Paroxysmal supraventricular tachycardia

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Classification

Pathophysiology

Causes

Differentiating Paroxysmal supraventricular tachycardia from other Diseases

Epidemiology and Demographics

Risk Factors

Screening

Natural History, Complications and Prognosis

Diagnosis

Diagnostic Study of Choice

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Case #1

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Noha Elzeiny, M.B.B.Ch, M.Sc.[2]

Synonyms and keywords:PSVT, Narrow QRS complex tachycardiaAtrioventricular nodal reentrant tachycardia, AVNRT, Supraventricular arrhythmia, Supraventricular tachycardia, Tachyarrhythmia, Arrhythmia.

Overview

Paroxysmal Supraventricular tachycardia (PSVT) is a subset of supraventricular tachycardia (SVT), characterized by its episodic nature with sudden onset, sudden offset, regular, rapid rhythm and narrow QRS complex on Electrocardiogram (ECG), usually the patient is normal in between attacks and except for patients with preexisting heart disease, the prognosis is usually good.

Historical Perspective

Catheter-based radiofrequency ablation has improved the treatment of PSVT by precise ablation of the abnormal accessory pathway.  First catheter ablations were in the early to mid-1980s, since then it has improved progressively especially in terms of safety and specificity.

Classification

SVTs are classified based on the origin and the regularity of the rhythm:

Atrial in origin:

  • Sinus tachycardia
  • Inappropriate sinus tachycardia
  • Sinoatrial nodal reentrant tachycardia
  • Atrial flutter
  • Atrial fibrillation
  • Multi atrial focal tachycardia

AV nodal in origin:

  • Junctional tachycardia
  • Atrioventricular nodal reentrant tachycardia
  •  Atrioventricular reentrant tachycardia

Regular SVT:

  • All tachycardia originating from the AV node
  • Sinus tachycardia
  • Inappropriate sinus tachycardia
  • Sinoatrial nodal reentrant tachycardia
  •  Atrial flutter

Irregular SVT:

  • Multifocal atrial tachycardia
  • Atrial flutter with variable block
  • Atrial fibrillation

Pathophysiology

PSVTs are due to abnormalities in impulse formation and conduction pathways. Often due to different reentry circuits in the heart, less frequent causes include enhanced or abnormal automaticity and triggered activity.

Causes

Reentry circuits  are the most common cause

a. About 60% are due to  AVNRT either within

  • AV node
  •  Perinodal atrial tissue.

b. 30% are due to Atrioventricular reciprocating tachycardia (AVRT)

  • Extranodal accessory pathway connecting the atrium and ventricle, e.g. Wolff-Parkinson-White syndrome (WPW).

c. 10% are due to pathways within or around the sinus node:

  • Focal atrial tachycardia
  • Intra atrial reentrant tachycardia (IART)
  • Sinoatrial nodal reentrant tachycardia (SANRT)

d. Other rare causes (Rare in adults, but can represent a larger portion of PSVTs in children) are due to

  • Junctional ectopic tachycardia
  • Non-paroxysmal junctional tachycardia

Differentiating Paroxysmal supraventricular tachycardia from other Diseases


Symptoms due to PSVT are often misdiagnosed as psychological disease e.g. panic attacks, stress, anxiety, or depression delaying referral for ablation.

Epidemiology and Demographics

  • In the United States, 1.1 to 1.4 million individuals before the age of 65 are affected annually
  • Sporadic and unpredictable
  • Slightly higher in females than in males
  • Positively correlated with age

Risk Factors

Any condition or drug that increases automaticity or triggers activity including:

  • Abnormal thyroid hormone level
  • Caffeine, nicotine, alcohol toxicity and Illicit drugs
  • Digoxin and electrolyte abnormalities
  • Sympathomimetic drugs
  • Stress and anxiety
  • Preexisting heart condition, e.g. Congenital heart disease, rheumatic heart disease, cardiomyopathy and previous myocardial infarction
  • Lung disease and hypoxia e.g. Chronic lung disease and infection

Screening

Natural History, Complications and Prognosis

  • In Absence of underlying heard disease, the PSVT prognosis is favorable.
  • Rarely PSVT can cause myocardial infarction, congestive heart failure and  even death.

Diagnosis

Diagnostic study of choice | History and Symptoms | Physical Examination | Laboratory Findings | Electrocardiogram | X-Ray Findings | Echocardiography and Ultrasound | CT-Scan Findings | MRI Findings | Other Imaging Findings | Other Diagnostic Studies

The clinical presentation is variable, ranging from asymptomatic to complicated palpitation.

History:

  • If present, history of previous self-limiting attacks.
  • In some patients there is a past history of preexisting heart disease

Symptoms:

  • Asymptomatic
  • Some experience episodes palpitations that starts and ends suddenly, may be associated with
  • Presyncope, syncope,
  • Lightheadedness, dizziness
  • Dyspnea, Shortness of breath
  • Diaphoresis and/or chest pain.

Physical examination:

  • In patients with no underlying disease, the patient is clinically free: If terminated episode of PSVT or in between attacks.
  • Tachycardia: Regular, Rapid, abrupt onset, with or without abrupt termination.
  • If present Hemodynamic instability and/or lung congestion. Both varies according to the presence of preexisting heart disease

Treatment

Acute treatment | Long term treatment | Prevention


According to 2019 ESC correction of 2015 AHA guidelines for the management of patients with supraventricular tachycardia.

Acute treatment

If hemodynamically unstable or resistant to other treatment modalities: Direct-current cardioversion.

If hemodynamically stable:

The first line of treatment is vagal maneuvers e.g. Valsalva maneuver or carotid sinus massage

If failed vagal maneuvers: Adenosine is recommended. Adenosine can be considered as both therapeutic and diagnostic agents in narrow-complex tachyarrhythmias

If failed adenosine Intravenous diltiazem, verapamil or betablockers

Long term treatment

Recommendations for treatment options (including drug therapy, ablation, or observation) must be considered in the context of frequency and duration of the SVT, along with clinical manifestations, such as symptoms or adverse consequences (e.g., development of cardiomyopathy)..

  • Clinical follow-up without pharmacological therapy or ablation in minimally symptomatic patients with AVNRT.
  • Catheter ablation of the slow pathway is recommended in patients with AVNRT
  • Oral verapamil,  diltiazem or beta blockers are recommended for ongoing management in patients with AVNRT who candidates for are not, or prefer not to undergo, catheter ablation
  • Flecainide or propafenone is reasonable for ongoing management in patients without structural heart disease or ischemic heart disease who have AVNRT and are not candidates for, or prefer not to undergo, catheter ablation and in whom beta blockers, diltiazem, or verapamil are ineffective or contraindicated
  • Oral sotalol, dofetilide, digoxin or amiodarone may be reasonable for ongoing management in patients with AVNRT who candidates for are not, or prefer not to undergo, catheter ablation
  • “Pill-in-the-Pocket” Approach • For patients with infrequent (i.e., no more than a few per year) but prolonged (i.e., lasting more than one to two hours) episodes of supraventricular tachycardia that are well tolerated hemodynamically, or  for patients who have had only a single episode of supraventricular tachycardia, another option is to prescribe single-dose pharmacologic therapy (the “pill in the pocket”) to be taken when needed for an arrhythmic event.

Case Studies

Case #1


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