1. Supraventricular arrhythmias, diagnosis and therapy

Page created on July 10, 2021. Not updated since.


Supraventricular arrhythmias are those which originate from the SA node, atria, or AV junction. They include the following:

  • Sinus arrhythmias
    • Sinus bradycardia
    • Sinus tachycardia
    • Sick sinus syndrome
  • Supraventricular premature beats
  • Atrial tachycardia
  • Atrial fibrillation
  • Atrial flutter
  • AV nodal reentry tachycardia (AVNRT)
  • AV reciprocating tachycardia (AVRT)

Atrial fibrillation


Atrial fibrillation (Afib) is the most important supraventricular arrhythmia. The characteristic ECG findings of atrial fibrillation is the lack of normal P-waves in all leads, and irregularly irregular ventricular rate. The ventricular rate is often high. We can distinguish three types of Afib:

  • Paroxysmal Afib – Afib that terminates spontaneously within 48 hours
  • Persistent Afib – Afib which lasts more than seven days or requires electrical cardioversion to restore sinus rhythm
  • Permanent Afib – Afib where a decision has been made to no longer try to achieve sinus rhythm, either because cardioversion or drugs have failed, or because a rhythm-control strategy is used instead

Afib usually progresses from paroxysmal to persistent to permanent with time.

Afib is problematic because of the following:

  • It increases the risk for stroke
  • It can cause tachycardia-induced heart failure (= arrhythmia-induced cardiomyopathy)
  • It can cause symptoms


Afib can be multifactorial and idiopathic, but in some cases it’s caused by treatable etiologies:

  • Hyperthyroidism
  • Hypovolaemia
  • Hypervolaemia
  • Intoxication
  • Heart failure
  • Respiratory failure

Clinical features

Most patients are asymptomatic, and Afib is discovered incidentally. Patients may also present with palpitations, syncope, dyspnoea, or symptoms of heart failure.


ESC uses an ABC pathway for the management of Afib:

  • Anticoagulation/avoid stroke
  • Better symptom control
  • Comorbidity management/cardiovascular risk factor reduction

In some cases, Afib is caused by a reversible etiology and does not return when the etiology is managed.


Stroke risk is increased in patients with atrial fibrillation, due to the Afib’s tendency to form thrombi in the atria which can embolise to the brain. All patients with Afib should have the CHA2DS2-VASc score calculated.

A score of 1 or more in men and 2 or more in women is an indication for anticoagulation. A score of 0 in males, or 1 or 0 in females has low risk for stroke and does not require anticoagulation. The bleeding risk (with the HAS-BLED score) should be calculated and considered, and risk factors for bleeding should be treated if possible. Anticoagulation should be with a DOAC, and it should be continued indefinitely.

Better symptom control

The symptoms of Afib can be controlled with either a rate-control strategy or a rhythm-control strategy. Choosing between them can be difficult. Generally, we use rhythm-control for patients who are young, have heart failure, have significant symptoms, have high cardiovascular risk, or if rate-control has failed. Rate-control is generally used for older or asymptomatic patients.

Rate control involves not doing anything to convert the rhythm to sinus rhythm, but to use drugs to reduce the ventricular rate. This improves symptoms and prevents development of heart failure. The first choice is a beta blocker, often metoprolol. Second choices include verapamil, amiodarone, or digoxin.

Rhythm control involves measures to convert the rhythm to sinus rhythm, and to maintain it. It’s usually tried if adequate rate control can’t be achieved, or if the onset of the Afib is recent (< 2 days). It can be performed in cases when it’s known that the Afib has lasted < 2 days, or if it’s lasted longer but the patient has been properly anticoagulated for 3 – 4 weeks, or if a TEE has been performed and excluded the presence of cardiac thrombus (which could embolise during cardioversion).

Usually, electrical cardioversion is performed to convert the rhythm back to sinus. Patients must usually remain on antiarrhythmic drugs after conversion to prevent recurrence. In some cases, electrical cardioversion cannot be performed. However, antiarrhythmic drugs alone may convert the rhythm to sinus as well. Antiarrhythmic drugs most commonly used include flecainide and amiodarone. In some cases the ectopic focus can be ablated, preventing further recurrence.

Comorbidity management/cardiovascular risk factor reduction

Tachycardia-induced heart failure should be treated like other types of heart failure, with ACEi/ARB, beta blockers, diuretics, etc. Other cardiovascular risk factors, like hypertension, diabetes, atherosclerosis, etc., should be managed as well.

Atrial flutter

Atrial flutter is generally managed similarly as atrial fibrillation, and in many cases it progresses to Afib. It requires anticoagulation and either rate or rhythm control. There are two types:

  • Typical atrial flutter
  • Atypical atrial flutter

On the ECG, P-waves are replaced by F-waves which have a frequency of about 300/minute. There is a fixed pattern of atrial:ventricular conduction (P-waves:QRS-complexes), usually 2:1 or 4:1.

Typical atrial flutter can be treated effectively with ablation because it’s caused by a macro-reentry circuit along the tricuspid anulus, which can be ablated.


AV nodal reentry tachycardia (AVNRT) is caused by the presence of an additional electrical pathway in the AV node, which forms a reentry circuit in the AV node. On the ECG there are fast, narrow, regular QRS complexes without normal P-waves. In some leads, small P-waves may be visible at the end of the QRS complex (retrograde P).

AVNRT can often be terminated by vagal manoeuvres or adenosine. Some patients can be managed by only performing vagal manoeuvres when they feel the AVNRT. Others require antiarrhythmic treatment with beta blockers, verapamil, or flecainide.


AV reciprocating tachycardia (AVRT) occurs in patients with an accessory pathway which circumvents the AV node, which causes pre-excitation of the ventricles. This occurs most commonly in patients with Wolff-Parkinson-White syndrome. It is triggered by a premature atrial or ventricular beat. Treatment involves ablation of the accessory pathway.

In patients with WPW (but not currently in AVRT), pre-excitation is visible as delta-waves, and the PQ-interval is decreased.

Other supraventricular arrhythmias

Sinus arrhythmias

Sinus bradycardia is a sinus rhythm with < 60 bpm. It’s physiological in well-trained persons but can be pathological in some cases.

Sick sinus syndrome (SSS) or sinus node dysfunction refers to the condition where the SA node is dysfunctional. This causes intermittent sinus bradycardia, sinus pauses, sinus arrest, or SA block, and is typically due to old age. Patients present with intermittent complaints of fatigue, dizziness, palpitations, syncope, etc. Patients often require implantation of a pacemaker.

Atrial tachycardia

Atrial tachycardia may be focal (originate from one focus in the atria) or multifocal (originate from multiple foci). The typical symptom is palpitations. In the focal type all P-waves have the same morphology, while in the multifocal type there are multiple P-wave morphologies.

Atrial tachycardia is associated with heart surgery, like CABG. Multifocal atrial tachycardia is associated with COPD.

Supraventricular premature beats

Supraventricular premature beats, also called supraventricular extrasystoles (SVES), are atrial contractions triggered by ectopic foci in the atria or AV node. They include atrial premature beats and junctional premature beats. Supraventricular premature beats rarely cause symptoms and therefore rarely require treatment.

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