The ECG demonstrates sinus tachycardia, with subtle P waves merging into the preceding T waves (as shown in the image). There is right axis deviation, QRS prolongation (>100 ms), and a distinct terminal R wave in aVR (also highlighted in the image). The QT interval is prolonged as well.
Although ST elevation in aVR and V1 may raise concern for acute MI, and a wide QRS can occur in hyperkalemia, the overall ECG pattern, combined with the patient’s symptoms (decreased level of consciousness and severely low blood pressure) strongly suggests sodium channel blocker toxicity, most classically TCA overdose given the patient’s history of depression , or toxicity from certain class I antiarrhythmic agents.
A 53 y woman with a history of peptic ulcer disease, depression, and hyperlipidemia is brought to the ER after being found unresponsive with severely low blood pressure.
A 62-year-old man was found to have an irregular heartbeat during a routine physical exam. He feels completely fine and denies chest pain, palpitations, or shortness of breath.
A 45 year old man comes to the ER with sudden onset rapid palpitations while at work. He has no prior cardiac history and says, “It started all of a sudden.”
This is a real arrhythmia, not an artifact. Careful review shows an irregular, continuously changing QRS morphology consistent with polymorphic VT. The arrhythmia begins with a PVC falling on the preceding T wave (R on T phenomenon), even though the QT interval is normal. Recognizing this pattern is crucial, as management differs entirely from a benign tracing or technical artifact.
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