Supraventricular Tachycardia (Tachyarrhythmias)

SVT is associated with advancing age and significant cardiac and pulm disease.

PSVT is associated with WPW, congenital heart disease, and mitral valve prolapse. It is more common in younger pts. The mechanism is reentrant in nature.

AAT may be automatic, triggered, or reentrant. It is seen more commonly in children and those with a Hx of prior atrial surgery. It is rare in adults, although it can be associated with digitalis toxicity and hypokalemia.

MAT is seen in adult pts with critical illness or advanced pulm disease.

Myocardial ischemia associated with tachycardia and resulting coronary insufficiency.

Circulatory compromise.

Increased risk of atrial thrombus.

Chronic sustained tachycardia can result in irreversible cardiomyopathy.

Lyte and acid-base balance (K ⁺ , Mg, alkalosis)

Digitalis toxicity

Tachycardia (HR >100 in adults) with origin above the bundle of His in sinus node, atrial, or junctional tissue. It may be reentrant, automatic, or triggered in origin.

SVT may be paroxysmal (PSVT) or gradual in onset (sinus tachycardia, atrial tachycardia, or multiform atrial tachycardia). Tachycardia mechanisms vary (reentrant vs. triggered and automatic); treatment varies accordingly.

PSVT is a reentrant arrhythmia usually seen more commonly in children. The reentrant circuit usually involves an accessory conducting pathway and the AV node.

AAT is more commonly seen in the pediatric population owing to the enhanced automaticity seen in children.

PSVT is due to reentry, which generally involves the AV node and an accessory pathway. Accessory pathways are relatively common in children. It is also assoc with WPW and LGL.

AAT is much more common in children and thought to stem from areas of enhanced automaticity of sites, which are usually found at the mouth of either atrial appendage, the orifices of the pulm veins, or the crista terminalis.