Supraventricular tachycardia (SVT) generally refers to atrioventricular nodal re-entry tachycardia (AVNRT), atrioventricular re-entry tachycardia (AVRT) and atrial tachycardia. It does not usually include atrial fibrillation.
SVT is usually paroxysmal (PSVT) and episodes may occur regularly or very infrequently (sometimes years apart). Episodes may only last for a few minutes or may last for up to several months.
SVT is caused by:
- Abnormalities of impulse conduction (re-entrant tachycardias).
- Disorders of impulse initiation (automatic tachycardias) causing a narrow complex tachycardia.
These are the most common type:
- Atrioventricular nodal re-entrant tachycardia (AVNRT):
- Due to the presence of two functionally and anatomically distinct conducting pathways in the atrioventricular node, one of which is fast-conducting, the other slow-conducting.
- During an episode of SVT one of these acts as the antegrade limb of a re-entrant circuit, while the other acts as the retrograde limb. AVNRT is the most common form of SVT.
- Atrioventricular re-entrant tachycardia (AVRT):
- Due to the presence of an accessory bypass pathway that bridges the normal insulation between the atria and ventricles. The pathway lies outside the atrioventricular node.
- Wolff-Parkinson-White (WPW) syndrome is the most well-known type of AVRT.
- Accessory pathways may be capable of antegrade or retrograde conduction, or both.
- Orthodromic AVRT is the term given to an activation pattern in which the conduction is down the AV node and the retrograde conduction is in the accessory pathway.
- In antidromic AVRT, which is rare, the direction of travel of the aberrant conduction is down the accessory pathway returning to the atrium through the AV node.
- Macro re-entrant atrial tachycardia:
- The re-entrant circuit involves a large area of the atrium
- Atrial flutter is the most common, where the re-entrant loop circles the right atrium.
- Focal junctional tachycardia:
- Due to abnormally rapid discharges from the junctional region.
- This type of SVT originates from the atrioventricular node, or bundle of His.
- This type is also known as automatic or paroxysmal junctional tachycardia.
- Focal atrial tachycardia:
- Due to regular atrial activation from atrial areas with centrifugal spread.
- Neither the sinus nor the atrioventricular node plays a role in the initiation or continuation of this type of SVT.
- Prevalence of SVT is approximately 2 per 1,000.
- Incidence of PSVT is about 36 per 100,000 people per year.
- Women have twice the risk of men of developing PSVT.
- The incidence of WPW pattern on ECG is 0.1-0.3% but not all patients with these changes experience PSVT.
SVT may occur at any age but often occurs in younger people in the absence of heart disease.
Risk factors include:
- Previous myocardial infarction
- Mitral valve prolapse
- Congenital heart disease
- Previous cardiac surgery
- Rheumatic heart disease
- Chronic lung disease
- Current alcohol intoxication
- Digoxin toxicity
- PSVT may be associated with minimal symptoms or present with syncope.
- Symptoms vary with the ventricular rate and duration of the SVT. Symptoms are more likely in those with underlying heart disease. They include:
- Palpitations and light-headedness, which are the most common symptoms reported.
- Palpitations of PSVT which start and end abruptly.
- Patients with AVNRT being more likely to describe 'shirt flapping' or 'neck pounding' than patients with AVRT, possibly due to right atrial contraction against a closed tricuspid valve.
- Other symptoms, including fatigue, chest discomfort, dyspnoea, polyuria and syncope (uncommon).
- Examination may be normal if seen after the attack, with normal cardiac function and no underlying heart abnormality.
- During an attack, tachycardia may be the only finding if the patient is otherwise healthy and there is no cardiac dysfunction. During an episode of SVT the pulse rate is 140-250 beats per minute (bpm).
- Resulting heart failure may cause tachypnoea, hypotension, raised JVP, third heart sound and basal lung crepitations.
- Drug adverse effects - eg, amiodarone, digoxin, beta-agonists; also amfetamines and cocaine.
- Narrow QRS-complex tachycardia:
- Irregular: atrial fibrillation.
- Sinus tachycardia - eg, due to anxiety, infection, medication, panic attack, thyrotoxicosis. The heart rate rarely exceeds 150 bpm except during exercise.
- No visible P waves: AVNRT.
- Visible P waves:
- Atrial rate greater than ventricular rate: atrial flutter or atrial fibrillation.
- Atrial rate not greater than ventricular rate: long RP interval: atrial tachycardia, permanent form of junctional re-entrant tachycardia, atypical AVNRT
- Short RP interval:
- Less than 70 ms: AVNRT.
- Longer than 70 ms: AVRT, AVNRT, atrial tachycardia.
- Wide QRS tachycardia (broad complex tachycardia):
- SVT with bundle branch block or aberration.
- SVT with atrioventricular conduction over an accessory pathway.
- Ventricular tachycardia (VT).
- Allows classification of the tachyarrhythmia (particularly its regularity) and may allow a precise diagnosis.
- P waves may not be visible; when present, they may be normal or abnormal depending on the mechanism of atrial depolarisation.
- Presence of pre-excitation on the resting ECG and a history of paroxysmal palpitations signifies an AVRT:
- Pre-excitation (WPW pattern) on ECG is defined as short PR (<0.12 s) and the presence of a delta wave (slurred, broad upstroke of QRS complex) which represents the more rapid conduction in the accessory pathway compared with conduction in the AV node.
- WPW syndrome refers to patients with a delta wave on their ECG who also experience palpitations; all such patients should be referred.
- A history of paroxysmal irregular palpitations - very likely to be atrial fibrillation - associated with baseline pre-excitation on the ECG; needs urgent specialist assessment, as there is a risk of sudden death.
- Ambulatory 24-hour Holter recording can be used for patients with frequent but transient tachycardias.
- Exercise ECG testing may be useful if arrhythmia is triggered by exercise.
- Cardiac enzymes: if there is chest pain; patients with risk factors for myocardial infarction and patients who are otherwise unstable and present with heart failure, hypotension, or pulmonary oedema.
- Electrolyte levels: electrolyte disturbances may be an underlying cause.
- FBC: helps assess whether anaemia is contributing to the tachycardia.
- Digoxin level for patients on digoxin: PSVT can be caused by high levels of digoxin.
- CXR: pulmonary oedema; infections such as pneumonia, which are associated with PSVT in certain cases.
- Echocardiogram may be helpful if structural heart disease is suggested.
See separate Atrial Flutter article.
An ECG should be performed as soon as possible.
If haemodynamically unstable, the most effective and rapid means of terminating any tachycardia is direct current (DC) cardioversion.
- In haemodynamically stable regular narrow QRS-complex tachycardia, vagal manoeuvres - eg, Valsalva, carotid massage, facial immersion in cold water:
- Carotid massage is usually reserved for young patients. Due to the risk of stroke from emboli, auscultate for bruits before attempting this manoeuvre. Do not perform carotid massage on both sides simultaneously.
- Valsalva manoeuvre may induce cardioversion in 5-20% of patients. A modified Valsalva manoeuvre, in which the patient is laid flat and their legs elevated after the end of the strain phase, was shown in one randomised controlled trial (RCT) to increase the rate of cardioversion to over 40%.
- If vagal manoeuvres fail, intravenous adenosine or verapamil can be used:
- Ensure resuscitation equipment is available in case of ventricular fibrillation or bronchospasm. AV nodal blockers in a patient with WPW and atrial fibrillation can result in ventricular fibrillation.
- Intravenous adenosine is the treatment of choice except for people with severe asthma. Adenosine has a rapid onset and short half-life. It blocks conduction through the atrioventricular node. Adenosine has a high incidence of minor but unpleasant side-effects (eg, nausea, chest tightness, shortness of breath and headache).
- Intravenous verapamil, although effective, is rarely used now. It has a more prolonged action than adenosine on blocking atrioventricular node conduction and there is a risk of prolonged depression of ventricular function and hypotension, especially if the person is taking a beta-blocker. It still has a place if adenosine is contra-indicated (eg, in somebody with severe asthma).
- Oral beta-blockers, diltiazem or verapamil may be appropriate for acute treatment of AVNRT.
- If vagal manoeuvres and adenosine fail or are contra-indicated, DC cardioversion is indicated.
Possible precipitating or aggravating factors - eg digoxin, caffeine, alcohol, nicotine intake, recreational drugs or hyperthyroidism - should be addressed.
The choice of long-term therapy depends on the exact nature of the tachyarrhythmia and the frequency and duration of episodes and risks associated with the arrhythmia (eg, heart failure, sudden death). The frequency and severity of the episodes of SVT need to be balanced against the risks of long-term therapy. Preventative treatment may not be required.
- Radiofrequency catheter ablation of the slow pathway is generally successful.
- Beta-blockers are first-line and diltiazem or verapamil are also effective.
- Flecainide or propafenone are alternatives.
- Valsalva manoeuvre can be taught to patients to do themselves.
- All patients with WPW syndrome should be referred to a cardiac electrophysiologist.
- Patients deemed to be at high risk of future arrhythmias should be considered for accessory pathway ablation.
- Sinus tachycardia:
- Exclude any secondary cause - eg, hyperthyroidism, excess caffeine or monosodium glutamate (MSG) intake, phaeochromocytoma, illicit drug use.
- Beta-blocker or non-dihydropyridine calcium-channel blocker - eg, diltiazem, verapamil.
- Focal atrial tachycardia:
- Calcium-channel blockers or beta-blockers are considered first-line.
- Flecainide, sotalol or amiodarone may also be effective.
- Catheter ablation is an alternative to pharmacological therapy.
- Multifocal atrial tachycardia:
- Therapy is mainly directed at chronic pulmonary disease (usually associated) and electrolyte disturbances, which may be the underlying cause. Digoxin toxicity is also an uncommon cause.
- Long-term therapy is otherwise with verapamil or diltiazem.
- Beta-blockers are usually contra-indicated because of pulmonary disease and there is no role for DC cardioversion or ablation.
Radiofrequency catheter ablation
- This is associated with a high success rate and low complication rate for people with SVT.
- Radiofrequency catheter ablation is indicated in the following situations:
- As first-line therapy as a curative option.
- If the SVT is refractory to antiarrhythmic drug therapy.
- If the person is intolerant of antiarrhythmic drug therapy.
- If antiarrhythmic drug therapy is contra-indicated.
- The available evidence does not justify the use of catheter ablation in the asymptomatic patient with WPW pattern on their ECG.
Driving and SVT
In the UK, Driver and Vehicle Licensing Agency (DVLA) advice is as follows:
- Group 1 (car or motorcycle):
- Must stop driving if the arrhythmia has caused or is likely to cause incapacity.
- Driving may be permitted when the underlying cause has been controlled for at least four weeks.
- Group 2 (lorry or bus):
- Disqualifies from driving if the arrhythmia has caused or is likely to cause incapacity. DVLA must be informed.
- Driving may be permitted when:
- The arrhythmia is controlled for at least three months.
- The LV ejection fraction is ≥40%.
- There is no other disqualifying condition.
Referral to an electrophysiologist
- Syncope with palpitations on exertion.
- Broad complex tachycardia.
- Pre-excitation (WPW pattern) on a 12-lead ECG.
- Structural heart disease.
- Severe symptoms.
- Drug resistance or intolerance.
- Preference not to take medication.
- Diagnostic uncertainty.
- Haemodynamic collapse can occur. This is more likely in people with underlying heart disease who are unable to tolerate increases in heart rate.
- Deep vein thrombosis.
- Systemic embolism.
- Cardiac tamponade.
- Rare complications include myocardial infarction, congestive heart failure, syncope, and sudden death.
- Patients with pre-excitation risk sudden cardiac death due to ventricular fibrillation induced by rapidly conducting atrial fibrillation.
- SVT that persists for weeks or months may lead to a tachycardia-mediated cardiomyopathy.
- Prognosis is dependent on any underlying structural heart disease.
- Patients with a structurally normal heart have an excellent prognosis.
- In the absence of manifest pre-excitation (WPW syndrome), the risk of sudden death is very small.
- Patients with pre-excitation risk sudden death:
- The risk is higher in patients who have experienced palpitations, in whom the risk is about 2.5 per 1,000 people per year, or 3-4% over a lifetime.
- Asymptomatic patients have a much lower risk of between 0.05-0.94 per 1,000 people per year.
- Electrophysiological studies and risk stratification in asymptomatic patients may be beneficial.
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