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Supraventricular tachycardia

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Supraventricular tachycardia

Supraventricular tachycardia (SVT) is an umbrella term for fast heart rhythms arising from the upper part of the heart. This is in contrast to the other group of fast heart rhythms – ventricular tachycardia, which starts within the lower chambers of the heart. There are four main types of SVT: atrial fibrillation, atrial flutter, paroxysmal supraventricular tachycardia (PSVT), and Wolff–Parkinson–White syndrome. The symptoms of SVT include palpitations, feeling of faintness, sweating, shortness of breath, and/or chest pain.

These abnormal rhythms start from either the atria or atrioventricular node. They are generally due to one of two mechanisms: re-entry or increased automaticity. Diagnosis is typically by electrocardiogram (ECG), Holter monitor, or event monitor. Blood tests may be done to rule out specific underlying causes such as hyperthyroidism, pheochromocytomas, or electrolyte abnormalities.

A normal resting heart rate is 60 to 100 beats per minute. A resting heart rate of more than 100 beats per minute is defined as a tachycardia. During an episode of SVT, the heart beats about 150 to 220 times per minute.

Specific treatment depends on the type of SVT and can include medications, medical procedures, or surgery. Vagal maneuvers, or a procedure known as catheter ablation, may be effective in certain types. For atrial fibrillation, calcium channel blockers or beta blockers may be used for rate control, and selected patients benefit from blood thinners (anticoagulants) such as warfarin or novel anticoagulants. Atrial fibrillation affects about 25 per 1000 people, paroxysmal supraventricular tachycardia 2.3 per 1000, Wolff-Parkinson-White syndrome 2 per 1000, and atrial flutter 0.8 per 1000.

Signs and symptoms can arise suddenly and may resolve without treatment. Stress, exercise, and emotion can all result in a normal or physiological increase in heart rate, but they can precipitate SVT in rare cases. Episodes can last from a few minutes to one or two days. They sometimes persist until treated. The rapid heart rate, if fast enough, reduces the opportunity for the "pump" to fill between beats decreasing cardiac output and consequently blood pressure. The following symptoms are typical with a rate of 150–270 or more beats per minute:

Symptoms of heart arrhythmias, such as SVT, are more difficult to assess in infants and toddlers because of their limited ability to communicate. Caregivers should watch for lack of interest in feeding, shallow breathing, and lethargy. These symptoms may be subtle and may be accompanied by vomiting and/or a decrease in responsiveness.

The main pumping chamber, the ventricle, is protected (to a certain extent) against excessively high rates arising from the supraventricular areas by a "gating mechanism" at the atrioventricular node, which allows only a proportion of the fast impulses to pass through to the ventricles. An accessory "bypass tract" can avoid the AV node and its protection so that the fast rate may be directly transmitted to the ventricles. This situation has characteristic findings on ECG. A congenital heart lesion, Ebstein's anomaly, is most commonly associated with supraventricular tachycardia.

Subtypes of SVT can often be distinguished by their electrocardiogram (ECG) characteristics. Most have a narrow QRS complex, although, occasionally, electrical conduction abnormalities may produce a wide QRS complex that may mimic ventricular tachycardia (VT). In the clinical setting, the distinction between narrow and wide complex tachycardia (supraventricular vs. ventricular) is fundamental since they are treated differently. In addition, ventricular tachycardia can quickly degenerate into ventricular fibrillation and death and merits different consideration. In the less common situation in which a wide-complex tachycardia may be supraventricular, a number of algorithms (such as the Brugada criteria) have been devised to assist in distinguishing between them. In general, a history of structural heart disease markedly increases the likelihood that the tachycardia is ventricular in origin.

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