Tachycardia

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Introduction

Differentiation between supraventricular tachycardias (SVT) and ventricular tachycardias (VT) can be challenging, especially in acute emergency settings. SVT's are rhythm disturbances in the atria or AV-nodal ring or rhythm disorders in which these structures are involved. VT's are rhythm disorders that only involve the ventricles. It can both take place in the myocardial tissue and the conduction system tissue.

Definitions:

Tachycardia:

heartrate > 100 bpm

Overview:

(Figure: Atrial ventricular)

Ventricular tachycardia

Ventricular tachycardias (VT's) are rhythm disturbances that arise in the ventricles.

History

Symptoms can arise in every ventricular tachycardia, depending on the heart rate, the presence of underlying heart disease and the degree of systolic heart failure. Various symptoms are:

• Palpitations
• Abnormal chest sensation
• Dyspnea
• Angina
• Presyncope (lightheadedness, weakness, diaphoresis)
• Syncope
• Cardiogenic shock

Additional information about drug use is mandatory. Toxic levels of digoxin and cocain can lead to VT's. Also additional information about family history of sudden cardiac death is helpfull, as it is a strong predictor of susceptibility to ventricular arrhythmias and sudden cardiac death.

Physical Examination

Although the diagnosis of VT is generally made by a 12 lead ECG, the following physical symptoms may be present:

• Cannon "A" waves on the jugular venous pulse in the neck. These represent intermittant retrograde propulsion of blood into the jugular veins during right atrial contraction against a closed AV valve. This is evidence of AV dissociation.
• Decreased or variable amplitude of the carotid or peripheral pulses. This is related to the intermittent periods of atrial and ventricular synchronization, which transiently augment cardiac output.
• Variable intensity of the first heart sound (although this is difficult with a rapid heart rate).
• Variable splitting of the first and second heart sounds, and intermittent presence of a third and/or fourth heart sound.

Diagnostic Evaluation

Exercise testing

Exercise testing is recommended in adult patients with ventricular tachycardias who have an intermediate or greater probability of having coronary heart disease by age, gender and symptoms. It is meant to provoke ischemic changes or ventricular arrhythmias.

Ambulatory (Holter) ECG

Ambulatory ECG is necessary if the diagnosis needs to be clarified, by detecting arrhythmias, QT-interval changes, T-wave alternans (TWA) or ST-segment changes.

Echocardiography, Cardiac CT, MRI

Echocardiography is recommended in patients with ventricular tachycardias who are suspected of having a structural heart disease. If echocardiography does not provide accurate assessment of the left and right ventricular function and/or structural changes, cardiac CT or MRI can be done.

Exercise testing with an image modality (echocardiography or nuclear perfusion)

Some patients with ventricular arrhythmias have an intermediate probability of coronairy heart disease, but their ECG is less reliabe (because of digoxin use, LVH, greater than 1mm ST-segment depression at rest, WPW syndrome or LBBB). For detecting silent ischemia in these patients exercise testing with an image modality can be done. If patients are unable to perform exercise, a pharmacological stress test with an imaging modality can be done.

Coronary angiography

Coronary angiography can diagnose or exclude the presence of significant obstructive coronairy heart disease in patients with ventricular arrhythmias who have an intermediate or greater probability of having coronairy heart disease.

Electrophysiological testing

Electrophysiological testing can be performed to guide and assess the efficacy of VT ablation in patients with ventricular arrhythmias. It can also be done to clarify the mechanism of broad complex tachycardias in patients with coronairy heart disease.

Ventricular tachycardia

Ventricular tachycardia (VT) is defined as a sequence of three or more ventricular beats. The frequency is often 110-250 bpm. Ventricular tachycardias often origin around old scar tissue in the heart, e.g. after myocardial infarction. Also electrolyte disturbances and ischemia can cause ventricular tachycardias. The cardiac output is often strongly reduced during VT resulting in hypotension and loss of conciousness. VT is a medical emergency as it can deteriorate into ventricular fibrillation and thus mechanical cardiac arrest.

Definitions:

• Non-sustained VT: three or more ventricular beats with a maximal duration of 30 seconds.
• Sustained VT: a VT of more than 30 seconds duration (or less if treated by electrocardioversion within 30 seconds).
• Monomorphic VT: all ventricular beats have the same configuration.
• Polymorphic VT: the ventricular beats have a changing configuration. The heart rate is 100-333 bpm.
• Biphasic VT: a ventricular tachycardia with a QRS complex that alternates from beat to beat. Associated with digoxin intoxication and long QT syndrome.

Localisation of the origin of a ventricular tachycardia:

Determination of the location (or exit site) where a ventricular tachycardia originated, can be helpful in understanding the cause of the VT and is very helpful when planning an ablation procedure to treat a ventricular tachycardia. (new page for localization)

Differential diagnosis

(Non)sustained VT may be idiopathic, but occurs most frequently in patients with underlying structural heart disease of various types including:

• Coronary heart disease (CHD) with prior myocardial infarction (is the most frequent cause in developed countries)
• Hypertrophic cardiomyopathy
• Dilated cardiomyopathy
• Mitral valve prolapse
• Aortic stenosis
• Complex congenital heart disease
• Cardiac sarcoidosis
• Arrhythmogenic RV cardiomyopathy/dysplasia

Ventricular fibrillation

VF is lethal if the patient is not treated immediately. It gives rise to a mechanical standstill of the heart, because the heart is not able to pump normally anymore.

Differentiation between SVT and VT

To differentiate between supraventricular tachycardias and ventricular tachycardias a 12 lead ECG is the cornerstone of the diagnostic process. At first, the physician has to make a differentiation between a small or broad complex tachycardia.

Definitions:

Small complex tachycardia:

QRS duration < 120 ms.

A small complex tachycardia is most likely to be a SVT. However, also a septal VT or His-tachycardia can appear as a small complex tachycardia.

Broad complex tachycardia:

QRS duration > 120 ms.

A broad complex tachycardia can be due to a SVT with aberration, pre-exited tachycardia (eg antidrome re-entry tachycardia) or VT.

Differentiation:

(Figure 1, small complex tachy algorithm) (Figure 2, broad complex tachy algorithm)

Treatment:

Haemodynamical instability (high heartrate, low blood pressure):

• electrical cardioversion

Haemodynamical stability in a regular small complex tachycardia:

• Carotid massage (after palpation and ausculatation of carotid arteries for exclusion of carotid occlusion/stenosis)
• Vasalva manoevre
• Adenosine bolus (if patient is not asthmatic or having COPD)
• Verapamil (if patient is not having systolic heart failure)
• Beta-blocker (if patient is not having systolic heart failure)

Haemodynamical stability in a regular monomorphic broadcomplex tachycardia (systolic blood pressure >100 mmHg):

• Procaïnamide
• Amiodaron