Sodium Bicarb

Hi guys, just got some questions on Sodium bicarbonate. So I know this is used to treat hyperkalemia and acidosis, but the thing is: you know you're going to get peaked t-waves and widen qrs with hyperkalemia, but how do you know the s/s of acidosis?

Granted a history would help, but is that all you're going on? For sure someone with DKA will have metabolic acidosis and you'll know by hx, BG, and fruity breath, but what about for other things?

Such as the case of Tricyclic antidepressant overdose, or even aspirin. It'll make them acidotic, but are there s/s of acidosis? Because when just going on hx I probably won't be as comfortable as getting more pieces that support your diagnosis.

Also, why don't we give sodium bicarb to shock or cardiac arrest pts. When their body is using anerobic metabolism, it produces lactic acid and makes their body acidic. Wouldn't sodium bicarb be the fix for that?

ParamedicStudent said:

Hi guys, just got some questions on Sodium bicarbonate. So I know this is used to treat hyperkalemia and acidosis, but the thing is: you know you're going to get peaked t-waves and widen qrs with hyperkalemia, but how do you know the s/s of acidosis?

Granted a history would help, but is that all you're going on? For sure someone with DKA will have metabolic acidosis and you'll know by hx, BG, and fruity breath, but what about for other things?

Such as the case of Tricyclic antidepressant overdose, or even aspirin. It'll make them acidotic, but are there s/s of acidosis? Because when just going on hx I probably won't be as comfortable as getting more pieces that support your diagnosis.

Also, why don't we give sodium bicarb to shock or cardiac arrest pts. When their body is using anerobic metabolism, it produces lactic acid and makes their body acidic. Wouldn't sodium bicarb be the fix for that?

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We do give sodium bicarb to arrest patients. I believe it used to be in ACLS algorithms, but it was removed in 2000 and now recommended at "the discretion of the treating physician" after ABG. But in my experience in the hospital, sodium bicarb is pushed after any sizable chunk of code time.

Especially crush injury codes, dialysis patient codes, and overdose codes

We use it as part of our "PEA/asystole bundle", which includes:
Saline bolus
Sodium Bicarb
Calcium Chloride
Narcan
and D50 (if hypoglycemic).

And it is given to TCA overdose patients not to combat acidosis, but to cause alkalosis, which speeds excretion of the drug and reduces its effects.

Sodium Bicarb raises the serum pH, but the effect is transient as it doesn't cure the underlying cause. I can't think of any scenario where giving bicarb is any more than a temporizing measure, in terms of using it to combat acidemia. This is why it is only used in ACLS when you are at the end of your rope and can't think of anything else to do.

It can affect the ionization of certain drugs, which could make them more or less potent, depending on the drug's pka, it's degree of protein binding, and other factors. It can also speed the renal elimination of some substances by raising the pH of the urine. In hyperkalemia it transiently stabilizes the cardiac membrane by reversing the ionic gradient in the conduction system, allowing the Na/K pump to work better.....or something like that

In tricyclic OD, you are giving bicarb primarily for its sodium load, not to reverse acidemia. The tricyclic drug's hemodynamic effects are primarily related to sodium blockade, which results in slowed cardiac conduction and vasodilation. A large enough dose of sodium (and Na Bicarb provides a lot of sodium) will combat that blockade.

The other big issue is hypernatremia (and/or metabolic alkalosis). As I recall, that was the main reason it was abandoned with ACLS protocols. I remember back in the 70's that the first drug we gave in a code (even a witnessed arrest in the ER) was two amps of bicarb "because you can't shock an acidotic heart", and we gave an amp every five minutes. "Hey doc, why is our pH 7.7 and the sodium 170?" We're finally relying on evidence-based medicine and figuring out what works and what doesn't. That is why the emphasis now is on high quality CPR, guided when possible by EtCO2 values to give you some clue of how you're doing, and bicarb ONLY guided by blood gases, and ONLY if the respiratory aberrancies are corrected first. Acidosis corrects pretty quickly on it's own with good CPR or decent ROSC.

There are not many overt signs or symptoms of a metabolic acidosis. Certainly, a patient who is able may have tachypnea to induce a compensatory respiratory alkalosis. However, beyond that the sings or symptoms are somewhat subtle. In severe acidosis you may see myocardial depression or even cardiovascular collapse. Hyperkalemia may be present from a shift of potassium from the intercellular compartment into the plasma.

As others have stated, it is a temporizing measure, not a fix. I personally use it for three reasons:
1. after cardiac surgery, the myocardium is relatively stunned, as you might imagine. These hearts do not tolerate acidosis well and the resulting myocardial depression is unmasked at an earlier point than you would see in a normal heart. There is much debate about whether normalizing the pH helps inotropes and vasopressors work more effectively. My own anecdotal experience is that in an acidotic patient post-op, normalizing the pH allows me to markedly decrease the doses of these drugs.
2. In other critically ill patients, I use it to treat acidosis refractory to other therapies, but only to a point I consider reasonable. So, I feel that we have adequately fluid resuscitated the sepsis patient and the pH is still 7.20 and the bicarb is 13 and I'm on high-dose pressors, I will give a dose of bicarb to attempt some degree of further normalization. I will not drive the bicarb to 24, but I will give a little extra. I have little evidence behind this practice.
3. I will drip bicarb in patients in acute renal failure who are otherwise doing well, just losing bicarb because of the kidney injury. I will usually continue this drip until the patient's native renal function recovers or we initiate dialysis.
4. After a few rounds of ACLS drugs, I will often slip in an amp of bicarb, though I recognize this is likely futile. Completely dogmatic.
5. In a patient with tenuous respiratory status and a recovering metabolic acidosis, I may supplement a low serum bicarb to prevent the patient from having to sustain the increased work of respiratory compensation. Respiratory compensation requires a lot of energy and may force you to intubate when the patient gets tired. If you keep their bicarb in a normal range, you may fend off that intubation. Again, little evidence for this practice as well.

Nova1300 said:

There are not many overt signs or symptoms of a metabolic acidosis. Certainly, a patient who is able may have tachypnea to induce a compensatory respiratory alkalosis. However, beyond that the sings or symptoms are somewhat subtle. In severe acidosis you may see myocardial depression or even cardiovascular collapse. Hyperkalemia may be present from a shift of potassium from the intercellular compartment into the plasma.

As others have stated, it is a temporizing measure, not a fix. I personally use it for three reasons:
1. after cardiac surgery, the myocardium is relatively stunned, as you might imagine. These hearts do not tolerate acidosis well and the resulting myocardial depression is unmasked at an earlier point than you would see in a normal heart. There is much debate about whether normalizing the pH helps inotropes and vasopressors work more effectively. My own anecdotal experience is that in an acidotic patient post-op, normalizing the pH allows me to markedly decrease the doses of these drugs.
2. In other critically ill patients, I use it to treat acidosis refractory to other therapies, but only to a point I consider reasonable. So, I feel that we have adequately fluid resuscitated the sepsis patient and the pH is still 7.20 and the bicarb is 13 and I'm on high-dose pressors, I will give a dose of bicarb to attempt some degree of further normalization. I will not drive the bicarb to 24, but I will give a little extra. I have little evidence behind this practice.
3. I will drip bicarb in patients in acute renal failure who are otherwise doing well, just losing bicarb because of the kidney injury. I will usually continue this drip until the patient's native renal function recovers or we initiate dialysis.
4. After a few rounds of ACLS drugs, I will often slip in an amp of bicarb, though I recognize this is likely futile. Completely dogmatic.
5. In a patient with tenuous respiratory status and a recovering metabolic acidosis, I may supplement a low serum bicarb to prevent the patient from having to sustain the increased work of respiratory compensation. Respiratory compensation requires a lot of energy and may force you to intubate when the patient gets tired. If you keep their bicarb in a normal range, you may fend off that intubation. Again, little evidence for this practice as well.

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@Nova1300, I really, REALLY appreciate your input on this forum. I always learn from your posts.

Remi said:

@Nova1300, I really, REALLY appreciate your input on this forum. I always learn from your posts.

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Good to know somebody gets something out of my ramblings.

I learn a lot from you folks as well.

I have read an article for the use of it in hyponatremia and elevated ICP.

MonkeyArrow said:

We do give sodium bicarb to arrest patients. I believe it used to be in ACLS algorithms, but it was removed in 2000 and now recommended at "the discretion of the treating physician" after ABG. But in my experience in the hospital, sodium bicarb is pushed after any sizable chunk of code time.

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It was in the algorithms. PEA (formerly EMD) was EBAC- epi, bicarb, atropine, calcium for example. Cardiac arrest was epi, bicarb, lidocaine.

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Routine use for cardiac arrest has been a Class III intervention since 2010.

"In some special resuscitation situations, such as preexisting metabolic acidosis, hyperkalemia, or tricyclic antidepressant overdose, bicarbonate can be beneficial (see Part 12: “Cardiac Arrest in Special Situations”). However, routine use of sodium bicarbonate is not recommended for patients in cardiac arrest (Class III, LOE B)."

http://circ.ahajournals.org/content/122/18_suppl_3/S729

For whatever reason sodium bicarbonate is the second most administered cardiac arrest drug in my EMS system (after epinephrine). I'd like to change that.

Tom