Paroxysmal tachycardia is a heart condition characterized by abrupt, unpredictable episodes of a rapid heartbeat, exceeding 100 beats per minute.
Symptoms and Triggers
During an episode of paroxysmal tachycardia, individuals experience symptoms such as:
- Palpitations, manifesting as a fluttering, pounding, or racing sensation in the chest, throat, or neck.
- Dizziness and lightheadedness, sometimes progressing to fainting (syncope).
- Shortness of breath.
- Chest discomfort or pain.
- General weakness or fatigue.
Episodes can be initiated by various non-medical factors, including:
- Caffeine.
- Alcohol.
- Nicotine use.
- Stress.
- Fatigue and dehydration.
- Vigorous exercise or certain medications (e.g., those for asthma or cold and allergy relief).
Types of Paroxysmal Tachycardia
Paroxysmal tachycardia encompasses different types, distinguished by their origin within the heart’s electrical system. These types include Supraventricular Tachycardia (SVT) and Ventricular Tachycardia (VT). Understanding the specific type is important for appropriate management and risk assessment.
Supraventricular Tachycardia (SVT)
Supraventricular tachycardia originates in the heart’s upper chambers (atria) or in the atrioventricular (AV) node, an electrical junction between the upper and lower chambers. This type results from abnormal electrical activity, often a “short circuit” or re-entry mechanism, where electrical signals cycle rapidly within the upper heart. SVT causes a heart rate between 120 and 230 beats per minute. While not usually life-threatening in individuals without other heart conditions, it can cause uncomfortable symptoms.
Common forms of SVT include Atrioventricular Nodal Reentrant Tachycardia (AVNRT), Atrioventricular Reentrant Tachycardia (AVRT), and Atrial Tachycardia. AVNRT is the most frequent type of SVT, involving two pathways within or near the AV node that create a continuous electrical loop. AVRT involves an extra electrical pathway (an accessory pathway) located outside the normal conduction system, such as in Wolff-Parkinson-White syndrome. Atrial tachycardia originates from an irritable electrical focus within the atria, firing rapidly outside the heart’s natural pacemaker.
Ventricular Tachycardia (VT)
Ventricular tachycardia originates in the heart’s lower chambers (ventricles), where other electrical areas take over pacing. It can cause the heart to beat at rates exceeding 120 beats per minute, sometimes reaching up to 200 beats per minute. Ventricular tachycardia can be more serious than SVT, especially if it lasts longer than 30 seconds (sustained VT). Sustained VT can prevent the heart from pumping enough blood to the body, leading to low blood pressure and potentially progressing to ventricular fibrillation or sudden cardiac death. VT is more common in individuals with underlying structural heart disease.
Underlying Causes and Diagnosis
Beyond immediate triggers, paroxysmal tachycardia stems from underlying structural or electrical abnormalities within the heart, such as:
- Coronary artery disease, which narrows the heart’s blood vessels.
- Cardiomyopathy (a disease of the heart muscle) and heart valve diseases.
- Certain congenital heart defects, like Wolff-Parkinson-White syndrome, involving extra electrical pathways.
- Electrolyte imbalances, particularly low levels of potassium or magnesium.
Diagnosis involves several medical tools and methods to identify the specific type:
- Electrocardiogram (ECG or EKG): Records the heart’s electrical activity to observe rhythm during an episode.
- Holter monitor: A portable device that continuously records heart activity for 24 to 48 hours to capture infrequent events.
- Event recorder: Worn for longer periods (typically around 30 days), allowing activation when symptoms occur or automatic recording of abnormal rhythms.
- Electrophysiology (EP) study: A more invasive procedure where thin, flexible tubes are guided into the heart to map electrical pathways and pinpoint the origin of abnormal signals.
Medical Interventions
Managing paroxysmal tachycardia involves interventions ranging from simple techniques to more involved procedures, depending on episode frequency and severity. The initial approach includes vagal maneuvers, simple physical actions designed to stimulate the vagus nerve. This nerve helps regulate heart rate; its stimulation can sometimes slow or stop a rapid heartbeat. Examples include bearing down as if straining during a bowel movement (Valsalva maneuver), coughing forcefully, or splashing ice-cold water on the face.
When vagal maneuvers are ineffective or for ongoing management, medications are prescribed. Beta-blockers (e.g., metoprolol, propranolol) work by slowing the heart rate and reducing its workload. Calcium channel blockers (e.g., verapamil, diltiazem) prevent calcium from entering heart cells, which can decrease heart rate and help terminate reentrant conduction. Anti-arrhythmic drugs, including flecainide or amiodarone, directly affect the heart’s electrical signals to restore and maintain a normal rhythm.
For severe or persistent episodes, electrical cardioversion is performed in a hospital setting. This procedure delivers a controlled electrical shock to the chest, synchronized with the heart’s rhythm, to reset the heart to a normal sinus rhythm. Patients are typically sedated for this brief procedure.
A more definitive treatment for recurrent paroxysmal tachycardia is catheter ablation. During this procedure, thin catheters are guided into the heart to locate and destroy the small area of heart tissue responsible for generating or perpetuating abnormal electrical signals using radiofrequency energy or cryoablation. This can provide a long-term solution by eliminating the source of the arrhythmia.