Paroxysmal Atrial Tachycardia (PAT) is a type of supraventricular tachycardia, characterized by episodes of a rapid heart rate that begin and end suddenly. During an episode, the heart rate can increase significantly, sometimes up to 250 beats per minute, compared to a typical resting heart rate of 60 to 100 beats per minute. This condition originates in the heart’s upper chambers, the atria.
The Heart’s Electrical Blueprint
The heart’s rhythmic pumping is orchestrated by a precise electrical system. The sinoatrial (SA) node, located in the right atrium, functions as the heart’s natural pacemaker, initiating electrical impulses that spread across the atria. These impulses cause the atria to contract, pushing blood into the ventricles.
The electrical signal then converges at the atrioventricular (AV) node, which acts as a gatekeeper, momentarily delaying the impulse. This delay ensures the ventricles have sufficient time to fill with blood before they contract. From the AV node, the impulse travels through specialized electrical pathways to the ventricles, prompting their synchronized contraction to pump blood out to the body. PAT arises when this normal electrical activity is disrupted, leading to an abnormally fast heart rhythm.
Direct Electrical Disruptions
Paroxysmal Atrial Tachycardia is directly caused by immediate physiological mechanisms within the heart’s electrical system. One primary mechanism is reentry, where an electrical impulse gets trapped in a continuous loop. This occurs when an electrical signal travels along a pathway, but instead of dying out, it finds a way to re-excite the tissue it just left, creating a self-sustaining circuit. Common examples include AV nodal reentry tachycardia (AVNRT) or AV reciprocating tachycardia (AVRT), which involve accessory pathways that bypass the normal conduction system.
Another mechanism is enhanced automaticity, where certain heart cells spontaneously begin to fire at an abnormally rapid rate. These cells, often located outside the SA node, can take over the heart’s rhythm, leading to a rapid atrial rhythm.
Triggered activity represents a third direct cause, where normal electrical activity can inadvertently trigger repetitive, abnormal firing. This happens when afterdepolarizations occur. If these oscillations are strong enough, they can generate a new, abnormal electrical impulse, leading to extra heartbeats or sustained rapid rhythms.
Predisposing Conditions and Triggers
Various internal and external factors can contribute to the direct electrical disruptions or trigger PAT episodes. Underlying heart conditions play a significant role. Structural heart disease, such as coronary artery disease, heart valve disorders, or a history of heart attack, can predispose individuals to PAT. Other heart rhythm disorders can also contribute.
Conditions outside the heart can also affect its electrical stability. Thyroid disorders, particularly hyperthyroidism (an overactive thyroid gland), are known to trigger PAT. Electrolyte imbalances, such as low potassium or magnesium levels, can disrupt the heart’s electrical signals. Chronic lung diseases, including chronic obstructive pulmonary disease (COPD), and severe infections, can also increase the risk of PAT episodes.
Lifestyle factors frequently act as triggers for PAT. Excessive intake of caffeine, alcohol consumption, high levels of stress, and insufficient sleep are common culprits. The use of certain illicit drugs, such as cocaine and other stimulants, can also induce PAT episodes.
Certain medications can inadvertently trigger PAT. Over-the-counter decongestants, some asthma medications, and specific cold remedies are known examples. Digoxin toxicity can also lead to PAT. In some instances, despite thorough investigation, no clear underlying cause or trigger for PAT can be identified, and such cases are referred to as idiopathic PAT.