Bicarb question

46Young

Level 25 EMS Wizard
Messages
3,063
Reaction score
90
Points
48
Fairfax County FRD asystole, PEA, and V-fib/pulseless V-tach protocols alike, at the end of their algorithms, state: If pt has known pre-existent metabolic acidosis, hyperkalemia (dialysis pt), or tricyclic antidepressant overdose, administer Sodium Bicarbonate (8.4%) 50mEq IV.

My question is involving pre-existent metabolic acidosis. In NYC the common rule of thumb I was taught was to push it after 20 mins of down time and after the algorithm(it was an OLMC option). Would anyone with in hospital experience of RN/RT or higher be able to give a rough estimate of how long a pt would need to be down before bicarb would be indicated? This would assume a witnessed arrest with timely BLS/ALS interventions. I do realize that every pt is different and there are many, many factors that influence this.

I'm thinking that there may be those with extensive experience working codes that may have made some correlations between ABG's and certain pt presentations.
 
My question would be, wouldn't the body be getting more acidic anyhow, even with "decent" CPR being done? If so, eventually the body wouldn't be able to function with the acidity, which is when the Bicarb would come in to play... but wouldn't you want to push it sooner rather then later? Isn't 20 minutes pushing the envelope?
 
We carry Calcium chloride for known or suspected hyperkalemia. I'm assuming excess potassium would bond more readily with cl2 than HCO3, actually changing the electrolyte balance rather than simply treating the pH issues in these patients.

I've worked codes where once we've made it through three rounds of drugs with no return in pulses bicarb has been pushed anyway, regardless of downtime. I suppose that's the "might as well try it anyway" mentality.

I'm sort of going on a limb here, but don't you give bicarb before arrest in a tricyclic overdose with widening QRS?

I'd also be interested to know how quickly the cardiac arrest patient becomes acidotic.
 
Last edited by a moderator:
I don't know of too many places where bicarb for TCA OD is a standing order, but if you contacted your on-line medical control, gave them that scenario and asked for a bicarb push, you would probably get an order for it. I'm sure the same could go for glucagon for a beta blocker OD, although it takes much more glucagon than 1 rig usually carries to counteract a BB OD.
 
I don't know of too many places where bicarb for TCA OD is a standing order, but if you contacted your on-line medical control, gave them that scenario and asked for a bicarb push, you would probably get an order for it.

Outside of Maryland (circa 2003) and apparently upstate New York, I've never seen it be a call-in. Calling in to get permission on a drug during a cardiac arrest is a waste of time and a sign that the protocols were not well thought out. We could give it as a standing order as EMT-Intermediates in that circumstance. Then again, we had maybe three skills/medications that required physician approval because our medical director trusted us and was actively involved in protocol development versus simply rubber stamping something from the state.
 
It is rare that we push bicarb even with documented acidosis. Of course that would also depend whether it is gap or nongap. Often we can turn around a patient once ROSC is achieved by fluids, pressor and ventilation to where the bicarb will not be needed. If the code is very lengthy, some ABGs surprise use by presenting with very little acidosis depending on the quality of the CPR and the patient's pre-existing conditions which may have made the patient acidotic before the code. Those that linger waiting for death and then have 911 called will have a greater chance of being metabolically acidotic. The COPD patient may have a respiratory acidosis with a profoundly low pH but that would not be one I would consider bicarb if it is a respiratory issue. The patient with N/V/D may or may not present with a gap acidosis.

So it is difficult to make a blanket statement.
 
be able to give a rough estimate of how long a pt would need to be down before bicarb would be indicated? This would assume a witnessed arrest with timely BLS/ALS interventions. I do realize that every pt is different and there are many, many factors that influence this.

It's going to rely on so many factors that I will not make a hard and fast statement since I know of no research addressing this specifically (at least not off the top of my head). The quality of the CPR, the patient's body temperature, the amount of ventilation, the drugs administered (?), and most importantly perhaps the patient's metabolic status before the arrest may all be factors that will effect the rate at which pH and other blood gas values are altered post-arrest. That said, if I know or strongly suspect someone was likely to be acidotic prior to arrest (sepsis, hyperthermia, diabetic ketoacidosis, etc) I will push sodium bicarbonate sooner rather than later in an arrest. Other than that, I only really would give it if I suspect hyperkalemia or TCA overdose. It really does not seem to have a place in your standard prolonged arrest unless you have ABG results to guide the administration. Now does that mean I won't occasionally give it at the end of an otherwise unsuccessful code just to see if it does anything? No, but at the same time, by the time you get to that point in a code, you are likely just reviving a potential organ or tissue donor anyhow.
 
My question would be, wouldn't the body be getting more acidic anyhow, even with "decent" CPR being done? If so, eventually the body wouldn't be able to function with the acidity, which is when the Bicarb would come in to play... but wouldn't you want to push it sooner rather then later? Isn't 20 minutes pushing the envelope?

Yes, what I'm asking is HOW soon? In NY it would take about 15- 20 mins form arrival to perform ALS interventions into play, call the doc in the box for orders(takes some time), and push the bicarb. That's probably where the 20 min rule of thumb came from.
 
We carry Calcium chloride for known or suspected hyperkalemia. I'm assuming excess potassium would bond more readily with cl2 than HCO3, actually changing the electrolyte balance rather than simply treating the pH issues in these patients.

I've worked codes where once we've made it through three rounds of drugs with no return in pulses bicarb has been pushed anyway, regardless of downtime. I suppose that's the "might as well try it anyway" mentality.

I'm sort of going on a limb here, but don't you give bicarb before arrest in a tricyclic overdose with widening QRS?

I'd also be interested to know how quickly the cardiac arrest patient becomes acidotic.

Yes, we carry calcium chloride for hyperK. We have glucagon, dopa, TCP, and OLMD CaCl for beta blocker/calcium channel blocker OD. We have CaCl for a mag OD, benadryl for dystonic reactions, and bicarb for TCO.
 
I don't know of too many places where bicarb for TCA OD is a standing order, but if you contacted your on-line medical control, gave them that scenario and asked for a bicarb push, you would probably get an order for it. I'm sure the same could go for glucagon for a beta blocker OD, although it takes much more glucagon than 1 rig usually carries to counteract a BB OD.

We have a standing odrers for 3 mg IV glucagon for a beta blocker OD followed by dopa 200/250Ns 60gtt 10mcg/kg/min, if hypotension/bradycardia refractory TCP, then CaCl 10% 10 ml IV over 10 minswith one repeat, both with OLMD.

This is assuming the pt is unstable. I'm not one that gets his kicks by emptying my drug box just because I can get away with it.

Bicarb for TCO OD is standing order after two 500ml boluses of NS.
 
It is rare that we push bicarb even with documented acidosis. Of course that would also depend whether it is gap or nongap. Often we can turn around a patient once ROSC is achieved by fluids, pressor and ventilation to where the bicarb will not be needed. If the code is very lengthy, some ABGs surprise use by presenting with very little acidosis depending on the quality of the CPR and the patient's pre-existing conditions which may have made the patient acidotic before the code. Those that linger waiting for death and then have 911 called will have a greater chance of being metabolically acidotic. The COPD patient may have a respiratory acidosis with a profoundly low pH but that would not be one I would consider bicarb if it is a respiratory issue. The patient with N/V/D may or may not present with a gap acidosis.

So it is difficult to make a blanket statement.

Thanks for the response. Bicarb is often arbitrary, given as part of the algorithm "just because". I'm trying to delve deeper. I don't like emptying my drug box just because the cookbook says so. Yes, I would be especially hesitant if it is a suspected respiratory issue.
 
It's going to rely on so many factors that I will not make a hard and fast statement since I know of no research addressing this specifically (at least not off the top of my head). The quality of the CPR, the patient's body temperature, the amount of ventilation, the drugs administered (?), and most importantly perhaps the patient's metabolic status before the arrest may all be factors that will effect the rate at which pH and other blood gas values are altered post-arrest. That said, if I know or strongly suspect someone was likely to be acidotic prior to arrest (sepsis, hyperthermia, diabetic ketoacidosis, etc) I will push sodium bicarbonate sooner rather than later in an arrest. Other than that, I only really would give it if I suspect hyperkalemia or TCA overdose. It really does not seem to have a place in your standard prolonged arrest unless you have ABG results to guide the administration. Now does that mean I won't occasionally give it at the end of an otherwise unsuccessful code just to see if it does anything? No, but at the same time, by the time you get to that point in a code, you are likely just reviving a potential organ or tissue donor anyhow.

That sounds about right. Also, all meds authorized for an arrest are standing orders.
 
Last edited by a moderator:
It's going to rely on so many factors that I will not make a hard and fast statement since I know of no research addressing this specifically (at least not off the top of my head). The quality of the CPR, the patient's body temperature, the amount of ventilation, the drugs administered (?), and most importantly perhaps the patient's metabolic status before the arrest may all be factors that will effect the rate at which pH and other blood gas values are altered post-arrest. That said, if I know or strongly suspect someone was likely to be acidotic prior to arrest (sepsis, hyperthermia, diabetic ketoacidosis, etc) I will push sodium bicarbonate sooner rather than later in an arrest. Other than that, I only really would give it if I suspect hyperkalemia or TCA overdose. It really does not seem to have a place in your standard prolonged arrest unless you have ABG results to guide the administration. Now does that mean I won't occasionally give it at the end of an otherwise unsuccessful code just to see if it does anything? No, but at the same time, by the time you get to that point in a code, you are likely just reviving a potential organ or tissue donor anyhow.

This, basically. Whether it was witnessed or not, plus the quality of CPR PTA will also determine how long I wait to push it.

Capnography can also be helpful, but it's not a determining factor of whether I give bi-carb or not. The CO2 reading can help you determine if the persons metabolism is still working at all, and roughly how well.
 
I don't know of too many places where bicarb for TCA OD is a standing order, but if you contacted your on-line medical control, gave them that scenario and asked for a bicarb push, you would probably get an order for it. I'm sure the same could go for glucagon for a beta blocker OD, although it takes much more glucagon than 1 rig usually carries to counteract a BB OD.

Here in NM we have standing orders for both of the ODs you've listed. For TCA we have to call in for orders for more than 1 round of bicarb though
 
In cardiac arrest Sodium Bic is recommended by our guidelines "after 15 minutes of ambulance personnel CPR" and earlier at the medics discretion for suspected TCA overdose.
 
As far as OP like everyone has said we usually will throw it in there around the 20min mark. As far as other use, if the pt is on a pressor gtt I have seen pressors work more effectively (needing lower doses) after Na Bicarb.
 
It is rare that we push bicarb even with documented acidosis. Of course that would also depend whether it is gap or nongap. Often we can turn around a patient once ROSC is achieved by fluids, pressor and ventilation to where the bicarb will not be needed. If the code is very lengthy, some ABGs surprise use by presenting with very little acidosis depending on the quality of the CPR and the patient's pre-existing conditions which may have made the patient acidotic before the code. Those that linger waiting for death and then have 911 called will have a greater chance of being metabolically acidotic. The COPD patient may have a respiratory acidosis with a profoundly low pH but that would not be one I would consider bicarb if it is a respiratory issue. The patient with N/V/D may or may not present with a gap acidosis.

So it is difficult to make a blanket statement.

Yes, sometimes the lactic acid dump off after ROSC can drop one's bicarb pretty low. Which is why most places wait for ABG's to determine whether or not to give NaHCO3.
 
Yes, sometimes the lactic acid dump off after ROSC can drop one's bicarb pretty low. Which is why most places wait for ABG's to determine whether or not to give NaHCO3.

Good article and the references at the end of it are also worth reading.
Sodium Bicarbonate for the Treatment of Lactic Acidosis

CHEST January 2000 vol. 117 no. 1 260-267
http://www.chestjournal.org/content/117/1/260.full

First, bicarbonate is not one of the independent determinants of the blood pH. Rather, these include the difference between the total concentrations of strong cations and anions (the strong ion difference, [SID]); the total concentration of weak acids; and the Paco2.44
Second, bicarbonate administration may engender metabolic reactions that may themselves alter (SID), the total concentration of weak acids, or Paco2. For example, in animals and humans, bicarbonate infusion can augment the production of lactic acid, a strong anion.454647484950 Mechanisms to explain this remain speculative, but include a shift in the oxyhemoglobin-saturation relationship51; enhanced anaerobic glycolysis, perhaps mediated by the pH-sensitive, rate-limiting enzyme phosphofructokinase; and changes in hepatic blood flow or lactate uptake.52
 
It does seem though that nobody really knows what the best practice is regarding pre-hospital sodium bic. I had a bit of a peruse through some old articles and it was all a bit inconclusive and theoretical.

This cochrane lit search also states that their isn't really alot out there as far as prehospital research goes (as of 2004).

http://www.jephc.com/full_article.cfm?content_id=195

Interesting article VENT, and an interesting conclusion.
 
Last edited by a moderator:
Back
Top