The Trickster

You may be asking yourself how Loki "the god of mischief" has anything to do with a medical blog. Well for one I am a huge Marvel fan and in the movies Loki is a trickster. He fools the audience - and other characters - into thinking he is dead several times and in one movie he actually does die.....but then he is back again because the Avengers travel back in time setting off an alternate time line. It's awesome!

But I digress. Loki is a trickster just like hyperkalemia. Patients who are hyperkalemic can appear very stable or unstable. The changes it can cause on an EKG can mimic other rhythms, myocardial infarction, or present very "textbook." It is easy to be fooled by your hyperkalemic patient's presentation and EKG findings. Today we will review this medical emergency and discuss some ways to heighten our suspicion for this "trickster."

Pathophysiology

Potassium plays an important part in the generation of action potentials and is an essential electrolyte for the normal function of our skeletal muscles, cardiac muscles, and neurons. Approximately 90% of our potassium stays in our intracellular space with the rest being extracellular. However, there are situations that can cause our potassium to shift where it does not belong (into the extracellular space) - hyperkalemia. Eventually we start to see this electrolyte shift affect the excitability of individual cardiac cells resulting in changes we can see on the EKG.

Initially, this shift causes increased excitability of the cardiac cells but, the body can only endure so long and we will see a decrease in cardiac cell excitability. The sodium potassium pump is used by our cardiac cells to initiate a contraction as well as recharge for the next contraction. High potassium decreases the efficiency of the sodium/potassium pump resulting in slower electrical impulse conduction through the heart and increased risk of arrhythmias. Eventually, the heart cells fail resulting in cardiac arrest. (Alila Medical Media, 2017)

Causes of Hyperkalemia/Patient Presentation

There is a laundry list of potential causes of hyperkalemia. By far the most common is diabetic ketoacidosis (DKA) and renal failure (especially if they have missed a dialysis appointment)! Other causes include: sepsis, blood pressure medication overdoses, excessive NSAID use/overdose, Addison's Disease, severe burns, crush injuries, excessive potassium supplement use, digoxin toxicity, the list goes on. History gathering and a story is crucial in developing differential diagnoses.

In the case of hyperkalemia, there is not a specific presentation to look out for. Signs and symptoms include: nausea/vomiting, dizziness, weakness, dyspnea, chest pain, palpitations, numbness, tingling, altered mental status, loss of consciousness/syncope. Often times there are other problems going on in addition to the hyperkalemia that can distract us. For example patient may have fallen and hit their head or attempted suicide by taking pills/medications causing a gastrointestinal bleed.

The overall point is that we must keep our differential broad and do sound detective work; this truly can be a silent killer unless you think hyperkalemia.

Recognizing Hyperkalemia

Getting a good history and story of what happened is key in suspecting hyperkalemia. If you have the ability to obtain labs with an iSTAT, that can be helpful; however, in some cases you just can't wait for the results or you may not have access to the test. Obtaining a 12 lead EKG is the last piece of information and the quickest way to identify hyperkalemia.

The classic textbook EKG changes for hyperkalemia are: tall and/or peaked T waves, widening QRS, prolonged PR interval, progressing to a very wide QRS complex (Sinusoidal wave). It is often taught that this is how the EKG changes progress as the patient's potassium rises. But remember hyperkalemia is the ultimate "Trickster."

There is "textbook" and then there is real life. Hyperkalemia can also cause EKG changes that mimic a STEMI, ventricular tachycardia, idioventricular rhythm, bundle branch blocks, heart blocks, or junctional rhythms (very tricky). When faced with these mimics we must understand that with every EKG there is a story/history/presentation that must be taken into account. Here are some EKG examples of how hyperkalemia can present:

(Dr. Smith EKG Blog, 2012)

This is the EKG of an adult male who presented to ED unconsious with a history of diabetes. Potassium level 8.7 mEq/L

(Dr. Smith EKG Blog, 2015)

This EKG looks like ventricular tachycardia and if this patient is unstable you should synchronize cardiovert. This was the EKG of an elderly male that missed his dialysis appointment and presented to ER with chest pain and dyspnea. He was treated for hyperkalemia due to his history/story and the rhythm did not change. He was synchronized cardioverted and the rhythm changed to sinus rhythm. If this patient had been given amiodarone/lidocaine (sodium channel blocker) it would have caused sudden cardiac arrest. Very rare but hyperkalemia sometimes can cause ventricular tachycardia. Your only clue to hyperkalemia is how extremely wide the QRS complex is and the story. His potassium was 7.6 mEq/L.

Treatment

In the prehospital setting, our treatment focuses on protecting the heart and rapid transport to the hospital. In critical care/flight/hospital you will have additional treatment that focuses on shifting the potassium back into the cells and excreting excess potassium. Before diving into treatments, recall normal potassium level is 3.5-5.0 mEq/L.

Calcium chloride or Calcium gluconate must be administered FIRST; the calcium has the opposite effect as potassium and will speed up electrical impulses. This temporarily stabilizes the cardiac membrane protecting the heart from arrhythmias. According to the US Pharmacist Resource for Clinical Excellence we administer calcium when the potassium level is "6.5 mEq/L or greater OR changes are seen on the EKG" (Ng & Lee, 2017). Dose is 1 gram calcium chloride or 3 g calcium gluconate IV/IO; make sure you push slow or infuse via drip. Calcium gluconate has 1/3 the amount of calcium as calcium chloride requiring the larger dose. For cardiac arrest due to hyperkalemia, the stated dose can be repeated.

Albuterol can be administered via nebulizer to a patient to begin shifting potassium back into the cells. It requires large doses: 10-20 mg and can lower potassium by 0.3-0.6 mEq/L (Ng & Lee, 2017).

Sodium bicarbonate (8.4% prefilled syringe) is still utilized but is falling out of favor for treatment. Initially it was thought that this medication had benefit for also combating acidosis related to hyperkalemia. We now realize that It can cause fluid shifting in patients with renal failure and heart failure and takes hours to start shifting potassium back into the cells. It may have some benefit for patients that are dehydrated (DKA). Dose is 1 mEq/kg IV/IO. This should be the very last drug you worry about giving or better yet just don't give it at all. It is also prudent to give this as an infusion instead of as a bolus.

In the prehospital setting, most of us only have the above treatment options. Those in critical care/flight/hospital have other options, which include: insulin (shifts potassium back into cells), diuretics (to excrete potassium out of body), medications that shift potassium into stool for excretion, and dialysis to remove excess potassium.

BEWARE that giving amiodarone/lidocaine for a rhythm that looks like ventricular tachycardia (but actually is hyperkalemia) will cause sudden cardiac arrest in your patient. Hyperkalemia is poisoning your sodium potassium pump and these medications are sodium channel blockers. Essentially you wipe out the pump and the patient quickly arrests.

Common Misconceptions/Myths

1. EKG changes are progressive and give you an idea of what range the potassium level is.
   1. This is false. You can have only peaked T waves on the EKG with very high potassium levels or a sinusoidal wave and moderately high potassium levels. EKG changes only tell us that the patient's heart is unstable.
2. Hyperkalemia only causes changes in the precordial leads and can only mimic a STEMI in the precordial leads.
   1. This is also false. Hyperkalemia can cause changes in any lead and can mimic inferior, anterior, or lateral STEMI. Often times you cannot identify whether your patient is having an MI until you clean up the EKG with the hyperkalemia treatment mentioned above.
3. My patient is stable so there is no need to treat emergently.
   1. Hyperkalemia is a "trickster", your patient can look remarkably stable before quickly decompensating. If there are EKG changes indicating hyperkalemia, TREAT your patient!
4. Calcium Chloride/Gluconate is dangerous to push and if you are wrong it can cause harm!
   1. This medication is necrotic and you must ensure the IV/IO is patent, just like we do when we give other necrotic medications (dextrose, levophed, etc.). We also need to flush the line well before giving other medications. Beyond that, calcium is safe to administer, so have no fear. As Dr. Amal Mattu says "You're patient will thank you...it makes their bones stronger!" (one of his favorite jokes).
5. Treating hyperkalemia in a patient with digoxin toxicity will cause stone heart/cardiac arrest!
   1. This is due to some case reports where patients with life threatening digoxin toxicity died after calcium administration. This was a biased conclusion and has since been proven false and that the digoxin toxicity itself caused the cardiac arrest. Calcium will not provide this specific patient any harm nor will it have any benefit; they need the antidote: Digibind.

Pro Tips

• If your patient is unstable and it looks like ventricular tachycardia or idioventricular rhythm go ahead and use your electrical therapy (synchronized cardioversion or pacing). This may work temporarily buying you time. If electrical therapy does not work, one differential that should pop up in your mind is hyperkalemia; other possibilities are beta blocker/calcium channel blocker overdose.
• Hyperkalemia often causes very slow and very wide QRS complex rhythms.
• Think hyperkalemia when you see a very slow and/or very wide complex tachycardia. If the heart rate is 100-140 that is abnormally slow for ventricular tachycardia AND/OR if the width of the QRS is one big box (0.2 seconds) or more, this is very wide. If the patient is stable don't rush, get a good history/story; giving amiodarone in this situation will result in cardiac arrest.
• Suspect hyperkalemia when working a cardiac arrest with a slow and wide complex PEA.
• An epinephrine drip for hypotension is a fantastic move in the hyperkalemic patient as it causes some potassium to shift back into the cells.

I leave you with a link to this awesome video: How To Avoid a Clean Kill - Wide Complex Tachycardia Mimics

In our next blog, we are going to continue along with our hyperkalemia topic and review several case studies so we can practice what we learned.

Stay safe my friends!

References:

Alila Medical Media. (2017, October 17). Hyperkalemia pathophysiology made easy with animation. Medical Information Illustrated. http://www.alilamedicalimages.org/2017/03/13/hyperkalemia-causes-effects-on-the-heart-pathophysiology-treatment/

Mayo Clinic. (2020, November 14). High potassium (hyperkalemia). https://www.mayoclinic.org/symptoms/hyperkalemia/basics/causes/sym-20050776

National Kidney Foundation. (2020, August 26). What is Hyperkalemia? https://www.kidney.org/atoz/content/what-hyperkalemia

Ng, Kimberly E & Lee, Chung-Shien. Kimberly Erin Ng, PharmD, BCPSAssistant ProfessorSt. John’s UniversityCollege of Pharmacy and Health SciencesDepartment of Clinical Health ProfessionsQueens, New York Chung-Shien Lee, PharmD, BCPS, BCOPAssistant ProfessorSt. John’s UniversityCollege of Pharmacy and Health SciencesDepartment of Clinical Health ProfessionsQueens, New York . (2017, February 16). Updated Treatment Options in the Management of Hyperkalemia. US Pharmacist. https://www.uspharmacist.com/article/updated-treatment-options-in-the-management-of-hyperkalemia

Weingart, S., & Farkas, J. (2020, September 23). Hyperkalemia. EMCrit Project. https://emcrit.org/ibcc/hyperkalemia/

Levine, M. (2011, January 4). The effects of intravenous calcium in patients with digoxin toxicity. PubMed. https://pubmed.ncbi.nlm.nih.gov/19201134/