Supraventricular Tachycardia - Diagnosis

Diagnosis

Individual subtypes of SVT can usually be distinguished by the electrical characteristics of the electrocardiogram (ECG).

Most supraventricular tachycardias have a narrow QRS complex although, occasionally, electrical conduction abnormalities may produce a wide-complex tachycardia 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. Ventricular tachycardia can quickly degenerate to ventricular fibrillation and death and merits different consideration. In the less common situation in which a wide-complex tachycardia may actually be supraventriculat, a number of algorithms have been devised to assist in determining which is which. In general, a history of structural heart disease markedly increases the likelihood that the tachycardia is ventricular in origin.

• Sinus tachycardia is physiologic or "appropriate" 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 fast rate (>100 beats per minute in adults). It is generally not considered SVT.
• 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 manoeuvres.
• Ectopic (unifocal) atrial tachycardia arises from an independent focus within the atria, distinguished by a consistent P-wave of abnormal morphology that falls before a narrow, regular QRS complex. It is caused by "automaticity" which means that some cardiac muscle cells, which have a primordial ability to generate electrical impulses that is 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.
• 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.
• Atrial fibrillation is not, by itself, a tachycardia, but meets the definition when associated with a ventricular response greater than 100 beats per minute. It is characterized as an "irregularly irregular rhythm" both in its atrial and ventricular depolarizations and is distinguished by fibrillatory atrial waves that, at some point in their chaos, stimulate a response from the ventricles in the form of irregular, narrow QRS complexes.
• Atrial flutter, is caused by a re-entry rhythm in the atria, with a regular atrial rate often of about 300 beats per minute. On the ECG, this appears as a line of "sawtooth" waves preceding the QRS complex. The AV node will not usually conduct at such a fast rate, and so the P:QRS usually involves a 2:1 or 4:1 block pattern, (though rarely 3:1, and sometimes 1:1 where class IC antiarrhythmic drug are in use). Because the ratio of P to QRS is usually consistent, A-flutter is often regular in comparison to its irregular counterpart, A-fib. Atrial Flutter is also not necessarily a tachycardia unless the AV node permits a ventricular response greater than 100 beats per minute.
• AV nodal reentrant tachycardia (AVNRT) involves a reentry circuit forming next to, or within, the AV node. The circuit most often involves two tiny pathways one faster than the other, within the AV node. Because the node is immediately between the atria and ventricle, the re-entry circuit often stimulates both, meaning that a retrogradely (backward) conducted P-wave is buried within or occurs just after the regular, narrow QRS complexes.
• Atrioventricular reciprocating tachycardia (AVRT), also results from a reentry circuit, although one physically much larger than AVNRT. One portion of the circuit is usually the AV node, and the other, an abnormal accessory pathway (muscular connection) from the atria to the ventricle. Wolff-Parkinson-White syndrome is a relatively common abnormality with an accessory pathway, the Bundle of Kent crossing the AV valvular ring.
  • In orthodromic AVRT, atrial impulses are conducted down through the AV node and retrogradely re-enter the atrium via the accessory pathway. A distinguishing characteristic of orthodromic AVRT can therefore be a P-wave that follows each of its regular, narrow QRS complexes, due to retrograde conduction.
  • In antidromic AVRT, atrial impulses are conducted down through the accessory pathway and re-enter the atrium retrogradely via the AV node. Because the accessory pathway initiates conduction in the ventricles outside of the bundle of His, the QRS complex in antidromic AVRT is often wider than usual, with a delta wave.
• Finally, junctional ectopic tachycardia (JET) is a rare tachycardia caused by increased automaticity of the AV node itself initiating frequent heart beats. On the ECG, junctional tachycardia often presents with abnormal morphology P-waves that may fall anywhere in relation to a regular, narrow QRS complex. It is often due to drug toxicity.