Recommended Citation: Roussas A and Feldman R. Cool County Cases - Recurrent and Refractory Torsades de Pointes [Internet]. Cook County Emergency Medicine Residency. 2023;Available from: https://cookcountyem.com/blog/2023/12/3/8dnvdo1yiiar5jqgl18pdmlfjs5ntz
The Case:
A 40-year-old female presents to the emergency department for palpitations and lightheadedness. She has a history of depression on citalopram, migraines on amitriptyline, and was recently prescribed tramadol after she broke her wrist. She is well-appearing, and while being placed on the monitor, she becomes anxious, stating the symptoms are recurring. An ECG is performed, with Figure 1 serving as a representative EKG. The patient is awake and talking. Defibrillator pads are placed and 2 g IV magnesium is administered twice each over ten minutes resulting in the termination of the prior rhythm. A repeat EKG is obtained and is similar to that in Figure 2. The patient remains stable, but then degenerates again into an aberrant rhythm. What do you do next?
Figure 2. Adapted from wikipedia. Source: https://en.wikipedia.org/wiki/Long_QT_syndrome
Discussion:
The initial EKG above shows polymorphic ventricular tachycardia (PVT). Although commonly referred to as torsades de pointes (TdP), not all PVT is TdP. A diagnosis of TdP is made by the combination of polymorphic ventricular tachycardia in addition to a prolonged QT-interval. This is an important distinction to make because treatment of PVT without prolonged QT will involve QT-prolonging agents such as amiodarone, procainamide, and beta-blockers. However, these medications must be avoided in patients with TdP, as the underlying cause of the rhythm is itself long QT. Similarly, the medications used to treat refractory TdP from acquired LQTS (aLQTS) will be harmful in treating PVT without prolonged QT or TdP from congenital long-QT syndrome (cLQTS) (1,2).
Table 1. Summary basic approach to TdP and PVT and the effect of beta-blockade.
This is due to differences in how TdP is triggered in aLQTS versus cLQTS. In both instances, TdP occurs when an early after depolarization (EAD) stimulus is generated during the repolarization phase of the cardiac action potential (also known as R on T phenomenon). The resulting electrical stimulus produced remains greater than the action potential threshold for multiple beats - i.e. the myocardium never returns to resting membrane potential - and this appears on a 12-lead ECG as a malignant ventricular arrhythmia. In aLQTS, an unstable cardiac membrane is prone to EADs. When the QT interval is lengthened, these asynchronous depolarizations are more likely to occur during depolarization and evolve into ventricular fibrillation or PVT. Intuitively, agents that slow down the heart (beta-blockers) will lengthen the QT interval and increase the risk of developing a malignant arrhythmia. Contrast this with cLQTS: the QT interval is always prolonged and EADs are not just produced by an unstable myocardium, but also due to the patient’s underlying membrane channel malfunctions rendering their myocardium hypersensitive to sympathetic input. As such, treatment should be focused on inhibiting sympathetic flow (beta-blockade), which results in improved control due to limiting sympathetic inflow and reducing EADs. However, nodal blocking agents used to treat ventricular tachycardia without QT prolongation, such as amiodarone or procainamide, must, again, be avoided, as these are QT-prolonging agents. A complete approach to treating cLQTS can be found in Wilde et al. (2).
Ultimately, TdP is ventricular tachycardia, and therefore, initial management consists of standard ACLS care with defibrillation. Initial management protocols for TdP are built to prevent recurrence, with a simplified protocol available in Table 2 (3). For stable patients, begin with 2 g IV (25-50 mg/kg in pediatrics) magnesium push over ten minutes, followed by additional doses as needed and a 1-4 g/hr (0.5-1.0 mg/kg/hr in pediatrics) magnesium infusion. Rapid pushes should be avoided as hypotension may occur, but it may be administered over 1-2 minutes in unstable patients in conjunction with ACLS. If the rhythm is terminated, assess the QT interval, evaluate for other causes of QT prolongation (hypo-kalemia, -calcemia, -magnesemia, -thermia, etc.), and maintain potassium between 4.5-5.0 per AHA guidelines (3). If the QT interval is prolonged, the patient is at high risk for recurrence - this is the purpose of the magnesium drip. Other mimics of TdP should be considered in refractory cases.
Table 2. GFR-directed magnesium resuscitation of TdP.
Some patients may develop “torsade storm,” which is defined as three or more episodes of TdP in 24 hours. If no infusion was given, a therapeutic level of magnesium was likely not obtained or not sustained given levels have been found to decrease significantly after only a few hours in patients with intact renal function (2). If serum magnesium is below 3.5 mg/dL, the magnesium protocol above can be repeated. Further interventions, such as chemical overdrive pacing with isoproterenol and overdrive transcutaneous/transvenous electrical pacing, can be utilized with a goal heart rate of 90-110 bpm (1,3,4). Be mindful that isoproterenol is contraindicated in patients with cLQTS, PVT without QT prolongation, acute MI, and severe hypertension. Other options include lidocaine, a type 1B antiarrhythmic that weakly blocks sodium channels and thereby shortening the QT via a decrease in the action potential and refractory period duration, and also phenytoin, a voltage-gated sodium channel blocker (1, 5-7). These options may be more attractive than isoproterenol as temporizing measures to electrical overdrive pacing given their availability in most EDs. In the stable patient, all of these should be initiated in collaboration with a cardiologist.
Table 3. Lidocaine and phenytoin dosing for refractory aTdP.
Authored by Adam Roussas, MD and Robert Feldman, MD
References:
Thomas SHL, Behr ER. Pharmacological treatment of acquired QT prolongation and torsades de pointes. Br J Clin Pharmacol. 2016;81:420-427.
Wilde AAM, Amin AS, Postema PG. Diagnosis, management and therapeutic strategies for congenital long QT syndrome. Heart. 2022;108:332.
Farkas J. Torsade de pointes. EMCrit Project.
Charlton NP, Lawrence DT, Brady WJ, Kirk MA, Holstege CP. Termination of drug-induced torsades de pointes with overdrive pacing. Am J Emerg Med. 2010;28:95-102.
Omar HR, Sprenker C, Karlnoski R, Mangar D, Camporesi EM. The use of isoproterenol and phenytoin to reverse torsade de pointes. Am J Emerg Med. 2014;32:683.e5-683.e7.
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Mukhopadhyay S, Chakraborty P, Yusuf J, Goyal A, Tyagi S. Phenytoin in treatment of amiodarone-induced Torsades de pointes. Indian J Pharmacol. 2012;44:264.