A 50s year old man with lightheadedness and bradycardia

 Written by Pendell Meyers with edits by Smith and Grauer

A man in his 50s with history of end stage renal disease on dialysis, prior bradycardia episode requiring transvenous pacemaker, diabetes, and hypertension, presented to the ED for evaluation of acute onset dizziness and lightheadedness starting several hours prior to arrival. These symptoms prevented him from going to dialysis, and his last session was three days ago. EMS found him with a heart rate of 30 bpm but normal blood pressure. He received 0.5 mg atropine with increased in heart rate to the 60s with improvement in symptoms. He denied chest pain or shortness of breath. 

Here is his triage ECG at 1533:

There is a regularly irregular rhythm with RBBB and possibly also LAFB morphology. The T waves are definitively peaked in many leads. The rhythm is possibly junctional with pauses or block, I'm not exactly sure. I asked Ken Grauer for help with this rhythm and he agrees it cannot be atrial fibrillation due to the irregular regularity, but with the artifact present also cannot definitively find atrial activity. His bottom line: "This rhythm is not 'following the rules' - so either hyperkalemia - or some other toxicity - or very severe and diffuse conduction system disease producing junctional escape with bifascicular block with some complex form of exit block." See his full comments reproduced at the end of the post. 

This ECG is diagnostic of significant hyperkalemia.

He was immediately given 2gm calcium gluconate, insulin and dextrose. Shortly after those therapies his heart rate is documented as improved to the 70s.

Initial labs showed a potassium level of 7.7 mEq/L.

Repeat ECG at 1801:

Improved heart rate and narrower QRS.

He later received a second dose of 2 gm calcium gluconate for down-trending heart rate.

He was emergently dialyzed and did well.

No more ECGs were recorded from this visit, unfortunately.

Approximately 1 year prior to this event, he had a similar event and presented with this ECG:

Junctional escape with similar RBBB and LAFB morphology, and peaked T waves. Notice the flat ST segments and narrow base of the T waves. This ECG was apparently not recognized as hyperkalemia (!). In my experience, these are some of the most commonly missed and dangerous hyperkalemia ECGs because many practitioners rely heavily on strikingly peaked T waves to start considering hyperkalemia on ECG. These T waves are in fact peaked, but they are more subtle than the textbook hyperkalemia ECG.

During this visit, the patient received transcutaneous pacing and an emergent transvenous pacemaker before the labs showed a potassium level of 7.3 mEq/L!

After treating his hyperkalemia, the pacemaker was successfully discontinued. He never received a permanent pacemaker.

After dialysis during that visit, a repeat ECG was recorded showing resolution of the RBBB/LAFB:

Notice the marked difference in the T-waves

Learning Points:

In medical school, I worry that the only consistent teaching you get about hyperkalemic ECG findings is peaked T waves and QRS widening. What should be taught includes the "Killer B's of Hyperkalemia": Broad (QRS widening), Brady (bradycardias), Blocks (AV blocks, bundle branch blocks), and Bizarre (bizarre morphology, OMI mimics, etc.). Some of the most important hyperkalemia ECGs are like the above: QRS widening that can be subtle or falsely blamed on RBBB alone, and T waves that are not perceived as classically peaked. Yet this ECG above is far more dangerous and far more hyperkalemic than the classic hyperkalemia ECG with only peaked T waves in the textbook.

Before you consider pacing a patient, consider hyperkalemia. I would go so far as to say that every patient about to be paced should receive calcium, unless there is certainty of a non-hyperkalemia diagnosis as the cause.

=====================================

Ken Grauer's comments on the rhythm in the first ECG of this case (he was completely blinded to all case details, just the ECG):

This is tough — and I do NOT have a definite answer. I labeled the tracing (Figure-1):

Figure-1: The 1st tracing in today's case.

Artifact makes it difficult to assess for the presence of atrial activity. I thought BLUE arrows might represent retrograde P waves (as their placement seems pretty consistent) — but there is a lot of “noise” in the baseline — so I’m not sure if this really represents retrograde atrial activity or not …

What we DO know — is that the QRS is wide, and NO P wave precedes any QRS. We also know (as per Pendell) — that this isn’t AFib, because there is a definite pattern ( = a “regular regularity” to the rhythm) — with both the short intervals (between #1-2; 4-5; 6-7) all equal — and the long intervals (between #2-3; 5-6; 7-8) also all equal.

My #1,2,3 questions are what is the serum K+ level? We have a wide QRS and T waves really are peaked in multiple leads (even though the base of these T waves isn’t as narrow as is usually seen with hyper-K+) — but Hyperkalemia is notorious for QRS widening, brady rhythms and ALL SORTS of conduction disorders that do not “obey the rules” …

So if K+ is normal — then we really have an RBBB/LAHB configuration without sinus P waves — so suggesting perhaps origin of a ventricular rhythm near the left anterior hemifascicle — vs junctional escape with bifascicular block … (the surprisingly narrow initial part of the QRS suggests origin not directly from ventricular myocardium).

What is unusual for a simple block (or “exit block”) — is that the duration of the pauses. You can have an ectopic ventricular focus (even VTach) with various degrees of “exit block” out of the ventricular focus — but against the usual form of exit block is the fact that the long intervals (between #2-3; 5-6; 7-8) is clearly MORE than twice the shortest interval …

Of note — the R-R interval between beats #3-4 is LONGER than that between #4-5. I do not think this is for chance — and this is what you tend to see with Wenckebach phenomenon — but unlike typical Wenckebach phenomena is the overly long pauses (more than twice the shortest R-R interval). NOTE — You CAN have a ventricular rhythm (including VTach) with a Wenckebach-type of exit block … 

BOTTOM LINE: This rhythm is not “following the rules” — so either hyperkalemia — or some other toxicity — or very severe and diffuse conduction system disease producing junctional escape with bifascicular block (vs ventricular escape near the anterior hemifascicle) with some complex form of exit block …

Hope the above is helpful. Let me know if you find out more clinically about the patient — :) Ken

==============================

Here are a couple other cases of hyperkalemia with small, but peaked, T-waves:

Patient with Dyspnea. You are handed a triage ECG interpreted as "normal" by the computer. (Physician also reads it as normal)

This is on a previous visit with K = 6.6:

After treatment: 

ST Elevation in I and aVL, with reciprocal ST depression in lead III