Supraventricular Arrhythmias

1. SAN RHYTHMS

Sinus arrhythmia

Phasic alteration of the heart rate (HR) during respiration – sinus rate (SR) ↑ during inspiration and ↓during inspiration
- Consequence of normal parasympathetic nervous system (PNS) activity

Sinus bradycardia

SR <60bpm may occur in healthy people at rest or athletes
Pathological causes – MI, sick sinus syndrome, hypothyroidism, drugs (BB, digoxin), carotid sinus pressure
IV atropine [0.6-1.2mg] for symptomatic patients

Sinus tachycardia

SR >100bpm
Due to ↑sympathetic NS activity – exercise, emotion, pregnancy
Pathologic causes – anxiety, fever, anaemia, thyrotoxicosis, heart failure, drugs (B-agonists)

Sick sinus syndrome

2. ATRIAL TACHYARRHYTHMIAS

Atrial ectopic beats (extrasystoles, premature beats)

Usually cause no symptoms. Sometimes a sensation of heaviness of the heart
ECG – shows a premature but normal QRS
- If visible, the P wave has a different morphology because the atria activate from an abnormal site
  Tx rarely needed – BB if sx are troubling

Atrial tachycardia

May be due to ↑atrial Automaticity, Triggered activity or Re-entry
ECG – narrow QRS complex (<0.12s) with abnormal P waves
Treatment
- BB (which ↓automaticity) or class I or III antiarrhythmics
- Ablation – to target the ectopic site

Atrial flutter

Characterised by a large re-entry circuit within the right atrium, circling around the tricuspid annulus
Atrial rate is 300bpm (if every beat conducts [rare])
Usually associated with AV block – 2:1 is MC
- Therefore every 2^nd beat conducts – giving a ventricular rate of 150bpm
ECG – saw toothed (flutter) waves
- Can be difficult to see flutter waves in 2:1 block as they are buried in the QRS complex
- Carotid sinus massage slows the AV block and reveal the flutter waves
Treatment
- DC cardioversion – to restore sinus rhythm
- Catheter ablation
- BB or amiodarone [200mg t.i.d] – to prevent recurrent episodes

Atrial fibrillation (AF)

Characterised by
- Accelerated automaticity
- And multiple interacting re-entry circuits looping around the atria
Episodes of AF are initiated by rapid bursts of ectopic beats arising from conducting tissue in the pulmonary veins or diseased atrial tissue
Then AF becomes sustained because of re-entrant conduction
- Re-entry is more likely to occur in enlarged atria e.g. in heart disease
During episodes of AF the atria beat rapidly but uncoordinated and ineffectively
- So the ventricles are activated irregularly – results in Irregularly irregular pulse
ECG – shows normal but irregular QRS. No p waves
- Oscillations of the baseline
AF can be paroxysmal (intermittent episodes that self-terminate within 7 days), An Persistent/permanent
Long term AF leads structural remodelling – atrial fibrosis and dilation
- Predisposes to further AF
Causes of AF – CAD, valvular heart disease, HTN, hyperthyroidism, cardiomyopathy
CF – palpitations, SOB, fatigue, chest pain
- Can precipitate or aggravate HF
- Associated with stroke and systemic embolism

Treatment

Tx primary disorder
Acute AF
- Control ventricular rate – see below
- Anticoagulation – warfarin
- Cardioversion – with DC shock or drugs (IV flecainide, propafenone)
Chronic AF
- Rate control – digoxin, BB or NDP-CCB (verapamil/diltiazem)
- Rhythm control
  - Patients with no heart disease – class Ia, Ic or III drugs
  - Patients with HF/Left ventricular hypertrophy – amiodarone
  - Patients with paroxysmal/early AF – LA ablation
- Anticoagulation
  - Indicated in pts with AF related to rheumatic mitral stenosis or in patients with prosthetic heart valve
  - In patients with non-valvular AF, CHA₂DS₂VASc system is used to determine need for anticoagulation
  - Prophylaxis against ischemic stroke with anticoagulation must be balanced against risk of haemorrhage using the HAS-BLED score
  - Warfarin – INR 2-3
  - Direct thrombin inhibitor – dabigatran
  - Direct factor Xa inhibitor – rivaroxaban

3. ATRIOVENTRICULAR JUNCTIONAL TACHYCARDIAS

AV nodal re-entrant tachycardia (AVNRT)

MC in women
CF – rapid, forceful, regular heart beat
Characterised by 2 different pathways in the AVN
- One with a short refractory period + slow conduction
- Other with long refractory period + fast conduction
In normal sinus rhythm, the atrial impulse that depolarises the ventricles conducts through the fast pathway
If an atrial premature beat occurs early when the fast pathway is still refractory, the slow pathway takes over in propagating the impulse to the ventricles
- It then travels back in a retrograde direction through the fast pathway, initiating the AVNRT
ECG – normal QRS at 140-240bpm
- P waves either invisible or are immediately before or after the QRS because of simultaneous atrial and ventricle activation

AV re-entrant tachycardia (AVRT)

This circuit comprises the AVN, His bundle, ventricle and an abnormal connection of myocardial fibres (accessory pathway [AP])
- Results from an incomplete separation of the atria and ventricles during fetal development
- MC accessory pathway is the Kent Bundles
- – in the septum
Atrial activation occurs after ventricle activation – so P wave is seen between QRS and T wave
Pathways that conduct in retrograde direction (ventricles→atria) are not seen on the ECG – concealed AP
Bidirectional APs are seen on the ECG
Conduction in sinus rhythm is mediated by both the AVN and the AP – this distorts the QRS
- Premature ventricular activation (pre-excitation) via the AP shortens the PR interval and produces a slurred deflection of the QRS – called the delta wave
- pts with a pre-excited ECG and palpitations have Wolff-Parkinson-White syndrome

Treatment