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Torsades de pointes is a distinctive polymorphic ventricular tachycardia in which the QRS amplitude varies and the QRS complexes announced to twist effectually the baseline. Torsades de pointes is associated with a prolonged QT interval, which may be congenital or acquired.^{[1, ii]}

Torsades de pointes is usually not sustained and terminates spontaneously merely often recurs unless the underlying cause is corrected. Torsades de pointes may degenerate into sustained ventricular tachycardia or ventricular fibrillation. Torsades is a life-threatening arrhythmia and may present equally sudden cardiac expiry in patients with structurally normal hearts.

Epidemiology^[3]

• The corrected QT interval is longer in the white population than in the black population, and longer in females than males. Therefore, torsades de pointes is more mutual in white races and in females.^[4]
• Torsades occurs at whatever age. If it occurs at an early on age, the cause is usually due to congenital long QT syndrome. In later years, the cause is usually due to acquired long QT syndrome.

Chance factors

• Built long QT syndromes - eg, Jervell and Lange-Nielsen syndrome, Romano-Ward syndrome.
• Acquired long QT syndromes:
  • Acute myocardial infarction.
  • Drugs - eg, antiarrhythmic agents of classes Ia and Iii, erythromycin, ketoconazole, tricyclic antidepressants, methadone, antipsychotics.^{[five, six]}
  • Electrolyte disturbances; hypokalaemia, hypomagnesaemia, hypocalcaemia.
  • Acute kidney injury, liver failure.
  • Metabolic; hypothyroidism, anorexia nervosa, malnutrition.
  • Bradycardia; sinoatrial disease, atrioventricular (AV) block.
  • Toxins; heavy metals, insecticides.

Presentation

• Episodes of torsades in patients with built long QT syndromes may be triggered by stress, fear or physical exertion.
• Patients with torsades usually present with recurrent episodes of palpitations, dizziness, and syncope.^[7] Sudden cardiac expiry tin can occur with the first episode.
• Nausea, pallor, cold sweats, shortness of breath and chest hurting may occur.
• A history of congenital deafness or a family history of sudden death may point a long QT syndrome.
• Concrete findings depend on the rate and duration of tachycardia and the degree of cerebral hypoperfusion. Findings include rapid pulse, depression or normal blood pressure, and transient or prolonged loss of consciousness.
• Other concrete signs depend on the cause - eg, features of a built disorder.

Differential diagnosis

• Ventricular tachycardia.
• Supraventricular tachycardia with abnormal conduction.
• Other causes of syncope or sudden cardiac death.

Investigations

• ECG:^[8]
  • Paroxysms of 5-20 beats, with a heart rate faster than 200 beats per infinitesimal. Sustained episodes are occasionally seen.
  • Progressive change in polarity of QRS about the isoelectric line occurs with complete 180° twist of QRS complexes in 10-12 beats.
  • Usually, a prolonged QT interval and pathological U waves are present. The most consistent indicator of QT prolongation is a QT of 0.60 seconds or longer or a QTc (corrected for eye rate) of 0.45 seconds or longer. QTc = QT interval divided by the square root of the interval (in seconds) between the onset of each QRS circuitous (Bazett's formula).
  • A short-long-short sequence between the R-R interval occurs earlier the trigger response.
• Electrolytes; hypokalaemia, hypomagnesaemia and hypocalcaemia.
• Cardiac enzymes; assessment for myocardial ischaemia.
• CXR and echocardiography, to rule out structural center illness.

Direction

Short-term treatment

• Resuscitation
• Defibrillation:
  • Although torsades is ofttimes self-terminating, it may develop into ventricular fibrillation, which requires defibrillation.^[9]
  • In an otherwise stable patient, direct current (DC) cardioversion is usually a terminal resort because torsades is paroxysmal in nature and ofttimes recurs afterwards cardioversion.
• Discontinuation of any offending agent (cease all QT-prolonging drugs) and correction of any underlying crusade such as hypokalaemia, hypomagnesaemia and bradycardia.
• Intravenous magnesium is the drug of choice for torsades de pointes. Magnesium is constructive fifty-fifty in patients with normal magnesium levels.
• Acceleration of the eye rate can be accomplished by using beta 1-adrenergic agonists such as isoprenaline or overdrive electrical pacing.
• Isoprenaline is used as an interim treatment until overdrive pacing can be started:
  • Isoprenaline accelerates AV conduction and decreases the QT interval.
  • Information technology can exist used in bradycardia-dependent torsades that is unremarkably associated with acquired long QT syndrome.
  • Isoprenaline is given as a continuous intravenous infusion to go on the middle rate faster than ninety beats per infinitesimal.
  • Beta-adrenergic agonists are contra-indicated in the congenital course of long QT syndrome.
• Temporary transvenous pacing:
  • Pacing tin can be effective in terminating torsades by increasing the heart charge per unit and and then reducing the QT interval.
  • Atrial pacing is the preferred mode because it preserves the atrial contribution to ventricular filling. In patients with AV cake, ventricular pacing can be used to suppress torsades.

Long-term treatment

• Patients without syncope, ventricular tachyarrhythmia or a family history of sudden cardiac decease can be observed without starting whatever treatment.
• Congenital long QT syndrome:
  • Beta-adrenergic antagonists are used as a outset-line long-term therapy in congenital long QT syndrome. Propranolol is has been the virtually extensively used.
  • Beta-blockers are contra-indicated in acquired cases because bradycardia produced by these agents can precipitate torsades. They should too be avoided in those congenital cases in which bradycardia is a prominent feature.
  • Permanent pacing benefits patients who remain symptomatic despite receiving the maximally tolerated dose of beta-blockers and tin can be used in addition to beta-blockers.
  • High left thoracic sympathectomy is effective in patients who remain refractory to beta-blockade and pacing.
  • Implantable cardioverter-defibrillators (ICDs) are useful in rare instances when torsades even so continues despite all of these treatments. Beta-blockers should be used along with ICDs considering shock can farther precipitate torsades by adrenergic stimulation.
• Acquired long QT syndrome:
  • Long-term treatment in acquired cases is usually non required considering the QT interval returns to normal once the predisposing factor has been corrected.
  • Pacemaker implantation is effective in cases that are associated with center block or bradycardia.
  • ICDs are indicated in cases that cannot be managed past avoidance of any specific precipitating factor.

Complications

• Ventricular tachycardia
• Ventricular fibrillation
• Sudden cardiac death

Prognosis

• Patients may revert spontaneously or catechumen to a not-polymorphic ventricular tachycardia or ventricular fibrillation.^[9]
• Torsades is a life-threatening arrhythmia and may nowadays as sudden cardiac death in patients with structurally normal hearts.
• In acquired long QT syndrome, the prognosis is excellent one time whatsoever precipitating factor has been removed.

Prevention^[9]

• Avoid offending drugs that prolong the QT interval.
• Prevent predisposing weather condition such every bit hypokalaemia, hypomagnesaemia, and hypocalcaemia, especially in patients shown to have long QT interval.
• Screen families of patients with torsades for whom the cause for prolonged QT is suggested to be congenital.

1. Kaye Advertising, Volpi-Abadie J, Bensler JM, et al; QT interval abnormalities: risk factors and perioperative management in long QT syndromes and Torsades de Pointes. J Anesth. 2013 Aug27(four):575-87. doi: x.1007/s00540-013-1564-1. Epub 2013 Feb fifteen.

2. Trinkley KE, Folio RL 2nd, Lien H, et al; QT interval prolongation and the risk of torsades de pointes: essentials for clinicians. Curr Med Res Opin. 2013 Dec29(12):1719-26. doi: ten.1185/03007995.2013.840568. Epub 2013 Sep 23.

3. Sauer AJ, Newton-Cheh C; Clinical and genetic determinants of torsade de pointes adventure. Circulation. 2012 Apr 3125(13):1684-94. doi: 10.1161/CIRCULATIONAHA.111.080887.

4. Kallergis EM, Goudis CA, Simantirakis EN, et al; Mechanisms, take chances factors, and management of acquired long QT syndrome: a comprehensive review. ScientificWorldJournal. 20122012:212178. doi: 10.1100/2012/212178. Epub 2012 April 19.

5. Pani PP, Trogu Due east, Maremmani I, et al; QTc interval screening for cardiac risk in methadone treatment of opioid dependence. Cochrane Database Syst Rev. 2013 Jun 206:CD008939. doi: 10.1002/14651858.CD008939.pub2.

6. Behr ER, Roden D; Drug-induced arrhythmia: pharmacogenomic prescribing? Eur Heart J. 2013 Jan34(2):89-95. doi: 10.1093/eurheartj/ehs351. Epub 2012 Oct 22.

7. Brignole M; Diagnosis and treatment of syncope. Heart. 2007 Jan93(1):130-six.

8. ECG Library

9. Drew BJ, Ackerman MJ, Funk M, 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. 2010 Mar 255(nine):934-47. doi: 10.1016/j.jacc.2010.01.001.

Source: https://patient.info/doctor/Torsades-de-Pointes

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