Paroxysmal supraventricular tachycardia: Difference between revisions

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* If present Hemodynamic instability and/or lung congestion. Both varies according to the presence of preexisting heart disease
* If present Hemodynamic instability and/or lung congestion. Both varies according to the presence of preexisting heart disease


=== Electrocardiogram: ===
* Electrocardiogram:
PSVT resolves at the time of presentation Holter is used or even a 30-day cardiac monitor.


===== PSVT resolves at the time of presentation, Holter, or even a 30-day cardiac monitor can be used. =====
Usually, ECG shows narrow QRS complexes and a regular, rapid rhythm; typically, between 150 and 240 beats per minute.   
Usually, ECG shows narrow QRS complexes and a regular, rapid rhythm; typically, between 150 and 240 beats per minute.   


In AVRT, The ECG shows delta waves during sinus rhythm if there is antegrade conduction via the accessory pathway, leading to a diagnosis of Wolff-Parkinson-White syndrome (WPW). The delta waves are lost during an episode of orthodromic AVRT, the most common tachyarrhythmia in patients with WPW.
===== Other changes can be detected =====


=== Electrophysiologic studies: ===
===== P WAVE : =====
 
*  Absent
* Abnormal Shape
* Embedded within  or even delayed after QRS complex
 
===== QRS complex : =====
 
* Tall complex
*  Bundle branch block pattern
 
===== ST segment: =====
 
* Depressed
 
===== T wave: =====
 
* Inverted
 
== Electrophysiologic studies: ==
Invasive electrophysiological study and/or catheter ablation, is recommended not only as a diagnostic but also as is a recommended therapeutic approach to ablate the slow pathway in patients with AVNRT according to ESC 2019 Guidelines
Invasive electrophysiological study and/or catheter ablation, is recommended not only as a diagnostic but also as is a recommended therapeutic approach to ablate the slow pathway in patients with AVNRT according to ESC 2019 Guidelines



Revision as of 22:28, 3 July 2020

Paroxysmal supraventricular tachycardia Microchapters

Home

Patient Information

Overview

Historical Perspective

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

History and Symptoms

Physical Examination

Laboratory Findings

Electrocardiogram

X-ray

Echocardiography and Ultrasound

CT scan

MRI

Other Imaging Findings

Other Diagnostic Studies

Treatment

Medical Therapy

Interventions

Surgery

Primary Prevention

Secondary Prevention

Cost-Effectiveness of Therapy

Future or Investigational Therapies

Case Studies

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. Can be either isolatd or on top of a heart disease. Usually the patient is normal in between attacks and except for patients with preexisting heart disease, the prognosis is usually good.PSVT

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.

Impulse Abnormalities:

The impulse is affected by the previous action potential. In PSVT the abnormal impulse is due to:

  • Early after-depolarization, which is promoted by:
    • Slow heart rate
    • Decreased or increased outward current
  • Delayed after-depolarization
    • Intracellular Ca++ overload
Conduction pathways:

Different reentry circuits in the heart.

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 (any population can be affected)
  • Affect all ages
    • PSVT is the most abundant neonatal and infantile arrhythmia
    • AT: Positively correlated with age.
  • Affect both genders
    • AVNRT: Slightly higher in females
    • AVRT: More often in males

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. Structurat heart disease, cardiomyopathy and previous myocardial infarction
  • Lung disease and hypoxia e.g. Chronic lung disease and infection

Screening


Natural History, Complications and Prognosis

  • Adults: In Absence of underlying heard disease, the prognosis is favorable.
  • Neonates: Usually undergo spontaneous resolution within the first year of life.
Complications:Rarely PSVT can cause:
  • Myocardial infarction
  • Cardiomyopathy
  • 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
  • Electrocardiogram:
PSVT resolves at the time of presentation, Holter, or even a 30-day cardiac monitor can be used.

Usually, ECG shows narrow QRS complexes and a regular, rapid rhythm; typically, between 150 and 240 beats per minute. 

Other changes can be detected
P WAVE :
  •  Absent
  • Abnormal Shape
  • Embedded within  or even delayed after QRS complex
QRS complex :
  • Tall complex
  •  Bundle branch block pattern
ST segment:
  • Depressed
T wave:
  • Inverted

Electrophysiologic studies:

Invasive electrophysiological study and/or catheter ablation, is recommended not only as a diagnostic but also as is a recommended therapeutic approach to ablate the slow pathway in patients with AVNRT according to ESC 2019 Guidelines

Laboratory findings:

Nonspecific, for detecting underlying conditions including:
  • Cardiac enzymes in any patient with a risk factor of myocardial infarction or presented with chest pain
  • Electrolyte levels
  • Complete blood count (CBC) as a contributor to the tachycardia or ischemia
  • Thyroid studies
  • Digoxin level if history of digitalis toxicity

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.

Prevention:

Lifestyle changes and stop any of the risk factors

Future episodes can be prevented by catheter ablation, a highly effective modality for patients with recurrent episodes.

Medications can be used to minimize the recurrence of PSVT, including calcium channel blockers, beta-blockers, or other antiarrhythmic medications

Case Studies

Case #1


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