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{{CMG}}; '''Associate Editor(s)-In-Chief:''' {{CZ}}
{{CMG}}; '''Associate Editor(s)-In-Chief:''' {{CZ}}

Revision as of 01:34, 15 October 2012

Torsade de pointes
DiseasesDB 29252
MeSH D016171

Torsades de pointes Microchapters

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Patient Information

Overview

Historical Perspective

Pathophysiology

Causes

Differentiating Torsades de pointes from other Diseases

Risk Factors

Natural History, Complications and Prognosis

Diagnosis

History and Symptoms

Physical Examination

Laboratory Findings

Electrocardiogram

EKG Examples

Echocardiography

Other Diagnostic Studies

Treatment

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Case #1

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-In-Chief: Cafer Zorkun, M.D., Ph.D. [2]

Overview

Torsade de pointes in French means "Twisting of the Points". It is characterized by a polymorphic ventricular tachycardia and can occur in the congenital long QT syndromes, electrolyte abnormalities (hypomagnesemia, hypokalemia), usage of certain drugs like antiarrhythmic (quinidine), nonsedating antihistamines (terfenadine); antibiotics (erythromycin) and neuroleptics (thioridazine). Torsade de pointes is characterized by constantly changing rhythm amplitude. The changing rhythm amplitudes comes from the ventricular depolarizing waves constantly shifting its axis. The underlying mechanism is thought to be triggered activity arising as a consequence of early after-depolarizations. Torsade de pointes is typically initiated by a short-long-short interval. A ventricle extrasystole (first beat: short) is followed by a compensatory pause. The following beat (second beat: long) has a longer QT interval. If the next beat follows shortly thereafter, there is a good chance that this third beat falls within the QT interval, resulting in the R on T phenomenon and subsequent Torsade de pointes. During Torsade de pointes the ventricles depolarize in a circular fashion resulting in QRS complexes with a continuously turning heart axis around the baseline (hence the name Torsade de Pointes). An understanding of the patho-physiology has led to development of treatment modalities like pacing, isoproterenol and drugs like magnesium and beta blockers. Although Torsades de Pointes (TdP) is a rare ventricular arrhythmia, it can degenerate into ventricular fibrillation, leading to death without rapid medical intervention. TdP is associated with long QT syndrome, a condition whereby prolonged QT intervals are visible on the ECG. Also, a more rare form of short coupled Torsade de pointes has been observed.[1]

Historical Perspective

  • The French term is largely due to the fact that the phenomenon was originally described in a French medical journal by Dessertenne in 1966, when he observed this rhythm disorder in an 80-year-old female patient with complete intermittent atrioventricular block.
  • There has been much debate in the Circulation journal among French and American scientist whether one should write Torsades de Pointes or Torsade de Pointes.
  • As for now Torsade is prefered (unless one sees rotations around more than one axis in one episode), but both forms are used in similar frequency.[3]

History and symptoms

Torsades is a rapid, polymorphic ventricular tachycardia with a characteristic twist of the QRS complex around the isoelectric baseline. It is also associated with a fall in arterial blood pressure, which gives rise to the syncopal symptoms experienced by patients. Although torsade de pointes is a rare ventricular arrhythmia, it can degenerate into ventricular fibrillation, which will lead to sudden death in the absence of medical intervention.

History

It is important to gather the following information from the patient:

Symptoms

Physical examination

Physical examination findings depends on the rate and duration of the episode and the effect on cerebral perfusion during the episode. The physical finding may include:

Causes

Long QT syndrome can either be inherited as congenital mutations of ion channels carrying the cardiac impulse/action potential or acquired as a result of drugs that block these cardiac ion currents.

Common causes for torsades de pointes include hypomagnesemia and hypokalemia. It is commonly seen in malnourished individuals and chronic alcoholics. Drug interactions such as erythromycin or Avelox, taken concomitantly with inhibitors like nitroimidazole, Diarrhea, dietary supplements, and various medications like methadone, Lithium, tricyclic antidepressants or phenothiazines may also contribute.

Factors that are associated with an increased tendency toward torsades de pointes include:

The List of Drugs that Causing Torsades de pointes

Drugs that are generally accepted to have a risk of causing torsades de pointes

Drugs that Possibly Cause Torsades de pointes

Drugs that in some reports have been associated with torsades de pointes and/or QT prolongation but at this time lack substantial evidence for causing torsades de pointes.

The List of Drugs that Causing Torsades de pointes in Certain Conditions

Drugs that, in some reports, have been weakly associated with torsades de pointes and/or QT prolongation but that are unlikely to be a risk for torsades de pointes when used in usual recommended dosages and in patients without other risk factors (e.g., concomitant QT prolonging drugs, bradycardia, electrolyte disturbances, congenital long QT syndrome, concomitant drugs that inhibit metabolism)

Differential diagnosis

Electrocardiography

EKG is the main diagnostic tool in patients with Torsade de pointes. EKG findings that can be seen are:

  • Progressive change in polarity of QRS about the isoelectric line occurs
  • Prolonged QT interval (QT ≥ 0.60 s or QTc ≥ 0.45 s)
  • Pathological U
  • Rotation of the heart's electrical axis by at least 180º
  • Preceded by short long and short RR-intervals
  • Triggered by an early premature ventricular contraction(R-on-T PVC)
  • Paroxysms of 5-20 beats at a rate ≥ 200 bpm
  • Patients may revert spontaneously to a nonpolymorphic ventricular tachycardia or ventricular fibrillation

Background

  1. The peaks of the QRS complexes appear to twist around the isoelectric axis.
  2. Polymorphic VT is distinguished from Torsades by the absence of QT prolongation in polymorphic VT.

EKG Findings

  1. Paroxysms of VT with irregular RR intervals.
  2. A ventricular rate between 200 and 250 beats per minute.
  3. Two or more cycles of QRS complexes with alternating polarity.
  4. Changing amplitude of the QRS complexes in each cycle in a sinusoidal fashion.
  5. Prolongation of the QT interval.
  6. Is often initiated by a PVC with a long coupling interval, R on T phenomenon.
  7. There are usually 5 to 20 complexes in each cycle.

Clinical Correlation

  1. Drugs: quinidine, PCA, norpace, amiodarone, phenothiazines, Tricyclic antidepressants, pentamidine.
    • with quinidine majority of the cases occur within one week of initiation, and with therapeutic levels
  2. Electrolyte imbalances: Hypokalemia, hypomagnesemia, hypocalcemia
  3. CAD
  4. MVP
  5. Variant angina
  6. Myocarditis
  7. Subarachnoid hemorrhage
  8. Congenital QT prolongation
  9. Liquid protein diets
  10. Hypothyroidism
    • because of bradycardia and a prolonged QT syndrome
  11. Organophosphate poisoning [4] [5]

Video: Torsade de pointes

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Torsade de pointes is characterized by constantly changing rhythm amplitude. 'Torsade de pointes' in French means "Twisting of the Points". The changing rhythm amplitudes comes from the ventricular depolarizing waves constantly shifting its axis. It is usually caused by hypomagnesemia, hypokalemia, and malnourished alcoholics. Although Torsades de Pointes (TdP) is a rare ventricular arrhythmia, it can degenerate into ventricular fibrillation, leading to death without rapid medical intervention. TdP is associated with long QT syndrome, a condition whereby prolonged QT intervals are visible on the ECG.

Other lab studies

Treatment

Acute Treatment

If the episode of does not terminate on its own and degenerates into ventricular fibrillation, cardioversion is required.

Lead II electrocardiogram showing Torsades being shocked by an Implantable cardioverter-defibrillator back to the patients baseline cardiac rhythm.

Once the patient is back in normal sinus rhythm, a vigorous search for and correction of conditions that predispose to torsades de pointes which include hypokalemia, hypomagnesemia, and bradycardia should be made. Magnesium sulfate (1-2 g IV over 30-60 seconds) reduces the influx of calcium thereby lowering the amplitude of early after depolarizations and should also be infused even if the magnesium is normal. [6][7] Administration of lidocaine is generally not effective, but mexiletene may be helpful in suppressing the recurrence of torsade de pointes.

Additional Information

Examples

EKG's shown below are courtesy of C. Michael Gibson MS MD, and copylefted


Examples from different resources

  • Arrhythmias in a patient with short coupled torsade de pointes[1]

    Arrhythmias in a patient with short coupled torsade de pointes[1]

  • Arrhythmias in a patient with short coupled torsades de pointes degenerating in ventricular fibrillation[1]

    Arrhythmias in a patient with short coupled torsades de pointes degenerating in ventricular fibrillation[1]


  • Arrhythmias in a patient with short coupled torsade de pointes: frequent short coupled extrasystoles[1]

    Arrhythmias in a patient with short coupled torsade de pointes: frequent short coupled extrasystoles[1]

  • Arrhythmias in a patient with short coupled torsade de pointes: frequent short coupled extrasystoles [1]

    Arrhythmias in a patient with short coupled torsade de pointes: frequent short coupled extrasystoles [1]


  • A 12 lead ECG recording example of TdP[8]

    A 12 lead ECG recording example of TdP[8]


Characteristic tracing showing the "twisting" (blue line) of Torsade de pointes

References

  1. ↑ 1.0 1.1 1.2 1.3 1.4 Leenhardt A, Glaser E, Burguera M, Nuernberg M, Maison-Blanche P, and Coumel P. Short-coupled variant of torsade de pointes. A new electrocardiographic entity in the spectrum of idiopathic ventricular tachyarrhythmias. Circulation 1994 Jan; 89(1) 206-15. PMID 8281648
  2. ↑ Dessertenne F (1966). "[Ventricular tachycardia with 2 variable opposing foci]". Archives des maladies du coeur et des vaisseaux (in French). 59 (2): 263–72. PMID 4956181.
  3. ↑ Moise NS. As Americans, we should get this right. Circulation 1999 Sep 28; 100(13) 1462. PMID 10500317
  4. ↑ Chou's Electrocardiography in Clinical Practice Third Edition, pp. 398-409.
  5. ↑ Sailer, Christian, Wasner, Susanne. Differential Diagnosis Pocket. Hermosa Beach, CA: Borm Bruckmeir Publishing LLC, 2002:194 ISBN 1591032016
  6. ↑ Hoshino K, Ogawa K, Hishitani T, Isobe T, Eto Y (2004). "Optimal administration dosage of magnesium sulfate for torsades de pointes in children with long QT syndrome". J Am Coll Nutr. 23 (5): 497S–500S. PMID 15466950. Unknown parameter |month= ignored (help)
  7. ↑ Hoshino K, Ogawa K, Hishitani T, Isobe T, Etoh Y (2006). "Successful uses of magnesium sulfate for torsades de pointes in children with long QT syndrome". Pediatr Int. 48 (2): 112–7. doi:10.1111/j.1442-200X.2006.02177.x. PMID 16635167. Unknown parameter |month= ignored (help)
  8. ↑ Khan IA. Twelve-lead electrocardiogram of torsade de pointes Tex Heart Inst J. 2001; 28 (1): 69. PMID 11330748

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