Supraventricular Tachycardia (SVT) is a common type of rapid heart rhythm that originates in the heart’s upper chambers, or atria, or the junctional area connecting the upper and lower chambers. The heart rate often exceeds 100 beats per minute. The appropriate treatment for SVT is highly dependent on the patient’s immediate condition, particularly whether they are stable or unstable. Understanding this distinction is the first step in determining the correct treatment path.
Understanding Supraventricular Tachycardia
Supraventricular Tachycardia is an umbrella term for fast heart rhythms that begin above the ventricles, often within the atria or the atrioventricular (AV) node. These rhythms are typically caused by a faulty electrical signal or a re-entry circuit, causing the heart rate to suddenly jump to 150 to 220 beats per minute.
Common symptoms include a fluttering sensation in the chest (palpitations), lightheadedness, dizziness, and sometimes chest discomfort. SVT is distinct from Ventricular Fibrillation (V-fib), which originates in the lower chambers and is a chaotic, immediately life-threatening rhythm. SVT treatment is often less aggressive because the rhythm is usually not immediately fatal, unlike V-fib which requires immediate defibrillation.
Initial Stabilization Methods
For the majority of patients experiencing SVT, the heart rhythm is considered stable, meaning they are not experiencing severe symptoms like profound hypotension or altered mental status. In these stable cases, the initial approach focuses on non-electrical methods to slow or stop the rapid rhythm, starting with vagal maneuvers. These simple physical actions stimulate the vagus nerve to slow conduction through the AV node.
The most effective technique is the modified Valsalva maneuver, where the patient forcefully exhales against a closed airway for up to 30 seconds while lying down, followed by immediately raising their legs. If vagal maneuvers fail, the next step is pharmacological intervention using intravenous medication.
Adenosine is the preferred first-line drug because it acts rapidly, causing a temporary block in the AV node to interrupt the re-entry circuit. It is administered as a rapid intravenous push, usually starting with a 6 milligram dose, followed immediately by a saline flush to ensure the medication reaches the heart quickly. If the first dose is ineffective, a higher dose of 12 milligrams may be given. If Adenosine is ineffective or contraindicated, Calcium Channel Blockers like Verapamil or Diltiazem serve as alternatives for stable patients.
When Electrical Cardioversion Is Necessary
Electrical cardioversion, the procedure involving an electrical shock, is reserved almost exclusively for patients with unstable SVT. A patient is considered unstable if the rapid heart rate is causing signs of hemodynamic collapse. These signs include severe low blood pressure (hypotension), acute confusion or altered mental status, ongoing chest pain suggesting a lack of blood flow to the heart muscle, or acute heart failure. In these situations, attempting to use medications first would delay the necessary restoration of a normal rhythm and could result in severe harm.
The procedure used for unstable SVT is called Synchronized Electrical Cardioversion. This technique differs from defibrillation because the electrical shock is timed precisely with the heart’s QRS complex, or the peak of the ventricular contraction. Synchronization prevents the electrical discharge from landing during the vulnerable period of the cardiac cycle, which could otherwise induce the chaotic and fatal rhythm of ventricular fibrillation.
The immediate application of a synchronized shock, typically starting with a lower energy dose between 50 and 100 Joules, aims to reset the heart’s electrical system to a normal rhythm. While recent evidence suggests a single trial of adenosine may be considered for unstable patients with a regular, narrow-complex SVT, the definitive and immediate treatment for any patient showing signs of collapse remains synchronized cardioversion. This intervention bypasses the waiting time for medications to work and quickly restores the heart’s ability to pump blood effectively.
Preventing Future Episodes
Once the acute episode of SVT has been managed, the focus shifts to long-term strategies for preventing recurrence. Lifestyle modifications are often recommended, including reducing or eliminating common triggers such as excessive caffeine, alcohol, and tobacco use. These substances can disrupt the heart’s normal electrical signaling and precipitate an episode.
For patients experiencing frequent or highly symptomatic episodes, maintenance therapy often involves daily medication. Beta-blockers or Calcium Channel Blockers are the preferred pharmacological agents for ongoing management, working to reduce the frequency and duration of SVT by slowing the heart rate. Antiarrhythmic drugs may be used if first-line medications prove ineffective.
Catheter ablation is increasingly considered a first-line treatment for long-term management because it offers a potentially definitive cure. This minimally invasive procedure involves guiding thin, flexible wires to the heart to locate and destroy the small area of heart tissue responsible for the faulty electrical pathway. Ablation success rates are high, often exceeding 95% for certain types of SVT, and this procedure can eliminate the need for lifelong medication.