Ventricular tachycardia

Ventricular tachycardia ( VT, ventricular tachycardia ) is a life -threatening tachycardia heart rhythm disorder, emanating from the ventricles.

Classification

After the shape of the chamber complex in the ECG, a distinction:

  • Monomorphic VT: the chamber complex always looks the same
  • Polymorphic VT: the chamber complex varies from heartbeat to heartbeat

After the duration of ventricular tachycardia, a distinction:

  • Nonsustained VT ( NSVT ): duration ≤ 30 seconds ( > 2 -consecutive ventricular complexes, frequency above 120 bpm )
  • Sustained VT ( sVT ): duration > 30 seconds

After the symptoms of ventricular tachycardia, a distinction:

  • Most ventricular tachycardias show an effective cardiac output and in extremely rare cases, even asymptomatic. Usually tolerated a heart as a heart rhythm disorder but only for a very short time and the heart rate can quickly turn into a pulseless ventricular tachycardia or ventricular fibrillation.
  • In a pulseless ventricular tachycardia, there is no effective pumping capacity of the heart, there is no pulse palpable. This arrhythmia has to be broken by defibrillation.
  • Very rarely, a VT is common in people with structurally normal hearts. This form is known as idiopathic ventricular tachycardia. As monomorphic VT is associated with a lower incidence of sudden cardiac death.

Pathogenesis

The morphology of ventricular tachycardia is dependent upon the underlying cause.

In monomorphic VT, all ventricular complexes appear the same as the excitation either from a single area of ​​increased arousal capacity ( automaticity ) from the left or right ventricle originates or by a reentry mechanism ( circulating excitation ) is generated within the ventricle.

Polymorphic VT, on the other hand, are most often caused by a failure of the ventricular muscle repolarization. This is usually in the ECG in the prolongation of the QT interval. A prolongation of the QT interval is either congenital or acquired (see also the table of the causes of ventricular tachycardia). The best known form constitutes torsade de pointes tachycardia ( Spitzenumkehrtachykardie )

Causes of ventricular tachycardia

  • Automaticity of a single area, in the left or right ventricle
  • Reentry ( circulating excitation ) from the ventricle or of supraventricular by myocardial scar by previous heart attack
  • Rare: right and left ventricular outflow tract VT ( RVOT )
  • Medication ( Class III antiarrhythmics, erythromycin, ketoconazole, tricyclic antidepressants, quinidine)
  • Abnormal serum electrolytes (sodium, magnesium, calcium )
  • Myocardial ischemia
  • Right ventricular dysplasia
  • Long QT syndrome ( Romano -Ward syndrome, Jervell and Lange -Nielsen syndrome)
  • Brugada syndrome
  • CPVT ( catecholaminergic polymorphic ventricular tachycardia; RYR2 or CASQ2 -channel mutation)

Clinical manifestations

Depending on the severity and duration of VT vary the symptoms of palpitations, shortness of breath over, heart pain (angina), to pulmonary edema or cardiogenic shock.

Electrocardiogram

In the ECG, the VT is usually regular (constant cycle length, heart rate 100-200 beats / min. ) With deformed legs blocky, wide chamber complexes ( QRS ≥ 120 milliseconds, " hairpin ").

Proving for a VT:

  • AV dissociation (that is, it can be seen as a sign of atrial activity, which prove that the atria are not included in the tachycardia P waves; atria and ventricles beat out of sync ).
  • In incomplete AV dissociation a sine excitation can be reconciled to the ventricle. We distinguish between excitement which the atrial to the ventricular ( ventricular captures, " Capture -beat ", normal QRS morphology) are transferred or supraventricular and ventricular mixed complexes ( Fusionssystole ) exist. The latter appears on the ECG as a mixed image of normal QRS complex and bundle branch block.

Differential Diagnosis

The distinction of one from the atria derived tachycardia ( supraventricular tachycardia, SVT) is sometimes difficult. SVT typically comprises a narrow chamber complex, but can at the so-called aberrant line also have a wide complex. While a SVT can be terminated by Vagusstimulus, this does not apply to VT!

  • Supraventricular tachycardia with pre-existing bundle branch block, with aberrant conduction or Präexzitationssyndrom ( WPW antidromic tachycardia, atrial fibrillation with rapid conduction)

Therapy

All ventricular tachycardias are an internist emergency. Until proof of the contrary any tachycardia should be treated with wide QRS as a ventricular tachycardia. In the acute therapy as a possible first digitalis and serum electrolytes ( potassium levels) should be checked. Sufficient oxygen administration by nasal tube is just as useful. The drug of choice is, with few exceptions, the immediate electrical cardioversion using defibrillator and hospitalization with the emergency physician.

Antiarrhythmic drug therapy

Means the first choice

  • Patients without heart failure: ajmaline ( under ECG control 50 mg slowly intravenously over 5 minutes).
  • Patients with heart failure: amiodarone ( under ECG monitoring 300 mg slowly intravenously over 5 minutes).
  • In polymorphic VT or torsades de pointes tachycardia magnesium infusion is the drug of choice.

Electrical cardioversion / defibrillation

Indication for electrocardioversion provide an imminent cardiogenic shock, threatening pulmonary edema, failure of medical therapy represents the electrocardioversion is performed under short anesthesia and should have an initial energy dose of

  • 200 joules ( biphasic defibrillator )
  • 360 joules ( monophasic defibrillator )

Carried out. To ensure the success of therapy is then recommended the administration of amiodarone.

Prevention

To ensure an adequate therapeutic success, it is important to treat the underlying cause (eg interventional reopening of a coronary artery in myocardial infarction ). Defibrillators, with frequent occurrence of tachycardia episodes, the patient to be implanted. Such a system is called an ICD. The ICD detects ventricular tachycardia and may be replaced by anti- tachycardic pacing (ATP ) or shock delivery schedule. In a state after myocardial infarction or in patients with heart failure, beta - blockers reduce the new onset of sudden cardiac death. If it is very frequently a ventricular tachycardia, may be cured by catheter ablation to reduce the rate of ICD intervention.

Cure views

Depending on the underlying cardiac disease and the prevention of relapse.

Cardiac dysrhythmia#Re-entry Antiarrhythmic agent Wolff–Parkinson–White syndrome Angioplasty Betablocker Eugene Braunwald Medical guideline Digital Object Identifier
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