R.E.B.E.L. ECG of the Week #4

29 Nov
November 29, 2013

R.E.B.E.L. EM ECG of the Week #462 year old male with chief complaint of weakness.  Patient had a complicated hospital course including necrotizing fasciitis which required surgical debridement and IV antibiotics.  Patient was discharged home with oral antibiotics and returned to the ED with a chief complaint of weakness, abdominal pain, and 3 weeks of loose bowel movements.

BP: 100/51     HR 93     RR 16     Temp 97.2     O2 Sat 98% on RA

ECG from triage is shown…

Before reading on, try to come up with your own interpretation of this ECG before moving on to the final impression

Hypokalemia U Wave

  • Rate: Ventricular rate 81
  • Rhythm: Normal Sinus Rhythm
  • Axis: Normal Axis
  • Final ECG Interpretation: U waves consistent with hypokalemia

Hypokalemia is the most common electrolyte abnormality encountered in clinical practice (i.e. K+ <3.6 mmol/L seen in over 20% of hospitalized patients) [1]. As serum potassium levels decline, the transmembrane potassium gradient is decreased causing an elevation in the resting membrane potential and a prolongation of the action potential (Phase 3 repolarization).  Therefore, the earliest ECG changes associated with hypokalemia is decreased T wave amplitude [2].  At extreme, low levels of potassium a positive deflection after the T wave (U wave) can be seen.  The U wave is best seen in the mid-precordial leads (i.e. V2 and V3) [2].

Action Potential

What are some electrocardiographic findings associated with hypokalemia? [2]

  • Flattening of T wave
  • T wave inversion
  • ST segment depression
  • Prominent U waves
  • Prolongation of QT (U) Interval
  • Ventricular tachycardia
  • Torsades de pointes

Case Conclusion:  Patient was diagnosed with C. Diff Colitis.  Initial K+ was 1.3 shown on the ECG above.  Potassium was aggressively replaced and ECG changes in lead V2 are shown as the potassium started to correct below.

Hypokalemia U Wave

References:

  1. El-Sherif N et al. Electrolyte Disorders and Arrhythmogenesis. Cardiol J 2011. PMID: 21660912
  2. Diercks DB et al. Electrocardiographic Manifestations: Electrolyte Abnormalities. JEM 2004. PMID: 15261358
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Salim Rezaie

Emergency Physician at Greater San Antonio Emergency Physicians (GSEP)
Creator & Founder of R.E.B.E.L. EM
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8 replies
  1. Adrian Baranchuk says:

    Nice case. I was wondering how the magnesium was. Hypomagnesemia can give rise to gigantic U-waves and it usually associates with hypokalemia. We published few years ago, the “tee-pee” sign for multimple electrolyte disorders in ANE (Johri et al, Annal Noninvasive Electrocardiology). I can send the PDF to those interested. Best wishes. AB

    Reply
  2. Hec Moon says:

    Nice case,.woul it be possible for you to send me the tee pee article? Thanks
    Hec Moon,MD
    Venezuela

    Reply
  3. Hec moon, MD says:

    Interesting case, very nicely presented. Congrats.
    Please I would like to read about the tee pee sign.
    Hec Moon , MD
    Venezuela

    Reply
  4. Ken Grauer, MD says:

    Nice case. Agree completely with Adrian – Magnesium is the “forgotten cation” – and it may produce virtually identical clinical and ECG signs as hypokalemia. I’d add several points regarding this tracing:
    i) The QRS looks to be a bit wide. It is almost in the morphology of LBBB, albeit not really wide enough for this – so perhaps IVCD (vs incomplete LBBB) may be the best terminology for this. ST-T wave changes may at least in part be a result of this conduction defect.
    ii) I’m not sure what to make of the small q in II,aVF and the deep Q in lead III – esp. in view of the conduction defect.
    iii) In general – the ECG is neither optimally sensitive nor optimally specific for diagnosing hypokalemia. That said – the U waves in this tracing are HUGE (esp. in V1,V2) – so this would seem a big clue to the diagnosis – together with the long QT (ie, “QU” interval).

    Reply

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