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 may include medications, medical procedures, or surgery. Directing patients to execute Vagal maneuvers such as the Valsalva maneuver, or conducting 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
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:
Pounding heart Rapid heart beat Shortness of breath Chest pain Rapid breathing Dizziness Sweating Loss of consciousness 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.
Pathophysiology
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.
Diagnosis
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.
Sinus tachycardia is physiologic when a reasonable stimulus, such as the catecholamine surge associated with fright, stress, or physical activity, provokes the tachycardia. It is identical to a normal sinus rhythm, except for its faster rate (>100 beats per minute in adults). However, sinus tachycardia is considered part of the diagnoses included in SVT by most sources. Sinoatrial node reentrant tachycardia (SANRT) is caused by a reentry circuit localised to the SA node, resulting in a P-wave of normal shape and size (morphology) that falls before a regular, narrow QRS complex. It cannot be distinguished electrocardiographically from sinus tachycardia unless the sudden onset is observed (or recorded on a continuous monitoring device). It may sometimes be distinguished by its prompt response to vagal maneuvers. Ectopic (unifocal) atrial tachycardia arises from an independent focus within the atria, distinguished by a consistent P-wave of abnormal shape and/or size that falls before a narrow, regular QRS complex. It can be caused by automaticity, which means that some cardiac muscle cells, which have the primordial (primitive, inborn, inherent) ability to generate electrical impulses that are common to all cardiac muscle cells, have established themselves as a 'rhythm center' with a natural rate of electrical discharge that is faster than the normal SA node. Some atrial tachycardias, rather than being a result of increased automaticity may be a result of a micro-reentrant circuit (defined by some as less than 2 cm in longest diameter to distinguish it from macro-reentrant atrial flutter). Still other atrial tachycardias may be due to triggered activity caused by after-depolarizations. Multifocal atrial tachycardia (MAT) is tachycardia arising from at least three ectopic foci within the atria, distinguished by P-waves of at least three different morphologies that all fall before irregular, narrow QRS complexes. This rhythm is most commonly seen in elderly people with COPD.
… excerpt ends here. Continue reading the full article.
