Friday, December 18, 2020

A woman with near-syncope, bradycardia, and hypotension

 Written by Pendell Meyers

A 59-year-old woman with diabetes, hypertension, prior stroke, and peripheral vascular disease presented with multiple near-syncopal events over the past 2 days, as well as ongoing back pain. EMS found her bradycardic in the 40s and administered atropine with no response. She was mentating and had a reasonable blood pressure (around 90s systolic), so they decided not to pace prehospital.


On arrival the patients blood pressure was 79/50 mm Hg. She was still awake and alert. Here is her first ECG (no baseline available):

What do you think?

 - junctional bradycardia (no P waves, slow regular QRS rhythm, QRS is slightly wide [computer 119ms] but not wide or disorganized enough to be ventricular in origin)
 - widened QRS (as above, must assume QRS widening is new until proven otherwise)
 - QRS with LAFB morphology
 - Peaked T waves in V2-V5

Diagnostic of severe hyperkalemia. No evidence of inferior OMI (which should always be scrutinized for to explain sick bradycardia, because the RCA usually supplies the SA and AV nodes).

The provider read this as a junctional bradycardia. There was no initial recognition of hyperkalemia. Dopamine was started as well as a fluid bolus, yet the heart rate was still in the high 30s. Cardiology was called emergently for advice as to whether they should start pacing.

The labs returned in time to show a potassium level of 7.1 mEq/L before pacing was performed.

She received calcium, insulin, dextrose, and lasix. The heart rate and blood pressure were reported to improve within minutes of calcium, however no ECG is recorded at that time. Further labs revealed acute renal failure. 

She had no further hemodynamic instability, and she was admitted.

The next morning her labs showed a potassium concentration of 4.5 mEq/L. Here is her ECG around that time:

Much improved. Sinus rhythm. QRS slightly narrower (computer says 110 ms), but LAFB morphology appears to be baseline. The T waves are still slightly peaked.

Learning Points:

Remember the "Killer B's" of hyperkalemia: Brady, Broad, Blocks, and Bizarre. These findings are associated with especially high risk of deterioration and cardiac arrest from hyperkalemia (peaked T waves less so, but do not be reassured). This patient has 2/4 (bradycardia and widening of the QRS complex).

Hyperkalemia treatment likely prevented cardiac arrest in this patient, and it could have been recognized and treated sooner.

Emergency medicine providers have to be the experts on acute severe hyperkalemia, and the ECG is the key to mastering this.

Never pace a patient without first considering calcium and hyperkalemia.


  1. Dr smith.
    Good case..
    Sir, How about
    Q Wave in V1 V2 ,
    Negative sinus P in V2 ,
    STE aVR .

  2. Q wave in V1 could be normal. Q wave in V2 is usually abnormal, could be prior anterior MI or other reasons. Normal sinus P waves in V1 are biphasic up-down (RA-LA). The p wave in V2 has the same appearance which to me looks normal. The STE in aVR I don't have a meaningful explanation for; usually STE in aVR is simply reciprocal to the rest of the ECG, but I don't really see a lot of STD elsewhere. Maybe a little in II. I would ignore it in this case.

  3. Sir can we call this as a junctional escape rhythm?

    1. It is hard to know for certain. Hyperkalemia often abolishes atrial depolarization even though the sinus node remains a pacemaker.


DEAR READER: I have loved receiving your comments, but I am no longer able to moderate them. Since the vast majority are SPAM, I need to moderate them all. Therefore, comments will rarely be published any more. So Sorry.

Recommended Resources