Pathophysiology of supraventricular tachycardia
Pathophysiology of supraventricular tachycardia Supraventricular tachycardia (SVT) refers to a rapid heart rhythm originating above the ventricles, primarily involving the atria or the atrioventricular (AV) node. Understanding the pathophysiology of SVT requires a grasp of the cardiac conduction system’s normal functioning and how abnormal electrical circuits or impulses disrupt this process.
Pathophysiology of supraventricular tachycardia Under normal circumstances, the heart’s electrical activity begins in the sinoatrial (SA) node, the heart’s natural pacemaker, which generates impulses that spread through the atria, causing them to contract. The impulse then reaches the AV node, which acts as a gatekeeper, slowing conduction before transmitting the signal to the ventricles via the bundle of His and Purkinje fibers. This orchestrated conduction ensures coordinated contractions, maintaining effective cardiac output.
Pathophysiology of supraventricular tachycardia In SVT, this orderly conduction is disturbed, leading to episodes of abnormally fast heart rates, typically ranging from 150 to 250 beats per minute. The most common mechanisms underlying SVT involve reentrant circuits, enhanced automaticity, or triggered activity. Reentry is particularly prevalent, accounting for many SVT episodes. It involves the formation of a self-sustaining loop of electrical activity that re-excites heart tissue repeatedly, producing rapid rhythms. For reentry to occur, there must be pathways with differing conduction velocities and refractory periods, allowing a premature impulse to travel through one pathway and re-enter via another, creating a continuous loop.
One typical reentrant mechanism involves an accessory pathway, such as in atrioventricular reentrant tachycardia (AVRT), which bypasses the normal AV node conduction route. In these cases, an abnormal conduction pathway connects the atria to the ventricles outside the normal conduction system. When a premature atrial impulse encounters this accessory pathway, reentry can be initiated, leading to rapid atrial and ventricular activity. Pathophysiology of supraventricular tachycardia
Another mechanism involves atrioventricular nodal reentrant tachycardia (AVNRT), where two pathways within or near the AV node— a fast and a slow pathway— facilitate reentry. A premature atrial beat can block the fast pathway but conduct down the slow pathway, setting up a reentrant circuit that perpetuates the tachycardia.
Enhanced automaticity involves abnormal pacemaker activity within atrial tissue or the AV node, where cells spontaneously generate impulses at a high rate, overriding normal sinus rhythm. Triggered activity, although less common, involves afterdepolarizations that reach threshold and initiate premature impulses, potentially leading to SVT episodes. Pathophysiology of supraventricular tachycardia
The clinical significance of the pathophysiology lies in the rapid and irregular heart activity, which can compromise cardiac efficiency and lead to symptoms such as palpitations, dizziness, or even syncope. Moreover, understanding the mechanisms guides treatment options; for example, medications that modify conduction properties or refractory periods can terminate reentrant circuits, while catheter ablation aims to disrupt the abnormal pathways responsible for reentry. Pathophysiology of supraventricular tachycardia
In summary, SVT primarily involves reentrant circuits within the atria or AV node, often facilitated by accessory pathways or dual pathways within the AV node. These abnormal electrical loops lead to rapid, repetitive firing that disrupts normal cardiac rhythm, emphasizing the importance of electrophysiological understanding for effective management.
