Hyperkalemia

 The Patient     This ECG was obtained from a 28-year-old woman who was found in her home, unresponsive.  She was hypotensive at 99/35.  No one was available to provide information about past medical history or the onset of this event.

Before you read my comments, pause to look at the ECG and see what YOU think.  We would welcome comments below from all our members!

The ECG     This ECG is quite challenging, as it illustrates the helpfulness of ECG changes in patient diagnosis, and also points out how important clinical correlation is when the ECG suggests multiple different problems. Forgive me in advance, but there is a lot to say about this ECG.

The heart rate is 148 bpm, and the rhythm is regular, although not perfectly. P waves are not seen, even though the ECG machine gives a P wave axis and PR interval measurement. The rate is fast enough to bury the P waves in the preceding T waves, especially if there is first-degree AV block. Differential dx: sinus tachycardia, PSVT, atrial flutter. The very slight irregularity points more towards sinus tachycardia.  The rate of nearly 150 suggests atrial flutter with 2:1 conduction, but the only lead that looks remotely like it has flutter waves is V2. The lack of an onset or offset of the rhythm makes it difficult to diagnose PSVT with any certainty.

This ECG is from a 57-year-old woman with extreme weakness.  We do not know her medical history or complete lab results, except that her serum potassium level was 8.8 mEq/liter at the time of this ECG.  

This ECG shows a fairly regular rhythm at about 75 bpm, with a few early beats raising the rate slightly. (Even though the machine's interpretation lists the rate as 54 bpm. The QRS duration is listed at 148 ms (.148 seconds), but it appears wider. It is difficult to see the excact location of the J point because the QRS slurrs into the ST segment.  Even though the ECG machine reports a P wave axis and a PR interval, P waves are not visible.

The QRS morphology appears to be an atypical right bundle branch block and left anterior hemiblock pattern. The T waves in leads I, II, aVF, and V3 through V6 are narrow, tall and peaked.

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.

This ECG was taken from an elderly man who was in acute renal failure, and had presented to the Emergency Department via EMS.  He was weak and hypotensive.  We have no other medical history or clinical information. 

The most noticeable feature of this ECG is the wide QRS, which is difficult to measure because there is no distinct J point at the end of the QRS complex.  As a result, the QRS blends into the ST segment and T wave.  The T waves are extremely wide.  At a rate of 61 bpm, it is almost bradycardic. It appears that P waves may be present in some leads (like Lead II) - but, if so, the PR interval looks short.  It is difficult to tell where the P wave ends and the QRS begins.  Also, there are occasional pacer spikes, which are not capturing.    

This is the “sine wave” rhythm of extreme hyperkalemia.  This pattern usually appears when the serum potassium levels are well over 8.0 mEq/L.  Had we seen the earlier ECGs, we might have had more warning, because the ECG in earlier stages of hyperkalemia shows us distinctive peaked, sharp T waves and a progressive intraventricular conduction delay (IVCD).  See example. The intervals progressively widen, the P waves lose amplitude until they disappear altogether.  It is as if someone is holding the tracing at each end, and stretching it apart. 

At this stage, this is an immediately life-threatening condition, but usually treatable.  Quick action must be taken to prevent cardiac arrest.

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.

For your collection, we present another interesting set of ECGs from Paramedic Erik Testerman.  They are from a 48 year old man who presented responsive only to painful stimuli, with deep, rapid (Kussmaul's) respirations.  His blood glucose in the field read as "HIGH" - too high for the glucometer to register a number.  He was treated with 3 large-bore IVs, 2 liters of NSS IV, O2.  At the hospital, his blood glucose again registered as "HIGH" on the glucometer, arterial O2 was 90%, CO2 15 (low), pH 6.8 (acidotic), HCO3 -2 (depleted).  His serum potassium was 7.0 ( greater than 5.5 is high ).  We do not have the rest of his chemistry panel.

The first ECG, at 5:59 am, shows some signs of early hyperkalemia.  One of these signs is wide QRS, at .188 sec (normal is less than .12).  This ECG even meets the criteria for LBBB, as noted in the machine's interpretation, but the widening is more likely due to the high potassium.  There is a right axis deviation.  Left axis deviation is more likely in LBBB. LBBB pattern with right axis deviation can be a sign of biventricular enlargement, but, again, this may be an intraventricular conduction delay that is NOT LBBB.  Another sign of hyperkalemia is that P waves are not evident.  They can either be flattened until they disappear, or the PR interval can become so long the P wave is lost in the preceding T wave.  The T waves are unusually tall and peaked in the chest leads - disproportionate to the wide QRS complexes.  There are ST depressions in the inferior leads.

For a good, systematic approach to the ECG changes associated with hyperkalemia, we recommend Life In The Fast Lane, by Ed Burns.

ECG number 2 was taken 13 minutes later, still in the pre-hospital phase.  The QRS is now .13 seconds, and the tall, narrow, peaked T waves are very evident in Leads V1 through V3.  There is  T wave inversion and ST depression in the inferior leads.  These are all possible signs of hyperkalemia, but also of other conditions.  Unfortunately, hyperkalemia is a "mimic" of many conditions on the ECG.  For a very interesting discussion of this topic, please go to Dr. Amal Mattu's ECG Discussion of the Week, October 14, 2013.