Arrhythmia

Question 1

What are supraventricular tachyarrhythmias & what are they characterised by?

Answer 1

• tachyarrhythmias that originate in the atria or AV junction
• this term is used when a more specific diagnosis of mechanism and site of origin cannot be made
• characterized by narrow QRS, unless there is pre-existing bundle branch block or aberrant ventricular conduction (abnormal conduction due to a change in cycle length)

Question 2

Px of SVT & what may SVT precipitate?

Answer 2

• presentation can include: palpitations, dizziness, dyspnea, chest discomfort, presyncope/syncope
• may precipitate congestive heart failure (CHF), hypotension or ischemia in patients with underlying disease
• untreated tachycardias can cause cardiomyopathy (rare, potentially reversible with treatment of SVTs)
• includes supraventricular and ventricular rhythms

Question 3

Risk factors for AFib & Aflutter

Answer 3

• high BP
• coronary artery disease
• mitral/tricuspid valve disorders
• alcohol abuse
• hyperthyroidism
• birth defect

Anything that causes atria to enlarge

Question 4

Pathophysiology of Atrial fibrillation

Answer 4

• electrical impulses are triggered from many areas in and around the atria rather than just one area (SA node)
• chaotic electrical activity rather than organized
• atrial walls quiver rather than contract.
• Irregular ventricle rhythm (irregular conduction of chaotic electrical impulses through the AV node)

Question 5

ECG of Atrial fibrillation

Answer 5

• no organized P waves due to rapid atrial activity (350-600 bpm) causing a chaotic fibrillatory baseline
• irregularly irregular ventricular response (typically 100-180 bpm), narrow QRS (unless aberrancy or previous BBB)
• wide QRS complexes due to aberrancy may occur following a long-short cycle sequence (“Ashman phenomenon”)
• loss of atrial contraction, thus no “a” wave seen in JVP, no S4 on auscultation

Question 6

ECG of Atrial flutter

Answer 6

sawtooth flutter waves (most common type of flutter) in inferior leads (II, III, aVF);

narrow QRS (unless aberrancy)

Question 7

Cx of AF

Answer 7

Blood clots in atria -> stroke

Rapid heart rate -> decreased CO

Question 8

Rx of atrial fibrillation

Answer 8

RACE

1. Rate control: β-blockers, diltiazem, verapamil (in patients with heart failure: digoxin, amiodarone)
2. Anticoagulation: use either warfarin, dabigatran, rivaroxaban, apixaban to prevent thromboembolism
3. Cardioversion (electrical)
   - if AFib 24-48 h, anticoagulate for 3 wk prior and 4 wk after cardioversion
   - if patient unstable (hypotensive, active angina due to tachycardia, uncontrolled heart failure) should cardiovert immediately
4. Etiology
   - HTN, CAD, valvular disease, pericarditis, cardiomyopathy, myocarditis, ASD, postoperative, PE, COPD, thyrotoxicosis, sick sinus syndrome, alcohol (“holiday heart”)
   - may present in young patients without demonstrable disease (“lone AFib”) and in the elderly without underlying heart disease

Question 9

Which control (Rate or rhythm) is better for long term survival in AF?

Answer 9

no difference in long-term survival when treating patients with a rhythm-control versus rate-control strategy

Question 10

Rx of newly discovered atrial fibrillation (c.f. recurrent/permanent)

Answer 10

Antiarrhythmics are not used.
( if the episode is self-limited and not associated with severe symptoms)

• if AFib persists, 2 options:

1. rate control and anticoagulation (as indicated above)
2. cardioversion (as above)

Question 11

Rx of recurrent/permanent atrial fibrillation (c.f. newly discovered)

Answer 11

Anti-arrhythmics are used (if symptoms are bothersome or episodes are prolonged)

• no or minimal heart disease: flecainide, propafenone or sotalol
• LV dysfunction: amiodarone
• CAD: β-blockers, amiodarone

Question 12

Rx of atrial flutter

Answer 12

Acute

• if unstable (hypotension, CHF, angina): cardioversion
• if stable: rate control (beta blocker, diltiazem, digoxin) & chemical cardioversion (sotalol, amiodarone)
• Anticoagulation same as Afib

Long term

• antiarrhythmics
• catheter radiofrequency ablation

Question 13

(4) other types of SVT than Afib & Aflutter

Answer 13

1. Sinus tachycardia
2. Premature beats
3. Multifocal atrial tachycardia
4. AV nodal re-entry

Question 14

Describe sinus tachycardia

Answer 14

• sinus rhythm with rate >100 bpm
• occurs in normal subjects with increased sympathetic tone (exercise, emotions, pain), alcohol use, caffeinated beverages, drugs (e.g. β-adrenergic agonists, anticholinergic drugs, etc.)
• etiology: fever, hypotension, hypovolemia, anemia, thyrotoxicosis, CHF, MI, shock, PE, etc.
• treatment: treat underlying disease; consider β-blocker if symptomatic, calcium channel blocker if β-blockers contraindicated

Question 15

Describe (2) types of premature beats

Answer 15

1. premature atrial contraction (PAC) (Figure 27)
   - ectopic supraventricular beat originating in the atria
   - P wave morphology of the PAC usually differs from that of a normal sinus beat
2. junctional (AV node) premature beat
   - ectopic supraventricular beat that originates in the vicinity of the AV node
   - P wave is usually not seen or an inverted P wave is seen and may be before or closely follow the QRS complex

Treatment usually not required

Question 16

Describe multifocal atrial tachycardia

Answer 16

• irregular rhythm caused by presence of 3 or more atrial foci (may mimic AFib)
• atrial rate 100-200 bpm; at least 3 distinct P wave morphologies and PR intervals vary, some P waves may not be conducted
• occurs more commonly in patients with COPD, and hypoxemia; less commonly in patients with hypokalemia, hypomagnesemia, sepsis, theophylline or digitalis toxicity

• treatment: treat the underlying cause; calcium channel blockers may be used (e.g. diltiazem,
verapamil), β-blockers may be contraindicated because of severe pulmonary disease

• no role for electrical cardioversion, antiarrhythmics or ablation

Question 17

Describe AV nodal re-entrant tachycardia

Answer 17

• re-entrant circuit using dual pathways (fast conducting β-fibres and slow conducting α-fibres) within or near the AV node; often found in the absence of structural heart disease – cause is commonly idiopathic, although familial AVNRT has been reported
• sudden onset and offset
• fast regular rhythm: rate 150-250 bpm
• usually initiated by a supraventricular or ventricular premature beat
• AVNRT accounts for 60-70% of all paroxysmal SVTs
• retrograde P waves may be seen but are usually lost in the QRS complex (see Figure 24)

• treatment

• acute: Valsalva or carotid massage, adenosine is first choice if unresponsive to vagal maneuvers; if no response, try metoprolol, digoxin, diltiazem, electrical cardioversion if patient hemodynamically unstable (hypotension, angina or CHF)
• long-term: 1st line – b-blocker, diltiazem, digoxin; 2nd line – flecainide, propafenone; 3rd line – catheter ablation