Atrial tachycardia (AT) is a heart rhythm disorder, or arrhythmia, where the heart’s upper chambers (atria) beat abnormally fast. This rapid rhythm originates from a location outside the heart’s natural pacemaker, the sinus node, causing the atria to contract between 100 and 250 times per minute. AT is classified under supraventricular tachycardia (SVT), which refers to any fast rhythm that starts above the heart’s lower chambers (ventricles).
The Heart’s Electrical Malfunction
The healthy heart rhythm is governed by the sinoatrial (SA) node, which generates a regular electrical impulse that spreads across the atria. In atrial tachycardia, an abnormal electrical focus, or “ectopic” site, within the atrial tissue takes over this pacing function. This site fires electrical signals at an accelerated rate, disrupting the heart’s normal sequence of contraction.
Atrial tachycardia is categorized into two main types based on the electrical fault mechanism. Focal atrial tachycardia arises from a single, localized area in the atria that fires rapidly, often due to enhanced automaticity or triggered activity. Macro-reentrant atrial tachycardia involves the electrical signal traveling in a continuous, abnormal circuit within the atrial tissue. This re-entry circuit often forms around areas of scar tissue resulting from prior cardiac surgery or underlying structural heart disease.
The rapid rate of atrial contractions means the chambers do not have enough time to fill completely with blood before the next beat. The resulting fast and inefficient heart rate can significantly reduce the amount of blood pumped out to the body, even if the ventricles do not follow every atrial beat. This reduction in cardiac output leads directly to the physical symptoms experienced by the individual.
Recognizing the Symptoms
The physical manifestations of atrial tachycardia vary widely; some people remain unaware of the condition, while others experience significant distress. A person may feel a distinct sensation of the heart pounding or fluttering in their chest or neck, known as palpitations. This feeling results directly from the rapid and forceful atrial contractions.
Since the fast heart rate decreases the heart’s pumping efficiency, the brain and body may not receive adequate blood flow. This lack of oxygenated blood can cause lightheadedness or dizziness, and in severe episodes, it may lead to fainting (syncope). Other common symptoms include shortness of breath, which occurs because blood can back up into the lungs, and fatigue or weakness. Chest discomfort or pain may also be reported when the rapid rate causes increased oxygen demand that the heart cannot meet.
Underlying Causes and Risk Factors
Atrial tachycardia can occur in individuals with otherwise healthy hearts, but it is frequently associated with pre-existing conditions that affect the heart’s structure or electrical stability. Structural heart disease, such as coronary artery disease, heart failure, or heart valve issues, can cause the atria to stretch or develop scar tissue, creating a substrate for the arrhythmia. Individuals who have undergone previous cardiac surgery are also at higher risk, as incisions can lead to scar tissue that promotes the formation of re-entry circuits.
Conditions that chronically stress the heart or lungs are strong predisposing factors. Chronic lung diseases, such as chronic obstructive pulmonary disease (COPD), are linked to atrial tachycardia, with multifocal atrial tachycardia being prevalent in these patients. Lifestyle factors and certain substances can act as triggers for episodes, including:
- Excessive intake of stimulants like caffeine.
- Alcohol.
- Illicit drugs.
- An imbalance in electrolytes, particularly potassium and magnesium.
Diagnosis and Treatment Approaches
The initial step in diagnosing atrial tachycardia involves documenting the rapid rhythm, most commonly through an Electrocardiogram (ECG or EKG). Because episodes can be intermittent, a physician may use ambulatory monitoring devices like a Holter monitor or an event recorder. These devices record the heart’s electrical activity over several days or weeks to capture the erratic rhythm and help determine its origin.
For persistent or highly symptomatic cases, an electrophysiology (EP) study may be required. During an EP study, thin, flexible catheters are threaded into the heart to precisely map the electrical pathways and pinpoint the location of the abnormal focus or re-entry circuit. This detailed mapping guides subsequent treatment.
Management of atrial tachycardia often begins with medication to control the heart rate or restore a normal rhythm. Rate-controlling drugs like beta-blockers and calcium channel blockers slow electrical conduction through the atrioventricular (AV) node, reducing the number of rapid beats that reach the ventricles. Antiarrhythmic drugs, such as flecainide or amiodarone, may also be prescribed to suppress ectopic activity and maintain a normal rhythm.
For patients whose symptoms persist despite medication, or for those who wish to avoid long-term drug use, catheter ablation is often a curative option. This minimally invasive procedure involves guiding a catheter to the precise location identified in the EP study. The catheter tip delivers energy, typically radiofrequency heat or cryoablation cold energy, to create a tiny scar that destroys the abnormal focus or interrupts the re-entry circuit. In acute situations where the patient is unstable, a controlled electrical shock, known as cardioversion, may be delivered externally to reset the heart’s rhythm.