Displaying 1 - 10 of 13
Dawn's picture

Tachycardia In An Unresponsive Patient

 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.

Dawn's picture

Early Hyperkalemia

This ECG was obtained from an elderly man with Type II diabetes and early chronic renal failure. His serum potassium level was 6.3 mmol/L, and his BUN was 52 mg/dL.  We don’t know his creatinine level.

This ECG shows the beginnings of the effects of hyperkalemia.  One of the early changes that increased serum K causes on the ECG is tall, peaked T waves.  The bases of those T waves becomes very narrow, making the T wave look sharp and thin.  In this ECG, we see the increased height of T waves in V2 and V3, with only Lead V2 having sharp peaks.  It is unlikely that hyperkalemia would be diagnosed on the appearance of the T waves alone, and in fact, the hyperkalemia was not confirmed until the lab results were available.  The patient’s history of known Type II diabetes and early renal failure help us know what to look for.

We also see in this ECG T wave inversion in Lead III (not an abnormality in itself) and biphasic T waves in aVF. 

 

It is good to remember that electrolyte imbalances are not usually diagnosed only from ECG changes.  It is also important to remember that the ECG changes of hyperkalemia can develop very rapidly in conditions that cause rapid increase in serum K. By the time we notice the ECG changes, the patient may very well be in a life-threatening situation.

Dawn's picture

Hyperkalemia

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.

Dawn's picture

Electrolyte Effects

This ECG is from a 46-year-old woman with diabetes mellitus.  She presented to the Emergency Dept. with a complaint of weakness.  Her BP was elevated at 186/102.  Her blood glucose was 936 mg/dL (normal 70-105). 

So, what does her ECG show?

1) Sinus bradycardia at 55 bpm.  The rhythm is regular, with no extrasystoles.

2) A slightly prolonged PR interval at 218 ms (.218 seconds). Normal is 120-200 ms. 

3) A “wide side of normal” QRS duration at 109 ms. Normal is 70-100, but can be a little longer in normal individuals.

4) A prolonged QTc interval at 520 ms.  Normal QTc is 460 ms or less in women. A helpful rule of thumb is that the QT should be less than half the preceding RR. 

5) Normal P waves.

6) Normal axes of P, QRS, and T waves.

7) A large Q wave in Lead III which is not repeated in aVL.  This can be inconsequential when confined to Lead III, or can be a pathological Q wave, especially if also seen in aVF. 

8) Flat ST segments.  Normal ST segments are convex upward, like a smile.

9) Tall, peaked T waves in precordial leads V2 through V6, and in Lead II. 

What does it mean?

Unfortunately, we do not have complete labs for this patient, or any information about her outcome.

We know that patients who have uncontrolled diabetes are at risk for renal failure, so we should consider electrolyte imbalances when we see abnormalities in the ECG. 

Dawn's picture

Extreme Hyperkalemia

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.

 

 

Dawn's picture

ECG Basics: Sinus Tachycardia, Peaked T Waves, and Baseline Artifact

This strip offers several good teaching opportunities.  If it were a 12-lead ECG, no doubt it would be a bonanza!  First, there is sinus tachycardia at a rate of about 138 per minute.  The P waves are all alike and regular.  The T waves are tall and narrow, with a sharp peak.  This is often a transient sign of hyperkalemia, and should be investigated with serum electrolyte tests and with a 12-lead ECG.  In addition, the baseline shows a wandering type of artifact.  This is due to the patient's deep breathing, and the fact that the arm electrodes were placed on the chest.  This patient was a diabetic in ketoacidosis with hyperkalemia. 

Dawn's picture

Hyperkalemia

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.

Dawn's picture

Hyperkalemia

This ECG was obtained from a patient who was suffering from renal failure and had a serum potassium level of 6.8 mEq/L.  It shows some of the earliest ECG signs of hyperkalemia.  There are tall, sharply-peaked T waves in many leads.  There is an irregular, bradycardic rhythm.  We can just barely see P waves, but they will soon flatten out and disappear.  At this level of hyperkalemia, we can expect to see conduction disturbances and bradycardia.  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.

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 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.

It is important the patient with hyperkalemia is treated rapidly, as it can be rapidly fatal.

Dawn's picture

Hyperkalemia in a DKA Patient

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.   

Dawn's picture

ECG Challenge From Dr. Ahmed - Patient With Hyperkalemia

This ECG was kindly donated to the ECG Guru website by Dr. Ahmed for open discussion among our members.  The patient was a 70+ year-old man who presented with a complaint of dizziness.  His serum potassium level was found to be 6.5 (normal is 3.5 - 5.0).  Upon correction of his K levels, his rhythm was atrial fibrillation at 130 / min.

WHAT DO YOU THINK ABOUT THIS INITIAL ECG?  What is causing the slow rate? Is there atrial activity?  Do you see QRS morphology changes?  What about the anterior ST and T wave changes? 

We look forward to hearing from our members!  And thanks to Dr. Ahmed for donating this interesting ECG.

 

Pages

All our content is FREE & COPYRIGHT FREE for non-commercial use

Please be courteous and leave any watermark or author attribution on content you reproduce.