An elderly patient with syncope, dyspnea, and weakness, but no Chest Pain, and mild hyperkalemia

An elderly patient had a fall from probable syncope, and could not get up.  He complained of weakness and shortness of breath, but no CP.  

Vital signs were normal.

Here is the first ED ECG:

COMPUTER INTERPRETATION:

Electronic Atrial Pacemaker.  Marked ST Elevation, ***ACUTE MI***

What do you think?

First, the QRS is incredibly wide!

You should ask for more history.  

Whenever a patient does not have chest pain, the pre-test probability of OMI is diminished.  Of course SOB, jaw pain, shoulder pain, etc can be a result of OMI, but the pretest probability is less and so you must scrutinize further.

The ECG: 

1.  It is NOT only atrial paced, it is ventricular paced. 

[Also: There is probably underlying atrial fibrillation (the computer will not tell you anything about atrial activity when there is a ventricular paced rhythm: Computer often fails to diagnose atrial fibrillation in ventricular paced rhythm, and that can be catastrophic]

2. A normal ventricular paced rhythm has a QRS duration of less than 200 ms.  This one is 320 ms!!

3.  Whenever the QRS is so wide, one must think of hyperkalemia or sodium channel blocker toxicity.

4. Although the ECG meets the Smith Modified Sgarbossa criteria, with proportionally excessively discordant STE in V2 - V4 and concordant STE in aVL (it appears to be a proximal LAD OMI), I suspect that there is no OMI here, but only toxicity.

Further history revealed that the patient is on flecainide to prevent paroxysmal atrial fibrillation (to keep him in sinus rhythm).  His Cr. was elevated.  Flecainide is renally excreted, and the patient's GFR was reduced to 20 mL/min.

He has a h/o 3rd degree heart block and has a pacemaker.  

The K was 5.8 mEq/L

Here is the PM Cardio Bot (Queen of Hearts) interpretation:

This is classic flecainide toxicity and the ST abnormalities are unlikely to be due to OMI (though possible)

Why syncope?

His pacemaker was interrogated and it was found that the pacemaker was not adquately capturing.  This can happen with hyperK, flecainide toxicity, or certainly both together.

The patient was taken off flecainide and 2 days later this was recorded with a Creatinine of 1.85 (down from 3.14) and K of 3.3.

The QRS is not approprately below 200 ms and there is no signs of Modified Sgarbossa Criteria

Other cases of flecainide effect or toxicity from this blog 

See even more cases of paced rhythm with hyperkalemia farther below

1.  Here, Flecainide toxicity mimics RBBB with anterior OMI:

Right Bundle Branch Block with New Anterior ST elevation 

2.  Here, Flecainide toxicity in the setting of ventricular paced rhythm mimics hyperK:

Weakness and Dyspnea with a Sine Wave. It's not what you think!

3.  Finally, a fascinating case of the odd aspect of"use dependence" with flecainide toxicity: it's effect on the QRS is often dependent on the heart rate.

Note how the QRS gets wider when the HR gets higher:

Hyperkalemia and Paced Rhythm

Paced rhythm with wide QRS due to K 8.2

Is This a Simple Paced Rhythm?

NO.

the K is 6.8 and it results in a paced sine wave

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MY Comment, by KEN GRAUER, MD (5/21/2023):

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Flecainide toxicity is a relatively uncommon — but extremely important condition to recognize. Dr. Smith provides links to a number of related cases we've presented on this ECG Blog. In Figure-1 — I've reproduced the initial ECG shown in today to illustrate key concepts associated with this entity.

• As per Dr. Smith — Although ECG #1 manifests eye-catching ST elevation in anterior leads V1-thru-V4 — this tracing is much more likely to represent Flecainide Toxicity, and not an acute OMI.
• That said, even more concerning to me than the anterior lead findings — is the shape of the ST elevation in lead aVL — and the ledge-like reciprocal ST depression in leads III, aVF and V6.
• 
  
• To Emphasize: I completely agree with Dr. Smith that the ECG abnormalities in Figure-1 will most probably resolve as this patient's Flecainide toxicity is treated — but ruling out the possibility of superimposed infarction with serial troponins will be prudent.

Why Is Flecainide Toxicity the Most Likely Diagnosis?

As per Dr. Smith — the QRS complex of the paced rhythm in Figure-1 is dramatically widened (ie, to 320 msec.). Hyperkalemia was not the primary cause of this — since serum K+ was only modestly elevated (to 5.8 mEq/L). Instead — the patient was predisposed to Flecainide toxicity given older age and renal insufficiency. Excessive Flecainide may result in the following (Levis — Permanente Journal 16(4): 53, 2012) (Strangio et al — Eur Heart J, 2022) (Andrikopoulos et al — World J Cardiol, 2015) (Dardas and Khan — Eur Soc Cardiol, 2021):

• Depressed contractility; hypotension (negative inotropic effect).
• Depression of all major conduction pathways (ie, in the AV Node; His-Purkinje system, in the ventricles). This may result in a series of conduction disorders including various forms of AV block; bundle branch blocks; impaired pacemaker function. The QRS may be markedly widened and bizarre in morphology.
• 
  
• Flecainide Toxicity is suggested when: i) There is ≥50% increase in QRS duration (typically producing a QRS ≥0.18 second); and/or, ii) A ≥30% increase in PR interval duration (typically to a PR ≥0.26 second). The QTc may also be increased (though much of this effect is the result of QRS rather than QT prolongation).
• Lethal arrhythmias may be a terminal event (VT/VFib; Asystole).
• 
  
• BOTTOM Line: As per Dr. Smith — Flecainide toxicity is the most likely primary cause of the ECG findings in Figure-1.

Figure-1: The initial ECG in today's case.