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PekkaRaatikainen

Ventricular Tachycardia

Essentials

  • Ventricular tachycardia (VT) is a broad complex arrhythmia which originates from the ventricles and has a rate exceeding 100 beats/min.
  • When suspecting VT, always refer the patient to a specialist for an assessment.
    • The referral should include a careful history and a copy of an ECG recording taken during the tachyarrhythmia and during the patient's normal rhythm.
  • VT must not be misdiagnosed as supraventricular tachycardia (SVT) - a misdiagnosis the other way round is not as dangerous Supraventricular Tachycardia (SVT).

Classification

  • Ventricular tachycardias may be classified into clinical sub-categories according to the underlying mechanism, duration and QRS morphology.
    • Non-sustained VT consists of more than 3 beats but lasts less than 30 seconds and causes no haemodynamic adverse effects. Sustained VT lasts for more than 30 seconds or causes haemodynamic adverse effects.
    • In monomorphic VT the QRS morphology is consistent but in polymorphic VT the morphology of the QRS changes from beat to beat. Sustained monomorphic VT is mostly seen in patients recovering from myocardial infarction or with heart disease.
    • Torsades de pointes is associated with a prolonged QT interval and is a form of polymorphic VT. Torsade de pointes is characterised by iterative runs of ventricular spindle-shaped waves. In congenital long QT syndrome, the mechanism behind the prolonged QT interval is a hereditary defect of the ion channels. In acquired long QT syndrome, an attack is usually precipitated by QT interval lengthening medication Long QT Syndrome (LQTS).
    • Ventricular flutter is so fast that it is impossible to distinguish the diastolic phase.
    • In ventricular fibrillation (VF) the pattern of the wave frequency is initially coarse but will quickly turn into a fine fibrillation pattern.
  • Classification into the sub-categories may be useful when assessing the seriousness and prognosis of VT and when deciding on appropriate treatment.

Clinical manifestation

  • The clinical manifestation of VT depends upon the patient's underlying disease as well as the type, duration and rate of the arrhythmia.
  • VT in a person with an otherwise normal heart usually manifests itself as paroxysmal palpitations which may be preceded by sensations of ectopic beats (felt like "thumps" or "somersaults" in the chest). Syncope is rare.
  • Sustained VT in a person with a diseased heart often leads to serious haemodynamic adverse effects. Syncope is common but some patients may tolerate VT well.

Diagnosis

  • Diagnosis of VT is based on a preliminary assessment derived from the patient history and on ECG recording during the arrhythmia.
    • QRS complex is wide and its shape is different from that seen during normal rhythm and the shape of the ventricular deflection in typical bundle branch block.
    • An experienced interpreter may be able to locate the site of origin of the VT by inspecting the shape of the QRS complex in a 12-lead ECG.
  • The patient's history and clinical examination are very important when differentiating VT from SVT with fixed bundle branch block or aberration.
    • Broad complex tachycardia (which has caused the patient to faint) in an elderly patient with myocardial infarction is almost without exception VT (picture ).
    • Tachycardia that has the form of a typical bundle branch block in a young, otherwise healthy person may be supraventricular in origin (aberration).
    • For principles of differential diagnosis of broad complex tachycardia, see Differential Diagnosis of Broad Complex Tachycardia
  • Important ECG changes, as regards the underlying mechanism of VT and its treatment, include: R on T phenomenon, the length of the QT interval, ST-T changes, changes in the rate (slowing down, increasing, pause).
  • Diagnosing VT wrongly as benign supraventricular tachycardia (SVT) is dangerous!

Treatment of an acute episode

  • Life-saving procedures should be focused on in the treatment of VF and other ventricular arrhythmias that induce haemodynamic instability. Electrical defibrillation is performed as soon as possible.
  • The first-line treatment of sustained VT is electrical cardioversion.
    • Similarly to VF, if the risk of recurrence is considerable the patient should be given a beta-blocker, amiodarone or lidocaine (bolus of 1 mg/kg followed by an infusion of 1-3 mg/min).
  • Other drugs may be considered if the underlying mechanism of sustained VT is known.
    • Idiopathic VT which originates from the region of the right ventricular outflow tract (RVOT) responds well to adenosine.
    • Fascicular VT will almost always terminate with verapamil.
    • In torsade de pointes VT, magnesium is administered (MgSO4 1-2 g over 1-2 min) and any drugs prolonging the QT interval are stopped; see Long QT Syndrome (LQTS).
  • In non-sustained VT the patient's condition should be carefully evaluated, and treatment should be commenced if the risk of a more serious arrhythmia is significant.
    • During the acute phase of myocardial infarction, non-sustained VT is of no prognostic significance. There is no need to treat it unless it recurs frequently or has an adverse effect on the patient's haemodynamics.
    • At the later stages of an infarction, a short run of VT, even if asymptomatic, is indicative of an increased risk of sudden death and cardiological investigations are warranted.

Investigations

  • After the acute phase, the patient is referred for further cardiological investigations.
    • The aetiology of the arrhythmia should be investigated and the need for further intervention evaluated.
    • Concerning the treatment choices it is essential that the possible existence of heart disease, or hereditary abnormalities in the functioning of the ion channels, is established.
  • The cornerstones of diagnostics include: history, clinical examination, 12-lead ECG and laboratory investigations (basic blood count, creatinine, electrolytes, cardiac enzymes, thyroid function tests etc.).
  • An echocardiogram is always needed to exclude a structural heart disease, and, if myocardial ischaemia is suspected, also an exercise stress test or coronary imaging should be performed, as necessary.
  • If the aforementioned investigations are normal and the patient has no close family members with a history of sudden death or serious arrhythmias, the arrhythmia can usually be classified as being benign VT in an otherwise normal heart.
  • If there are signs and symptoms of heart disease (e.g. heart failure, sequela of myocardial infarction), the patient should be referred to an arrhythmia cardiologist for cardiac and coronary artery angiography, MRI of the heart, and electrophysiological studies.
  • Based on the assessment of the arrhythmia cardiologist, myocardial biopsy and genetic studies may also be carried out.

Prognosis and follow-up treatment Amiodarone for Prevention of Sudden Cardiac Death

  • Planning the treatment of ventricular arrhythmias should be carried out by a cardiologist.
    • Good treatment of an underlying heart disease is of paramount importance, but anti-arrhythmic medication, an implantable cardioverter-defibrillator, a pacemaker, and sometimes also ablation therapy may be needed in addition.
    • The prescribed treatment should always be based on adequate cardiological investigations, since empirical (by trial and error) anti-arrhytmic drug treatment may be more dangerous than the arrhythmia itself.
  • Implantable cardiac defibrillators have proved to be the only effective form of treatment for patients who have successfully been resuscitated from VF or VT. The implantation of a cardiac defibrillator should always be considered for patients who have been resuscitated after a cardiac arrest if no transient or reliably treatable cause for the cardiac arrest can be identified.
  • In other cases, the treatment is principally dependent on the patient's other heart diseases.

VT in an otherwise normal heart

  • The most common form of ventricular arrhythmia in an otherwise normal heart is VT originating in the right ventricular outflow tract (RVOT).
    • The QRS complex in ECG resembles LBBB and the activation is directed downwards (positive deflections in inferior wall leads).
    • The origin of a VT may also be in the left ventricular outflow tract (LVOT) or at the base of the aorta. In these cases the ECG differs from the aforementioned.
  • Another form of tachycardia in a normal heart is fascicular tachycardia. The underlying mechanism is re-entry in the left ventricular conductive system
    • In VT the QRS complex typically resembles RBBB and LAFB.
  • VT in an otherwise normal heart is usually benign and treatment is symptomatic.
  • Medication should be chosen according to the underlying mechanism of the arrhythmia.
    • In RVOT-VT, beta-blockers are the drug of choice. If they prove not to be of benefit, verapamil may be tried or, after consultation with a specialist physician, Class IC antiarrhythmics.
    • In fascicular tachycardia the first-line drug is verapamil.
  • If the arrhythmia reacts poorly to drug treatment, it can often be cured by catheter ablation.

VT associated with hereditary ion channel abnormalities

  • Treatment of VT in a patient with hereditary ion channel abnormalities (for example long QT syndrome, Brugada syndrome, short QT syndrome, catecholamine-sensitive polymorphic VT) requires specialist intervention, and these patients should always be referred to a cardiologist with expertise in rhythm disorders.
  • Beta-blockers are the drug of choice in long QT syndrome. If they are ineffective, an implantable cardiac defibrillator should be considered Long QT Syndrome (LQTS).
  • Drug treatment is of little benefit in the other ion channel abnormalities, and an implantable cardiac defibrillator is the treatment of choice.
  • Genetic counselling and testing of close family members form an integral part of treatment in these patients.

VT associated with heart disease

  • As a general rule, both non-sustained and sustained VT is dangerous and will not be treatable with drugs but requires an implantable cardioverter defibrillator, especially if the patient's left ventricular ejection fraction is < 35%.
    • Before a cardiac defibrillator is implanted, the patient's overall condition should be considered. It might be advisable to refrain from using the device if, based on the patient's other illnesses, his/her prognosis is poor.
  • When managing VT associated with heart disease it is important that emphasis is given to treating ischaemia, heart failure and any other underlying cardiac condition. Basic medications that have been shown to improve the prognosis of ischaemic heart diseases:
  • Class I anti-arrhythmic drugs (quinidine, disopyramide, flecainide, propafenone) are contraindicated after myocardial infarction and in heart failure.
  • Amiodarone may have a beneficial effect on prognosis. Amiodarone should initially only be prescribed under specialist supervision, but a general practitioner may be responsible for follow-up care. At discretion of a specialist, also sotalol may be used in some cases.
  • If monomorphic VT is repeatedly detected and drug treatment is ineffective, the patient should be referred for catheter ablation. With the new electroanatomic mapping methods, the results of catheter ablation are good even in haemodynamically unstable VT.