Should we push Bicarbonate in patients with Acidemia?

Acidemia is a serious condition that leads to hemodynamic repercussions if unattended. Acidemia decreases cardiac output by affecting myocardial contractility and reducing afterload, also causes a relative tachycardia, which decreases the filling time of the ventricle. However, the evidence to give bicarbonate is not that robust. For example, should we give bicarbonate during cardiac arrest? Should we supplement bicarbonate to patients with severe DKA?

To answer these questions I will be summarizing a very well done Podcast reviewing the topic from Pulmcast.

Let’s start by understanding what happens to the body when we inject 1 ampule of Sodium Bicarbonate. 1 pre-filled ampule of Bicarbonate has 50 mEq of Sodium and same amount of Bicarbonate. The tonicity of such is almost seven times the tonicity of plasma. If we think about it, we even transfer patients to ICU when 3% saline is going to be infused, but we are definitely more tolerant to push bicarbonate, leave alone if we decided to push 3 ampules or 4 at a time. Let’s continue with the sodium effect on the body. The sodium level will increase by 2 mEq after injecting 1 ampule, and the effect will be a shift of intracellular fluid that has been roughly quantified by 125 mL. Not only we are increasing the plasma sodium, we are dehydrating the cells by directly injecting sodium Bicarbonate.  What about Bicarbonate itself? The answer depends on the level of acidemia. Under acidosis, the HCO3 will convert to CO2 and H2O generating even more acid! If there is no Acidemia, the kidney will buffer the bicarbonate load by excreting it in the urine.  However, here comes the tricky part that almost no one remembers about pushing Bicarbonate. In order to increase the pH, you need to maintain a constant CO2 level, which means, you need to increase the minute ventilation on the ventilator, otherwise the pH won’t be touched. When giving bicarbonate, Calcium levels decrease and it is recommended to check ionized calcium levels or empirically supplement it.

Now that we know the effects of Sodium Bicarbonate in the body, let’s review when should it be given. We have no question, that in non-anion gap acidosis where the main problem is bicarbonate loss like in renal tubular acidosis, diarrhea, etc. The right answer is to replace bicarbonate. Hyperkalemia is another accepted indication as well as TCA intoxication, overdose with antiarrhythmics that block sodium channels like Flecainide, local anesthetics, Carbamazepines and finally salicylate intoxication. No one will ever question the use of bicarbonate on those groups of patients.   What about DKA? In DKA the problem is acid production in the form of ketones. Giving bicarbonate is almost always the wrong answer, even in the pH is less than 7.0. Let’s think through it: A patient in severe DKA is alive by having Kussmaul’s breathing. They are already at their capacity in terms of minute ventilation. If we give them bicarbonate, they will produce more CO2 that they cannot buffer by breathing more –because they are already at capacity- and the result will be the generation of even more acid; total opposite of what we want. Whenever you’re considering giving bicarbonate to a patient with pure DKA (no mixed acid base disturbance), rather given them another bolus of crystalloids and another bolus of Insulin. Let’s move to the anion-gap metabolic acidosis. Difficult topic. Very scarce literature about it, quite honestly, almost absent. In one hand by giving them bicarbonate acid will increase by action of carbonic anhydrase. In the other hand, by giving bicarbonate we may improve hemodynamics by increasing cardiac contractility and cardiac output. What to do? In general may consider using it if pH < 7.15 and be more restrictive if pH > 7.15. These are not absolutes. These are just some guiding principles. What patient with anion-gap acidosis definitely will benefit from bicarbonate? Those who have both anion and non-anion acidosis and those who have anion gap acidosis AND renal failure as demonstrated in the BICARB-ICU trial. Last, but not least, what about the patient in cardiac arrest? If the arrest is due to hyperkalemia or TCA intoxication, by all means, otherwise the AHA recommends against the use of bicarbonate in cardiac arrest.  Be aware that trials have not demonstrated survival benefit or faster achievement of ROSC by giving bicarbonate. If you still decide to do it –which you can- consider supplementing calcium.

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