The ventricular tachycardia (VT, ventricular tachycardia ; English ventricular tachycardia ) is a tachycardia arrhythmia , as the impulse formation disorder of the heart chambers runs out. It occurs in healthy people, but it can also be a sign of a heart disease that needs treatment.
According to the shape of the chamber complex in the EKG, one differentiates:
- monomorphic VT : the ventricular complex always appears the same
- polymorphic VT : the ventricular complex changes from heartbeat to heartbeat
A distinction is made according to the duration of a ventricular tachycardia:
- Non-sustained VT (nsVT from non-sustained): Duration ≤ 30 seconds (> 2 consecutive ventricular complexes, frequency over 120 bpm)
- Sustained VT (sVT from sustained): duration> 30 seconds
Furthermore, it has the ventricular fibrillation and pulseless ventricular tachycardia are (PVT) delimited. Both patients with ventricular fibrillation and pVT have cardiac arrest and are therefore subject to resuscitation . In this context, rapid defibrillation can save lives.
The morphology of a ventricular tachycardia depends on the underlying cause.
In monomorphic VTs, all ventricular complexes appear the same, as the excitation either comes from a single area with increased excitability (automatism) in the left or right ventricle or is generated by a reentry mechanism ( circular excitation ) within the ventricle.
Polymorphic VTs, on the other hand, are most commonly caused by disruption of ventricular muscle repolarization . This is usually shown in the ECG as the QT time lengthened . A prolongation of the QT time is either congenital or acquired (see also the table of causes of ventricular tachycardia). The best-known form, the torsades de pointes -Tachykardie ( Spitzenumkehrtachykardie is).
|monomorphic VT||polymorphic VT|
In the ECG , the VT is usually regular (constant cycle length, heart rate 100–200 beats / min.) With broad ventricular complexes deformed like bundle branches (QRS ≥ 120 milliseconds, “hairpin shape”).
Proof of a VT:
- AV dissociation (i.e., P-waves can be seen as a sign of atrial activity, proving that the atria are not involved in the tachycardia; the atria and ventricles are out of sync).
- If the AV dissociation is incomplete, sinus excitation can be transferred to the ventricle. A distinction is made between excitation which is transferred from the atrium to the ventricle (ventricular captures, “ capture beat ”, normal QRS morphology) or which consist of supraventricular and ventricular mixed complexes ( fusion systole ). The latter appears in the ECG as a mixed picture of the normal QRS complex and bundle branch block .
Differentiating it from atrial tachycardia ( supraventricular tachycardia , SVT) is sometimes difficult. The SVT typically has a narrow chamber complex, but with so-called aberrant conduction can also have a wide complex. While SVT can be terminated by vagal stimulus, this does not apply to VT!
- Supraventricular tachycardia with pre-existing bundle branch block, with aberrant conduction or with pre-excitation syndrome ( antidromic WPW tachycardia , atrial fibrillation with rapid conduction)
Non-sustained ventricular tachycardias in healthy people do not require therapy. A life-shortening effect has so far only been observed in certain heart diseases and impaired heart function.
All persistent ventricular tachycardias are an internal medical emergency. Unless proven otherwise, any broad QRS complex tachycardia should be treated as ventricular tachycardia. In acute therapy, any digital therapy and the serum electrolytes (potassium level) should be checked first. Adequate oxygen administration via a nasogastric tube is also useful. With a few exceptions, the method of choice is immediate electrical cardioversion using a defibrillator .
Antiarrhythmic drug therapy
1st choice means
- Patients without heart failure : Ajmaline (50 mg slowly intravenously over 5 minutes under ECG monitoring).
- Heart failure patients: amiodarone (300 mg slowly intravenously over 5 minutes under ECG monitoring).
- Magnesium infusion is the drug of choice for polymorphic VT or torsade de pointes tachycardia.
Electrical cardioversion / defibrillation
The indication for an electrocardioversion is an impending cardiogenic shock, impending pulmonary edema, failure of the drug therapy. The electrocardioversion is performed under short anesthesia and should have an initial absorbed dose of
- 200 joules (biphasic defibrillator)
- 360 joules (monophasic defibrillator )
respectively. Subsequent administration of amiodarone is recommended to ensure the success of the therapy .
In order to ensure adequate therapy success, it is important to treat the underlying cause (e.g. interventional reopening of a coronary artery in the event of a heart attack ). Defibrillators can be implanted in the patient if tachycardia episodes are frequent. One such system is called an ICD . The ICD detects ventricular tachycardia and can terminate it with anti-tachycardia pacing (ATP) or by delivering a shock. Beta-blockers can reduce the chance of sudden cardiac death in people who have had a post-heart attack or heart failure . If ventricular tachycardia is very common, catheter ablation can be used to attempt to reduce the ICD intervention rate.
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