ECG Pointers: Hyperkalemia – The Great Imitator

Author: Manpreet Singh, MD (@MPrizzleER – Assistant Professor of Emergency Medicine / Department of Emergency Medicine – Harbor-UCLA Medical Center)  // Edited by: Jamie Santistevan, MD (@jamie_rae_EMdoc – EM Physician, Presbyterian Hospital, Albuquerque, NM) and Brit Long (@long_brit  – EM Attending Physician, San Antonio, TX)

Welcome to this edition of ECG Pointers, an emDOCs series designed to give you high yield tips about ECGs to keep your interpretation skills sharp. For a deeper dive on ECGs, we will include links to other great ECG FOAMed!

The Case:

It’s flu season and it seems like all your patients have the same thing. Your next patient is a 68-year-old male who had a syncopal episode at his SNF. The nursing notes say he has been feeling weak and dizzy for the last three days and attributes his symptoms due to influenza-like-illness. He has been having multiple bouts of nausea, vomiting and diarrhea. While reviewing his ECG, you are called overhead to the patient bedside for a cardiac arrest. You quickly run to bedside while reviewing the EKG in front of you.

There is atrial-sensed, ventricular-paced rhythm with a rate of approximately 95 and a very wide QRS complex (about 220ms) but the QRS morphology is not typical for right or left bundle branch block.

How does hyperkalemia typically manifest on an ECG?

Classically, we have been taught that ECG changes¹ in hyperkalemia have the following progression (see Table 1 below):

1. Prominent “peaked” T-waves
   • Typically considered the first manifestation
   • Note, the polarity of the T-wave can also change (ie Lateral T-waves normally inverted in LVH can become upright)
   • Q: What else should be in your differential when you see “peaked” T-waves?
     • Hyperkalemia
     • Hyperacute T-waves from ischemia
     • De Winter’s T-waves
     • Benign Early Repolarization

2. PR interval prolongation
   • AV conduction delay as atrial tissue is more sensitive than other cardiac tissues
3. Loss of the P wave
   • SA node dysfunction
4. QRS-widening
   • May resemble bundle-branch blocks at times, though not typical pattern
5. Sinusoidal QRS-complex (“sinoventricular rhythm”)
   • This can degenerate into ventricular fibrillation and asystole

However, keep in mind that the changes are NOT always predictable and sequential.^2,3,4,5 Significant variation is found among patients at any particular serum potassium level. In general, sudden serum potassium increases can lead to significant ECG abnormalities, while those that occur progressively over time can produce fewer ECG manifestations. The most recent study on hyperkalemia in ECGs has shown the progression of ECG changes (not just peaked T-waves) predicts adverse outcomes, which can function as a risk stratification tool for hyperkalemia with further research.⁶ Keeping all this in mind, management of hyperkalemia should be guided by your clinic scenario.

How can hyperkalemia masquerade on an ECG?

As a famous man told us, hyperkalemia is the syphilis of ECGs. It is the great imitator presenting as bradyarrhythmias, tachyarrhythmias, AV blocks, bundle-branch blocks, STEMI-mimics, and more! In the setting as a STEMI-mimic, keep in mind you MAY see a rightward axis in the presence of a wide QRS rhythm that appears to be ST elevations.

It is always important to put hyperkalemia in your differential, especially if the ECG does not add up to your clinical scenario or your interpretation. Point of care potassium at bedside is a quick way to give you the information you need to make your clinical decision if you encounter a bizarre ECG.

Case Conclusion

Though you say to yourself this is a useless ECG as this is a ventricular-paced rhythm, which can obscure ischemia, you notice that the QRS complexes are a bit wide and merge with the T-waves. Your team initiates ACLS and you wisely decide to push two amps of calcium chloride, epinephrine 1mg and 100 mEq of sodium bicarbonate before obtaining ROSC. The post-ROSC ECG shown below shows narrowed QRS duration, greater amplitude and sharper morphology. Labs soon return showing a critical high potassium of 7.5 mEq/L. You initiate further hyperkalemia treatment and look for the underlying etiology.

What are the main ECG pointers for hyperkalemia?

• Though it is good to know the classic ECG progression of hyperkalemia, do not be fooled by a normal or nonspecific ECG in hyperkalemia.
  • The relationship between serum potassium and ECG manifestation is not cut and dry as we are taught. Don’t get into a false sense of security…treat the patient in front of you!
  • Keep hyperkalemia in the differential diagnosis for a patient with an ECG showing a very wide QRS complex
• Keep in mind the differential of a “peaked” T-wave:
  • Hyperkalemia
  • Hyperacute T-waves from ischemia
  • De Winter’s T-waves
  • Benign Early Repolarization
• Hyperkalemia is a great mimicker – think about it in your STEMI-mimics, bradyarrhythmias, tachyarrhythmias, AV blocks, etc., especially if the ECG is not adding up on your interpretation.

But wait, here’s some more ECG FOAMed:

• Amal Mattu highlight’s some great STEMI-mimic pearls in his ECG Case of the Week.
• EmCrit intern H. Pendell Meyers tackles hyperkalemia in a deep dive, including the most recent literature on hyperkalemia in ECGs.
• R.E.B.E.L. EM breaks down the latest evidence of ECG changes in hyperkalemia.
• EM Lyceum goes over some hyperkalemia questions and answers.
• Dr. Stephen Smith has a variety of hyperkalemia cases showing how it is the great masquerader.
• emDOCs article discusses the latest hyperkalemia treatment updates.

References:

1. Mattu, Amal, William J. Brady, and David A. Robinson. “Electrocardiographic manifestations of hyperkalemia.” The American journal of emergency medicine6 (2000): 721-729.
2. Rafique, Z., et al. “61 Electrocardiogram Changes Are Not Reliably Associated With Hyperkalemia or Its Severity.” Annals of Emergency Medicine4 (2017): S25-S26.
3. Montague, Brian T., Jason R. Ouellette, and Gregory K. Buller. “Retrospective review of the frequency of ECG changes in hyperkalemia.” Clinical Journal of the American Society of Nephrology2 (2008): 324-330.
4. Martinez-Vea, Alberto, et al. “Severe hyperkalemia with minimal electrocardiographic manifestations: a report of seven cases.” Journal of electrocardiology1 (1999): 45-49.
5. Dittrich, Kenneth L., and Ron M. Walls. “Hyperkalemia: ECG manifestations and clinical considerations.” The Journal of emergency medicine6 (1986): 449-455.
6. Durfey, Nicole, et al. “Severe Hyperkalemia: Can the Electrocardiogram Risk Stratify for Short-term Adverse Events?.” Western Journal of Emergency Medicine 18.5 (2017): 963.
7. ECGs obtained from: Bahl et. al. “ECG changes of Hyperkalemia during Paced Rhythm.” Indian Heart Journal. 2009; 61:93-94