Monday 2 February 2015

ECG of the Week - 26th January 2015 - Interpretation

These ECG's are from a 70 yr old male who presented to the Emergency Department following an overdose of unknown agent / agents.
The first ECG was performed on arrival the second ECG following intervention. 
Check out the comments on our original post here. 


Vital signs on arrival: 

  • GCS 8 (V=1 E=2 M=5)
  • BP 103/67
  • Temp 36.4 C (97.5 F)
  • BSL 5.8 mmol/L

ECG 1 On arrival to the Emergency Dept
Click to enlarge
Rate:
  • ~115 bpm
Rhythm:
  • Regular
  • Sinus rhythm
Axis:
  • Marked LAD / Extreme axis
Intervals:
  • PR - Normal (~180ms)
  • QRS - Prolonged (120-130ms)
  • QT - 360ms 
  • QTc - 500 ms (Bazette's)
Segments:

  • ST Elevation leads V1-3
  • ST Depression lead V6

Additional:

  • Terminal R wave lead aVR >3mm & R/S ratio >0.7
  • Prominent T waves in leads V1-4

Interpretation:

  • Broad Complex Tachycardia
  • QTc Prolongation
  • Terminal R wave aVR


In the setting of suspected or known overdose there are several agents that could cause this ECG picture. As a single agent the most likely culprit is a sodium channel blocking agent given the QRS prolongation and findings in lead aVR. Many of the sodium channel blocking drugs can also cause QT prolongation, although multiple non-sodium channel blocking drugs can also cause QT prolongation. The prominent T waves could be secondary to drug effects, acid-based disturbance but I'd also want an urgent potassium on this patient. 

So what did they do to this patient ?

We've got a patient after a suspect overdose of unknown agents, ECG features consistent with sodium channel toxicity +/- other ingestants and the patient has a significantly reduced conscious level. The patient received sodium bicarbonate bolus and was promptly intubated. Post intubation they were hyperventilated to a pH of 7.5 and given nasogastric charcoal. The following ECG is below.


ECG 2 Post Intervention
Click to enlarge
Rate:
  • ~72 bpm
Rhythm:
  • Regular
  • Sinus rhythm
Axis:
  • Normal
Intervals:
  • PR - Normal (~200ms)
  • QRS - Normal (80ms)
  • QT - 480ms
  • QTc - 530 ms (Bazette's)
Segments:

  • Minor ST elevation in leads V1 & V2
  • Significantly reduced ST elevation and QRS voltage when compared with 1st ECG

Additional:

  • Resolution of terminal R wave in lead aVR
Interpretation:

  • Resolution of features of sodium channel toxicity
    • QRS Narrowed
    • Terminal R wave resolved
  • Persistent QT Prolongation
The persistent QT prolongation in this case may be multi-factorial and could be caused by one or a combination of:
  • Hyperventilation / Respiratory Alkalosis
  • Drug toxicity either additional agents to sodium channel blocker or from single agent

The patient made an uneventful medical recovery with no episodes of TdP, seizure or other post-overdose complication. The agents ingested were never clearly identified as the patient had access to multiple drugs and would not reveal which were taken.

Management of Sodium Channel Toxicity

This is an ECG blog and I never wanted to re-invent the FOAM wheel so for more on sodium channel blocker toxicity check out these great cases from Life in the Fast Lane.



References / Further Reading

Life in the Fast Lane

Textbook
  • Chan TC, Brady WJ, Harrigan RA, Ornato JP, Rosen P. ECG in Emergency Medicine and Acute Care. Elsevier Mosby 2005.

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