The supraventricular tachycardia pathophysiology
The supraventricular tachycardia pathophysiology Supraventricular tachycardia (SVT) is a common arrhythmia characterized by a rapid heart rate originating above the ventricles. Understanding its pathophysiology involves exploring the complex electrical system of the heart, particularly the mechanisms that give rise to abnormal electrical circuits or impulses. The heart’s conduction system, comprising the sinoatrial (SA) node, atrioventricular (AV) node, bundle of His, and Purkinje fibers, coordinates normal heartbeat rhythms. In SVT, disruptions within this system lead to episodes of rapid heart beating, often sudden in onset and termination.
One primary mechanism behind SVT is the presence of an abnormal electrical pathway that creates a reentrant circuit. Reentry occurs when an electrical impulse continues to circle within the heart tissue, repeatedly activating the atria or the atrioventricular node. This phenomenon relies on the presence of at least two pathways with different conduction velocities and refractory periods. For example, in atrioventricular nodal reentrant tachycardia (AVNRT), a common type of SVT, there are two pathways within or near the AV node: a fast pathway and a slow pathway. Under certain conditions, an impulse can travel down the slow pathway and then retrogradely travel up the fast pathway, establishing a reentrant loop that results in rapid atrial and ventricular contractions.
Another mechanism involves an accessory pathway, such as in Wolff-Parkinson-White (WPW) syndrome. In WPW, an extra electrical connection between the atria and ventricles bypasses the normal conduction system, creating a pathway that can facilitate reentry. If an impulse travels down the normal AV node and then retrogrades through this accessory pathway, a reentrant circuit forms, leading to SVT. This pathway allows impulses to circulate rapidly, causing episodes of tachycardia. The supraventricular tachycardia pathophysiology
In addition to reentry, enhanced automaticity of atrial tissues or the AV node can also trigger SVT. Automaticity refers to the heart tissue’s inherent ability to generate electrical impulses spontaneously. Abnormal automaticity can result from various factors, including ischemia, electrolyte disturbances, or sympathetic stimulation, which increase the likelihood of premature impulses that can initiate or sustain a tachycardia. The supraventricular tachycardia pathophysiology
The supraventricular tachycardia pathophysiology Furthermore, triggered activity, caused by afterdepolarizations, can contribute to SVT episodes. These are abnormal depolarizations occurring during or after repolarization phases of cardiac action potentials, potentially leading to repetitive firing and perpetuation of rapid rhythms.
The clinical significance of SVT’s pathophysiology lies in its impact on cardiac output and patient symptoms. Rapid rhythms reduce filling time, impair cardiac efficiency, and can precipitate symptoms like palpitations, dizziness, or even syncope. Understanding the underlying mechanisms helps guide targeted treatments, whether pharmacologic, ablative, or device-based, to disrupt reentrant circuits or suppress abnormal automaticity. The supraventricular tachycardia pathophysiology
The supraventricular tachycardia pathophysiology In summary, the pathophysiology of supraventricular tachycardia primarily revolves around reentrant circuits facilitated by accessory pathways or dual pathways within the AV node, as well as automaticity and triggered activity. Recognizing these mechanisms is essential for effective diagnosis and management of this arrhythmia, improving patient outcomes and quality of life.
