Torsades de pointes and the classic short-long-short activation sequence in the setting of atrial fibrillation 

Torsades de pointes (TdP) is an ominous form of rapid polymorphic ventricular tachycardia occurring in the setting of QT prolongation that must be addressed immediately as it often leads to ventricular fibrillation. TdP is associated with many factors that prolong the QT interval, including hypokalemia, hypomagnesemia, hypocalcemia, drugs (antiemetics, antipsychotics, SSRI's, TCA's, macrolide and fluoroquinolone antibiotics) and congenital long QT syndrome. We present a case of TdP in the setting of electrolyte abnormalities and atrial fibrillation with a classic short-long-short (SLS) activation sequence on EKG prior to deteriorating into TdP.

An 88-year-old female with a history of atrial fibrillation and dementia presented to the emergency room with progressive weakness. Patient requires total care from her son at baseline. Her vitals were stable on arrival. Chemistry revealed hypokalemia, hypocalcemia, and hypomagnesemia which were contributed to poor appetite. Her troponin was elevated. Urinalysis revealed pyuria suggestive of urinary tract infection. Patient's EKG revealed atrial fibrillation and old left bundle brand block on arrival. She was given magnesium oxide and potassium chloride for electrolyte replacement.

Shortly thereafter, the patient was noted to have several episodes of non-sustained ventricular tachycardia. Multiple EKGs were performed and exhibited prolonged QTc greater than 500 ms. While in the emergency room, patient was noted to have seizure-like activity and found to be pulseless. The EKG during this period showed a run of atrial fibrillation that progressed to TdP after a SLS activation sequence. The patient required chest compressions, one round of epinephrine and defibrillation before achieving ROSC with spontaneous movement and breathing. She was admitted to ICU and received aggressive electrolyte replacement and non-QT prolonging antibiotic treatment for her urinary tract infection. Her home medication list was reviewed and trazadone was discontinued due to potential QTc prolongation. Her troponin was concluded to be type 2 myocardial infarct in the setting of active infection and defibrillation. She did not have any additional arrhythmia throughout her hospital stay.

TdP is an uncommon but well recognized polymorphic ventricular tachycardia pattern that involves a twisting of the QRS complexes around the isoelectric line. In the setting of QTc prolongation, a SLS activation sequence has been observed to precede TdP. The sequence was theorized to promote heterogeneity of myocardial repolarization that creates potential reentry that results in TdP. Our case demonstrated another layer of arrhythmia as patient has underlying atrial fibrillation. The R-R variation in atrial fibrillation makes the widely used Bazett formula difficult to access QTc. Additionally, atrial fibrillation has been described in literature to be associated with TdP when treated with Class III antiarrhythmic for rhythm control. TdP occurring in atrial fibrillation in the absence of antiarrhythmic drugs is poorly understood. Prompt recognition of this life-threatening arrhythmia and prompt defibrillation to restore perfusion rhythm continues to be the cornerstone of treatment for an unstable patient with TdP. A careful history and medication reconciliation often guide prompt action to prevent future occurrence.