Supraventricular arrhythmias (atrial tachycardia, atrial flutter, atrial fibrillation) – etiology, pathogenesis, and clinical manifestations
Supraventricular arrhythmias are abnormal heart rhythms originating above the ventricles, usually in the atria or AV node.
1 Atrial tachycardia
Etiology
Structural heart disease (e.g., cardiomyopathies, valvular diseases).
Coronary artery disease.
Chronic lung disease ( cor pulmonale).
Digitalis (digoxin) toxicity.
Electrolyte imbalances ( hypokalemia, hypomagnesemia).
Pathogenesis
Enhanced automaticity of atrial ectopic focu s- Normally, the sinoatrial (SA) node is the natural pacemaker of the heart.
In atrial tachycardia, another site in the atrium (ectopic focus) starts firing impulses on its own at a faster rate.
This happens because that focus has increased automaticity, meaning it spontaneously depolarizes faster than the SA node
Triggered activity (delayed afterdepolarizations), especially in digoxin toxicity - After each heartbeat, heart cells normally reset (repolarize).
Delayed afterdepolarizations (DADs) are extra small depolarizations that occur after full repolarization, often due to abnormal calcium handling inside the cells.
DADs can become large enough to trigger an extra beat or sustained rapid rhythm.
Digoxin toxicity is a classic cause because it disrupts calcium balance, making DADs more likely.
Usually a single ectopic focus overrides the SA node → regular rapid atrial rate (about 150–250 bpm) - Because this abnormal atrial focus fires rapidly (about 150–250 beats per minute ), it overrides the normal SA node control.
The atria then follow this new "pacemaker," leading to a regular but rapid atrial rhythm.
Clinical manifestations
Palpitations (rapid, regular).
Dizziness, fatigue.
Dyspnea.
Possible heart failure symptoms in patients with reduced cardiac reserve.
2 Atrial flutter
Etiology
Structural heart diseases (e.g., mitral valve disease, dilated atria).
Ischemic heart disease.
Chronic obstructive pulmonary disease (COPD).
Post- cardiac surgery.
Pathogenesis
Macro- reentrant circuit within the right atrium (most common: counterclockwise loop around the tricuspid annulus). As this loop keeps circulating, it continuously depolarizes the atrial muscle very rapidly.
Atrial rate typically about 250–350 bpm Because of this continuous loop, the atria contract very quickly, However, the atria cannot contract effectively at this rate, so atrial mechanical function is impaired.
AV node conducts some impulses (often in 2:1 or 3:1 ratio) → ventricular rate is slower and regular.
Clinical manifestations
Sudden onset of palpitations (often regular but rapid).
Dyspnea.
Fatigue.
Hypotension, presyncope (if rapid ventricular response).
Possible signs of heart failure
3 Atrial fibrillation (AF)
Etiology
Hypertension (most common risk factor).
Valvular heart diseases (especially mitral stenosis).
Coronary artery disease.
Heart failure.
Hyperthyroidism (thyrotoxic AF).
Alcohol ("holiday heart syndrome").
Pathogenesis