Supraventricular Arrhythmia: Definition, Causes, Signs, Symptoms, Diagnosis, Treatments and Tips

They are a type of abnormal heartbeat (arrhythmias), so your heart beats too fast.

Causes of supraventricular arrhythmia

This condition is caused by faulty electrical signals in your heart originating from your ventricles (the lower chambers of your heart).

Supraventricular arrhythmias are the most widespread group of arrhythmias and affect all age groups. Atrial fibrillation is the most common arrhythmic disorder and is even more common among the elderly.

Due to their prevalence, the physician must be informed about these arrhythmias and treatment considerations.


In the normal heart, impulse formation occurs in the sinoatrial node. It leads sequentially to the atrioventricular (AV) node, the bundle of His, bundle branches, and finally, Purkinje fibers located in the ventricles.

The mechanism of cardiac arrhythmias involves disturbances in impulse formation (often called automatic) or abnormalities in impulse conduction (often called reentrant).

Improved or abnormal automation, reentry, and reflection (reflected reentry) are SVT and ventricular tachycardia mechanisms.


Automaticity is the inherent property of myocardial cells to depolarize spontaneously (i.e., impulse formation), whereas reentry refers to abnormalities in impulse conduction.


The high incidence of atrial arrhythmias is mainly due to AF. However, sinus tachycardia, another atrial arrhythmia, is a typical physiological response to stressors such as pain, fever, exercise, or anxiety.

Other arrhythmias from the atrium include multifocal AT, which is commonly seen in elderly patients with lung disease, and AFL, which is often associated with cardiomyopathy, hyperthyroidism, and electrolyte imbalance.

As mentioned above, AF is the most common arrhythmia, and its prevalence increases with advanced age, with a higher prevalence in patients older than 69 years.

More than 2.2 million people in the United States alone are affected by AF and have a 1.5-1.9-fold increased risk of death.

The incidence of new-onset AF doubles with each decade of age, regardless of other risk factors. AF patients are predicted to increase 2.5 times by 2050, affecting more than 5.6 million American adults.

There are distinct gender differences in the risk of mortality from AF, with a 1.5-fold increase for men compared to a 1.9-fold increase for women.

Risk factors for the development of AF include hypertension (HTN), diabetes mellitus, male sex, congestive heart failure, and valve disease, with HT as the dominant risk factor.

In both men and women, HTN and diabetes were significant independent predictors of AF, with HT conferring a 1.5-fold risk in men and a 1.4-fold risk in women, while diabetes conferring risk of 1.4 in men and a risk of 1.6 times in women.

Risk assessment includes left atrial diameter, left ventricular wall dimensions, and left ventricular systolic function.

Due to the risks, especially the strokes associated with this arrhythmia, much attention has been paid to preventing and treating AF, which is responsible for 15% -25% of all strokes in the United States alone.

Numerous clinical trials have not documented any advantage of rhythm over rate control in the treatment of AF.

Risk factors for stroke due to AF include:

  • Male.
  • Rheumatic valve disease.
  • Congestive heart failure
  • HA.
  • Diabetes.
  • History of stroke or transient ischemic attack.
  • Advanced age.
  • Global left ventricular dysfunction.
  • Coronary artery disease.
  • Mitral stenosis or the presence of a prosthetic valve.

This reentrant arrhythmia is more common in the elderly, with a higher prevalence in men than women. It is associated with hypoxia, hyperthyroidism, cardiomyopathy, alcohol consumption, electrolyte imbalance, and pheochromocytoma.

While two-thirds of patients with AFL have hypertension or coronary artery disease, the remaining third do not have heart disease.

This arrhythmia is quite rare and is generally seen in elderly, predominantly male patients with lung disease. The hallmark of this arrhythmia is the presence of three or more distinct P wave morphologies.

These arrhythmias occur less frequently than atrial arrhythmias and involve the AV node. The two most common types are VNRT and AVRT. AVNRT is more common in women than men, accounting for 50% -60% of narrow QRS atrioventricular tachyarrhythmias.

Both AVNRT and AVRT occur more frequently in younger patients, but unlike AVNRT, AVRT is more common in men (2: 1 ratio) and affects less than 0.5% of the population.

AVRT commonly presents at a younger age than AVNRT and is associated with Ebstein’s anomaly. However, most patients have no evidence of structural heart disease. AVRT results from two or more conduction pathways (that is, the AV node and one or more diversion pathways).

Other less common AV arrhythmias include non-paroxysmal junctional tachycardia and ectopic junctional tachycardia. These rare arrhythmias are generally seen after vascular surgery, post-myocardial infarction, digoxin toxicity, and in children after congenital heart surgery.

Signs and symptoms of supraventricular arrhythmia

Common signs and symptoms include:

  • Palpitations
  • Fatigue.
  • Chest pain.
  • Dyspnoea.
  • Dizziness/lightheadedness
  • Sickness.
  • Diaphoresis.
  • General discomfort.
  • Polyuria.
  • Presence.
  • Rarely syncope.

However, the patient may be asymptomatic, with a higher risk of morbidity and mortality due to the unrecognized presence of these arrhythmias.

Atrial contraction against a closed AV valve causes an increase in atrial pressure with subsequent release of atrial natriuretic peptide, resulting in polyuria.

The rapid ventricular rates that commonly occur with AF can cause or exacerbate myocardial ischemia (predisposing the patient to sustained ventricular tachyarrhythmia) or induce or worsen heart failure (tachycardia-mediated cardiomyopathy).

Diagnosis of supraventricular arrhythmia

A history of arrhythmia-related symptoms is essential and should include the presence and pattern of pulses (regular or irregular) and whether the arrhythmia has a gradual or abrupt onset and end.

The diagnosis is based on the medical history and whether or not the arrhythmia may end with vagal maneuvers.

Regular paroxysmal palpitations with sudden onset and displacement, terminated by vagal maneuvers, maybe due to AVRT or AVNRT, whereas irregular palpitations may be due to AF or multifocal atrial tachycardia.

The diagnosis of many of these arrhythmias can be made by documenting a 12-lead electrocardiogram (ECG).

A 12-lead resting ECG with evidence of pre-excitation and a history of regular paroxysmal palpitations suggests AVRT. In contrast, pre-excitation with a history of irregular paroxysmal palpitations is more likely to be AF.

In addition, narrow QRS complex tachycardia must be differentiated from wide QRS complex tachycardia on the ECG for diagnostic and treatment purposes.

This latter group of patients requires immediate evaluation by an electrophysiologist. They are at increased risk of sudden death due to atrial fibrillation. The rapid ventricular response (caused by an accessory pathway with rapid repetitive conduction to the ventricles) deteriorates ventricular fibrillation.

Since many of these arrhythmias are paroxysmal, with rapid onset and movement, event monitors such as loop recorders may be necessary to capture a brief and infrequent episode.

Twenty-four-hour Holter monitors can be used if the episodes are frequent. Laboratory tests rule out possible electrolyte imbalances, drug toxicity, and thyroid disorders.

Treatment of supraventricular arrhythmia

Treatment of supraventricular arrhythmias varies with rhythm, rate, and hemodynamic stability. Therapeutic modalities include drug therapy, electrical cardioversion, ablation, and stimulation.

Atrial pacing therapies (delivered by an implantable dual-chamber cardioverter-defibrillator) are currently under investigation for use in the treatment and prevention of AT or AF.

Regular, narrow QRS complex tachycardias are usually supraventricular and are initially treated with vagal maneuvers.

However, wide QRS complex tachycardia can be present in SVT with bundle branch block or AV conduction on an accessory pathway and ventricular tachycardia.

Treatment for SVT versus ventricular tachycardia is very different, and when in doubt, the patient should be treated as if ventricular tachycardia is present.

The traditional approach to the treatment of AF involves anticoagulation and antiarrhythmic pharmacological agents.

However, advances in knowledge and technology have resulted in the development and use of radiofrequency catheter ablation in or around the pulmonary veins and the Maze surgical procedure.

Also recently, anti-tachycardia pacing, atrial pacing, and atrial defibrillation therapies for treatment. And prevention of AF.

In patients with intractable arrhythmia and poor ventricular rate control (i.e., AF with rapid ventricular response refractory to drug therapy), AV nodal ablation may be used to disconnect the atria from the ventricles.

However, AV nodal ablation produces complete heart block and subsequently requires implantation of a permanent pacemaker.

It is essential to recognize that this treatment option does not eliminate the symptoms associated with loss of atrial output (atrial kick) or the risk of stroke.

Therefore, the patient must remain on anticoagulation therapy as their underlying rhythm (below the accelerated rate) remains in AF.

Cardiac resynchronization therapy (also known as biventricular pacing) involves pacing both ventricles to correct mechanical dyssynchrony in patients with heart failure and conduction disorders.

The first study was prospective and randomized in the trial of biventricular pacing after ablation compared to right ventricular therapy (PAVE).

This study evaluated biventricular pacing after pacing therapy. Biventricular pacing resulted in a statistically significant improvement in functional ability (Presented by Rahul Doshi, MD, at the American College of Cardiology Annual Scientific Session, March 7-10, 2004; New Orleans, LA).

Preventive atrial pacing therapy is currently being investigated as a strategy to reduce the incidence of AF by eliminating the triggers and modifying the AF substrate.

Compared with ventricular pacing, atrial or dual-chamber pacing has been shown to prevent or delay progression to permanent AF in elderly patients.

Atrial resynchronization pacing is being studied in treating patients with advanced delay in atrial conduction.

Pacing from different sites in the atria, specific pacing algorithms targeting potential AF triggers, and TA pacing termination are strategies that are incorporated into newer defibrillators and implantable pacemakers.

Atrial defibrillators are being investigated as a treatment modality for recurrent, symptomatic, and persistent AF.

The Maze surgical procedure, which creates zoning of the atria, is highly effective in treating AF. Still, its use is limited as it involves major thoracic surgery in cardiopulmonary bypass and is generally performed in conjunction with another procedure, such as Como mitral valve repair.

Pulmonary vein isolation/ablation of focal triggers for paroxysmal AF has a higher success rate in patients with a single focus than in patients with multiple areas of focal stimuli.

Possible complications of pulmonary vein ablation include pulmonary vein stenosis, systemic embolization, pericardial effusion and tamponade, and phrenic nerve palsy.

The use of hybrid therapy consisting of two or more treatment strategies can help reduce the morbidity and mortality of AF.

In elderly patients and those with heart failure, the risks of proarrhythmia derived from antiarrhythmic drug therapy can be reduced or eliminated with preventive anti-tachycardia stimulation.

Treatment of narrow QRS complex tachycardia includes:

  • Vagal maneuvers.
  • Intravenous adenosine (to aid in rhythm diagnosis).
  • Non-dihydropyridine calcium channel blockers.

Wide QRS complex tachycardia of unknown origin is treated with amiodarone or direct current cardioversion if it is hemodynamically unstable.

Tips for Living with Supraventricular Arrhythmias

When you have a supraventricular arrhythmia, your heart’s electrical system sometimes causes it to beat faster than usual.

You can have a supraventricular arrhythmia attack even when not stressed or exercising hard. When your heart beats too fast, it can’t pump enough blood.

You may feel tired, breathless, or dizzy due to this condition that begins in the upper chambers of your heart.

Your doctor can prescribe medications and other treatments to get your heart back into a regular rhythm. But there are also many positive things you can do to stay on track.

Eat foods that are good for you.

A well-balanced diet with whole grains, fruits, vegetables, and lean protein is always intelligent. With supraventricular arrhythmias, you may need to be even more careful about what you eat, especially if you are overweight or have other heart conditions.

Ask your doctor how many calories you should eat each day to maintain your current weight or lose a few pounds. You put extra pressure on your heart if you are too heavy.

Certain foods can trigger arrhythmias, while others are packed with minerals that help keep your heart beating. Put potassium and magnesium on your list.

Find potassium in foods like:

  • Albaricoques.
  • Bananas
  • Melons
  • Lime beans.
  • Oranges
  • Peas.
  • Low-fat, skim milk.
  • Spinach.
  • Sweet potatoes.
  • Tomatoes.
  • Yogurt.

All of these foods are high in magnesium:

  • Almonds
  • Avocados
  • Black beans
  • Integral rice.
  • Peanuts and cashews.
  • Spinach.

Also, try to cut down on foods and drinks that could trigger a faster heart rate. They include:

  • Alcohol.
  • Caffeine, chocolate, and some soft drinks and herbal teas.
  • Spicy food.
  • Icy drinks.

Exercise safely

A quick run or strenuous exercise can trigger an SVT attack in some people, even if you don’t stop exercising. It is a crucial way to keep your heart strong. Just be more careful about your physical condition.

Check with your doctor to see how much exercise and which types are safest for you. You may need a stress test to determine how much activity you can handle.

Start any new exercise program slowly. Add more time and effort only when your heart can do so. Learn to check your pulse while you exercise, and ask your doctor what to do if your heart rate is racing.


A hectic day can make your heart rate skyrocket.

You can try these things to help you relax:

  • Meditate for 5-10 minutes throughout the day. Sit in a quiet place, close your eyes, and take a deep breath.
  • Take a yoga class.
  • Relax with a hot bath or listen to soft music.
  • Get a massage.


Treatment begins with your doctor, but it does not end there. You are also a big part of your own “healthcare team.”

To play that role, you need to know a lot about your condition and how to manage it. Please read it and ask your doctor to explain anything you don’t understand.

Learn what triggers your SVT fights. Keep a journal to help you identify your triggers. Write down when your heart breaks down and what you were doing at the time.


  • Cigarettes and other forms of tobacco.
  • Diet pills.
  • Energy pills.
  • Herbal supplements.
  • Illegal drugs such as cocaine and methamphetamine (crystal meth).
  • Over-the-counter cold and cough medicines.

Manage your medications

Your doctors may recommend medicines called “beta-blockers” or “calcium channel blockers.” They can help your heart keep pumping at the correct rate. They work best when taken as prescribed, usually every day.

If you have any questions about side effects, ask your doctor or pharmacist. Do not skip a dose or stop taking medicine without first checking with your doctor. Also, ask if the medication could interact with other drugs.

Your doctor should carry out regular follow-ups. Keep these appointments, so your plan stays on track.