Paroxysmal supraventricular tachycardia
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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 tachycardia, Atrioventricular 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).PSVT can occur in any age and gender. PSVT can be either isolated or on top of heart disease. In the pediatric population, it usually presents with signs and symptoms of heart failure. In adult patients are asymptomatic or presented of signs and symptoms of tachycardia and tachycardia-induced complications. Usually, the patient is normal in between attacks and except for patients with preexisting heart disease, the prognosis is usually good. Reentry phenomena constitute a major pillar in the pathogenesis of PSVT. In most of patients, catheter ablation of the abnormal slow pathway is considered the treatment of choice to prevent recurrence.
Historical Perspective [1]
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
- Peri nodal atrial tissue.
b. 30% are due to Atrioventricular reciprocating tachycardia (AVRT)
- Extra nodal 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 diseases 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
- A preexisting heart condition, e.g. Structural heart disease, cardiomyopathy, and previous myocardial infarction
- Lung disease and hypoxia e.g. Chronic lung disease and infection
Natural History, Complications and Prognosis
- Adults: In the absence of underlying heart 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
History and Symptoms | Physical Examination | Laboratory Findings | Electrocardiogram | Other Diagnostic Studies
The clinical presentation is variable, ranging from asymptomatic to complicated tachycardia.
History:
In adults:
- If present, a history of previous self-limiting attacks.
- In some patients, there is a history of preexisting heart disease
In newborns and small children
- Usually tolerates tachycardia, most cases are presented with heart failure
- To a lesser extent occasional detection by parents
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.
·Newborns and small children presented with symptoms of congestive heart failure as vomiting
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
In newborns and small children presented with signs of congestive heart failure as diaphoresis, increased respiratory rate and pale cold skin
=== 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 including:
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:
Catheter ablation is recommended not to diagnose and detect the exact location of the reentry pathway, but also as is the recommended therapeutic approach to ablate the slow pathway in patients with AVNRT according to ESC 2019 Guidelines
=== Laboratory findings: ===
Nonspecific to PSVT, directed towards conditions including:
- Cardiac enzymes in any patient with a risk factor of myocardial infarction or presented with chest pain
- B-type natriuretic peptide to detect heart failure
- 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 and 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 beta-blockers
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 are not candidates, 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
- ↑ Ghzally Y, Gerasimon G. Catheter Ablation. [Updated 2020 Feb 6]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2020 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK470203/