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Torsades de pointes is a distinctive polymorphic ventricular tachycardia in which the QRS aamplitude 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 caused.^{[1, 2]}

Torsades de pointes is unremarkably non sustained and terminates spontaneously just frequently 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 common 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 built long QT syndrome. In later on years, the cause is ordinarily due to caused long QT syndrome.

Hazard 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.^{[5, 6]}
  • Electrolyte disturbances; hypokalaemia, hypomagnesaemia, hypocalcaemia.
  • Astute 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 exist triggered by stress, fear or physical exertion.
• Patients with torsades commonly 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 breath and breast hurting may occur.
• A history of congenital deafness or a family history of sudden death may signal a long QT syndrome.
• Physical findings depend on the rate and duration of tachycardia and the caste of cerebral hypoperfusion. Findings include rapid pulse, low or normal blood pressure level, and transient or prolonged loss of consciousness.
• Other concrete signs depend on the cause - eg, features of a congenital disorder.

Differential diagnosis

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

Investigations

• ECG:^[8]
  • Paroxysms of five-20 beats, with a heart rate 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 ten-12 beats.
  • Ordinarily, a prolonged QT interval and pathological U waves are present. The well-nigh consequent indicator of QT prolongation is a QT of 0.60 seconds or longer or a QTc (corrected for center charge per unit) of 0.45 seconds or longer. QTc = QT interval divided by the foursquare root of the interval (in seconds) between the onset of each QRS complex (Bazett'southward formula).
  • A short-long-short sequence betwixt the R-R interval occurs before the trigger response.
• Electrolytes; hypokalaemia, hypomagnesaemia and hypocalcaemia.
• Cardiac enzymes; cess for myocardial ischaemia.
• CXR and echocardiography, to rule out structural heart illness.

Direction

Brusque-term treatment

• Resuscitation
• Defibrillation:
  • Although torsades is often self-terminating, it may develop into ventricular fibrillation, which requires defibrillation.^[9]
  • In an otherwise stable patient, directly current (DC) cardioversion is ordinarily a last resort because torsades is paroxysmal in nature and frequently recurs afterwards cardioversion.
• Discontinuation of whatsoever offending agent (finish all QT-prolonging drugs) and correction of whatever underlying cause such as hypokalaemia, hypomagnesaemia and bradycardia.
• Intravenous magnesium is the drug of option for torsades de pointes. Magnesium is effective even in patients with normal magnesium levels.
• Acceleration of the middle rate can be achieved by using beta 1-adrenergic agonists such as isoprenaline or overdrive electrical pacing.
• Isoprenaline is used as an acting treatment until overdrive pacing can exist started:
  • Isoprenaline accelerates AV conduction and decreases the QT interval.
  • It can be used in bradycardia-dependent torsades that is usually associated with acquired long QT syndrome.
  • Isoprenaline is given as a continuous intravenous infusion to go on the middle charge per unit faster than 90 beats per infinitesimal.
  • Beta-adrenergic agonists are contra-indicated in the congenital grade of long QT syndrome.
• Temporary transvenous pacing:
  • Pacing tin can be effective in terminating torsades by increasing the heart rate and so reducing the QT interval.
  • Atrial pacing is the preferred mode considering it preserves the atrial contribution to ventricular filling. In patients with AV block, ventricular pacing tin can be used to suppress torsades.

Long-term handling

• Patients without syncope, ventricular tachyarrhythmia or a family unit history of sudden cardiac death tin be observed without starting any treatment.
• Congenital long QT syndrome:
  • Beta-adrenergic antagonists are used as a first-line long-term therapy in congenital long QT syndrome. Propranolol is has been the well-nigh extensively used.
  • Beta-blockers are contra-indicated in acquired cases considering bradycardia produced by these agents can precipitate torsades. They should as well be avoided in those built cases in which bradycardia is a prominent characteristic.
  • Permanent pacing benefits patients who remain symptomatic despite receiving the maximally tolerated dose of beta-blockers and 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 still continues despite all of these treatments. Beta-blockers should be used forth with ICDs because daze tin can further precipitate torsades past adrenergic stimulation.
• Acquired long QT syndrome:
  • Long-term handling 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 centre cake or bradycardia.
  • ICDs are indicated in cases that cannot be managed by avoidance of whatsoever specific precipitating factor.

Complications

• Ventricular tachycardia
• Ventricular fibrillation
• Sudden cardiac death

Prognosis

• Patients may revert spontaneously or catechumen to a non-polymorphic ventricular tachycardia or ventricular fibrillation.^[9]
• Torsades is a life-threatening arrhythmia and may present equally sudden cardiac expiry 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]

• Avoid offending drugs that prolong the QT interval.
• Preclude predisposing conditions such every bit hypokalaemia, hypomagnesaemia, and hypocalcaemia, peculiarly in patients shown to take long QT interval.
• Screen families of patients with torsades for whom the crusade for prolonged QT is suggested to be congenital.

1. Kaye AD, Volpi-Abadie J, Bensler JM, et al; QT interval abnormalities: take chances factors and perioperative direction in long QT syndromes and Torsades de Pointes. J Anesth. 2013 Aug27(4):575-87. doi: 10.1007/s00540-013-1564-i. Epub 2013 Feb 15.

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: 10.1185/03007995.2013.840568. Epub 2013 Sep 23.

3. Sauer AJ, Newton-Cheh C; Clinical and genetic determinants of torsade de pointes hazard. Circulation. 2012 April 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 Apr 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(ii):89-95. doi: 10.1093/eurheartj/ehs351. Epub 2012 October 22.

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

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 Middle Association and the American Higher of Cardiology Foundation. J Am Coll Cardiol. 2010 Mar 255(9):934-47. doi: 10.1016/j.jacc.2010.01.001.

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

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