Rhythm Nation: December 2015 ANSWER!

Published by carmellig on

First, lets interpret the initial ECG:

 

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  • My Interpretation:
    • Sinus rhythm with junctional bigeminy, occasional unifocal premature ventricular complexes. There is also a reported QTc of 548ms, which is significantly prolonged.

 

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The next Rhythm on the cardiac monitor was:

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  • My Interpretation:
    • This was a polymorphic, wide complex tachycardia

 

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Question 1: DDx for this rhythm

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  • The rhythm is polymorphic ventricular tachycardia and more specifically, Torsades de Pointes (TdP)
  • A little background on Torsades de Pointes (TdP)
    • TdP is defined as a polymorphic ventricular tachycardia in a patient with a preceding, prolonged QT interval1.
    • TdP accounts for fewer than 5% of SCD cases, and death usually occurs when TdP degenerates into the more deadly ventricular fibrillation1.

 

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Question 2: Risk factors for Torsades de Pointes (TdP)
  • TdP occurs in a patient with a Long QT syndrome (LQTS). There are two types:
    • Congenital LQTS
      • Congenital LQTS results from an autosomal dominant mutation resulting in a channelopathy1,2
    • Acquired LQTS (Many causes. Here are a few:)
      • Medications with QT-prolonging effects are the most frequent causes of acquired LQTS, estimated to occur with approximately 2-3% of all prescriptions written3,4
        • Most medications prolong the QT interval through direct inhibition of the outward flow potassium channels that allow repolarization5,6
        • The list of medications is vast and constantly growing. You can find up-to-date lists at one of the following websites:
        • Methadone has an FDA-approved black-box warning for its known effects on QT prolongation7,8.
      • Electrolyte disturbances:
        • Hypokalemia and hypocalcemia are known causes, and hypomagnesemia is a possible cause; hypomagnesemia may directly cause hypokalemia (further evidenced by the reversal of the TdP dysrhythmia when magnesium infusion is given)6,9.
        • Calcium and potassium ions are important during repolarization in both stabilizing the cell membrane potential and returning it to a more negative charge, below the threshold level. When concentrations are low, it takes longer to repolarize the cell back to a negative potential; thus the repolarization phase is prolonged9.
      • Bradycardia
        • There is a direct inverse relationship between heart rate and duration of repolarization, wherein slower heart rates have delayed repolarization times3.
        • This may occur from any type of bradycardia, such as benign sinus bradycardia, bradycardia with AV nodal block, or sick sinus syndrome3.
        • Sleep itself is characterized by bradycardia. Polysomnographic studies of healthy individuals have shown heart rates as low as 30/min during sleep, along with associated, temporary QT prolongation10-16.
      • Cardiac abnormalities
        • Many cardiac abnormalities can lead to a prolonged QT, including congestive heart failure, ischemic heart disease, rheumatic heart disease, myocarditis, and mitral valve prolapse6,9.
      • Dialysis
        • QT prolongation and decreased adaptability of QT interval to changes in heart rate have been shown to occur during dialysis17
        • Patients have been shown to be in an increased dysrhythmogenic state hours after dialysis sessions17

 

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Question 3: Describe the treatments for Torsades de Pointes (TdP)
  • When clinically unstable, the patient with TdP requires defibrillation
  • When stable, the treatment is as follows:
    • Magnesium sulfate has been shown to be a safe an effective treatment in TdP and is considered to be the first-line therapy18-21
    • Magnesium was perhaps less important in this case, in which TdP appeared to be temporally related to bradycardia from somnolence. Therefore, accelerating the heart rate in order to counter the cardiovascular effects of sleep was the next step in management.
    • There are two proven methods for heart rate acceleration
      • Atrial/Ventricular pacing
        • Studies show that pacing at rates of about 90-110 bpm (however sometimes up to 140 bpm), can sufficiently elevate the heart rate enough to both terminate and prevent recurrence of TdP22
      • Isoproterenol infusion:
        • A b-adrenergic agent, resulting in an increase in heart rate and vasodilation18,19
      • Keep in mind, that if TdP recurs and the patient became unstable at any point, then immediate defibrillation is warranted18
  • Diagnosis and treatment of the underlying pathology that is responsible for prolonging the depolarization phase must also be performed18.
  • It is important to treat any electrolyte abnormality or myocardial ischemia and discontinue any QT prolonging medication – in this case, methadone.

 

For more information on understanding the risk factors and pathophysiology of Torsades de Points, I found this textbook very helpful: Clinical Arrhythmology and Electrophysiology: A Companion to Braunwald’s Heart Disease(see citation below).

 

Reviewed by Dr. deSouza

 

Citations:
  1. Ashworth SW, Levsky ME, Marley CT, Kang CS. Bradycardia-associated torsade de pointes and the long-QT syndromes: a case report and review of the literature. Military medicine 2005;170:381-6.
  2. Issa Z, Miller J, Zipes D. Clinical Arrhythmology and Electrophysiology: A Companion to Braunwald’s Heart Disease. Philadelphia, PA 19103-2899: Elsevier saunders; 2012.
  3. Letsas KP, Efremidis M, Filippatos GS, Sideris AM. Drug-induced long QT syndrome. Hellenic journal of cardiology : HJC = Hellenike kardiologike epitheorese 2007;48:296-9.
  4. De Ponti F, Poluzzi E, Montanaro N, Ferguson J. QTc and psychotropic drugs. Lancet (London, England) 2000;356:75-6.
  5. Miranda H, McMain C, Smith A. Medication-Induced QT-Interval Prolongation and Torsades de Pointes US Pharm.; 2011.
  6. Barnes BJ, Hollands JM. Drug-induced arrhythmias. Critical care medicine 2010;38:S188-97.
  7. Martin JA, Campbell A, Killip T, et al. QT Interval Screening in Methadone Maintenance Treatment: Report of a SAMHSA Expert Panel. Journal of addictive diseases 2011;30:283-306.
  8. Nelson LS, Lewin NA, Howland MA, Hoffman RS, Goldfrank LR, Flomenbaum NE. Goldfrank’s Toxicologic Emergencies. 9th edition ed: McGraw-Hill; 2011.
  9. Choudhuri I, Pinninti M, Marwali MR, Sra J, Akhtar M. Polymorphic ventricular tachycardia-part I: structural heart disease and acquired causes. Current problems in cardiology 2013;38:463-96.
  10. Holty JE, Guilleminault C. REM-related bradyarrhythmia syndrome. Sleep medicine reviews 2011;15:143-51.
  11. Tobe TJ, de Langen CD, Bink-Boelkens MT, et al. Late potentials in a bradycardia-dependent long QT syndrome associated with sudden death during sleep. Journal of the American College of Cardiology 1992;19:541-9.
  12. Fleg JL, Kennedy HL. Cardiac arrhythmias in a healthy elderly population: detection by 24-hour ambulatory electrocardiography. Chest 1982;81:302-7.
  13. Serafini A, Dolso P, Gigli GL, et al. Rem sleep brady-arrhythmias: an indication to pacemaker implantation? Sleep medicine 2012;13:759-62.
  14. Rotondi F, Marino L, Lanzillo T, Manganelli F, Zeppilli P. Prolonged ventricular pauses in an asymptomatic athlete with “apparent Mobitz type II second-degree atrioventricular block”. Pacing and clinical electrophysiology : PACE 2012;35:e210-3.
  15. Adlakha A, Shepard JW, Jr. Cardiac arrhythmias during normal sleep and in obstructive sleep apnea syndrome. Sleep medicine reviews 1998;2:45-60.
  16. Gillis AM, MacLean KE, Guilleminault C. The QT interval during wake and sleep in patients with ventricular arrhythmias. Sleep 1988;11:333-9.
  17. Martindale JL, Aherne A, Sinert R. Sudden cardiac death in a dialysis patient: hyperkalemia reconsidered. The Journal of emergency medicine 2014;47:e73-6.
  18. American Heart Association. Web-based Integrated Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care – Part 7: Adult Advanced Cardiovascular Life Support. ECCguidelines.heart.org © Copyright 2015 American Heart Association, Inc.
  19. Shah M, Carter C. Long QT syndrome: A therapeutic challenge. Annals of pediatric cardiology 2008;1:18-26.
  20. Kaye P, O’Sullivan I. The role of magnesium in the emergency department. Emergency medicine journal : EMJ 2002;19:288-91.
  21. Tzivoni D, Banai S, Schuger C, et al. Treatment of torsade de pointes with magnesium sulfate. Circulation 1988;77:392-7.
  22. Charlton NP, Lawrence DT, Brady WJ, Kirk MA, Holstege CP. Termination of drug-induced torsades de pointes with overdrive pacing. The American journal of emergency medicine 2010;28:95-102.

 

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