Back in 2012, there were two times that hyperkalemia caught me with my pants down. Between the two, I had the pleasure of feeling pretty damn stupid, twice, due to the same condition — which felt unfair because the presentation was… So. Damn. Different.
The first round in my battle with hyperkalemia, the ST-segment and T wave morphology changes fooled me into thinking I needed to rush a patient directly to a cath lab. The appearance of ST-segment elevation, or what I thought was ST-segment elevation, screamed, “GET TO DA CHOPPA!” A middle-aged female with a heart rate in the high 90's, occasional ectopy, with atypical ACS complaints; it just didn't feel right. So, I did what I felt was right. I took the patient to the nearest hospital with a cath lab and advanced cardiac care/capabilities… I called the presenting 12 Lead a STEMI and requested cath lab activation. Shortly after arrival, the patient was rushed into an ER room, and the physician took a peek at my 12 lead ECG — The cath lab wasn’t ready at this time, so the patient would get initial care in the ER. The physician doesn’t say much after quickly looking at my print-out; he simply requests immediate labs and wants to perform a 12 lead of his own.
Well, it turns out the potassium was 6.2 mEq/dL… The 12 Lead ECG showed dynamic changes very consistent with hyperkalemia. But, having not been a medic for too long, my knowledge of hyperkalemia was… Spiked T waves… Yeah’p, that's it! Outside of that, I had no idea what I would be looking for.
With my minimal knowledge of hyperkalemia, I knew nothing about how I should have taken care of this patient. But my time with the patient was up, and they took over care. After I finished making my cot, I went into the room to see if there was anything else they needed before I left. Those "changes" that I had mistaken for the possible STEMI were gone... Or the changes weren't as apparent. I wanted to inquire about the treatment they rendered, but the nurses and physicians appeared very busy so I let my curiosity be.
Round one of my battle with hyperkalemia went to the opponent and I made no preparation for round two... Shame on me...
The second time, or ROUND 2, again happened in 2012. I had a bradycardic patient with a heart rate in the high 20’s to low 30’s complaining of severe lethargy/weakness. I was hesitant to start pacing or attempt other interventions in the ambulance because all of my other numbers were within normal ranges (Judge me, I know you are 😉). So, of course, shortly after arrival at the ED, the patient begins to “crump.” We opt to pace and continue with other care (blood draws, establish another IV, fluid, pressor preparation, and oxygen…). Our EMS service works in the ED we transported to, so we get to assist with the continuation of care. The pacer is set to 60 and 60 (60 mA with a rate of 60). The physician chooses to transfer this patient and requests a flight team. My partner and I debate whether we — our own crew — should take the transfer or fly. I won the debate; we’re gonna fly the patient. My partner would be attending this transfer, and since we were unable to obtain mechanical and electrical capture while pacing, he gets nervous and agrees… we should fly this patient.
The flight team arrives, sees that with our pacer settings, the patient isn’t getting appropriate capture even after I increased the mA to 100 (could have been higher, I just can’t remember; it was 8 years ago, BACK OFF!). The flight team recognizes this, and while switching to their equipment, the medic sees the underlying rhythm. He immediately asks, “What is the potassium?” Minutes after he asked, we finally got the results back. 7.6 mEq/dL!!! After hearing this, the flight team took the controller from my hands and finished the game for me, just as my brother would do back in the day. They requested medications from our ED, and in what seemed like only minutes, a beautiful sinus rhythm is seen on the monitor… Stable hemodynamics to follow… it was like they used some sort of cheat codes.
Now, I was left with the question: Where did they get this cheat code, and how did they get their hands on it? Magic? Witchcraft?
This time I wasn't gonna leave myself with curiosity. I saw the treatment work right in front of my eyes, and I wanted to know it before this 💩 happened again. But before I get into the cheat code for hyperkalemia, I think we should cover the basics.
WHAT IS HYPERKALEMIA?
Hyperkalemia: Higher amounts of the electrolyte Potassium (K+) in the blood or serum. For whatever the reason, there is a surplus of potassium floating around in the blood, be it from the body's inability to rid itself of potassium or the cells not containing the potassium intracellularly.
Potassium is vital for regulating the normal electrical conduction of the heart. Increased extracellular potassium reduces myocardial excitability, with depression of both pacemaking and conducting tissues. Worsening hyperkalemia leads to ineffective impulse generation by the SA node and reduced conduction by the AV node and the conduction system to follow. This can result in conduction abnormalities, bradycardia, and eventually… Cardiac arrest.
HOW IS IT MEASURED?
Potassium is measured following a blood draw. A BMP (Basic Metabolic Panel) or a Chem7/Chem8 is often ordered, which provides information about the body’s metabolism. It measures glucose, fluid balance, renal function, and electrolytes such as sodium, chloride, and potassium.
Potassium is measured within this “test” with a normal range of 3.5 - 5.0 mEq/dL (some institutions may have varying values, but all are within this range, normally). Hyperkalemia is usually diagnosed when the serum potassium level is greater than 5.5 mEq/dL.
Some sources delineate these levels even further:
Hyperkalemia = Level > 5.5 mEq/dL
Moderate Hyperkalemia = Level > 6.0 mEq/dL
Severe Hyperkalemia = Level > 7.0 mEq/dL
Now, why do I say serum potassium level and not just potassium level? That’s because there is a difference between the total body potassium and the serum potassium that we measure. What is that difference? It’s where the potassium is located within the body.
Extracellular Potassium: Or, better put, potassium outside of the cell. This is the potassium that we are measuring and using to guide our treatment of the patient. The extracellular components consist of potassium found in the intravascular and interstitial spaces.
Intracellular Potassium: Or, better put, potassium inside the cell. This part of the potassium is found… well… in the cell. A vast majority of our total body potassium is found within the cell — Approximately 97-98%, whereas the rest is extracellular. The concentration inside the cell is approximately 150 mEq/dL, and outside the cell, it’s approximately 4.5 mEq/dL.
Understanding that our total body potassium is the sum of extracellular and intracellular potassium is a concept that can help us understand the etiologies of hyperkalemia and the “why” behind how we are treating it. Where did the excess potassium come from? Where is it going when we treat it? Often, our patients don’t have an excessive amount of total body potassium. It has just been released by the cells for one of many reasons. Maybe it just needs “put back.” Other times, there is simply too much, and we may need to remove it completely…
WHAT ARE THE SIGNS AND SYMPTOMS OF HYPERKALEMIA?
This is where it gets easy… or hard.
The signs and symptoms of hyperkalemia are very non-specific, including but not limited to:
So as you can tell, this could be make up a solid majority, or more, of our patients. But that’s where and why we have to play detective and include other things such as ECG findings to see if we can’t pinpoint this down to potential hyperkalemia.
Which brings up common ECG findings encountered with our hyperkalemic patient’s…
HYPERKALEMIA ECG FINDINGS
Before I get into this, It is worth mentioning that the ECG changes associated with hyperkalemia do not always happen in a step-wise fashion with predictable serum potassium levels. Although it is generally true that higher levels of potassium correlate with progressive ECG changes, the more acute or, the faster the levels rise, the more likely it is for life-threatening changes to occur, and they may not occur predictably. An acute rise in potassium may have more “dramatic” effects, whereas the body adapts with a slow rise. A hyperkalemic patient can progress rapidly from a normal ECG to ventricular fibrillation.
Here is the “Textbook progression” of hyperkalemia:
Serum Potassium > 5.5 mEq/dL:
Tall, peaked T waves
Serum Potassium > 6.5 mEq/dL:
P wave widens and flattens.
P waves disappearing, eventually
Serum Potassium >7.0 mEq/dL
Prolonged QRS interval; wide and bizarre appearing
Sine wave appearance
Blocks and ventricular escape rhythms
Serum Potassium > 9.0
Usually cardiac arrest…
PEA; usually with a sine wave appearance (Wide, bizarre)
Again, this is just a guide to determine the possible severity of the patient’s condition correlated with the ECG findings. ECG's have low sensitivity and a “meh” specificity when predicting the potential for hyperkalemia. Also, keep in mind, patients with chronically high potassium levels may not fit the above description, either — The slower the potassium rises, the better the body adapts to it.
So, as you can see with the above picture, hyperkalemia can present in many different ways, fooling us as providers. The morphology changes can be hard to interpret, especially with amplitude increasing in some cases forcing us to believe there is ST-segment elevation or abnormal rhythm morphology related to another condition.
^^ Similar 12-Lead to my "Round One" Cath Lab Activation ^^
Taken from Life in the Fast Lane ECG Blog
^^ Similar rhythm to that of which I paced in "round 2" ^^
Taken from Dr. Smith's ECG Blog
^^ Potassium Level - 7.0 mEq/dL ^^
Taken from Life in the Fast Lane ECG Blog
WHAT CAUSES HYPERKALEMIA?
So when you are thinking of the potential causes of hyperkalemia… think CRAP! Which stands for:
*** The original acronym is CRAM, with the “M” standing for medications, which originated from our fellow FOAMed educators at Heavy Lies the Helmet. I’m just immature and after having heard this simple letter change, couldn’t not use it ***
Cell death, or lysis of the cell, causes a release of potassium into the blood.
Renal failure cause an inability of the body to remove potassium from the body. The kidneys play a huge role in potassium excretion… If they don’t work properly, the patient may retain potassium — they have impaired potassium excretion.
Acidosis has an increase in hydrogen ions. These hydrogen ions “bump” potassium off of the cell and take its place, causing an increase in serum potassium.
Pharm/Medications can cause an increase in serum potassium levels as well. Potassium replacement supplements. Beta-blockers keep potassium from pressing into the cell. Potassium-sparing diuretics prevent the removal of the potassium in the urine. and ACE inhibitors block aldosterone, causing less potassium secretion and retained potassium leading to hyperkalemia.
Pseudohyperkalemia: Not mentioned in the "C-R-A-P" acronym, but is very much worth mentioning (maybe it could be added to the P too). If the blood specimen was damaged or hemolyzed during the draw, a falsy elevated potassium level can be reported. If you are in hospital, often times the lab techs will report this information to you, telling you that you have an elevated potassium level, but a hemolyzed specimen. Not everyone has this leisure, especially if you do labs via EPOC or iStat. Consider a re-draw if the potassium doesn't seem to correlate with the patient's presentation.
AND, NOW, TO THE CHEAT CODES….
HOW DO YOU TREAT IT????
Obviously, cheat codes weren’t actually used, or at least I don’t think so. But I just so happen to work for this service today, so I’ll be honest, maybe it could have been witchcraft… after meeting some of them… 😁 😉
*** COUGH.. 🚁💙 LifeFlight 💙 🚁 .. COUGH ***
With hyperkalemia, in most cases, we can’t directly treat it by attacking the cause. The more acceptable way to approach it, in the EMS/HEMS, critical care transport, or acute setting must be focused on reversing or avoiding dysrhythmic effects and other related complications. Our management will be focused on cardiac membrane stabilization, shifting the potassium back into the cell, and assisting with excretion of the electrolyte.
Cardiac Membrane Stabilization (DO THIS FIRST!):
Calcium — Gluconate or Chloride:
There is no good literature to help guide whether calcium gluconate or calcium chloride is better for stabilizing the cardiac membrane in hyperkalemia. The most important difference to remember is that calcium chloride has 3 times more elemental calcium than calcium gluconate (6.8 mEq/10 mL vs 2.2 mEq/10 mL) and has greater bioavailability. However, calcium gluconate has less risk of local tissue necrosis at the IV site. Therefore, if you decide to give calcium gluconate, ensure you are giving sufficient doses of calcium since one amp may not be enough. Three amps of calcium gluconate are often required to start to see the ECG changes of hyperkalemia resolve. Remember that calcium does not lower the potassium level.
Within minutes, calcium decreases hyperkalemia’s depolarization effects and reduces the threshold potential of cardiac myocytes. This stabilizes the cardiac membrane, essentially combatting arrhythmias commonly seen with hyperkalemia. But we have to remember that this does not shift or excrete the potassium.
Indication/When to Give it:
Controversial. Many resources and guidelines call for calcium administration when ECG changes (peaked T waves or worse) related to hyperkalemia are visibly seen. Others require a serum potassium level to be drawn with levels > 6.5 mEq/L. As a good rule of thumb though, we should all have a low threshold to administer calcium.
1 gram Calcium Chloride or 1 - 3 grams Calcium Gluconate; both SIVP. Repeat q 5 minutes until the ECG normalizes — continue administration if the ECG changes persist or worsen.
Within minutes (no difference in the time of onset between the two — first-pass metabolism is a myth)
20 - 30 minutes (many sources report up to 60 minutes). Repeat dosing may be required during longer transports or continue dosing every 5 minutes if ECG changes persist or worsen.
*** Stone Heart has mostly been debunked; if the patient is on Digoxin, document the necessity of calcium in detail ***
Shifting Potassium Back into the Cell:
Insulin and Glucose
This should be the first treatment after the administration of calcium. It works by shifting potassium back into the cell, reducing the serum potassium level. It does this by enhancing the activity of the Na-K-ATPase pump within skeletal muscles. Glucose is given in conjunction with insulin to combat the development of hypoglycemia. Glucose should reportedly be withheld, and insulin is given alone, in patients with serum glucose > 250 mg/dL. Either way, continuous monitoring of blood glucose levels should occur.
Dose: 10 Units of Regular Insulin IV with 25 grams of dextrose (1 amp of D50) IV.
Onset: 10 to 30 minutes*
Duration: Several hours, reportedly*
Albuterol is a beta-agonist that proves useful in rapidly shifting potassium back into the cell. But it only proves useful with very large doses which essentially require continuous nebulization. It has been reported that there can be a paradoxical increase in potassium after administration has stopped, so it is recommenced that albuterol isn’t given as a monotherapy and should be followed by administration of insulin and glucose. Albuterol and insulin have an additive effect, decreasing the concentration by approximately 1.2 to 1.5 mEq/L.
Dose: 10 to 20 mg; usually 4 - 8 albuterol bullets. Continuous nebulization.
Onset: Less than 15 minutes, typically.*
Duration: 30 - 60 minutes*
As time goes on this is used less and less… It is believed that since Bicarb is typically given in its hypertonic form, it may cause a solvent drag and pull potassium from the intracellular space to the extracellular space, worsening the hyperkalemia. If Bicarb is to be given, it is recommended to give it in an isotonic form, which is generally obtained by adding three amps of Bicarb to a liter of D5W. Administration of isotonic bicarb works to decrease potassium in three ways: 1. Dilution 2. Shifting potassium into muscle cells. 3. Renal potassium excretion which is promoted by alkalosis. This has been demonstrated to work only in patients with metabolic acidosis.
Dose: IF, and only IF, the patient is in metabolic acidosis (typically a non-anion gap acidosis such as patients with renal tubular acidosis)… then 1 - 2 liters of isotonic bicarb may be recommended.
Assisting with Excretion:
"There is no role for diuretics in the routine management of hyperkalemia unless the patient is hypervolemic." Many resources report something like this or something along these lines. I won't say that we shouldn't use a diuretic such as Lasix... But in the acute transport setting, we likely have no way to prove the patient is truly hypervolemic and our administration of diuretics may be misguided or harmful.
No benefit was shown in the acute phase with many experts concluding that there is no role for Kayexalate in the ED. AND, if it’s been given… it’s gonna be a shit show! 💩 💩
This is definitive treatment/care for many of our hyperkalemic patients. At this point... I'm unsure of the specific dose, onset, and duration at this time as it's not within my scope of practice 😉
There you have it, the cheat codes to treating hyperkalemia. Obviously, I couldn't include absolutely everything about hyperkalemia, but I will leave you guys with some additional links that I personally suggest for some research of your own.
Hyperkalemia can often mime, or "mimic" that of a STEMI. Here is another blog I wrote that includes some information about hyperkalemia as a "STEMI Mimicking" rhythm:
CHECK THESE OUT TOO!
Life in the Fast Lane:
Jared Patterson, CCP-C, One Rad Medic
Killin' It Since 1989
UpToDate. (2020). Retrieved 8 December 2020, from https://www.uptodate.com/contents/treatment-and-prevention-of-hyperkalemia-in-adultssearch=Hyperkalemia&source=search_result&selectedTitle=1~150&usage_type=default&display_rank=1
American Academy of Orthopaedic Surgeons (AAOS), American College of Emergency Physicians (ACEP), & U. (2017). Critical Care Transport (2nd ed.). Jones & Bartlett Learning.