Sodium bicarbonate push

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I pushed 3amps of bicarbonate through a midline catheter per doctors orders and about an hour prior to transferring a pt to a different unit. We drew it up in 10ml syringes and did not dilute it. The pt's BP shot up to over 200, but we were able to get it down within minutes. My question is this- after the fact, I've read it should be diluted and given slower. Could I have potentially harmed this pt, and how long after administration would it be clear if she was experiencing adverse effects. I haven't been able to find these answers on online or in my books. This pt was acidotic, on a vent with spontaneous breathing. I'm a new grad and feel lost in these high pressure situations, and don't really know how to manage checking my actions before I perform them when there's really no time to do so, so I end up relying on veterans' advice. I realize this could be very unsafe practice. Our charge nurse is off unit a lot, and I've been told to lean on the veteran resources, but still, if it's my pt it's my butt on the line.

Specializes in Critical Care.
IV push sodium bicarbonate (8.4%, 50 ml, bristojet syringe) is usually indicated in Code Blue situations. It's not directly listed in the ACLS algorithms but is indirectly alluded to when you look for Reversible Causes in the Cardiac Arrest Algorithm. Remember the 5 H's and 5 T's where Hydrogen Ion means Acidosis? that's an indication when you would push IV sodium bicarbonate.

However, I've seen some surgical specialties particularly Adult Cardiac Surgery use IV push sodium bicarbonate in their fresh post-op patients with metabolic acidosis that are not even on the verge of cardiac arrest. Metabolic acidosis affects cardiac function negatively and an acidic medium also makes pressors (except vasopressin) not work well. It does almost instantaneously make hemodynamics better in this subset of patients, hence, the transient rise in BP you saw.

There is a caveat though because sodium bicarbonate as an IV push is actually short acting (8-10 minutes in some literature as far as duration) so I guess it's more of a temporizing measure until the reason for the acidemia is sorted out and corrected. You also can't push the bristojet too fast anyway as it's a 50 ml syringe not unless you are injecting it on to an introducer catheter/Cordis or you have really strong fingers.

In many cases, you could use sodium bicarbonate infusion in patients with metabolic acidosis and the results would be more sustained though you run the risk of contributing to fluid overload in patients who have poor kidney function and dwindling urine output.

I've never heard of sodium bicarb as having what can be described as a "half-life", it's a normally occurring electrolyte, so it's similar to saying potassium or sodium has a "half life". It will go through metabolism and eventual excretion, but it doesn't become inert in a predictable period of time.

Bicarb isn't in the ACLS algorithm. Does that mean the docs who wrote the guidelines don't know what they are doing too?

im not saying we don't give it where I work.

just saying that there is no evidence I have seen that it works.

treating the underlying problem makes more sense to me than "fixing" the pH

Specializes in Critical Care.
Bicarb isn't in the ACLS algorithm. Does that mean the docs who wrote the guidelines don't know what they are doing too?

im not saying we don't give it where I work.

just saying that there is no evidence I have seen that it works.

treating the underlying problem makes more sense to me than "fixing" the pH

It is actually in the ACLS algorithm under the H's and T's to consider; H for Hydrogen ion (acidosis).

Like any electrolyte deficiency, treating the cause of the deficiency is necessary, but often take some time, so while the process of treating the cause is ongoing a more immediate improvement in the deficiency might be necessary to avoid problems it may cause.

Specializes in Critical care.
It is actually in the ACLS algorithm under the H's and T's to consider; H for Hydrogen ion (acidosis).

Like any electrolyte deficiency, treating the cause of the deficiency is necessary, but often take some time, so while the process of treating the cause is ongoing a more immediate improvement in the deficiency might be necessary to avoid problems it may cause.

Precisely. It was de rigueur to give it during prolonged codes. A few cycles ago, it seemed to be totally removed from the algorithm on face value, but one only has to run down the "H's and T's" to see it's still there for correctable causes of asystole. Aside from increasing serum Na+, another big contraindication commonly cited is "rebound acidosis". That is to say, a worry exists that the CO2 produced from metabolizing NaHCO3 actually increases acidosis. This is only true in cases where the pt is hypoventilating. If adequate ventilation is provided/already exists, the pt will readily exhale excess CO2.

Specializes in Family Nurse Practitioner.
I pushed 3amps of bicarbonate through a midline catheter per doctors orders and about an hour prior to transferring a pt to a different unit. We drew it up in 10ml syringes and did not dilute it. The pt's BP shot up to over 200, but we were able to get it down within minutes. My question is this- after the fact, I've read it should be diluted and given slower. Could I have potentially harmed this pt, and how long after administration would it be clear if she was experiencing adverse effects. I haven't been able to find these answers on online or in my books. This pt was acidotic, on a vent with spontaneous breathing. I'm a new grad and feel lost in these high pressure situations, and don't really know how to manage checking my actions before I perform them when there's really no time to do so, so I end up relying on veterans' advice. I realize this could be very unsafe practice. Our charge nurse is off unit a lot, and I've been told to lean on the veteran resources, but still, if it's my pt it's my butt on the line.

Was this patient on pressors? First thought was that the bicarb corrected the acidic environment which made the pressors start working to the max... Normally, pushing bicarb does not have such a huge response in BP right away. It definitelty will help with mottling/cyanosis though pretty quickly.

It has to do with how the bicarb is converted/eliminated. It gets converted to co2 (as I recall) so if you don't actively hyperventilate the patient by bagging them or increasing their set rate you essentially help their acidosis for a short period of time (with the resultant rise in ph and thus BP and then the resultant crashing once again).

So sure..if they are dying go ahead and push some bicarb. But at that point I'd argue you are fighting a losing battle anyway. They probably needed a diluted bicarb drip hours ago.

Also I love that blog/podcast (emcrit) just in case anyway likes FOAMed

I've never heard of sodium bicarb as having what can be described as a "half-life", it's a normally occurring electrolyte, so it's similar to saying potassium or sodium has a "half life". It will go through metabolism and eventual excretion, but it doesn't become inert in a predictable period of time.

It doesn't become inert, it disassociates to sodium and CO2. And that happens as soon as it buffers hydrogen ions. It's why giving a lot of it requires Na+ monitoring and very good ventilation.

Specializes in ACNP-BC, Adult Critical Care, Cardiology.
I've never heard of sodium bicarb as having what can be described as a "half-life", it's a normally occurring electrolyte, so it's similar to saying potassium or sodium has a "half life". It will go through metabolism and eventual excretion, but it doesn't become inert in a predictable period of time.

Sodium Bicarbonate as a compound is not a naturally occurring substance...they exist separately in the body. It's quite simplistic to compare that compound to naturally occuring electrolytes such as potassium and sodium.

Pharmacokinetics

Sodium bicarbonate in water dissociates to provide sodium (Na+) and bicarbonate (HC03-) ions. Sodium is the principal cation of the extracellular fluid. Bicarbonate is a normal constituent of body fluids and the normal plasma level ranges from 24 to 31 mEq/L. Plasma concentration is regulated by the kidney. Bicarbonate anion, at a proper concentration of hydrogen ion (H+), may be converted to carbonic acid (H2CO3), then to its volatile form, carbon dioxide (CO2) excreted by the lung. Normally, a ratio of 1:20 (carbonic acid:bicarbonate) is present in the extracellular fluid. In a healthy adult with normal kidney function, practically all the glomerular filtered bicarbonate ion is reabsorbed; less than 1% is excreted in the urine.

And also as the article I mentioned the sodium helps absolutely nothing for the acidosis

"This is only true in cases where the pt is hypoventilating."

Which is the majority of cases

It has to do with how the bicarb is converted/eliminated. It gets converted to co2 (as I recall) so if you don't actively hyperventilate the patient by bagging them or increasing their set rate you essentially help their acidosis for a short period of time (with the resultant rise in ph and thus BP and then the resultant crashing once again).

So sure..if they are dying go ahead and push some bicarb. But at that point I'd argue you are fighting a losing battle anyway. They probably needed a diluted bicarb drip hours ago.

Also I love that blog/podcast (emcrit) just in case anyway likes FOAMed

You're certainly correct that a patient needs adequate ventilation in order to fully metabolize bicarb and raise their pH. But I believe there are some other mechanisms at work behind that common pattern where bicarb 'saves' a patient briefly only to have them crash again before long.

Specifically, I've read that bicarb can cause a kind of paradoxical intracellular acidosis by creating excess co2 molecules that can easily be absorbed through cell walls rather than being transported out of the body via ventilation. And also that bicarb can cause a worsening of a lactic acidosis because acidemia inhibits anaerobic glycolysis and bicarb's reversal of acidemia without reversing the other driving causes of a patient's lactic acidosis can kick start the production of more lactic acid. There are scant proven benefits of bicarb administration to overall mortality, IIRC.

The take home point is more or less unchanged, as I understand it. There's not much controversy in giving bicarb when the main cause of a patient's acidosis is loss of bicarb (low anion gap acidosis - most often excreted renally or in diarrhea), and this should be fairly routine. But for other kinds of metabolic acidosis, give it when you don't have much of a choice (scary low pH in shock with pressors not working, etc), try to fix the cause of the acidosis, and realize that you're not out of the woods yet despite seeing a few promising signs soon after administration.

Specializes in Critical Care.

Our computers have a clinical pharmacology link on the desktop and accessible via our charting software. I use it all the time to check IV compatibilities. Maybe you have something similar?

Even if it takes an extra sixty seconds, it's better to be safe and sure than being the cause of harm. I learned this the hard way. Although in this instance I've never seen sodium bicarb given as a slow push; I wouldn't worry about it.

Serious question - does anyone push IV meds over the full recommended time? I can't imagine standing around to push Vasotec for example over five minutes every few hours.

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