The human heart normally beats in a steady, regular rhythm, but electrical malfunctions can lead to a rapid heart rate called tachycardia. These fast rhythms originate in different areas of the heart, resulting in complex classifications. For people trying to understand a recent diagnosis, the distinctions between terms like Supraventricular Tachycardia and Atrial Tachycardia can be confusing. Clarifying the relationship between these rhythms is important for understanding both the diagnosis and the tailored approach to treatment.
Understanding Supraventricular Tachycardia
Supraventricular Tachycardia (SVT) is an overarching term for any fast heart rhythm originating in structures located above the ventricles, the lower pumping chambers. This means the abnormal focus is located in the atria (upper chambers) or the atrioventricular (AV) node, which acts as the heart’s electrical relay station. The heart rate during an SVT episode is generally over 100 beats per minute at rest, often ranging between 150 and 220 beats per minute. Because the abnormal electrical activity occurs high up, the resulting signal usually travels down normal conduction pathways, typically resulting in a narrow-complex tachycardia on an electrocardiogram (ECG).
SVT is not a single diagnosis but a category encompassing many specific rhythm disorders. The most common types involve a re-entry mechanism, where a continuous electrical loop forms, causing the heart to beat rapidly. Other forms are due to increased automaticity, where a group of cells spontaneously fires electrical impulses faster than the heart’s natural pacemaker. The specific mechanism and location determine the exact type of SVT, which guides management.
What is Atrial Tachycardia
Atrial Tachycardia (AT) is a specific type of rapid heart rhythm that originates exclusively within the atrial muscle tissue. This rhythm is defined by a heart rate over 100 beats per minute, and the abnormal electrical impulse starts outside the sinoatrial (SA) node, the heart’s natural pacemaker. The mechanism often involves a single, localized source, known as an ectopic focus, which fires repeatedly and rapidly, usurping control from the SA node.
The electrical impulse generated by this ectopic focus spreads outward through the atria, causing them to contract quickly and regularly. Unlike some other SVT types, Atrial Tachycardia does not rely on the AV node or the ventricles to sustain the rapid rhythm. The rate of atrial contraction in AT is typically between 100 and 250 beats per minute. This focus can arise from various locations in the atria, such as the area where the pulmonary veins enter the heart.
The Relationship Between Atrial Tachycardia and SVT
The core difference between the two terms is classification: Atrial Tachycardia is specifically defined as a subtype of Supraventricular Tachycardia. SVT serves as the broad umbrella term for all fast rhythms originating above the ventricles, making AT one member of this larger group. This hierarchical relationship means that every episode of Atrial Tachycardia is technically a Supraventricular Tachycardia, but not every SVT is an Atrial Tachycardia.
The SVT category also includes other common rhythms, such as Atrioventricular Nodal Re-entrant Tachycardia (AVNRT) and Atrioventricular Re-entrant Tachycardia (AVRT). AVNRT involves a re-entry circuit within the AV node itself. AVRT requires an extra electrical connection between the atria and ventricles, known as an accessory pathway. The ability to distinguish AT from these other SVT mechanisms is important because the most effective treatment for each rhythm can differ significantly.
How These Rhythms Are Identified
Patients experiencing an SVT, including Atrial Tachycardia, commonly report sudden-onset palpitations, a feeling of the heart racing, or a fluttering sensation in the chest. Other symptoms can include light-headedness, dizziness, shortness of breath, or chest discomfort, especially if the heart rate is extremely fast or the patient has underlying heart disease. Since these episodes can start and stop abruptly, diagnosis relies on a combination of patient history and objective testing.
The primary diagnostic tool used to identify and classify the specific rhythm is the Electrocardiogram (ECG). During an episode, the ECG captures electrical activity, allowing doctors to analyze the rhythm characteristics. Specifically, the shape and timing of the P wave (atrial contraction) and its relationship to the QRS complex (ventricular contraction) help pinpoint the origin. Atrial Tachycardia often displays an abnormal P wave, suggesting the electrical impulse is driven from an atrial focus. If the rhythm is not present during a clinic visit, a Holter monitor or an event recorder may be used to capture electrical activity over an extended period.
General Approaches to Management
The general strategy for managing these rapid rhythms involves two main phases: acute termination of the ongoing episode and long-term control to prevent recurrence. For an acute episode of a stable SVT, the first step is often to attempt vagal maneuvers, which are physical actions like bearing down that stimulate the vagus nerve and can help slow or stop the rhythm. If vagal maneuvers are unsuccessful, intravenous medications such as adenosine or calcium channel blockers may be administered in a controlled setting to interrupt the abnormal electrical circuit.
For long-term management of frequent or symptomatic episodes, treatment is tailored to the specific SVT subtype. Options include daily oral medications, such as beta-blockers or antiarrhythmic drugs, to suppress the abnormal firing or slow the heart rate. A definitive treatment option for many patients is catheter ablation, a minimally invasive procedure where a thin, flexible tube is guided into the heart. Once the exact location of the abnormal focus or circuit is mapped, radiofrequency energy is applied to create a small scar that permanently blocks the errant electrical signal.