SupraVentricular Tachycardia (SVT)

1. SupraVentricular Tachycardia (SVT) PBL patient case 1

2. Basically… • Tachycardia = rapid heart beat over 100bpm • Supraventricular = upper chambers (atria) • Usually involves an alternative/re-entry pathway

3. Symptoms • Palpitations – this is common symptom where patients have sensation that their heart is racing or fluttering • Lightheadedness • Dizziness • LOC / Syncope – rare occurrence • Chest pain • Shortness of breath • May be asymptomatic In general SVT is not life threatening but patient should seek medical attention. Rapid beating of the heart decreases time for ventricle filling = heart is a less effective pump = CO decreases and BP drops

4. Classification • Based on the path that the electrical signal takes from the atria… • Technically SVT involves any tachycardia not of ventricular origin, however clinically it is PAROXYSMAL SVT’s that are the “real” SVT’s  these involve accessory pathway and have sudden onset and are regular.

5. SVT’s from Sinoatrial Source Don’t have immediate development so not clinically considered as SVT’s. • Physiological: hyperthyroidism, fever, stress = normal response • SANRT (SA node re-entrant tachycardia): uncommon, rarely causes symptoms, p waves still appear normal

6. SVT’s from ATRIAL source • Ectopic Atrial tachycardia (EAT): small cluster of cells within atrium with abnormal automaticity. Most commonly a paediatric condition. ECG shows clear P wave before QRS, but rapid rate. • Atrial fibrillation and Atrial Flutter are technically SVT’s but if identified clinically they are considered seperately (also AF is not regular so not clinically an SVT).

7. SVT’s from an AV source (also termed Junctional SVT’s) • AVNRT (AV nodal re-entrant tachycardia): electrical impulse travels in a circle using extra fibres in and around the AV node. • Most common type of Junctional SVT • More females than males • Don’t usually occur till atleast age 20 • Physiology: dual conduction pathways (usually a fast and slow path) in the AV node and tissue in close proximity to it which allow electrical impulses to recycle within the AV nodal region at rate of 150-250 bpm. The impulse travels down one pathway to the point where it converges with another path. If the second pathway has recovered its ability to conduct (ie. past refractory period), the impulse travels back up the second pathway to where the pathways converge "upstream". The impulse then travels down the first pathway again and the cycle repeats. Basically the atrium and ventricles end up contracting at the SAME TIME. • ECG: p wave morphology normal so resembles sinus tachycardia but abrupt onset and offset • Treatment: need to transiently block the AV node: • Valsalva manouvre or carotid sinus massage to activate vagus nerve • AV nodal slowing drugs (adenosine, B blockers, Ca channel blockers) • Catheter Ablation which blocks the slow pathway is often curative

8. SVT’s from an AV source (also termed Junctional SVT’s) • AVRT (AV re-entrant tachycardia): electrical impulse travels down AV node to ventricles and BACK to atrium via extra fibres from the atria to the ventricles. (ie. the re-entry pathway is OUTSIDE the AV node. Can occur two main ways (can have both): • 1. Accessory pathway is retrograde only (ie. from ventricles back to atria) – termed “concealed pathway” as not evident on ECG • 2. Accessory pathway is antegrade so from atria to ventricles • Includes Wolff-Parkinson-White Syndrome (see next slide) • Physiology: signal going down accessory pathway often reaches the ventricle before the signal going through the AV node  results in pre-excitation of the ventricle seen on an ECG as an extra “bump” termed delta wave (characteristic of WPW). • Problems: because accessory path can conduct much faster than AV node (ie. up to 300bpm) can result in low BP and death. This is rare and usually only occurs if patient develops AF aswell Treatment: same as AVNRT – valsalva manouvre, pharmacological to slow conduction, catheter ablation of accessory pathways.

9. Wolf-Parkinson-White Syndrome • 0.1-0.3% of population, M>F • Thought to be present at birth but only occasionally genetic. Presents sporadically (usually incidentally found). • Often asymptomatic but associated with other cardiac defects – ASD, mitral valve prolapse, hypertrophic cardiomyopathy etc.