Junctional Tachycardia (JT) is a type of supraventricular tachycardia (SVT) characterized by an abnormal, rapid heart rhythm. This condition occurs when the heart’s natural pacemaker in the upper chamber is overridden by a secondary electrical site in the lower part of the heart. JT is diagnosed when this secondary pacemaker fires at a rate exceeding 100 beats per minute (bpm). This rapid rhythm leads to inefficient pumping because the heart chambers lack adequate time to fill with blood between beats.
How the Heart’s Electrical System Works
The heart’s rhythm is normally orchestrated by electrical signals starting at the sinoatrial (SA) node, located in the upper right chamber. The SA node generates an impulse that spreads across the upper chambers, causing them to contract and send blood into the lower chambers. This impulse then converges at the atrioventricular (AV) node, situated between the upper and lower chambers.
The AV node briefly delays the signal to allow the upper chambers to fully empty before transmitting the impulse down the Bundle of His and Purkinje fibers into the lower chambers. This process ensures a coordinated contraction. The AV node and the surrounding tissue, including the Bundle of His, constitute the “junctional area.”
The cells within this junctional area possess an inherent, slower firing rate, serving as a backup system if the SA node fails. Junctional tachycardia occurs when this secondary pacemaker in the AV junction becomes hyperactive and fires faster than the SA node. This enhanced automaticity causes the AV junction to seize control of the heart’s rhythm, resulting in the characteristic rapid heart rate.
Triggers and Signs of Junctional Tachycardia
Junctional tachycardia can be caused by various factors that disrupt the heart’s normal electrical balance. A frequent cause, particularly in children, is inflammation or injury following open-heart surgery to correct congenital heart defects. This postoperative form typically manifests within 6 to 72 hours after the procedure.
Specific medications, most notably toxicity from the cardiac drug digoxin, can trigger this rapid rhythm. Inflammation of the heart muscle (myocarditis) or damage from an acute myocardial infarction can also cause the AV junction to become irritable. Furthermore, metabolic disturbances, such as electrolyte imbalances, contribute to the rhythm’s onset.
The physical manifestations of junctional tachycardia range from being unnoticed to causing severe distress, depending on the heart rate. Common symptoms include palpitations, described as a racing or fluttering heart. The rapid, inefficient beating reduces the heart’s output, leading to signs of decreased blood flow.
Patients may experience dizziness, lightheadedness, or fatigue. In more serious cases, the rhythm can cause shortness of breath, chest discomfort, or fainting (syncope). These symptoms occur because the ventricles lack enough time to properly fill with blood, reducing the amount pumped out to the body.
Confirming the Diagnosis
The definitive method for identifying junctional tachycardia is the Electrocardiogram (ECG), which records the heart’s electrical activity. The ECG allows clinicians to distinguish JT from other rapid heart rates. A signature finding is a regular rhythm with a narrow QRS complex, indicating the impulse travels via normal conduction pathways.
Since the impulse originates in the AV junction, it can travel backward into the upper chambers and forward into the lower chambers simultaneously. On the ECG, this often results in the disappearance of the P wave (upper chamber contraction signal), as it is hidden within the QRS complex. Alternatively, the P wave may be visible but appears inverted or immediately follows the QRS complex, a pattern called retrograde conduction.
For patients with intermittent symptoms, a Holter monitor or event recorder tracks the heart rhythm over a longer period. Physicians may also order blood tests to check for underlying causes like electrolyte abnormalities or drug toxicity. An echocardiogram (ultrasound) assesses the heart’s size and pumping function.
Managing and Treating Junctional Tachycardia
Treatment depends on the patient’s symptoms, heart rate, and underlying cause. The first step is to identify and reverse reversible triggers, such as discontinuing toxic medication or correcting electrolyte imbalance. If the patient is unstable due to the rapid rate, immediate intervention, including synchronized electrical cardioversion, is necessary to reset the rhythm.
For stable patients, medical management aims to slow the heart rate and restore SA node control. Acute treatment involves administering intravenous medications, such as beta-blockers or calcium channel blockers like diltiazem or verapamil. These drugs slow conduction through the AV node, suppressing the rapid firing of the junctional pacemaker cells.
Long-term management for recurrent JT involves daily oral medication, typically beta-blockers. If drug therapy is ineffective, catheter ablation may be considered. This procedure uses radiofrequency energy or cryotherapy to precisely destroy the heart tissue responsible for the abnormal firing.
Catheter ablation is effective but risks damaging the normal electrical pathway, potentially requiring a permanent pacemaker. Cryoablation, which uses extreme cold, may be preferred in some cases as it poses a lower risk to the adjacent conduction system. In pediatric cases, overdrive atrial pacing may also be used to temporarily control the rhythm.