Recurrent Syncope in the Emergency Department

Clinical Review & Education

Challenges in Clinical Electrocardiography

Recurrent Syncope in the Emergency Department A Lethal Cause Not for the Faint Hearted Derek S. Chew, MD; Saman Rezazadeh, MD, PhD; Robert J. Miller, MD

A woman in her 50s with a history of hypertension and alcohol abuse presented to the emergency department with 4 episodes of syncope in the preceding 24 hours. She denied prodromal symptoms of chest pain, dyspnea, palpitations or presyncope. Her medications included perindopril, metoprolol, and a magnesium supplement. On examination, her blood pressure was 121/79 mm Hg, heart rate was 65 bpm, and her respiratory rate was 24 breaths/min. She was afebrile and had normal oxygen saturations on room air. A 12-lead electrocardiogram (ECG) was obtained (Figure 1). Questions: What is the likely etiology of her syncope, and what should you do next?

ECG Interpretation The ECG revealed sinus rhythm at approximately 60 bpm, with diffuse nonspecific ST-segment changes, giant U waves, and slurring of the T waves into the U waves. It is challenging to assess the precise corrected QT(U) interval in the context of R-R interval variability and the presence of giant U waves; however, the QT(U)

interval is markedly prolonged and likely approximates 732 milliseconds. A couplet of premature ventricular contractions (PVCs) with different morphologies initiate on the T wave of the preceding beat.

Clinical Course While awaiting assessment in the emergency department, she suffered a cardiac arrest secondary to polymorphic ventricular tachycardia (VT) requiring cardiopulmonary resuscitation for several minutes with spontaneously recovery of sinus rhythm (Figure 2). During her cardiac arrest, she received intravenous magnesium 5 mg but did not require defibrillation. She was also given intravenous amiodarone 300 mg and began an infusion of 1 mg/min. Her heart rate decreased to 50 bpm, and she continued to have brief episodes (<30 second) of polymorphic VT. Her initial blood tests revealed a serum potassium value of 1.9 mmol/L (to convert to mEq/L, divide by 1.0) and serum magnesium of 1.07 mmol/L (to convert to mEq/L, divide by 0.5). She was admitted to the hospital, and a tem-

Figure 1. Initial 12-Lead Electrocardiogram

I

aVR

V1

V4

II

aVL

V2

V5

III

aVF

V6

V3

II

The electrocardiogram revealed sinus rhythm at approximately 60 bpm, with diffuse nonspecific ST-segment changes, giant U waves, and slurring of the T waves into the U waves. The QT(U) interval is markedly prolonged and

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approximates 732 milliseconds. A couplet of premature ventricular contractions with different morphologies initiate on the T wave of the preceding beat.

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Clinical Review & Education Challenges in Clinical Electrocardiography

Figure 2. Telemetry Monitoring in the Emergency Department Showing Torsades de pointes

The telemetry monitor revealed frequent premature ventricular contractions with "R on T" phenomenon that trigger runs of Torsades de pointes. The first episode of Torsades de pointes was self-terminating. The second episode of Torsades de pointes required defibrillation.

porary transvenous pacemaker was placed for overdrive pacing at a rate of 90 bpm while her electrolyte abnormalities were reversed. Amiodarone was also discontinued. Within 24 hours of her hospital admission, she developed significant alcohol withdrawal that required sedation and intubation. Upon review of her home situation, her family found many empty bottles of vodka and cough syrup that contained dextromethorphan.

Discussion Torsades de pointes (TdP) is a specific form of polymorphic VT that occurs in the setting of congenital or acquired QT(U) interval prolongation, typically with rates of 200 to 250 bpm. The original description of TdP or “twisting of the points” was coined in 1966, because the QRS complexes of changing amplitudes appeared to twist around the isoelectric line and reminded the authors of the TdP movement in ballet.1 Importantly, TdP is not simply a description of the twisting QRS morphology. Its definition also requires the presence of a prolonged QT(U) interval, generally exceeding 500 milliseconds. Other features of TdP include a short-long-short initiation pattern for VT, which consists of a short-coupled PVC followed by a compensatory pause and another PVC that falls close to the peak of the T wave (the so-called “R on T” PVC). This is due to the fact that the QT(U) interval is partially determined by the length of the preceding R-R interval, with a longer R-R interval generating a longer subsequent QT(U) interval. The resulting TU wave changes (ie, further QT[U] prolongation and abnormal morphology of the TU complex) following the postextrasystolic pause is one of best predictors of TdP.2 In addition, TdP episodes usually exhibit a warm-up phenomenon, with the first few beats E2

of exhibiting longer cycle lengths compared with subsequent beats. Finally, TdP often terminates spontaneously, with the last 2 to 3 beats showing slowing of the arrhythmia. However, TdP can degenerate into ventricular fibrillation resulting in sudden cardiac death.3 Accurate identification of TdP is critically important because the etiology and management of TdP is distinct from other types of polymorphic or monomorphic VT. The cornerstones of TdP management include correction of underlying causes, use of pharmacologic agents or temporary pacing to shorten the ventricular refractory period, and avoidance of antiarrhythmic drugs that may exacerbate TdP.4 Importantly, the use of class IA antiarrhythmics (such as procainamide) can prolong the QT(U) interval further, perpetuating the arrhythmia. Amiodarone, which also results in QT prolongation, is infrequently associated with TdP in the absence of electrolyte disorders and concomitant QT-prolonging agents.5 Intravenous magnesium should be given as a first-line agent regardless of the serum magnesium level, as a normal serum level may not reflect the intracellular stores which account for 99% of total body magnesium. Magnesium can attenuate episodes of TdP by decreasing calcium influx, thus lowering the amplitude of early afterdepolarizations that lead to TdP. As previously mentioned, increasing the heart rate with temporary pacing shortens the QT(U) interval and prevents pauses that lead to initiation of TdP. Isoproterenol can also be used to increase the heart rate until temporary pacing can be initiated.6 However, its use requires caution in patients with known coronary artery disease, older age, or other cardiac risk factors, because isoproterenol may increase myocardial oxygen demand resulting in ischemia. Immediate defibrillation should be per-

JAMA Internal Medicine Published online April 10, 2017 (Reprinted)




Challenges in Clinical Electrocardiography Clinical Review & Education

formed for patients with TdP that does not terminate spontaneously or that degenerates into ventricular fibrillation. This patient presented with multiple episodes of syncope likely due to episodes of TdP. Her initial ECG revealed a markedly prolonged QT(U) interval of 732 milliseconds, resulting from severe hypokalemia and potentially dextromethorphan ingestion.7 Upon replacement of serum potassium and clearance of her dextromethorphan, her QT(U) interval normalized to 440 milliseconds and her arrhythmias resolved.

Take-Home Points • Torsades de pointes is a specific form of polymorphic ventricular tachycardia requiring the presence of a prolonged QT(U) interval as part of its definition and is often preceded by a short-coupled premature ventricular contractions (PVC) followed by a compensatory pause and another PVC that falls close to the peak of the T wave (ie, short-long-short initiation pattern). ARTICLE INFORMATION Author Affiliations: Department of Cardiac Sciences, Libin Cardiovascular Institute of Alberta, University of Calgary, Calgary, Alberta, Canada. Corresponding Author: Derek S. Chew, MD, FRCP(C), Foothills Medical Center, 1403 29th St NW, Calgary, AB T2N 1T9, Canada ([email protected]). Section Editors: Zachary D. Goldberger, MD, MS; Nora Goldschlager, MD; Elsayed Z. Soliman, MD, MSc, MS. Published Online: April 10, 2017. doi:10.1001/jamainternmed.2017.0580 Conflict of Interest Disclosures: None reported. Additional Contributions: We thank Sheila Klassen, MD, for her helpful comments on an earlier draft of this manuscript; she was not compensated for her contributions.

• Torsades de pointes is usually self-terminating but can be associated with hemodynamic instability or degenerate into ventricular fibrillation. • The recognition of TdP and its differentiation from other forms of ventricular tachycardia are important for initiating specific management strategies (ie, intravenous magnesium, overdrive pacing). • The cornerstones of TdP management include: (1) the correction of underlying causes; (2) use of pharmacologic agents or temporary pacing to shorten the ventricular refractory period; and (3) avoidance of antiarrhythmic drugs that may exacerbate TdP. • Intravenous magnesium is a first-line agent regardless of the serum magnesium level, because a normal serum level may not reflect the intracellular stores which account for 99% of total body magnesium. Magnesium may attenuate episodes of TdP by decreasing calcium influx and lowering the amplitude of early afterdepolarizations that lead to TdP.

2. Cho MS, Nam GB, Kim YG, et al. Electrocardiographic predictors of bradycardia-induced Torsades de pointes in patients with acquired atrioventricular block. Heart Rhythm. 2015;12(3):498-505. 3. Drew BJ, Ackerman MJ, Funk M, et al; American Heart Association Acute Cardiac Care Committee of the Council on Clinical Cardiology, the Council on Cardiovascular Nursing, and the American College of Cardiology Foundation. Prevention of Torsade de pointes in hospital settings: a scientific statement from the American Heart Association and the American College of Cardiology Foundation. Circulation. 2010;121(8):1047-1060. 4. Vukmir RB. Torsades de pointes: a review. Am J Emerg Med. 1991;9(3):250-255.

REFERENCES

5. Hohnloser SH, Klingenheben T, Singh BN. Amiodarone-associated proarrhythmic effects: a review with special reference to Torsade de pointes tachycardia. Ann Intern Med. 1994;121(7): 529-535.

1. Dessertenne F. [Ventricular tachycardia with 2 variable opposing foci]. Arch Mal Coeur Vaiss. 1966; 59(2):263-272.

6. Zipes DP, Camm AJ, Borggrefe M, et al; American College of Cardiology/American Heart Association Task Force; European Society of Cardiology


Committee for Practice Guidelines; European Heart Rhythm Association; Heart Rhythm Society. ACC/AHA/ESC 2006 Guidelines for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death: a report of the American College of Cardiology/American Heart Association Task Force and the European Society of Cardiology Committee for Practice Guidelines (writing committee to develop Guidelines for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death): developed in collaboration with the European Heart Rhythm Association and the Heart Rhythm Society. Circulation. 2006;114(10):e385e484. 7. Kaplan B, Buchanan J, Krantz MJ. QTc prolongation due to dextromethorphan. Int J Cardiol. 2011;148(3):363-364.

(Reprinted) JAMA Internal Medicine Published online April 10, 2017



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Recurrent Syncope in the Emergency Department

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