an ABG for the heck of it. At this point all VS and other parameters were normal.

Came back 7.28 with base excess -10 and HCO3 at 18. My attending happened to pass by and I said I was about to give bicarb using the formula BE x KG x 0.3. She said to give absolutely no bicarb as she didn't want to make the pt hypernatremic.

Of course, a little while later her relief came by and went ballistic because I hadn't given any bicarb.

What would you have done?

Hard to make much of this without an actual measured serum Bicarb and serum lactate.

Sounds like you work with a couple of pretty dogmatic anesthesiologists who obviously know it all and are just out to make your life miserable.

 

[VolatileAgent]

9 grams of Sodium Chloride.

Atomic weight of Na is about 23
Atomic weight of Chloride is about 35...

so only about 40% of the 9 grams is actual Sodium....3.5 grams.

you are correct. and the "recommended" daily na+ load may be 2.4 grams (per U.S. RDA), but this is not realistic. most americans in the average (read that "bad") U.S. diet get probably around 4.5-7 grams of sodium per day, far more than the oft-quoted 3.5 g. if you're well-hydrated and have functioning kidneys you'll be able to rid the excess. (didn't we cover this already?)

and no one needs to quote me the DASH diet findings. i am aware of them. i see plenty of hypertensive patients everyday. we're talking about what happens in the real world, folks. just go park your butt in a wendy's sometime.

 

[militarymd]

you are correct. and the "recommended" daily na+ load is not 2.4 grams anyway, unless you are on a salt restricted diet. most americans in an average U.S. diet get probably around 4.5-7 grams of sodium per day. it's no problem if you're well-hydrated and have functioning kidneys. (didn't we cover this already?)

Yes ...we have covered it....and obviously you still don't get it......ability to handle sodium loads has little to do with amount of water consumed......and having normal kidneys doesn't mean anything.......How many CHF patients have you treated who have normal kidney function? AND they definitly CANNOT have 4 gram per day of sodium intake.

 

[VolatileAgent]

How many CHF patients have you treated who have normal kidney function?

ummm.... none. you can't look at the kidney in isolation in a failure patient.

by definition, their kidneys are perfused inadequately when they're overloaded. if you look at their chem numbers, you may think they have "normal" kidney function. but, they don't. the problem is in the pump. and, if you've got a bad pump, you're not going to keep up with forward flow which is necessary for the kidneys to work properly. dump a ton of salt and fluidin them, and they're going to back up. salt alone won't do a damn thing. problem is, salt acts on the hypothalamus and says "drink" and the patient gets in trouble. heart can't keep up with the forward flow, kidney's are inadequately perfused, and now you got a problem.

if you give a failure patient a bag of potato chips and nothing else, they'll be fine... until they start drinking water.

 

[militarymd]

ummm.... none. you can't look at the kidney in isolation in a failure patient.

by definition, their kidneys are perfused inadequately when they're overloaded. if you look at their chem numbers, you may think they have "normal" kidney function. but, they don't. the problem is in the pump. and, if you've got a bad pump, you're not going to keep up with forward flow which is necessary for the kidneys to work properly. dump a ton of salt and fluidin them, and they're going to back up. salt alone won't do a damn thing. problem is, salt acts on the hypothalamus and says "drink" and the patient gets in trouble. heart can't keep up with the forward flow, kidney's are inadequately perfused, and now you got a problem.

if you give a failure patient a bag of potato chips and nothing else, they'll be fine... until they start drinking water.

typical resident answer........

next time you actually TAKE CARE of a patient with CHF (which I know will be never...because obviously you have NEVER actully taken care of one..putting one to sleep doesn't count)....and have to check their Cardiac output...you will find that their Cardiac Outputs are normal despite low EF's.

Most CHF patients have normal LVF

Oh...and separation from CPB is NOT CHF...that is myocardial failure from being on pump....that is another very typical resident and junior attending misconception.

 

[Monty Python]

My thoughts.. you probably got behind on your fluids.... time start squeezing in some blood and crystalloid. Check coags as well... FFP if oozing.


Was there a central line? CVP? Pt in Supine position?
EBL? Etc....

(Previous: the crit has drifted down from 30 to 27, and the surgeon warned me he was about to get into more blood loss. I gave two units and ran an ABG for the heck of it. At this point all VS and other parameters were normal.

Came back 7.28 with base excess -10 and HCO3 at 18)

Reply: We were still supine, and CVP was in the 3-4 range. EBL was around 500. Urine was brisk and very pale yellow. There was no visible dampening of the arterial line waveform when the bellows cycled.

To answer another inquiry: ETCO2 was low 30s, and PaCO2 was 39.

Thanks for the very interesting electrolyte answers/debates.

 

[EtherMD]

This happens all the time and the outcomes are usually similar. I'm on the no bicarb fence. Base deficit of -10 can be corrected with volume easily and the PRBC's will suffice. I reserve bicarb for cases were the pressors are not very effective b/c of the acidosis.

Agree. Have THOUSANDS of case experience with this situation. No Bicarb needed for this level of base deficit and PH. No data showing any difference in outcome and I prefer to see my correction occur with therapy (fluids, blood, etc.) rather than bicarbonate.

 

[urgewrx]

I wouldn't give bicarb myself, but I have worked with a senior ABA examiner who liked giving it for just about anything. It's just a matter of style. I'll agree with ether, fixing the acidosis without bicarb is more rewarding.
​

 

[urgewrx]

typical resident answer........

I'll have to agree with volatile on this one. The reason CHF pts get renal insufficiency, or CRF, is poor perfusion of the kidney. One week in the ICU will be evidence enough. Yes, in the beginning of Systolic Dysfunction the EF drops, but the heart dilates keeping the Stroke Volume the same, and hence the Cardiac Output. These patients tend not to be symptomatic. Later, the EF keeps dropping and the heart cannot dilate accordingly. These patients will have a low cardiac output and will be symptomatic. These are the patients that are labeled as CHF. Also, there is a thing called Diastolic Dysfunction, where the heart cannot relax enough in diastole to maintain a good Stroke Volume, causing CHF due to low SV/CO. In summary, there is a wide expectrum of ventricular dysfunction. Don't assume they all have good CO.

A Congestive Hert Failure patient cannot have good Left Ventricular Function.

 

[Noyac]

I'll have to agree with volatile on this one. The reason CHF pts get renal insufficiency, or CRF, is poor perfusion of the kidney. One week in the ICU will be evidence enough. Yes, in the beginning of Systolic Dysfunction the EF drops, but the heart dilates keeping the Stroke Volume the same, and hence the Cardiac Output. These patients tend not to be symptomatic. Later, the EF keeps dropping and the heart cannot dilate accordingly. These patients will have a low cardiac output and will be symptomatic. These are the patients that are labeled as CHF. Also, there is a thing called Diastolic Dysfunction, where the heart cannot relax enough in diastole to maintain a good Stroke Volume, causing CHF due to low SV/CO. In summary, there is a wide expectrum of ventricular dysfunction. Don't assume they all have good CO.

A Congestive Hert Failure patient cannot have good Left Ventricular Function.

Oh no, you didn't.😱













Just joking

 

[militarymd]

A Congestive Hert Failure patient cannot have good Left Ventricular Function.

That is just PLAIN WRONG.

Read some of the current literature on the CHF "syndrome".

What you're saying is the state of the art understanding of CHF in the 1970's....when beta blockers were contraindicated in patients of low EFs..

 

[urgewrx]

Militarymd> gotta love how you back up you stance. Find another one to look for the pot of gold under the rainbow.

I already talked about this but maybe another time around will help. A third of the pts in CHF have normal EF (systolic function) but have Diastolic Dysfunction. That's why they are on CHF. LVF includes systole and diastole. If diastole is dysfunctional, how can you claim that "most pt in CHF have normal LVF"? WTF, half the cardiac cycle is dysfunctional. You seem to only care about systole. "Good EF, Good LVF!" Wrong!
Any high school student can grasp this concept: A pt that is symptomatic due to a bad heart (CHF) cannot have a good functioning heart.


​

 

[urgewrx]

Oh no, you didn't.😱

I had to. Cannot let the residents learn wrong concepts.

 

[Monty Python]

.... Also, there is a thing called Diastolic Dysfunction, where the heart cannot relax enough in diastole......

Could you elaborate a little please? What's keeping it in a contracted state? Are the muscle fibers constantly tensed due to whatever reason?

 

[militarymd]

Militarymd> gotta love how you back up you stance. Find another one to look for the pot of gold under the rainbow.​

I already talked about this but maybe another time around will help. A third of the pts in CHF have normal EF (systolic function) but have Diastolic Dysfunction. That's why they are on CHF. LVF includes systole and diastole. If diastole is dysfunctional, how can you claim that "most pt in CHF have normal LVF"? WTF, half the cardiac cycle is dysfunctional. You seem to only care about systole. "Good EF, Good LVF!" Wrong!
Any high school student can grasp this concept: A pt that is symptomatic due to a bad heart (CHF) cannot have a good functioning heart.​

Are you a doctor? Or are you a medical student?

Have you EVER taken care of a CHF patient who gets admitted to the hospital with a volume overload syndrome....I'm not talking about putting someone to sleep...I'm talking about treating them, and making them better, so they can go home.

I'm sorry, but I'm just so tired of this medical student BS that is being spouted like it's gospel.

Pick up a journal (other than A&A or Anesthesiology) .....spend some time OUTSIDE of the OR actually managing patients for god sakes....be a doctor for crying out loud.

 

[Darwin]

diastolic dysfunction can be caused by a number of things, most commonly long standing hypertension. Rather than resulting in an eccentric hypertrophy, it causes concentric hypertrophy. A thickened myocardial wall, often times 14-18mm on posterior wall and septal measurements, and usually have E/A wave form ratio's of <1. On swan or right heart cath the PCWP (and thus LVEDP in absence of valve dysfunction) is elevated because of the "steak like" ventricle and reduced compliance. Other things that cause this are aortic stenosis, and, by definition, hypertrophic cardiomyopathyies (with or without obstruction). These people present with classic CHF symptoms, give the typical "boot shaped" heart on CXR, and have an S4 on auscultation (rather than an S3). Unless decompensated, or concomitant ischemic cardiomyopathy, meth/alcohol cardiomyopathy, etc, they usally have a normal EF% (or increased EF to compensate for reduced filling).

 

[urgewrx]

Are you a doctor? Or are you a medical student?

Have you EVER taken care of a CHF patient who gets admitted to the hospital with a volume overload syndrome....I'm not talking about putting someone to sleep...I'm talking about treating them, and making them better, so they can go home.

I'm sorry, but I'm just so tired of this medical student BS that is being spouted like it's gospel.

Pick up a journal (other than A&A or Anesthesiology) .....spend some time OUTSIDE of the OR actually managing patients for god sakes....be a doctor for crying out loud.

Nothing to bring to the table? I see.
Don't be upset. I didn't mean to make you look like a buffon. Nothing personal.

 

[dhb]

Pick up a journal (other than A&A or Anesthesiology) .....spend some time OUTSIDE of the OR actually managing patients for god sakes....be a doctor for crying out loud.

Hey Mil like others i acknowledge your experience and clinical judgment but you could do with a little more explanation for the lowly residents on the forum. If you come to this forum to educate people (like i think you've said before) then give us more than the "i know it but i'm not telling" type of posts... thanks

 

[aredoubleyou]

Im not all that bright, but in chronic congestive heart failure, I've always understood it as the heart operating at higher end diastolic pressures, thus higher wedge and r atrial pressures, and thus the findings of pulmonary oedema (from high L atrial P) and peripheral oedema, etc (high R sided pressures). Acute treatment is aimed at lowering filling pressures (lasix, nitro, morphine) and not increasing cardiac output - although the mechanism of salt retention is secondary to renal hypoperfusion, with the kidney compensating for what it perceives as hypovolaemia. A major focus of chronic treatment is aimed at interupting salt retention (diet, lasix, ACEi). If this cycle spirals out of control, the heart operates at even higher pressures, causing its systemic manefestations as well as worsening renal hypoperfusion causing worsening fluid retention.

 

[Planktonmd]

Im not all that bright, but in chronic congestive heart failure, I've always understood it as the heart operating at higher end diastolic pressures, thus higher wedge and r atrial pressures, and thus the findings of pulmonary oedema (from high L atrial P) and peripheral oedema, etc (high R sided pressures). Acute treatment is aimed at lowering filling pressures (lasix, nitro, morphine) and not increasing cardiac output - although the mechanism of salt retention is secondary to renal hypoperfusion, with the kidney compensating for what it perceives as hypovolaemia. A major focus of chronic treatment is aimed at interupting salt retention (diet, lasix, ACEi). If this cycle spirals out of control, the heart operates at even higher pressures, causing its systemic manefestations as well as worsening renal hypoperfusion causing worsening fluid retention.

Correct!
We just need to remember that CHF is a clinical diagnosis based on symptoms and signs not based on pressure measurments or Echographic findings.

 

[SoroptomistMini]

You guys are on fire! I can't get enough of these heart vs. kidneys misconceptions. There seems to be a strong correlation between quality of grammar and physiological understanding on the posts above. And for the resident who didn't get the blood gas - just use the internet to interpret them for you in future! There's a foolproof analyser here: http://www.altitude.org/calculators/ABGcalculator.htm

 

[Planktonmd]

Yesterday I was doing a 10 hour A+P spinal fusion with multi-level hardware.
Pt was a 40 y/o smoker, otherwise generally healthy (except for very impressive osteomyelytic lesions of the vertebral bodies on MRI).

About two hours into the case the crit has drifted down from 30 to 27, and the surgeon warned me he was about to get into more blood loss. I gave two units and ran an ABG for the heck of it. At this point all VS and other parameters were normal.

Came back 7.28 with base excess -10 and HCO3 at 18. My attending happened to pass by and I said I was about to give bicarb using the formula BE x KG x 0.3. She said to give absolutely no bicarb as she didn't want to make the pt hypernatremic.

Of course, a little while later her relief came by and went ballistic because I hadn't given any bicarb.

What would you have done?

Why do you want to give bicarb?
and what would happen if you don't?

 

[Planktonmd]

Oh, I didn't realize that this was an old discussion, but why not we can revisit it.

 

[Strength&Speed]

9 grams of Sodium Chloride.

Atomic weight of Na is about 23
Atomic weight of Chloride is about 35...

so only about 40% of the 9 grams is actual Sodium....3.5 grams.

thanks. something looked fishy about that

 

[Strength&Speed]

Yes ...we have covered it....and obviously you still don't get it......ability to handle sodium loads has little to do with amount of water consumed......and having normal kidneys doesn't mean anything.......How many CHF patients have you treated who have normal kidney function? AND they definitly CANNOT have 4 gram per day of sodium intake.[/QUOTE]

I dont agree with this statement. First of all, there is a huge range of CHF patients, ranging from mild to serious. I can tell you for the number of buckets of chicken consumed relative to hospital admits, there are quite a few CHF patients who can tolerate 4 grams per day of sodium or more, especially if they are on their meds. I don't recommend it, but to say they definitely cannot have 4 grams per day is a little overstating the case.

 

[Strength&Speed]

Could you elaborate a little please? What's keeping it in a contracted state? Are the muscle fibers constantly tensed due to whatever reason?

you get left ventricular hypertrophy leading to difficulty of the heart "relaxing" in diastole...thus impairing diastolic filling. Yes, the muscle overgrowth distorts the normal shape of the left ventricle, leading to the problems.

However, the muscular overgrowth leads to an excellent or normal ejection fraction. It's really somewhat similar to restrictive lung diseases. Low TLC but good fev1.

 

[militarymd]

What happened to my friend VolatileAgent?

 

[Gern Blansten]

What happened to my friend VolatileAgent?

He evaporated??😕

 

[Planktonmd]

He evaporated??😕

 

[pgg]

What happened to my friend VolatileAgent?

He got a job?

 

[cchoukal]

you get left ventricular hypertrophy leading to difficulty of the heart "relaxing" in diastole...thus impairing diastolic filling. Yes, the muscle overgrowth distorts the normal shape of the left ventricle, leading to the problems.

However, the muscular overgrowth leads to an excellent or normal ejection fraction. It's really somewhat similar to restrictive lung diseases. Low TLC but good fev1.

and add in some neurohumoral changes that lead to restructuring of the sarcomere! And although they have a high EF, the actual stroke volume is low. This is one of those instances where the LVEDP is a poor proxy for LVEDV and the starling curve shifts left.

 

[nutmegs]

and add in some neurohumoral changes that lead to restructuring of the sarcomere! And although they have a high EF, the actual stroke volume is low. This is one of those instances where the LVEDP is a poor proxy for LVEDV and the starling curve shifts left.

the real question is, have you ever seen an echo report of a patient over fiddy that DIDN'T include "EDLVD"?

 

[urge]

Wow. I was on fire back then. I have mellowed out over 1 yr. GUS FRABA, GUS FRABA......

Sorry guys.

 

[Tenesma]

i think the original issue with this post is that

1) you don't transfuse a 40 year old for a hematocrit of 27

2) you don't check an ABG on a 40 year old 2 hours into the case just for the heck of it...

3) and once you do check an ABG don't rely on crap like base excess/deficit(which is a distorted calculation anyways)... just look at your PH and your PCO2 - the whole story is right there...

4) i would NOT use bicarbonate - there are other simpler ways to make those numbers look better

5) this argument about CHF/Renal Function/LV fxn is hilarious - i was saddened that it ended abruptly...

 

[Strength&Speed]

i think the original issue with this post is that

1) you don't transfuse a 40 year old for a hematocrit of 27

2) you don't check an ABG on a 40 year old 2 hours into the case just for the heck of it...

3) and once you do check an ABG don't rely on crap like base excess/deficit(which is a distorted calculation anyways)... just look at your PH and your PCO2 - the whole story is right there...

4) i would NOT use bicarbonate - there are other simpler ways to make those numbers look better

5) this argument about CHF/Renal Function/LV fxn is hilarious - i was saddened that it ended abruptly...

Can't disagree with any of that, but you can't leave us hanging on #5. Toss us a bone here

 

[militarymd]

i think the original issue with this post is that

1) you don't transfuse a 40 year old for a hematocrit of 27

2) you don't check an ABG on a 40 year old 2 hours into the case just for the heck of it...

3) and once you do check an ABG don't rely on crap like base excess/deficit(which is a distorted calculation anyways)... just look at your PH and your PCO2 - the whole story is right there...

4) i would NOT use bicarbonate - there are other simpler ways to make those numbers look better

5) this argument about CHF/Renal Function/LV fxn is hilarious - i was saddened that it ended abruptly...

I transfuse 40 year olds with a hct of 27 who is about to undergo additional significant blood loss..you don't have to.

I will check labs (not just ABGs) 2 hours into cases that are major and invasive...it's called monitoring....you don't have to.

The pH and pCO2 yields some of the story....but without knowing the anion gap....serum lactate...and other parameters of perfusion...you really are flying with only one eye open....but you can do that if you want.

Although I wouldn't use Bicarb....it IS the simplest way to make an ABG "look better".

And finally....there is nothing funny about posting on the internet......people kill themselves over them

 

[jetproppilot]

Wow. I was on fire back then. I have mellowed out over 1 yr. GUS FRABA, GUS FRABA......

Sorry guys.

I think you mean SORRY, MIL.😀

 

[Leverage]

Sodium Birabonate has a pka of 6.1. With a pH of 7.2 Sodium bicarbonate is a worthless buffer. Check out its titration curve. For it to be of any use as a buffer your patient's pH has them pretty much seeing the light. I also think the typical nabicarb solution has a PCO2 load which the lungs have to end up blowing off anyhow. I never really understand why folks like this stuff anyhow. Like others have mentioned treat the cause of the ABG disturbance (volume in this case) not the ABG. If anything the slight acidosis increases catecholomaines which may increase CO and buy you some time while you get your volume in.

 

[militarymd]

Sodium Birabonate has a pka of 6.1. With a pH of 7.2 Sodium bicarbonate is a worthless buffer. Check out its titration curve. For it to be of any use as a buffer your patient's pH has them pretty much seeing the light. I also think the typical nabicarb solution has a PCO2 load which the lungs have to end up blowing off anyhow. I never really understand why folks like this stuff anyhow. Like others have mentioned treat the cause of the ABG disturbance (volume in this case) not the ABG. If anything the slight acidosis increases catecholomaines which may increase CO and buy you some time while you get your volume in.

then why do we use it in ARDS when the lungs can't blow off CO2

 

[Leverage]

then why do we use it in ARDS when the lungs can't blow off CO2

Probably to make us feel better. Only thing that really affects mortality is keeping the Pplat less than 30, which requires some permissive hypercapnia anyhow secondary to the low TV, thus a little extra PaCO2 load wont hurt, right? I think it may be in some NIH protocol for really low pHs but I think increaseing the RR is the first thing you do if you have a low pH.

At what pH threashold to you decide to treat the acidosis with Na Birab? If it isn't less than 7.1 you really are not really treating it anyhow with a pka of 6.1. I guess I am wondering a what level of acidemia do you feel hydrogen Ions are causing organ dysfuction if CaO2 is adequeate (ie no evidence of dysoxia)???

 

[jetproppilot]

I'm asking since I don't know the answer.

Great thread started by TRINITY on acid-base balance and potential sequelae.

We all know that the inotropes/vasopressors we use in critical situations are less efficacious when patient's pH is awry.

So lets say you're knee-deep-in-s hit with a hemodynamically unstable patient for whatever reason.

Got epi running at fifty mikes a minute (or whatever appropriate inotrope/vasopressor) just to maintain a systolic pressure of eighty.

ABG comes back like the ABG on Trins post....say with a BD of -10 to -15.

So my question is:

Volume problems take time to correct. Maybe 20-30 minutes to catch up. Would acute treatment with NaHCO3 make the drugs being used to keep parameters acceptable more effective until clinician can catch up volume wise? Or catch up with whatever physiologic insult has occurred if it isnt volume?

In other words, if your patient's hemodynamics are dependent on some inotrope/vasopressor you've initiated, is immediate correction of pH abnormality with bicarb a wise choice since its gonna take time to correct the underlying problem?

Is there any literature out there addressing this?