NaHCO3 for BP?

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Last night I saw an order I have never seen before and I was hoping someone (Pawpaw John?!), could enlighten me. s/p code pt was very hypotensive - on Levophed @ 80 mcg/min, Dopamine @ 20 mcg/kg/min, Epinephrine @ 1 mcg/min and still kept dropping to SBP 40-50. Doc wrote for NaHCO3 1 amp IVP if SBP drops below 60. I asked and someone said that NaHCO3 can support the pressors by "recruiting more catecholamines"? Pt was also on a HCO3 gtt (3 amps) @ 200 ml/hr. Code ABG showed pH = 6.89, CO2 = 8, pCO2 = 48 and lactate = 42! We got the ABG corrected pretty quickly, but surely those numbers are incompatible with life...he was (obviously) non-responsive and showing strong decorticate posturing! Family wanted everything done so when I left he was on CRRT!

Thanks in advance for your input.

Terri Finney

in sunny NC!

Specializes in ICUs, Tele, etc..

You can google ''Sodium Bicarbonate for Persistent Hypotension with Acidosis" ....Hope that can help

You can google ''Sodium Bicarbonate for Persistent Hypotension with Acidosis" ....Hope that can help

Thanks, will do. Now I remember him saying something about the pressors not working well in too acidic of an environment...guess that makes sense.

Terri

Specializes in CCU/CVU/ICU.
Last night I saw an order I have never seen before and I was hoping someone (Pawpaw John?!), could enlighten me. s/p code pt was very hypotensive - on Levophed @ 80 mcg/min, Dopamine @ 20 mcg/kg/min, Epinephrine @ 1 mcg/min and still kept dropping to SBP 40-50. Doc wrote for NaHCO3 1 amp IVP if SBP drops below 60. I asked and someone said that NaHCO3 can support the pressors by "recruiting more catecholamines"? Pt was also on a HCO3 gtt (3 amps) @ 200 ml/hr. Code ABG showed pH = 6.89, CO2 = 8, pCO2 = 48 and lactate = 42! We got the ABG corrected pretty quickly, but surely those numbers are incompatible with life...he was (obviously) non-responsive and showing strong decorticate posturing! Family wanted everything done so when I left he was on CRRT!

Thanks in advance for your input.

Terri Finney

in sunny NC!

Terri, that patient was a corpse on life support and is surely dead by now. Whoever told you bicarb will 'recruit catecholomines' was wrong. It has nothing to do with bp....rather, in a persitent hypotensive state the patient will become more and more acidotic d/t lactic acidosis. The bicarb will help neutralize the acidosis...and prolong her suffering(in the case you presented). Occaisionally a patient will become hypotensive BECAUSE of acidosis but it's USUALLY the other way around. Nothing to do with catecholomines.

Hey Y'all!!!

Ditto you dinith. The only thing that makes sense to me in this scenario, is that acidosis like 'neutralizes' most meds. The acidosis is (as has been said) from Lactic Acid produced by dying cells. The bicarb 'really' neutralizes the acid and and the code drugs work better. Once upon a time, every 'code' was started with an amp of bicarb for just this reason. Unfortunately, the code drugs don't work so well in an alkaline environment, either. So the AMA reasonably said, go by the ABGs.

Anyhow--Bicarb used in resuscitation is pretty much part of the 'art' of medicine instead of the 'science', unless specifically used to treat ABGs.

Papaw John

Specializes in Critical Care.

NaHCO3 is used for severe acidosis...but with this patient...with a lactate level of 42...he would have benefited with fluid resuscitation to correct the base deficit - possibly improving his acidosis.

Specializes in ICU's, every type.

A very simple explanation (pharmacology aside) is that your pressers don't work well in an acidic environment, at this point with your patient, you only option (last ditch) was to correct the acidosis. In CABG pt's we'll give Bicarb with an acidosis and sometimes see a remarkable rebound blood pressure (can't let the new grafts collapse while your stabalizing the ph). but unless you're able to correct the underlying acidosis, you're just buying time.

Terri, that patient was a corpse on life support and is surely dead by now. Whoever told you bicarb will 'recruit catecholomines' was wrong. It has nothing to do with bp....rather, in a persitent hypotensive state the patient will become more and more acidotic d/t lactic acidosis. The bicarb will help neutralize the acidosis...and prolong her suffering(in the case you presented). Occaisionally a patient will become hypotensive BECAUSE of acidosis but it's USUALLY the other way around. Nothing to do with catecholomines.

Actually, it does have something to do with catecholamines. Severe acidosis, with pH

Specializes in CCU/CVU/ICU.
Actually, it does have something to do with catecholamines. Severe acidosis, with pH

Yeah, other posters have said that. However, the OP asked if bicarb will 'recruit' catecholomines, and the answer is no. And, although pressors may work better if patient is not severly acidotic, they still work. You dont give bicarb to correct a blood pressure or pulse. In fact, have you ever seen someone dramatically improve (respond better to pressors or become normotensive) because of a bicarb bolus or drip? . In a severely acidotic environment, pressors may be less effective, but the 'effect' of acidosis on pressors is minimal...people will respond to them even in the face of ph

Of course, in the face of severe acidosis bicarb will be given in any event...to correct ph...not (primarily) to facilitate pressor effect.

Specializes in CCU/CVU/ICU.
"recruiting more catecholamines"?

Terri Finney

in sunny NC!

OR...i may be misunderstanding the 'recruit catecholamines' statement. I took it to mean that the bicarb will cause a release of endogenous catecholamines.

If, by 'recruit' the person meant 'help the pressors work a little better by reversing the acidosis' then maybe i was blubbering unneccesarily(sp?).

Specializes in ICU, Education.

Actually Dinith88, I HAVE seen patient's bp's drastically improve after bicarb bolus's (albeit it is usually short lived). I am sure others here will atest to this. I have had patients on EPI, LEVO, NEO,well above the max & dumping in fluid that remain severely hypotensive & after the bicarb boluses they actually get a short lived bp. It is the severely acidotic patient that does respond like this. Again, the outcome is always poor and it only goes so far. But, pressors do not work well with severe acidosis, and severe acidosis does cause hypotension.

Specializes in CCU/CVU/ICU.
Actually Dinith88, I HAVE seen patient's bp's drastically improve after bicarb bolus's (albeit it is usually short lived). I am sure others here will atest to this. I have had patients on EPI, LEVO, NEO,well above the max & dumping in fluid that remain severely hypotensive & after the bicarb boluses they actually get a short lived bp. It is the severely acidotic patient that does respond like this. Again, the outcome is always poor and it only goes so far. But, pressors do not work well with severe acidosis, and severe acidosis does cause hypotension.

It's funny, but i happened to be at work while reading this post. So, i grabbed the nearest cardiologist to get his input on the matter. Anyway, his opinion (of course he's only one of gazillions of cardiologists) was that bicarb wont improve a severly acidotic patient's blood pressure...and also that it's not current medical 'thought' that bicarb will potentiate/improve pressor response in these patients. Apparently, in the past, the thought among doctors used to be that by correcting/attempting to correct severe acidosis with bicarb would help to alleviate the hemodynamic compromise 'caused' by the acidosis itself..NOT by potentiating pressors. However, that theory has since been disregarded.

So...i did a quick google looking for info on this business and came on this article/study regarding bicarb effect on hemodynamics in acidotic patients... it's a fairly interesting read if you're interested. A revealing quote at the conclusion of the paper is "the oft-cited rationale for bicarbinate use, that it might ameliorate the hemodynamic depression of metabolic acidemia, has been disproved convincingly".

this study is 14 years old.

http://www.chestjournal.org/cgi/content/full/117/1/260

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