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SVT
- During an episode of SVT the pulse rate is 140-250 beats per minute (bpm)
- Most often due to the junctional tachycardias, atrioventricular nodal re-entrant tachycardia (AVNRT) or atrioventricular re-entrant tachycardia (AVRT).
SVT is caused by:
- Abnormalities of impulse conduction (re-entrant tachycardias)
- Disorders of impulse initiation (automatic tachycardias) causing a narrow complex tachycardia
- Atrioventricular nodal re-entrant tachycardia (AVNRT)
- Due to the presence of two functionally and anatomically distinct conducting pathways in the atrioventricular (AV) node. One of these is fast-conducting, the other slow-conducting.
- During an episode of SVT one of these acts as the antegrade limb of a re-entrant circuit, while the other acts as the retrograde limb. AVNRT is the most common form of SVT.
- Atrioventricular re-entrant tachycardia (AVRT)
- Due to the presence of accessory pathways that connect the atria and ventricles, but that lie outside the AV node.
- Accessory pathways may be capable of antegrade or retrograde conduction, or both.
- Wolff-Parkinson-White syndrome is the most well-known type of AVRT.
- Delta wave, which is a slurred upstroke in the QRS complex that is associated with a short PR interval.
Epidemiology
- Incidence of supraventricular tachycardia (PSVT) is approximately 1-3 per 1,000.
- Prevalence is twice as high in women compared with men and the prevalence increases with age.
Risk factors
- Previous myocardial infarction, Mitral valve prolapse, Rheumatic heart disease, Pericarditis, Pneumonia, Chronic lung disease, current alcohol intoxication, Digoxin toxicity
Presentation
- Minimal symptoms or present with syncope. Palpitations and dizziness, which are the most common symptoms reported.
- During an attack, tachycardia may be the only finding if otherwise healthy and no cardiac dysfunction. Resulting heart failure may cause tachypnea, hypotension, raised JVP, third heart sound and basal lung crepitations.
Differential diagnosis
- Drug adverse effects, eg amiodarone, digoxin, theophylline
- Narrow QRS-complex tachycardia
- Wide QRS tachycardia (broad complex tachycardia):
Management
- Possible precipitating factors, eg digoxin, caffeine, alcohol, nicotine intake, recreational drugs or hyperthyroidism, should be addressed.
- The most effective and rapid means of terminating any hemodynamically unstable tachycardia is direct current (DC) cardioversion.
- In hemodynamically stable regular narrow QRS-complex tachycardia:
- Vagal manoeuvres, eg Valsalva, carotid massage, facial immersion in cold water. Carotid massage is usually reserved for young patients. Due to the risk of stroke from emboli, auscultate for bruits before attempting this manoeuvre. Do not perform carotid massage on both sides simultaneously.
- Intravenous adenosine is the treatment of choice except for people with severe asthma.
- Adenosine has a rapid onset and short half-life.
- Blocks conduction through the atrioventricular (AV) node.
- Intravenous verapamil
- It has a more prolonged action than adenosine
- Blocks AV node conduction
- irsk of prolonged depression of ventricular function and hypotension, especially if the person is taking a betablocker.
- Long-term preventative treatment:
- Not required in all people.
- The choice of maintenance therapy depends on the underlying type of SVT.
- Radiofrequency catheter ablation:
- Is associated with a high success rate and low complication rate for people with SVT.
- Radiofrequency catheter ablation is indicated in the following situations:
- As first-line therapy as a curative option.
- If the SVT is refractory to antiarrhythmic drug therapy.
- If the person is intolerant of antiarrhythmic drug therapy.
- If antiarrhythmic drug therapy is contra-indicated.
Complications
- Hemodynamic collapse can occur. This is more likely in people with underlying heart disease who are unable to tolerate increases in heart rate.
- Deep vein thrombosis/ Systemic embolism.
- Cardiac tamponade
- Rare complications include MI, CHF, syncope, and sudden death.
- Supraventricular tachycardia (SVT) that persists for weeks or months may lead to a tachycardia-mediated cardiomyopathy.
Prognosis
- Prognosis is dependent on any underlying structural heart disease.
- Patients with a structurally normal heart have an excellent prognosis.
In the absence of manifest pre-excitation (Wolff-Parkinson-White syndrome), the risk of sudden death is very small.
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The views expressed on this blog are the author's own and do not reflect the views of their employer. Please read our full disclaimer here. Any references to clinical cases refer to patients treated at a virtual hospital, Janus General Hospital.
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Jay Khadpe MD
Editor in Chief of "The Original Kings of County"
Assistant Professor of Emergency Medicine
Assistant Residency Director
SUNY Downstate / Kings County Hospital
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