Ventricular tachycardia I47.2

It was not until the 1960s and 1970s that researchers discovered that patients without structural heart disease can also suffer from ventricular tachycardia (Heeger 2024).

Ventricular tachycardia (VT) is defined as 3 or more consecutive depolarizations below the His bundle with a ventricular rate that is more than 20 % higher than the previous rate. If the heart rate is lower, this is referred to as an accelerated / idioventricular rhythm. This usually does not require any therapy (Paul 2018).

A palpable pulse may or may not be present (Thierbach 2002).

VT can be a potentially fatal cardiac arrhythmia with the risk of sudden cardiac death (Samuel 2022), but ventricular arrhythmias can also occur in healthy hearts and be completely harmless (AlMohameed 2019).

VT can only be terminated by active intervention such as external cardioversion, an implanted cardioverter defibrillator or intravenous medication (Kasper 2017).

Depending on the duration, a distinction is made between:

• Non-sustained VT (non- sustained): Non-sustained VTs are defined as ventricular bursts that begin with a triplet and last < 30 s.
• Sustained VT (sustained): These are defined by a duration of at least 30 s (Weber 2008) or the occurrence of circulatory collapse (Paul 2018).

Morphologically, depending on the shape of the ventricular complex in the ECG, a distinction is made between:

• Monomorphic VT: The monomorphic form occurs most frequently. Here, regular and uniform ventricular complexes with a frequency variability < 10 % are found (von Olshausen 1996)
• Polymorphic VT: Here, changing configurations of the ventricular complex occur and the frequency behavior is more restless. In terms of differential diagnosis, torsade de pointes in particular must be distinguished (Börger 1995).

On average, around 25% of all deaths are due to sudden cardiac death, which is partly the result of VT (Samuel 2022).

The excitation origin of a VT is usually distal to the bundle trunk division, i.e.: Tawara leg, Purkinje fibers and working myocardium. In most cases there is a macro reentry tachycardia from the left ventricle (von Olshausen 1996).

The cause of ventricular tachycardia can be:

• Structural heart diseases such as:
  • Cardiomyopathies:
    • ischemic
    • dilated
    • non-ischemic
    • hypertrophic
    • arrhythmogenic such as right ventricular cardiomyopathy (ARVC)
    • genetic
• Structurally healthy heart, so-called idiopathic cause such as:
  • Outflow tachycardia from the right outflow tract (RVOT) or left outflow tract (LVOT)
  • Idiopathic left ventricular tachycardia (ILVT)
  • Primary electrical diseases of the heart such as SQTS, LQTS, CPVT, Brugada syndrome
  • Bidirectional ventricular tachycardia (Herold 2023)
  • Overdose or intoxication with antiarrhythmic drugs or digitalis (Herold 2023)

Ventricular tachycardia is usually triggered by critically timed ventricular extrasystoles (Herold 2023).

Mechanisms of pathogenesis in ventricular tachycardia are:

• Triggered activity
• Reentry mechanism
  • In reentry, the excitation circles through borderline vital myocardial channels and within scarred areas
• Increased autonomy
  • Here, the focus is often in the RV or LV outflow tract (Herold 2023)

Clinical symptoms depend on the frequency and duration of ventricular tachycardia and also on the extent of structural heart disease (Herold 2023).

Symptoms may include:

• Dyspnea
• palpitations
• angina pectoris
• up to pulmonary edema and cardiogenic shock (Herold 2023)

12-channel ECG

The diagnosis is made by means of an ECG recording. This can show:

• Deformed wide ventricular complexes (QRS ≥ 0.12 sec)
• Tachycardia with > 100 / min.
  • Monomorphic VT with uniform ventricular complexes
  • Polymorphic VT with alternating ventricular complexes
  • Sustained VT with a duration of ≥ 30 sec or where there is a need for termination by cardioversion
  • Non-sustained VT with > 2 consecutive ventricular complexes lasting < 30 sec.
  • Torsade de pointes (TdP) tachycardia with prolonged QT time, recognizable by ventricular complexes with alternating deflection direction around the zero line (Herold 2023)
• Capture beat and fusion beat: Both are evidence of the presence of VT. They can occur with a rather slow VT. In this case, sinus excitation can be transmitted to the ventricle via the AV node or His-Purkinje conduction system. In this case, the ECG shows a normal QRS morphology (so-called capture beat) or a mixed image of normal QRS complexes and VT QRS complexes, the so-called fusion beat (Herold 2023).
• VA dissociation: This is also known as pararhythmia. It is characterized by 2 different stimulus formation centers that do not cancel each other out (Halhuber 1978). The atrial rate occurs independently of the ventricular rate. Therefore, more QRS complexes than P waves can be recognized in the ECG. It is also evidence of a VT, but is often difficult to detect on the surface ECG (Herold 2023).
• QRS width: Either a right bundle branch block morphology with > 140 ms or a left bundle branch block morphology > 160 ms is found. The QRS width is only a weak criterion. It can also be influenced by antiarrhythmic drugs and electrolyte imbalances (Herold 2023).
• North-west axis or also known as "aVR sign": A pure R wave in lead aVR or a position type between - 90 ° and - 180 ° indicate a ventricular tachycardia (Herold 2023).
• Negative or positive concordance: In this case, all chest wall leads are either positive, so that only R-waves are found, or they are exclusively negative and only QS-waves are seen. This sign also indicates a VT (Herold 2023).

In the case of tachycardia with wide bundle branch block-like QRS complexes, the differential diagnosis may include

• Supraventricular tachycardia with frequency-dependent bundle branch block
• Supraventricular tachycardia with pre-excitation syndrome (rarely occurring)
• Supraventricular tachycardia with pre-existing bundle branch block
• Pacemaker pacing: This is more common with bipolar pacing configuration, as pacing artifacts are then difficult or impossible to detect (Herold 2023).

Ventricular tachycardia can lead to ventricular fibrillation and sudden cardiac death (Erdmann 2009).

Until proven otherwise, any tachycardia presenting with wide QRS complexes should be treated as VT, as VT is an acutely life-threatening situation (Herold 2023).

The primary emergency treatment is external cardioversion (Paul 2018).

The other treatment strategy is to implant a cardioverter defibrillator, as this has been shown to reduce the mortality rate. However, this has no influence on the recurrence rate of VTs (Samuel 2022).

In the past, VT without structural heart disease was treated with antiarrhythmic drugs. However, since a study by Klein et al. in 1992, these patients have also been treated exclusively with catheter ablation (Heeger 2024).

The prognosis of VT without the presence of structural heart disease is significantly better than in cases with structural heart disease. However, even without structural heart disease, there is an increased mortality rate, which makes further diagnosis and treatment necessary (Heeger 2024).

1. AlMohameed S T, Ziv O (2019) Ventricular arrhythmias. Med Clin North Am. 103 (5) 881 - 895
2. Börger H H, von Olshausen K (1995) EKG- Information: Grundlagen - Vektorielle Deutung - Morphologische Interpretation - Klinische Symptome - Rhythmstörungen - Schrittmacher _ EKG - EKG- Technik und Artefakte. Springer Verlag Berlin / Heidelberg 258
3. Erdmann E (2009) Clinical cardiology: diseases of the heart, circulation and cardiovascular system. Springer Medizin Verlag Heidelberg 103
4. Halhuber M J, Günther R, Ciresa M, Schumacher P. Newesely W (1978) EKG- Einführungskurs: Eine praktische Propädeutik der klinischen Elektrographie. Springer Verlag Berlin / Heidelberg 127
5. Heeger C H, Tilz RR (2024) VT - without structural heart disease: historical overview. Herzsch Elektrophys 35 (1) 102 - 109 doi: https://link.springer.com/article/10.1007/s00399-024-01007-z
6. Herold G et al. (2023) Internal medicine. Herold Publishers 291 - 293
7. Kasper D L, Fauci A S, Hauser S L, Longo D L, Jameson J L, Loscalzo J et al. (2015
8. Kobayashi Y (2018) Idiopathic Ventricular Premature Contraction and Ventricular Tachycardia: Distribution of the Origin, Diagnostic Algorithm, and Catheter Ablation. J Nippon Med Sch. 85 (2) 87 - 94 doi: 10.1272/jnms.2018_85-14.
9. Kasper D L, Fauci A S, Hauser S L, Longo D L, Jameson J L, Loscalzo J et al. (2015) Harrison's Principles of Internal Medicine. Mc Graw Hill Education 1489 - 1491
10. von Olshausen K, Börger H H (1996) ECG information: basics - morphological interpretation - clinical syndromes. Springer Verlag Berlin / Heidelberg 261 - 262
11. Paul T, Gebauer R, Kriebel T, Schneider H, Janousek J (2018) Guideline Pediatric Cardiology: Tachycardic arrhythmias in children, adolescents and young adults (EMAH patients). AWMF Register No. 023 / 022
12. Samuel M, Elsokkari I, Sapp J L (2022) Ventricular Tachycardia Burden and Mortality: Association or Causality? Can J Cardiol. 38 (4) 454 - 464
13. Thierbach A (2002) Lexicon of emergency medicine. Springer Verlag Berlin / Heidelberg 390
14. Weber H (2008) Heart failure: from symptom to therapeutic success. Springer Verlag Vienna / New York 104