Alright, in this lesson here we're going to be talking about sodium bicarbonate, commonly referred to as bicarb. So bicarb has a history that's really long-standing history, going back to 1791 when a French chemist actually made the first sodium carbonate. Then kind of fast forward from there, our first use of IV sodium bicarbonate was actually in the 1950s, and today it's now considered one of the essential medications according to the World Health Organization. So bicarb is the most widely used buffering agent for treatment of persistent metabolic acidosis due to a prolonged low flow state, so think hypoperfusion, diabetic ketoacidosis, lactic acidosis, and hyperkalemia.
The use of this medication increases our plasma bicarbonate level and really buffers excess hydrogen ions, so our acid concentration, thus ultimately raising our patient's pH and then reversing the clinical manifestations of acidosis. When we look at this medication as a whole, there's a lot of different uses in which it can be used, medically, non-medically, critical care versus not. So I'm just going to be covering the cases in which we're typically going to be using this in the ICU. So first is going to be metabolic acidosis. It's really important that we want to correct this acidosis for our patients in a lot of cases, and especially when we're using vasopressors, because those are going to be less effective when they're in an acidic environment, especially a very acidic environment, so less than 7.1.
Cardiac arrest is another indication, so be careful though about just administering this blindly during cardiac arrest, because it can actually produce paradoxical acidosis from CO2 production. So we typically want to withhold this at least early on in the code unless acidosis is something that's clearly present for the patient. Another use would be for severe hyperkalemia, so typically if our potassium is greater than six.
And so here this is going to be driving extracellular potassium into the cells, lowering our serum potassium levels. Another use is for diabetic ketoacidosis, but this definitely depends on the facility and the provider. Outcomes are similar to patients though who are treated with or without bicarb, so Whether it's an effective treatment or not definitely remains up for debate. Another potential use that you could hear about it or see it is in a hydration protocol prior to contrast injection.
So again, we've got conflicting evidence here, but there may be some benefit to using bicarb to help to prevent post-contrast nephropathy. And we can also use bicarb in certain drug toxicities. Examples here include aspirin, tricyclic antidepressants, methanol, salicyates, and barbiturate overdoses. Now some contraindications for its use would include patients who have a metabolic or respiratory alkalosis. So if they're already in an alkaline state, we don't want to give them bicarb and push them further that way.
Also patients who have a loss of chloride from either excessive vomiting or excessive continuous GI suction. So here think like your decompression with an OG or an NG. If they've got a significant loss in chloride, this might not be a good choice for them.
And we do want to use it cautiously in people who have renal insufficiency. heart failure, or other edematous sodium retaining conditions. So just some quick adverse effects.
So the first and most obvious one is going to be alkalosis. So obviously we are increasing their pH, which is creating a more alkaline environment for the patient. This can actually cause something we call a left shift in our oxyhemoglobin dissociation curve. This can ultimately compromise the release of oxygen to the tissue.
leading to lactic acidosis, which kind of works against us. And then another adverse effect potentially of this medication is edema. All right, so common concentrations that we can see this.
Typically, we've got an IV push and an IV infusion. IV push is going to be 50 mEq and 50 mL vial. This is typically what's referred to as an amp of bicarb. Then from there, for IV infusions, we can either have it mixed with fluid, so typically like 150 mEq and a liter of fluid.
or we can have a one-to-one bicarbon fusion. So this is 250 mEq and 250 mLs. So this is typically going to be that bicarbon fusion for the sicker patients that we're using.
And then from there, our common dosing. So IV push, typically we're going to be giving 1A, which is that 50 mEq. For IV infusion, this can range anywhere from 0.5 to 1 mEq per kilogram per hour.
For our pharmacokinetics, IV administration is going to be immediate onset, immediate peak, Duration is usually about one to two hours, or again, if we have an infusion for the duration of that infusion. And then our plasma concentration is actually regulated by the kidneys. So we have acidification of the urine if we have a deficit of bicarb.
So we're needing to get rid of the rid of those hydrogen ions out through the urine or through alkalinization of the urine when we have an excess. So the kidneys will release bicarb into the urine, causing a more alkaline urine in order to get rid of that excess bicarb. And then some things for you to consider when you do have a patient that's getting this medication. We want to be avoiding the risk of alkalosis.
So we want to obtain a blood pH, PO2, PCO2, and serum electrolytes. We want to make sure that we're monitoring our relevant lab values. So This could be our potassium, our sodium, our CO2 levels, potentially lactate, again on our ABG, like I talked about the P8, CO2, or bicarb level there. We do want to monitor the patient closely during our IV administration as fluid or solute overload can actually cause the dilution of serum electrolytes, overhydration, and thus heart failure and pulmonary edema. And then also make sure that you guys don't administer this in the same line as calcium as a strong precipitate will form.
And then for our lab studies, this could potentially increase our sodium and lactate levels, so definitely make sure and keep an eye on those. It may actually decrease our potassium levels as that pH increases, so make sure we're monitoring that as well. And then monitor our serum CO2 or on ABG, our bicarb level as well.
And so that was our review of sodium bicarb. Hopefully you guys got some good information from this lesson. So I hope that you guys found this information useful.
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