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Hyperkalemia

Dawn's picture
Sun, 08/23/2015 - 14:06 -- Dawn

This ECG was obtained from a patient who had a serum potassium level of 7.4 mEq/L.  It shows some of the earliest ECG signs of hyperkalemia.  There are tall, sharply-peaked T waves in many leads.  The P waves have not yet widened and lost amplitude, but they will soon flatten out and disappear.  At this level of hyperkalemia, we can expect to see conduction disturbances (first-degree AV block in this case) and bradycardia (not yet). It is a bit surprising that the QRS complexes have not yet widened at this serum K level.    Caution:  hyperkalemia can progress and become life-threatening very quickly.

Potassium is primarily an intracellular electrolyte.  It is necessary for proper electrical functioning of the heart.  Extracellular  serum potassium can rise due to renal failure, or taking potassium supplements, potassium-sparing diuretics, or ACE inhibitors.  Occasionally, serum K levels may be artificially elevated by drawing the blood with too much syringe pressure, or using too small a needle, as the red blood cells can be damaged and release intracellular K into the serum.

ECG signs may vary among people with hyperkalemia, but in general:

Serum K levels of 5.5 mEq/L or greater can cause repolarization abnormalities like tall, peaked T waves.

Serum K levels of 6.5 mEq/L or greater cause progressive paralysis of the atria.  The P waves will lose amplitude, widen and flatten.   The PR segment will lengthen. Eventually, the P waves will disappear.

Serum K levels of 7.0 mEq/L or greater can cause conduction abnormalities.  The QRS will widen and the rate will slow.  There may be bundle branch blocks or fascicular blocks.  The QRS morphology will be bizarre - not necessarily showing a typical bundle branch block pattern.  AV blocks may occur, with either ventricular or junctional escape rhythms.

As the patient's condition worsens and the serum potassium rises, the QRS and T waves lose amplitude, widen, and may seem to blend together.  

At levels above 8.0 mEq/L, we may see what looks like a bizarre idioventricular rhythm, or a sine wave pattern.  This sine wave pattern signals cardiac arrest is imminent.

For a comprehensive discussion of hyperkalemia on the ECG with many examples of the different phases, go to Life In The Fast Lane.  Ed Burns has compiled a very instructive collection of ECGs that illustrate the progression of this deadly condition.

Dr. Steve Smith's blog has several very good discussions on the subject.  For a comparison of tall T waves caused by several factors, including hyperkalemia, go to Dr. Smith's Blog.

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Comments

ekgpress@mac.com's picture
 
As per Dawn — the ECG shown shouts out, “Hyper-K, Hyper-K, Hyper-K” !
 
While as a general rule, there is sequential evolution of the ECG changes of hyperkalemia — many patients fail to “read the textbook” along the way. So numerous variations on the general themes put forth by Dawn may be seen. For example, in this case — I would not call the dramatically tall and pointed T waves with exceedingly narrow base in numerous leads an “early sign” of hyperkalemia despite lack of QRS widening. Instead, I would fully expect a serum K+ in the ~ 7.0-8.0 mEq/L range.
 
  • KEY POINT: What is often forgotten, is that the ECG is the composite effect of all clinical events. For example, if a patient’s baseline ECG showed significant ST segment depression — then development of hyperkalemia might not manifest the tall peaked T waves one expects, because what you see with be the combination of baseline ST depression + changes from hyperkalemia. It is for this reason, that one should NOT attempt to assess for ST-T wave changes of ischemia/infarction until hyperkalemia has been corrected. You never know what you will see after serum K+ has returned toward normal ...
For those interested — I discuss in detail essential ECG Changes with Electrolyte Disorders in Section 11.0 (from my ECG-2014-ePUb). CLICK HERE for free download of this Section. Discussion of Hyperkalemia begins in Section 11.3 of this pdf.
 
 

Ken Grauer, MD  www.kg-ekgpress.com   [email protected] 

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