Pathophysiology of paroxysmal supraventricular tachycardia
Pathophysiology of paroxysmal supraventricular tachycardia Paroxysmal supraventricular tachycardia (PSVT) is a common arrhythmia characterized by episodes of rapid heart rate that originate above the ventricles. Understanding the pathophysiology of PSVT involves exploring the cardiac conduction system, specific electrical pathways, and the mechanisms that facilitate abnormal rapid rhythms.
Pathophysiology of paroxysmal supraventricular tachycardia The heart’s electrical activity is orchestrated through a specialized conduction system, primarily involving the sinoatrial (SA) node, atrioventricular (AV) node, bundle of His, and Purkinje fibers. Under normal circumstances, impulses originate in the SA node, propagate through the atria to the AV node, then travel via the His-Purkinje system to coordinate synchronized ventricular contraction. This system ensures a controlled heart rhythm, typically ranging between 60 to 100 beats per minute.
Pathophysiology of paroxysmal supraventricular tachycardia In PSVT, abnormal electrical circuits or pathways cause episodes of tachycardia that originate suddenly and terminate spontaneously. These episodes are generally caused by reentrant mechanisms, which are loops of electrical activity that perpetuate themselves. The most prevalent type involves a reentrant circuit within or around the AV node, known as AV nodal reentrant tachycardia (AVNRT). Another common form involves accessory pathways—abnormal muscular connections between the atria and ventricles—that can form a reentrant circuit, leading to atrioventricular reentrant tachycardia (AVRT).
The reentrant circuit in AVNRT typically involves two pathways within or near the AV node: a fast pathway and a slow pathway. Under normal conditions, impulses travel down the fast pathway. However, in certain situations, a premature atrial contraction can block conduction in the fast pathway but conduct slowly through the slow pathway. When the fast pathway recovers, it can conduct the impulse back through the slow pathway, creating a loop that sustains rapid atrioventricular conduction. This results in a rapid, regular heart rate often exceeding 150 beats per minute.
Pathophysiology of paroxysmal supraventricular tachycardia AVRT, on the other hand, involves an accessory pathway, such as the bundle of Kent, that bypasses the AV node. During sinus rhythm, impulses travel from atria to ventricles via the normal pathway. During an episode, an atrial impulse can travel down the normal pathway to the ventricles and then retrogradely back to the atria through the accessory pathway, establishing a reentrant loop. This circular conduction accelerates the heart rate significantly and produces characteristic findings on electrocardiogram (ECG), such as a narrow QRS complex with a short RP interval.
In both types of PSVT, triggers like premature atrial contractions, stress, or stimulants can initiate episodes by setting off the reentrant circuit. The episodes often recur because the underlying electrophysiological substrate remains unchanged, making the individual susceptible to future episodes. Pathophysiology of paroxysmal supraventricular tachycardia
In conclusion, the pathophysiology of PSVT centers on reentrant circuits involving either the AV node or accessory pathways, resulting in rapid, coordinated, but abnormal heart rhythms. Understanding these mechanisms is essential for diagnosis and management, which may include medications, vagal maneuvers, or catheter ablation to interrupt the reentrant pathways and restore normal rhythm. Pathophysiology of paroxysmal supraventricular tachycardia