Contents
Dysrhythmia originating at or above the atrioventricular (AV) node and defined by a narrow complex (QRS < 120 ms) at a rate of > 100bpm.
- M/C symptomatic dysrhythmia in infants in children
Classification
SVT is caused by 1 of 3 mechanisms: reentry, increased automaticity, or triggered activity.
Atrioventricular nodal reentrant tachycardia (AVNRT):
Patients with AVNRT demonstrate dual atrioventricular nodal inputs with differing electrophysiologic properties, the fast and slow pathways that act as the 2 limbs of the reentrant circuit.
- M/C paroxysmal SVT
Atrioventricular reentrant tachycardia (AVRT):
Accessory pathways are anomalous, extranodal conduction pathways between atrium and ventricle. The accessory pathway and the atrioventricular node can act as the 2 limbs of the AVRT reentrant circuit.
Accessory pathways are classified based on their location along the mitral or tricuspid annuli, conduction characteristics, and directionality of conduction (antegrade, retrograde, or both).
- Antegrade conduction:
- Orthodromic: Antegrade conduction occurs via AV node
- Antidromic: Antegrade conduction occurs via accessory pathway
- Retrograde conduction
Wolff-Parkinson-White (WPW) pattern: Accessory pathways capable of antegrade conduction demonstrate a delta wave on ECG
Accessory pathways capable only of retrograde conduction do not exhibit a delta wave on the surface ECG (concealed pathways) but can still form a reentrant loop with the atrioventricular node and result in AVRT.
Atrial tachycardia:
Group of atrial arrhythmias whose mechanisms may be focal or macroreentrant.
- Focal atrial tachycardia: Results in a centrifugal wavefront spread throughout the atria from a focus of (1) enhanced automaticity, (2) triggered activity, or (3) a small area of reentry (microreentry).
- Macroreentrant atrial tachycardia: Results from a large intraatrial reentrant loop >2 cm in length. Note that the term macroreentrant atrial tachycardia is synonymous with the term atrial flutter.
Both focal and macroreentrant atrial tachycardia may result from prior structural heart disease or surgery for congenital heart disease, may follow surgical or catheter ablation of atrial fibrillation, or may be due to idiopathic phenomena.
- Right atrial tachycardia often arises from the crista terminalis but can also arise from the tricuspid annulus, compact atrioventricular node, and coronary sinus ostium
- Left atrial tachycardias often arise from the pulmonary veins, as well as the mitral annulus and left atrial appendage
Atrial flutter:
Form of macroreentrant atrial tachycardia that may result in stroke and cardiomyopathy, and is highly amenable to catheter ablation.
Aetiology
Risk factors:
- Congenital heart disease (children)
- In children younger than 12 years old, an accessory atrioventricular pathway causing reentry tachycardia is the most common cause of SVT.
Triggering factors:
- Medications
- Caffeine
- Alcohol
- Physical/emotional stress
- Cigarette smoking
Clinical features
The clinical presentation of SVT is variable- ranging from asymptomatic to severe palpitation.
- Mild cases: Anxiety, palpitations, chest discomfort, lightheadedness, syncope, or dyspnea
- Severe cases: Shock, hypotension, signs of heart failure, lightheadedness, or exercise intolerance
- Signs of hemodynamic instability: Hypotension, hypoxia, shortness of breath, chest pain, shock, evidence of poor end-organ perfusion, or altered mental status.
Diagnosis
ECG:
- Narrow QRS complex, regular tachycardia of 180-220 bpm rate
- P waves not detectable (if detectable, consider sinus tachycardia or atrial fibrillation/flutter as a potential etiology)
Management
Immediate synchronized cardioversion: For haemodynamically unstable cases
Defibrillator synchronized with the QRS complex, to prevent the shock from being delivered during the T-wave, while the heart is depolarized.
Vagal maneuvers: For haemodynamically stable patient
Act to stimulate the parasympathetic system. This slows impulse formation at the sinus node, slows conduction velocity at the AV node, lengthens the AV node refractory period, and decreases ventricular inotropy.
- Valsalva maneuver: Expiring against a closed glottis, and needs to be held for 10 seconds to 15 seconds.
- Carotid massage: Placing patient in supine position with neck extended, and applying pressure to one carotid sinus for approximately 10 seconds.
Chemical cardioversion:
If vagal maneuvers prove ineffective
- Adenosine 6 mg IV (pediatric dose 0.1 mg/kg, maximum of 6 mg)
- If initial dose ineffective, 2nd dose at 12 mg IVP (pediatric dose 0.2 mg/kg, maximum dose 12 mg)
- Second line medfications:
- Diltiazem (0.25 mg/kg IV loading dose followed by 5mg/hr to 15 mg/hr infusion)
- Esmolol (0.5 mg/kg IV loading dose, then 0.5 mg/kg/min up to 0.2 mg/kg/min, will need to repeat bolus for every up-titration)
- Metoprolol (2.5-5 mg IV every 2-5 minutes, not exceeding 15 mg over 10-15 minutes)
Overdrive pacing:
Pacing the heart at a faster rate than its native rhythm, can help discontinue SVT. Performed if chemical cardioversion still prove ineffective
Maintenance therapy:
Indicated in recurrent SVT without a .pre-excitation syndrome
- Oral beta-blockers or CCBs to maintain sinus rhythm
- Radio-frequency ablation (if accessory pathway identified)
- Patients should be counseled on how to perform vagal maneuvers on their own for long-term management of recurrent SVT
