Torsade de Pointes

Torsade de Pointes

The term Torsade de Pointes (TdP) refers to a polymorphic ventricular tachycardia (VT) associated with a prolonged QT interval and electrocardiographically characterized by QRS complexes of changing amplitude that appear to twist around the isoelectric line, hence the name torsade de pointes, or “twisting of the points”

Onset of Torsade de Pointes during the recording of a standard 12-lead electrocardiogram (ECG) in a young male with a history of drug addiction treated with chronic methadone therapy who presented to a hospital emergency department after ingesting an overdose of prescription and over-the-counter drugs from his parent’s drug cabinet.

Classic ECG features evident in this rhythm strip include a prolonged QT interval with distorted T-U complex, initiation of the arrhythmia after a short-long-short cycle sequence by a PVC that falls near the peak of the distorted T-U complex, “warm-up” phenomenon with initial R-R cycles longer than subsequent cycles, and abrupt switching of QRS morphology from predominantly positive to predominantly negative complexes (asterisk).

From Drew BJ et al: Prevention of torsade de pointes in hospital settings: a scientific statement from the American Heart Association and the American College of Cardiology Foundation, J Am Coll Cardiol 55:934-947, 2010.

Torsade is typically initiated by a short-long-short sequence of ventricular beats but can also be initiated by a short-coupled variant. Typically, TdP occurs in the setting of a markedly prolonged QT interval (>500 msec); the QTc prolongs even further during the long diastolic interval of a compensatory pause after an early beat, followed by an early PVC on the T wave, leading to a polymorphic VT with a ventricular rate of 160 to 250 beats per min, irregular RR intervals, and a cycling of the QRS axis through 180 degrees every 5 to 20 beats. It may be repetitive, nonsustained, or sustained and may degenerate into ventricular fibrillation. In some cases, the result is sudden cardiac death.





How common is Torsade de Pointes?

The precise incidence of TdP is unclear but accounts for fewer than 5% of all sudden cardiac arrests. In congenital long QT syndromes (LQTS), TdP may occur in up to 6% of cases at rest and 9% of cases during an exercise test. Among drug-induced causes of TdP, the incidence may vary between <1% in cases of antibiotics and antipsychotics to 2% to 4% when caused by class III antiarrhythmics such as sotalol, ibutilide, and dofetilide.

Predominant Sex & Age

Because testosterone shortens the QT interval, women have a longer baseline QT interval, which is believed to be the reason for a two- to threefold increased incidence of TdP in women.

What are the Risk Factors

  • •TdP in patients with congenital LQTS is often initiated by an external trigger ( Table 1 ). Triggers can include exercise, noise, emotion, sudden waking from sleep by an alarm clock, telephone ringing, thunder, swimming, or diving. TdP in LQT1 patients is classically triggered by vigorous exercise or swimming; in LQT2 by emotion, pregnancy, or noise; and in LQT3 when at rest or asleep. Risk factors for drug-induced TdP are outlined in table 2.

Causes and Triggers of Torsade de Pointes

Congenital•Romano-Ward syndrome (autosomal dominant)•Jervell and Lange-Nielsen syndrome (autosomal recessive)•LQTS channelopathies
Metabolic syndromes•Hypokalemia•Hypocalcemia•Hypomagnesemia•Starvation•Anorexia nervosa•Liquid protein diets•Hypothyroidism
Bradyarrhythmias•Sinus node dysfunction•Second- or third-degree AV block
Antiarrhythmic drugs•Quinidine•Procainamide•Disopyramide•Amiodarone and dronedarone•Sotalol•Dofetilide, ibutilide, azimilide
Antimicrobial drugs•Erythromycin, clarithromycin, azithromycin•Pentamidine•Azole antifungals like voriconazole•Fluoroquinolones such as levofloxacin and moxifloxacin•Chloroquine
Psychiatric drugs•Phenothiazines•Thioridazine•Tricyclic antidepressants•Haloperidol•Risperidone•Selective serotonin reuptake inhibitors
Antineoplastic agents•Tyrosine kinase inhibitors such as sunitinib, dasatinib•Vorinostat•Arsenic
Gastric motility agents•Cisapride, domperidone
Opioid dependence drugs•Methadone
Other factors•Myocardial ischemia•Hypothermia•Intracranial disease•HIV infection•Connective tissue disease with anti-Ro/SSA antibodies•Periodic paralysis (Andersen syndrome)•Cocaine
Risk Factors for Drug-Induced Torsade de Pointes
From Gowda RM et al: Torsade de pointes: the clinical considerations, Int J Cardiol 96(1):1-6, 2004.
•Congenital long QT
•Female gender
•Electrolyte abnormalities (hypokalemia, hypomagnesemia, hypocalcemia)
•Diuretic use
•Cardiac hypertrophy
•Myocardial fibrosis
•Congestive heart failure
•Renal and liver insufficiency
•Coadministration of drugs blocking P450 isoenzyme CYP3A4
•High doses or rapid intravenous infusion of the drug
•Baseline electrocardiographic abnormalities (prolonged QT, T-wave lability)

The risk factors for developing TdP in patients with acquired long QT are extensive and are outlined in Table 3.

  • Risk Factors for Torsade de Pointes in Hospitalized PatientsFrom Drew BJ et al: Prevention of torsade de pointes in hospital settings: a scientific statement from the American Heart Association and the American College of Cardiology Foundation, Circulation 121(8):1047, 2010.
    • •Clinically recognizable risk factors
    • •QTc >500 msec
    • •LQT2-type repolarization: Notched or “bifid” T-wave
    • •Use of QT-prolonging drugs
    • •Concurrent use of more than one QT-prolonging drug
    • •Rapid infusion by intravenous route
    • •Structural heart disease
    • •Congestive heart failure
    • •Myocardial infarction
    • •Advanced age
    • •Female sex
    • •Hypokalemia
    • •Hypomagnesemia
    • •Hypocalcemia
    • •Treatment with diuretics
    • •Impaired hepatic drug metabolism
    • •Bradycardia
    • •Sinus bradycardia, heart block, incomplete heart block with pauses
    • •Premature QRS complexes leading to short-long-short cycles
    • •Multiple clinically recognizable risk factors
    • •Occult (latent) congenital LQTS
    • •Genetic polymorphisms


  • •Of the congenital LQTS channelopathies, long QT syndromes 1, 2, and 3 account for >70% of all cases. In general, the risk of TdP increases as the QT lengthens; however, there are also genotype-phenotype relationships that help define risk; for example, LQTS3 carries a higher risk of TdP than LQTS1. Similarly, the Jervell and Lange-Nielsen syndrome and Romano-Ward syndrome may lead to TdP.
  • •It is also likely that genetic factors are at play in acquired LQT and in the development of TdP. For example, in large populations, the QT interval prolongs very little with the administration of QT-prolonging drugs such as fluoroquinolones; however, certain individuals will have markedly exaggerated QT prolongation that leads to TdP; this is likely due to some underlying genetic factor.


  • •Changes in the balance of transmembrane ionic currents lead to lengthening of the QT interval and to abnormal action potentials called early afterdepolarizations (EADs). An EAD, in the setting of electrical instability induced by the prolonged QT, initiates the torsades. Perpetuation may be caused by transmural entry, triggered activity, or abnormal automaticity. A distinct group of cells called the M cells, located in the mid-myocardium, has a less rapid delayed rectifier potassium current (IKr), and these cells are central to the genesis of TdP.
  • •Drugs with the potential to cause TdP most frequently inhibit the rapid potassium channels and result in prolongation of the action potential duration, producing a prolonged QT on ECG.

Physical Findings & Clinical Presentation

  • •Clinical features depend on whether the TdP is caused by acquired or congenital long QT syndrome. Congenital LQTS patients may have certain specific triggers, such as noise, exercise, and emotions (see “Risk Factors”).
  • •Symptoms of the tachycardia itself include palpitations, presyncope, syncope (sometimes with jerking movements from myoclonus, often misinterpreted as seizures), and sudden cardiac death (SCD).
  • •Patients resuscitated from SCD have an especially ominous prognosis, with a relative risk of 12.9% of experiencing another cardiac arrest.

What causes Torsade de Pointes?

The etiology or triggers of TdP may be congenital or acquired causes of QT prolongation. For a comprehensive list of drugs that can cause or have the potential to cause TdP, see “Patient/Family Education.”

Differential Diagnosis

Other causes of syncope:

  • •Other causes of broad complex tachycardia such as:
    • 1.Polymorphic VT
    • 2.Wolff-Parkinson-White (WPW) syndrome with rapid atrial fibrillation
    • 3.ECG artifact


  • •ECG and telemetry are the mainstays of diagnosing TdP as they detect the arrhythmia, the preceding prolonged QT interval, and the long-short cycles that trigger it.
  • This lead I, III, and V rhythm strip shows sinus bradycardia with left bundle branch block and marked QT prolongation with premature ventricular contractions (R-on-T) that initiates a very rapid polymorphic ventricular tachycardia with the characteristic twisting of the QRS complex around the isoelectric baseline. Torsade de Pointes literally means “twisting of the points.”From Olshansky B et al: Arrhythmia essentials, ed 2, Philadelphia, 2017, Elsevier.
  • •Determination and treatment of the etiology of TdP (see Table 1 ) is key.

Laboratory Tests

  • •Electrolytes: Assess for hypokalemia, hypocalcemia, and hypomagnesemia
  • •Thyroid function tests
  • •Genetic studies if suspicion of congenital LQT syndrome

Imaging Studies

  • •Echocardiography to rule out structural heart disease as a cause of VT
  • •Stress test to rule out myocardial ischemia. Stress ECG with dynamic assessment of the QT interval during varying heart rates may be diagnostic of long QT syndromes and related TdP
  • •Computed tomography scan of the head if intracranial disease is suspected


The cornerstone of treatment comprises intravenous magnesium and acceleration of the heart rate, either by mechanical overdrive pacing or by infusion of isoproterenol. Withdrawal of causative drugs and correction of underlying causes such as electrolyte imbalances, hypothermia, and ischemia are also important. The 2017 American Heart Association and the American College of Cardiology (AHA/ACC) guidelines for management of patients with ventricular arrhythmias provide an overview and recommendations for treatment of TdP. 1

Nonpharmacological Therapy

  • •Withdrawal of any offending drugs and correction of electrolyte abnormalities are recommended in patients presenting with TdP (Class I recommendation).
  • •Temporary atrial or ventricular overdrive pacing is a Class I recommendation for all causes of TdP if intravenous magnesium fails.
  • •Acute and long-term pacing is recommended for patients presenting with TdP due to heart block and symptomatic bradycardia (Class 1) or those with recurrent pause-dependent torsades (Class IIa).
  • •Active internal and external rewarming if hypothermia is the etiology.
  • •If TdP degenerates into ventricular fibrillation, defibrillation and advanced cardiac life support protocol should be followed.

Acute General Treatment

  • •Intravenous magnesium sulfate 1 to 2 g given over 1 to 2 min is first-line therapy for patients who present with LQTS and few episodes of TdP (Class IIa). Magnesium is not likely to be effective in patients with a normal QT interval.
  • •Isoproterenol is reasonable as temporary treatment in patients with acute disease who present with recurrent pause-dependent TdP and who do not have congenital LQTS (Class IIa).
  • •Beta-blockade combined with pacing is reasonable acute therapy for patients who present with TdP and sinus bradycardia (Class IIa).
  • •Potassium repletion to 4.5 to 5 mmol/L may be considered for patients who present with TdP and hypokalemia (Class IIb).
  • •Intravenous lidocaine, oral mexiletine, or phenytoin may be considered in patients who present with LQT3 and TdP (Class IIb).
  • •TdP is usually self-limited, and cardioversion should be performed only as a last resort in the setting of pulseless VF because of the high likelihood of immediate recurrence of the TdP after cardioversion.

Chronic Treatment

  • •TdP resulting from congenital LQTS is treated with beta-blockade (propranolol or nadolol are preferred), pacing, and implantable cardioverter-defibrillator in high-risk cases. For patients who continue to have syncope despite maximal drug therapy, cervical-thoracic sympathectomy may be considered.
  • •Long-term pacing is recommended for patients presenting with TdP due to heart block and symptomatic bradycardia.
  • •Avoid use of QT-prolonging drugs.
  • •Lifestyle modification in case of congenital LQTS.
  • •In patients with eating disorders, nutritional rehabilitation will correct the QT prolongation over the long term (3 to 18 mo).
  • •Psychiatric evaluation of patients with drug overdose and eating disorders.


Patients with TdP should be monitored in an intensive care setting.


Patients should have an urgent cardiology consultation.

Pearls & Considerations

  • •Identification of the etiology for TdP is key in diagnosis, management, and prognosis of this condition.
  • •Drugs associated with TdP vary greatly in their risk for arrhythmia; an updated list can be found at . The risk-benefit ratio should be assessed for each individual to determine whether the potential therapeutic benefit of a drug outweighs the risk for TdP.
  • •Risk factors for drug-induced TdP include older age, female sex, heart disease, electrolyte disorders (especially hypokalemia and hypomagnesemia), renal or hepatic dysfunction, bradycardia or rhythms with long pauses, treatment with more than one QT-prolonging drug, and genetic predisposition.
  • •After initiation of a drug associated with TdP, ECG signs indicative of risk for arrhythmia include an increase in QTc from predrug baseline of >60 msec, marked QTc interval prolongation >500 msec, T-U wave distortion that becomes more exaggerated in the beat after a pause, visible T-wave alternans, new-onset ventricular ectopy, and couplets and nonsustained polymorphic ventricular tachycardia initiated in the beat after a pause.


The 2011 AHA/ACC scientific statement on prevention of TdP suggests a strategy of documenting the QTc interval before and at least every 8 to 12 h after the initiation, increased dose, or overdose of QT-prolonging drugs. If QTc prolongation is observed, documentation of more frequent measurements is recommended. The duration of QTc monitoring depends upon the duration of treatment with the QT-prolonging drug and the drug half-life. 2

Patient & Family Education

  • •Patients should be educated about avoiding use of QT-prolonging drugs. A complete list of these drugs can be found at .
  • •First-degree relatives of all patients with congenital LQTS should undergo genetic testing.
  • •Congenital LQTS patients should avoid certain specific triggers (e.g., swimming and exercise in LQTS 1 and LQTS 2 and acoustic stimuli in LQTS 2).
  • •It is recommended that all patients affected by LQTS avoid competitive sports activity.


1.Al-Khatib S.M., et al.: 2017 AHA/ACC/HRS guideline for management of patients with ventricular arrhythmias and the prevention of sudden cardiac death . Circulation 2018; 138 (13): pp. e272.

2.Drew B.J., et al.: 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): pp. 1047.


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