Supraventricular Tachycardia (SVT) is an abnormally fast heart rhythm originating in the upper chambers (atria), causing the heart to beat over 100 times per minute at rest. This rapid rhythm, often between 150 and 220 beats per minute, impairs the heart’s ability to pump blood effectively. Treatment focuses on restoring a normal rhythm, which sometimes requires cardioversion. This procedure uses controlled electrical energy or medication to reset the heart’s electrical activity. This article explores the circumstances that determine when cardioversion is necessary for SVT.
Understanding Supraventricular Tachycardia (SVT)
Supraventricular Tachycardia is a term for arrhythmias caused by faulty electrical signaling originating above the ventricles, often involving the atrioventricular (AV) node or the atria. While the heart’s normal electrical impulse begins in the sinoatrial (SA) node, SVT involves an alternate circuit or focus overriding this natural pacemaker. This rapid firing shortens the time the heart chambers have to fill with blood, which reduces overall cardiac output.
A person experiencing SVT may notice a sudden onset of symptoms related to inefficient pumping. Common complaints include palpitations (a fluttering or pounding sensation in the chest) or a bounding pulse. Reduced blood flow can lead to lightheadedness, dizziness, shortness of breath, weakness, or fatigue. Although episodes can resolve spontaneously, persistent or severe symptoms require immediate medical attention.
Initial Treatment Approaches for SVT
When a patient presents with SVT but remains hemodynamically stable (meaning blood pressure and mental status are normal), less aggressive interventions are attempted first. The first-line approach is vagal maneuvers, which stimulate the vagus nerve to increase parasympathetic tone to the heart. These maneuvers temporarily slow conduction through the AV node, interrupting the electrical circuit causing the rapid rhythm.
The Valsalva maneuver, performed by bearing down against a closed airway, is the most effective vagal technique, especially when the patient is placed supine immediately afterward. If vagal maneuvers fail, the next step involves administering intravenous antiarrhythmic medication. The medication of choice is typically Adenosine, given as a rapid intravenous bolus followed by a saline flush.
Adenosine has an extremely short half-life of only a few seconds; its effects are immediate but transient, and it works by temporarily blocking the AV node. This drug is highly effective for most types of SVT, often reaching over 90% success for specific re-entrant tachycardias. If Adenosine is unsuccessful or contraindicated, other agents like intravenous beta-blockers or calcium channel blockers may be used.
Determining the Need for Cardioversion
Cardioversion is reserved for situations where initial, less invasive treatments have failed or the patient’s condition is rapidly deteriorating. The decision hinges on the patient’s hemodynamic status, differentiating between instability and stability refractory to medication. Immediate synchronized electrical cardioversion is indicated for hemodynamically unstable patients, as this condition poses an immediate threat to life.
Hemodynamic instability is defined by severe symptoms linked to the rapid heart rate. These include significant hypotension, acute altered mental status, signs of shock, or chest pain suggesting myocardial ischemia. The speed of the electrical shock is necessary to rapidly restore a normal rhythm and prevent further organ damage.
For stable patients whose SVT fails to convert after receiving maximum doses of first-line medications, the next step involves a choice between pharmacological or electrical cardioversion. Pharmacological cardioversion uses intravenous administration of potent antiarrhythmic drugs, such as Amiodarone, to chemically reset the rhythm. While this approach is less successful than electrical cardioversion, it avoids the need for procedural sedation.
Electrical cardioversion is often preferred, even in stable patients, due to its higher success rate, typically ranging from 80% to 90%. The procedure involves delivering a controlled, synchronized electrical shock to the heart muscle. This shock interrupts the abnormal electrical circuit, allowing the heart’s natural pacemaker to regain control. Synchronization of the shock to the heart’s electrical cycle is mandatory to prevent inducing a more dangerous rhythm, such as ventricular fibrillation.
What Happens During Cardioversion
When electrical cardioversion is necessary, the procedure is performed in a monitored setting, such as an emergency room or a dedicated cardiac unit, with a team of healthcare professionals present. Before the shock is delivered, large electrode pads are placed on the patient’s chest and potentially on the back, connected to the cardioversion machine. These pads deliver the therapeutic electrical energy needed to reset the heart.
Because the electrical shock can be painful, procedural sedation is administered intravenously to ensure the patient is asleep and comfortable throughout the brief procedure. The medical team continuously monitors the patient’s heart rhythm, blood pressure, and oxygen levels during the shock delivery. Once the shock successfully restores a normal sinus rhythm, the patient is slowly awakened from the short-acting sedative.
The entire process of delivering the shock takes only a few minutes, though the recovery period is longer to allow the sedative effects to wear off. Patients typically wake up feeling drowsy and may experience minor redness or tenderness where the pads were placed. Most individuals are able to go home the same day but are advised not to drive for at least 24 hours until the effects of the anesthesia have dissipated.