A woman in her 50s with dyspnea and bradycardia

Written by Pendell Meyers

A patient in her 50s presented with shortness of breath and fatigue worsening over 1 week. Her vital signs were within normal limits except for bradycardia at 55 bpm.

Here is her ECG recorded at triage:

What do you think?

It is probably sinus bradycardia with very small/depressed P-waves and prolonged PR interval. The QRS is about 150 ms, and has morphology consistent with LAFB. The T-waves are peaked. All findings are concerning for hyperkalemia.


Here was the baseline ECG on file:

The hyperkalemia was not yet identified, and the chemistry was pending.

To us, this is clearly hyperkalemia, and we only present what should be an obvious diagnosis because people continue to miss this.  Repetition. Repetition. Repetition.

Another ECG was recorded when a "change in the monitor" was noted:

The first half of the ECG is the same as above, but the second half shows a suddenly wider QRS complex with RBBB morphology. This likely represents an escape rhythm (possibly originating in the LBB). The QRS width of the RBBB beats is just over 200 msec. This is far too wide for normal RBBB, and also implies hyperkalemia or other QRS widening disturbance. The T-waves are markedly hyperacute.

The potassium level came back at 7.8 mEq/L.

The patient was treated for hyperkalemia and this was the repeat ECG:

Much improved, narrower QRS.

The patient did well.




Learning Points:

Always consider hyperK with slow, wide QRS complexes, among other patterns.

It is extremely rare for RBBB to have a QRS width greater than 190ms outside the influence of hyperkalemia or other QRS widening abnormality.


See these other related cases:

A patient with cardiac arrest, ROSC, and right bundle branch block (RBBB).

Is this just right bundle branch block?

Is This a Simple Right Bundle Branch Block?

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MY Comment by KEN GRAUER, MD (1/26/2020):

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Dr. Smith’s ECG Blog has presented too-numerous-to-count cases of hyperkalemia (See My Comment in the 12/11/2018 post — there are many others!). Clearly, recognition of Hyperkalemia is among the most important challenges faced by emergency providers because: i) this electrolyte disorder is potentially life-threatening; ii) there is an empiric treatment (ie, calcium) that can be life-saving, and which should often be given prior to lab confirmation of hyperkalemia, because cautious administration is safe — and not-to-promptly treat the patient risks losing the patient; and, iii) Not-to-recognize hyperkalemia as the cause of QRS widening and/or ST-T wave abnormalities will lead you down the path of potentially serious mis-diagnosis.

• BOTTOM Line: Emergency providers must be expert in recognizing hyperkalemia (and in recognizing those cases in which a presumptive diagnosis of hyperkalemia must be made until proven otherwise — knowing that in the meantime while waiting for lab confirmation, they should treat accordingly for presumed hyperkalemia).

It was not always this way! I trained in the mid-1970s. At that time, far fewer patients lived long enough with kidney failure to receive dialysis. End-stage renal failure (to the point of predisposing to frequent episodes of hyperkalemia) — was simply not a common disorder. So, in earlier days of my career — I saw much less hyperkalemia. 

• Nowadays, any provider who frequents any of the many international ECG internet forums will see numerous cases of hyperkalemia posted daily. We need to always keep this diagnosis in the forefront of our differential diagnosis!

For clarity — I’ve added in Figure-1 the “textbook” sequence of ECG findings seen with progressive degrees of hyperkalemia. While fully acknowledging that “not all patients read the textbook” — I have found awareness of the ECG generalizations in Figure-1 to be extremely helpful.

• PEARL #1 — Even if in an individual patient — these “general rules” are not strictly followed (ie, if QRS widening in your patient is seen before the serum K+ level = 8 mEq/L) — in any given patient, the sequence for development of the ECG findings suggested in Figure-1 tends to be surprisingly accurate (in my experience) over the patient’s early hospital course.

Figure-1: The “textbook” sequence of ECG findings with hyperkalemia (See text).

PEARL #2 — I love the image of the Eiffel Tower — and I have taught this visual aid for decades. Like the Eiffel Tower — the T wave with progressive degrees of hyperkalemia becomes tall, peaked (pointed) with a narrow base. While patients with repolarization variants or acute ischemia (including the DeWinter T wave pattern) often manifest peaked T waves — the T waves with ischemia or repolarization variants tend not to be as pointed as is seen with hyperkalemia — and, the base of those T waves tends not to be as narrow as occurs with hyperkalemia.

• Take a Look at Figure-2 — in which for clarity, I have reproduced the first 3 tracings shown in this case. Don’t YOU See the Eiffel Tower effect for the T waves in ECG #1 — and especially for the T waves in ECG #3?

Figure-2: The first 3 ECGs in this case (See text).

PEARL #3 — In my experience, “All bets are OFF regarding QRS morphology” in the presence of significant hyperkalemia. For example, in ECG #1 — Despite the markedly leftward axis — this is not the typical picture of LAHB because: i) the inferior r waves are so tiny; and, ii) there are virtually no positive forces in lateral chest leads (ie, there is no more than a tiny r wave in leads V4-thru-V6). As a result — I immediately suspected something else was going on!

• Also — Although there is a tall R wave in lead V1 of ECG #3 — there should be NO way this picture is confused with RBBB because: i) this QRS in lead V1 is both amorphous and very wide (nearly 0.20 second); ii) the QRS complex in ECG #3 is already all negative by lead V3, and stays virtually all negative through to lead V6 (and you virtually never see this with RBBB); and, iii) the Eiffel Tower effect is especially obvious in ECG #3 — so we should KNOW that “All Bets are OFF” regarding QRS morphology with an ECG like this, in which the reason for QRS widening is almost certain to be hyperkalemia.

PEARL #4 — In my opinion, it is not worth wasting time trying to figure out the specific rhythm diagnosis of a bradycardia when there is hyperkalemia. I used to spend hours trying to do this — but after years of doing so, I finally realized: i) That a specific rhythm diagnosis is rarely possible when there is significant hyperkalemia — and, even if you succeed in making a diagnosis such as Wenckebach — chances are as serum K+ intra/extracellular fluxes change, that the cardiac rhythm will also soon change; and, ii) Clinically — it does not matter what the specific rhythm diagnosis is once you recognize hyperkalemia that needs to be immediately treated — because usually within minutes after giving IV calcium, the “bad” rhythm will probably “go away” (often with surprisingly rapid reestablishment of sinus rhythm).

PEARL #5 — Reasons why assessment of the rhythm with significant hyperkalemia is so difficult are: i) As serum K+ goes up, P wave amplitude decreases, and eventually P waves disappear (See Panels D and E in Figure-1); and, ii) As serum K+ goes up — the QRS widens.

• Think for a moment what the ECG is going to look like IF you can’t clearly see P waves (or can’t see P waves at all) — and, the QRS is wide? ANSWER: The ECG will look like there is a ventricular escape rhythm, or like the rhythm is VT if the heart rate is faster.
• Ultimately, patients with progressively worsening degrees of hyperkalemia may die — and, VT/VFib is one of the likely mechanisms of death. (See THIS CASE — in which we never knew for certain IF the wide QRS was the result of hyperkalemia alone, or of hyperkalemic-induced VT — though this did not matter clinically, since in either case the immediate treatment of choice would be IV calcium that this patient was given).

PEARL #6 — As noted above, with progressive hyperkalemia — P wave amplitude decreases until ultimately P waves disappear. Interestingly, the sinus node is often still able to transmit the electrical impulse to the ventricles, even though no P wave may be seen on ECG. This is known as a sinoventricular rhythm.

• Take Another Look at the rhythm in ECG #1. It is extremely difficult to know IF there are (or are not) P waves in this tracing (ie, some small amplitude deflections that might be P waves seem to be present in the long lead V1 rhythm strip in front of beats #2 and 4, and perhaps elsewhere — or perhaps not ...). In addition — Note slight-but-real irregularity of the R-R interval in this tracing (ie, the initial R-R interval is 7.0 large boxes, but then decreases and remains slightly irregular). Rather than AFib — I suspect we are seeing a sinoventricular rhythm in ECG #1 — with some sinus arrhythmia.

PEARL #7 — We can use calipers to assist with rhythm interpretation. I used them to verify the slight-but-real irregularity present for the rhythm in ECG #1. This is relevant — because this underlying irregular sinoventricular rhythm intermittently slows enough to allow a slightly accelerated ventricular escape rhythm at a slightly faster rate to take over.

• Note that beginning with beat #5 in ECG #3 — the QRS complex widens markedly! This does not reflect sudden development of RBBB (as we discussed in PEARL #3). Further support that beat #5 instead marks the beginning of a ventricular escape rhythm — is forthcoming from measurement of R-R intervals in the long lead V1 rhythm strip. Calipers make such measurement fast, EASY and accurate. Note that the R-R interval for the sinoventricular rhythm ( = beats #2, 3 and 4 in ECG #3) is longer (ie, 6.6-to-6.8 large boxes) — than the R-R interval for the slightly accelerated ventricular escape focus (which measures 6.3 large boxes for the first 2 beats). Thus, there is a reason why the ventricular escape focus takes over the rhythm — which is, that the ventricular escape focus is slightly faster than the underlying sinoventricular rhythm.
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• Beyond-the-Core — Did YOU Notice what happens before beat #2 in the long lead V1 rhythm strip of ECG #3? Unfortunately, the beginning of this rhythm strip was cut off — but we DO see a very wide and deep T wave (just above the #1) that tells us that beat #1 was from the ventricular escape focus! The reason the sinoventricular rhythm was able to prevail for beats #2, 3 and 4 — is that the R-R interval prior to beat #2 is shorter than the R-R interval of the ventricular escape focus. This confirms that change to a much wider QRS in the rhythm strip of ECG #3 is rate-related — with the ventricular escape focus taking over when the sinoventricular rate drops below the slightly accelerated ventricular focus.

PEARL #8 — It is impossible to know how much the hyperkalemia is influencing QRS width and ST-T wave morphology until you normalize serum K+ and then REPEAT the ECG! Appreciation of this PEARL #8 is important for assessing ischemia — because hyperkalemia may either mimic or mask ischemic ECG changes!

• In the case at hand — it turned out that the unusual QRS morphology in ECG #1 was in fact indicative of LAHB, despite how tiny the initial r waves in each of the inferior leads were. We know this because the baseline ECG ( = ECG #2) showed a nearly identical QRS morphology in the inferior leads (albeit the QRS was narrower in this baseline tracing).
• That said — QRS morphology in virtually all chest leads is significantly different in the baseline tracing ( = ECG #2) — compared to the initial ED tracing ( = ECG #1). Note how the peaked, hyperkalemic T waves in ECG #1 masked the shallow, ischemic T wave inversion in the baseline tracing. Hyperkalemia shows the net effect of what underlying ST-T waves looked like + T wave peaking with narrow base from increased serum K+. Only after correcting hyperkalemia — will you be able to determine whether ischemic ST-T wave changes exist.

Our THANKS to Dr. Meyers for presenting this truly interesting case!