Stop Giving Amps of Bicarb!

Chapter 1: What dafuq is in an amp of bicarb?

Take a look!

• 50mL

• 8.4% NaHCO3 -> 50mEq

• The osmolarity of this solution is 2,000mOsm/L - twice that of 3% saline. < (click for emcrit)

Chapter 2: Sodium bicarbonate doesn't just magically raise pH...

Remember this thing?

CO2 + H20 <=> H2CO3 <=> HCO3 + H

It's complicated. Bicarb binds to acid. Then it turns to CO2 and water, so you can breathe it out.

Basically if you're giving bicarb, you can only raise your pH as long as you can breathe off your CO2, increasing your RATE or VOLUME.

**This is particularly a problem in patients who are not in control of their breathing (vented), aren't breathing (arrest), or who have maximized the efficiency of their breathing (Kussmal breathing in DKA).**

That's right - you need to increase your minute ventilation to have a change in pH.

Here's Weingart's take.

Chapter 3: Sodium bicarb amps can cause harm!

FIRST:

One amp of bicarb is like giving 100cc of 3% hypertonic saline!! But as Josh Farkas points out, we typically have no hesitation giving "a couple of amps of bicarb."
This is a huge osmotic load which can lead to huge fluid shifts - prepare for that amp to increase intravascular fluid by 1/4 liter with every push. (Is this what you want to give to your renal failure pt? Your heart failure pt?)

SECOND:

You are worsening acidosis.
What? Huh? But I thought...
No. Stop. Shush. You're worsening acidosis.

Remember, you're increasing CO2 - whether you can breathe it off or not, this CO2 rises in but blood BUT ALSO rises in the tissues and may worsen acidosis in these tissues. < (click for litfl.com article)

THIRD:

Be ready to cause hypernatremia - expect a rise of 1mEq Na per amp of bicarb.

FOURTH:

Extravasation can cause tissue necrosis.

FIFTH:

CSF acidosis, hypocalcemia. Increased lactate. (Some may argue that's not a bad thing.)

If you do manage to fix the acidosis, you can overshoot and create an alkalosis and even screw up the oxygen dissociation curve (in a bad way).

Chapter 4: It just doesn't f&$%ing work
Cardiac arrest: it doesn't do anything. No increased survival. and AHA says it should not be given routinely.

Lactic acidosis: There's a whole section on UpToDate - there's minimal research for pH < 7.1 so you can consider it at that point... but otherwise, nah.

DKA: Take it from a nephrologist: In ketoacidosis, it is almost never necessary to give bicarbonate even though the patient is bicarbonate deficient unless renal function is permanently impaired. Therapy with fluids and electrolytes restores extracellular volume and renal blood flow, thus enhancing the renal excretion of acid and regenerating bicarbonate.

Hyperkalemia: Amps of bicarb, even in hyperK emergencies, have not been shown to lower potassium. Click that UpToDate link or listen to Scott Weingart talk about it on EMRAP.
Patients with hyperK should be started on isotonic bicarbonate drips for 4-6hours, a treatment that works better in acidotic patients.

CHAPTER 5: Soooo who gets bicarb?
AMPS:

• Bicarb ampules in sodium channel blockade (like TCAs) are, as Dr. Bogoch said yesterday, the cornerstone of therapy

• Bicarb ampules may be appropriate to alkalinize urine in certain toxicities

• Seizing hyponatremic patients

DRIPS:

• Appropriate in hyperK patients who can handle fluid

• Appropriate in patients with AKI and pH < 7.2 (BICAR-ICU Trial)

• May be appropriate for pH < 7.0 or 7.1, depending on who you talk to...

**If the pH is < 7.1 and you wanna give an amp of bicarb, there isn't enough data to say you're wrong. If it's a last-ditch effort, you might as well.

https://www.uptodate.com/contents/bicarbonate-therapy-in-lactic-acidosis?search=sodium%20bicarbonate&source=search_result&selectedTitle=3~148&usage_type=default&display_rank=2

Other references embedded in text.

EMS Protocol of the Week - Excited Delirium

This week’s protocol was requested from one of our residents following the recent surge in coverage of Elijah McClain’s 2019 death and the associated controversy around the use of ketamine as a sedation agent. Protocol 530, Excited Delirium, discusses more than just ketamine administration, and I’d like to use this space to discuss the protocol overall without making this a ketamine-specific email. That being said, this is the only one out of all the NYC REMAC protocols to even mention ketamine, so I’ll touch on it a bit here, and hopefully we can use this to kick off a conversation about our own perspectives and experiences with administering ketamine, whether in-hospital or out-of-hospital. First thing to note about this protocol is that it is not a protocol for anxiety, nor is it for simple agitation. This is not supposed to be the go-to for the little granny with dementia who’s shouting expletives at passerby. Excited delirium is intended to encapsulate the belligerent, aggressive, potentially violent patient, for a couple of key reasons. For one, same as in the ED, you want to be able to quickly intervene on patients that pose an acute threat to themselves and/or first responders. Further than that, depending on etiology, you want to be able to quickly control the patient that is truly hypermetabolic, preferably without prolonged physical restraint, in order to prevent worsening hyperthermia or acidosis, either of which can be rapidly lethal if unmitigated. Protocol 530 starts with reference to BLS procedures, which put a large emphasis on rapidly ensuring scene safety, both by attempting verbal de-escalation but also having a low threshold for requesting assistance from law enforcement. For the ALS component, note that the default Standing Order for continued patient resistance is 10mg of IM midazolam. Not “up to,” not a weight-based calculation, just a flat 10mg dose. A quick note about that. The reasoning is, broadly, to quickly control the potential threat to first responders with the lowest potential for needlestick injuries in the process (whether from placing an IV or from attempting multiple IM injections). Yes, there is controversy about this dosing strategy. Ideally, if ALS has a 30kg geriatric in true excited delirium requiring medication, the paramedic will be cognizant enough to call OLMC for a Discretionary Order for a lower dose. What I can tell you is that during my time with FDNY, we looked at data surrounding administering 10mg midazolam IM for excited delirium in NYC and found it to be relatively safe, with the most common complication being hypotension that was responsive to IV fluids (the next SO in the protocol). If adequate sedation is achieved with the SO midazolam, great, EMS will package the patient and transport. If that dose somehow isn’t enough, expect an OLMC call for one of the MCO’s listed in the attached pdf. The request may be for a repeat dose of IM midazolam (this time “up to 10mg”) or IM lorazepam if the crew carries it. Another option is IN benzos (although these tend to not be preferred due to patients spitting them back at providers), or IV/IO benzos if the initial SO midazolam briefly calmed the patient enough for the crew to obtain vascular access. Finally, there is the option for ketamine, either IN (again, often not preferred) or IM. Now, a few things about ketamine. Recognize that many EMS services in NYC do not yet carry ketamine (although obviously our own Maimo medics do). This has been another example of how practice in the prehospital setting has developed somewhat behind that in the ED or the rest of the hospital. Similarly to how ketamine has surged in popularity in the ED over the last several years, so too is it now getting lots of attention in EMS systems. However, the “ketamine can do no wrong” mentality started to stall a few years ago after some studies began to show some adverse effects from its use. One of the most impactful papers was the 2016 study from Hennepin County, MN, comparing prehospital ketamine to haloperidol, which showed superior sedation but a worse side effect profile, specifically a significantly increased rate of subsequent intubation. Why? While this may be partially related to ketamine-induced laryngospasm, there is an argument that a large part of this is explained by inexperience with ketamine and unfamiliarity with how to manage a dissociated patient. There is also a question of correlation between ketamine dosing and adverse effects. The Hennepin study, along with many other EMS systems, utilizes a 5mg/kg dosing strategy for IM ketamine; for context, Elijah McClain appears to have been given a good deal more. Our own protocol here in NYC calls for 2-4mg/kg IM. Of note, a more recent study by the same Hennepin group comparing prehospital ketamine to midazolam was suspended after public backlash over informed consent with regards to ketamine administration. Finally, note that this protocol explicitly states in its title that it is for adults only. For NYC EMS, although you are considered a minor until the age of 18, you are only a pediatric patient until the age of 15. What this means is that you very well may encounter 16-year-olds who have received midazolam as Standing Order, and you may receive OLMC calls for large, violent 14-year-olds requesting a Discretionary Order for sedation. In the latter case, use your judgment, but remember to consider patient and provider safety, and if you do authorize the use of sedation, be sure to get an accurate weight for dosing. Very interested in hearing all of your takes on prehospital management of excited delirium, in-hospital and out-of-hospital (CLINICAL) ketamine use, and anything in between! Feel free to reply to this email chain, and in the meantime, keep checking out www.nycremsco.org and the protocols binder!

–– David Eng, MD Assistant Medical Director, Emergency Medical Services Attending Physician, Department of Emergency Medicine Maimonides Medical Center

Hyperthemia and Rapid Cooling

There are a number of causes for hyperthermia that isn’t just fever and r/o sepsis. There is certainly environmental hyperthermia – particularly the elderly in poorly or non- air-conditioned buildings, the runner training for a marathon, and the lost hiker.

Today though, I want to focus on sympathomimetics and psychostimulants. In these settings, rapid cooling is often needed as there is high mortality if not cooled promptly. 

Sympathomimetic/psychostimulant highlights:

• hyperthermia, mydriasis, tachycardia, diaphoresis, hypertension, agitation, psychosis

• cocaine, PCP, amphetamines, MDMA, LSD, bath salts, etc.

• can get the phenomenon of “excited delirium” where there is excess catecholamines and/or overstimulation of dopamine and NMDA receptors

In clinical practice…

-Get a rectal temp to asses someone’s core temperature!

-High body temperatures can cause protein unraveling, severe rhabdo -> AKI ->hyperkalemia

-When agitated and hyperthemic, consider benzodiazepines or dissociating with ketamine as we are trying to stop hypermetabolism and muscle contractions that generate further heat.

-If intubation is needed, rocuronium > succylcholine to avoid hyperkalemia.

-Ways to rapidly cool somebody: remove clothing, cold IV fluids, ice packs, ice baths, and even bladder irrigation.

-With an ice or cold water bath, you can cool somebody and drop their temperature about 3°F for every 5 min in the bath.

How might we set up an ice bath here at Maimonides? Get a body bag from the charge nurse, place the patient in it, grab ice from the ice machine if it’s working (inevitably 2 out of 3 machines in the department aren’t) or go to 3-in-1 and borrow their ice (order an iced coffee with just ice, no coffee). Place the ice in the body bag with the patient, or perhaps in large biohazard bags filled with ice around the patient.

Lastly, the evidence for dantrolene when rapid cooling is needed is very limited/non-existent. It’s expensive. It’s efficacy is mostly anecdotal. That being said, some of our event medicine teams have used it in the past at music festivals for excited delirium patients.