Electrocardiographic artefacts mimicking atrial tachycardia resulted in unnecessary diagnostic and therapeutic measures
The patient was a 30-year-old female, with a past history of a traffic accident, which resulted in tetraplegia and autonomic dysreflexia as sequelae of trauma to the neck region. Since the accident, the patient had experienced repeated attacks of severe renal colic and urinary tract infections. These attacks were associated with episodes of hypertension and headache.\nThe patient was admitted to the intensive care unit to receive epidural anaesthesia after new repeated severe attacks of abdominal pain. During observation at the intensive care unit, the electrocardiogram monitor showed an apparent narrow QRS tachycardia with a QRS frequency of 150 to 180/min. She received repeated metoprolol injections 2 to 5 mg which had a doubtful effect. A few hours later, the apparent tachycardia worsened and the QRS frequency increased to 200 to 300/min. Her blood pressure was normal. The arrhythmia was interpreted as rapid atrial fibrillation by the managing internal medicine team, who administered intravenous sotalol 40 + 20 + 20 mg, which had no apparent effect on the arrhythmia.\nThe 12-lead surface ECG showed irregular narrow QRS complex tachycardia (). Two rhythms with two different QRS complex morphologies were noted in the same ECG. The first rhythm was irregular and had a frequency of 250 to 300/min (the rapid rhythm). The second was regular with a frequency of 130/min (the slower rhythm). The patient was very anxious, panic-stricken, and quivering all over. Because the initial drug treatment was ineffective, and the arrhythmia was at times apparently regular, further evaluation of the case by esophageal ECG recording was performed and repeated adenosine injections were administered ().\nThe esophageal ECG recording was made under chaotic circumstances. The patient did not like having the electrode in her esophagus. The esophageal electrode was inserted deeply in the esophagus and then pulled back very slowly while recording the ECG, including the esophageal lead, at a paper speed of 50 mm/sec and an amplification of 10 mm/mV. Adenosine 5, 10, and 15 mg were administered via the jugular vein. It was not possible to conclude what the esophageal ECG showed at the moment of examination, and the adenosine had no effect on the rapid tachycardia. A decision was made to perform electrical cardioversion. For anesthetic induction, sodium pentothal was administered. Surprisingly, the "resistant arrhythmia" terminated abruptly during sodium pentothal administration, and the ECG showed regular sinus tachycardia thereafter ().\nUpon review of the esophageal ECG recording (), P waves were noted before every QRS complex of the slower rhythm; this P wave was unrelated to the rapid rhythm. After identification of P waves in the esophageal ECG recording, a closer review of the 12-lead surface ECG () also revealed P waves before every QRS complex of the slower rhythm. Injection of adenosine 10 mg intravenously via the jugular vein reduced the slower rhythm to about 45 to 50 beats/min, and adenosine 15 mg caused further slowing (total block) of the slower rhythm, with the maximum recorded R-R interval of 3.5 seconds (). Even the blocked P waves can be seen clearly in leads V2 to V6 in the same figure (asterisk) continuing through the rapid rhythm. No change in the rapid rhythm was seen during or after bolus adenosine administration. We concluded that the slower rhythm was, in fact, the regular cardiac (native) rhythm and the rapid rhythm, which did not respond to antiarrhythmic drugs but disappeared completely after sodium pentothal injection, was most probably an extracardiac artefact, mimicking atrial fibrillation.\nFortunately, the purported rapid "arrhythmia" relapsed about 30 minutes after terminating the sodium pentothal. Blood pressure monitoring showed a normal, regular tracing, with a frequency that corresponded to the slower rhythm of about 130/min. Once again, the patient was shaking all over. Palpation of the radial pulse and cardiac auscultation revealed a regular rhythm with a frequency corresponding to the blood pressure tracing and the slower rhythm on the ECG monitor. The body movements and the apparent rapid arrhythmia disappeared completely after administration of 5-mg intravenous diazepam. Thus the rapid "arrhythmia" was diagnosed as an ECG artefact due to tremulous, quivering body movements.