Forex: Aprenda A Investir De Maneira Responsavel,

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

Torsades de pointes is commonly non sustained and terminates spontaneously but 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 as sudden cardiac death in patients with structurally normal hearts.

Epidemiology^[3]

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

Risk factors

• Congenital 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.^{[5, 6]}
  • 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 congenital long QT syndromes may be triggered past stress, fear or concrete exertion.
• Patients with torsades unremarkably nowadays with recurrent episodes of palpitations, dizziness, and syncope.^[7] Sudden cardiac death can occur with the first episode.
• Nausea, pallor, common cold sweats, shortness of jiff and chest pain may occur.
• A history of congenital deafness or a family history of sudden expiry may indicate a long QT syndrome.
• Physical findings depend on the charge per unit 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 physical signs depend on the cause - eg, features of a built disorder.

Differential diagnosis

• Ventricular tachycardia.
• Supraventricular tachycardia with aberrant conduction.
• Other causes of syncope or sudden cardiac decease.

Investigations

• ECG:^[8]
  • Paroxysms of five-20 beats, with a heart charge per unit faster than 200 beats per minute. Sustained episodes are occasionally seen.
  • Progressive change in polarity of QRS most 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.lx seconds or longer or a QTc (corrected for heart 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 complex (Bazett's formula).
  • A short-long-curt sequence between the R-R interval occurs before the trigger response.
• Electrolytes; hypokalaemia, hypomagnesaemia and hypocalcaemia.
• Cardiac enzymes; assessment for myocardial ischaemia.
• CXR and echocardiography, to rule out structural heart disease.

Management

Short-term treatment

• Resuscitation
• Defibrillation:
  • Although torsades is frequently self-terminating, it may develop into ventricular fibrillation, which requires defibrillation.^[9]
  • In an otherwise stable patient, straight electric current (DC) cardioversion is usually a concluding resort because torsades is paroxysmal in nature and frequently recurs later cardioversion.
• Discontinuation of whatsoever offending agent (stop all QT-prolonging drugs) and correction of any underlying cause such as hypokalaemia, hypomagnesaemia and bradycardia.
• Intravenous magnesium is the drug of choice for torsades de pointes. Magnesium is effective even in patients with normal magnesium levels.
• Acceleration of the middle rate can exist accomplished by using beta 1-adrenergic agonists such as isoprenaline or overdrive electrical pacing.
• Isoprenaline is used as an interim handling until overdrive pacing tin can exist started:
  • Isoprenaline accelerates AV conduction and decreases the QT interval.
  • It can exist used in bradycardia-dependent torsades that is usually associated with acquired long QT syndrome.
  • Isoprenaline is given as a continuous intravenous infusion to keep the heart rate faster than 90 beats per minute.
  • Beta-adrenergic agonists are contra-indicated in the built form of long QT syndrome.
• Temporary transvenous pacing:
  • Pacing can be constructive in terminating torsades past increasing the heart rate and then reducing the QT interval.
  • Atrial pacing is the preferred mode because information technology preserves the atrial contribution to ventricular filling. In patients with AV block, ventricular pacing can exist used to suppress torsades.

Long-term treatment

• Patients without syncope, ventricular tachyarrhythmia or a family history of sudden cardiac death can be observed without starting any treatment.
• Congenital long QT syndrome:
  • Beta-adrenergic antagonists are used as a kickoff-line long-term therapy in built long QT syndrome. Propranolol is has been the nigh extensively used.
  • Beta-blockers are contra-indicated in acquired cases because bradycardia produced by these agents can precipitate torsades. They should as well 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 be used in addition to beta-blockers.
  • High left thoracic sympathectomy is constructive in patients who remain refractory to beta-occludent and pacing.
  • Implantable cardioverter-defibrillators (ICDs) are useful in rare instances when torsades still continues despite all of these treatments. Beta-blockers should be used forth with ICDs because shock tin can further precipitate torsades past adrenergic stimulation.
• Acquired long QT syndrome:
  • Long-term handling in caused cases is usually not required because the QT interval returns to normal once the predisposing factor has been corrected.
  • Pacemaker implantation is effective in cases that are associated with heart cake or bradycardia.
  • ICDs are indicated in cases that cannot exist managed by abstention of whatsoever specific precipitating factor.

Complications

• Ventricular tachycardia
• Ventricular fibrillation
• Sudden cardiac death

Prognosis

• Patients may revert spontaneously or convert to a non-polymorphic ventricular tachycardia or ventricular fibrillation.^[9]
• Torsades is a life-threatening arrhythmia and may present as sudden cardiac death in patients with structurally normal hearts.
• In acquired long QT syndrome, the prognosis is excellent one time any precipitating factor has been removed.

Prevention^[9]

• Avert offending drugs that prolong the QT interval.
• Forbid 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 AD, 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(4):575-87. doi: 10.1007/s00540-013-1564-1. Epub 2013 Feb 15.

2. Trinkley KE, Page RL 2d, Lien H, et al; QT interval prolongation and the gamble of torsades de pointes: essentials for clinicians. Curr Med Res Opin. 2013 Dec29(12):1719-26. doi: 10.1185/03007995.2013.840568. Epub 2013 Sep 23.

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

4. Kallergis EM, Goudis CA, Simantirakis EN, et al; Mechanisms, run a risk factors, and direction of caused long QT syndrome: a comprehensive review. ScientificWorldJournal. 20122012:212178. doi: 10.1100/2012/212178. Epub 2012 Apr 19.

5. Pani PP, Trogu Due east, Maremmani I, et al; QTc interval screening for cardiac adventure 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(two):89-95. doi: 10.1093/eurheartj/ehs351. Epub 2012 Oct 22.

7. Brignole M; Diagnosis and treatment of syncope. Middle. 2007 Jan93(1):130-6.

8. ECG Library

9. Drew BJ, Ackerman MJ, Funk Thou, et al; Prevention of torsade de pointes in hospital settings: a scientific statement from the American Heart Association and the American Higher of Cardiology Foundation. J Am Coll Cardiol. 2010 Mar 255(9):934-47. doi: x.1016/j.jacc.2010.01.001.

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

Posted by: mooreseeting92.blogspot.com

Share this post