Junctional tachycardia (JT) is an abnormally fast heart rhythm that originates from a secondary pacemaker site within the heart’s electrical system. This rapid rhythm begins in the atrioventricular (AV) junction, which is the area connecting the heart’s upper and lower chambers. JT is classified as a type of supraventricular tachycardia (SVT) because its source is located above the ventricles, specifically in the AV node or the tissue immediately surrounding it. The heart rate in this condition exceeds 100 beats per minute, which is faster than the heart’s normal resting rate.
The Electrical Mechanism of the Heart
The normal electrical pathway begins with the sinoatrial (SA) node, the heart’s natural primary pacemaker, initiating a regular impulse. This signal travels across the upper chambers, the atria, before collecting at the atrioventricular (AV) node. After a brief delay, the impulse is conducted down the His-Purkinje system, spreading quickly to cause the contraction of the ventricles.
Junctional tachycardia develops when the cells in the AV junction become overly excitable and begin firing electrical impulses faster than the SA node. This is known as enhanced automaticity, where the junctional cells take over the role of the primary pacemaker. While the AV junction’s intrinsic escape rate is typically 40 to 60 beats per minute, during JT, this rate accelerates beyond 100 beats per minute.
The rapid rate originating from the junction overrides the normal rhythm, causing the upper and lower chambers to contract in an uncoordinated manner. This lack of proper sequencing means the atria and ventricles do not fill and empty efficiently, which can compromise the heart’s ability to pump blood effectively.
Physical Symptoms of Junctional Tachycardia
The physical presentation of junctional tachycardia can vary greatly; some individuals experience no symptoms at all, particularly if the heart rate is only moderately elevated. For those who do, the most common complaint is palpitations, described as a racing, fluttering, or pounding sensation in the chest.
The rapid, inefficient heart rate reduces the volume of blood pumped with each beat, leading to signs of decreased blood flow to the body. Patients may experience lightheadedness or dizziness, which can progress to fainting or near-fainting episodes, known as syncope.
Other physical signs include shortness of breath and a general feeling of fatigue or weakness, as the body struggles with the heart’s diminished output. Some people may also report chest discomfort or pain, often described as tightness. In infants and young children, who are more commonly affected, symptoms may manifest as poor feeding, lethargy, or unusually rapid breathing.
Interpreting the ECG Electrical Signature
The most definitive way to diagnose junctional tachycardia is through an electrocardiogram (ECG), which records the heart’s electrical activity. The rhythm is characterized by a heart rate exceeding 100 beats per minute that is typically regular, often ranging from 100 to 180 beats per minute. This rate range is the defining factor distinguishing it from an accelerated junctional rhythm.
A distinguishing feature of JT is the appearance, or lack thereof, of the P wave, which represents the electrical activation of the atria. Because the impulse starts in the AV junction, it travels backward (retrogradely) to the atria while simultaneously moving forward to the ventricles. This retrograde activation results in P waves that are often inverted (negative deflection) in the inferior ECG leads (II, III, and aVF).
The P wave is frequently hidden or buried within the QRS complex, which represents the ventricular contraction. This occurs because the atria and ventricles are often depolarized at the same time. Alternatively, the inverted P wave may be visible immediately before or immediately after the QRS complex, depending on the precise location of the impulse origin within the junction.
The QRS complex itself usually appears narrow and normal in shape, since the electrical signal follows the standard His-Purkinje system for ventricular conduction. This narrow QRS is consistent with a supraventricular origin, helping to differentiate JT from rhythms that originate lower down in the ventricles.
Common Triggers and Underlying Conditions
Junctional tachycardia does not usually occur spontaneously in otherwise healthy adults but is frequently a consequence of other underlying issues. One common cause is digitalis toxicity, often related to the heart medication digoxin, which can increase the automaticity of the AV junction cells.
The condition is also frequently observed as a complication following heart surgery, particularly procedures to repair congenital heart defects in children. This postoperative junctional tachycardia is thought to be a result of inflammation and swelling of the surrounding heart tissue following the surgical trauma.
Other physiological stressors can trigger the rhythm, including acute inferior wall myocardial ischemia or infarction, which affects the blood supply to the region of the AV node. Inflammatory conditions of the heart, such as myocarditis, and systemic infections like Lyme disease are also recognized causes of enhanced junctional automaticity. Addressing the root cause often helps resolve the abnormal rhythm.