Arrhythmia Treatment in Hyderabad

Classification of Arrhythmias

By Rate

Tachycardia: heart rate above 100 beats per minute. Bradycardia: heart rate below 60 beats per minute. Tachycardias are further classified as narrow-complex (supraventricular) or broad-complex (ventricular or aberrantly conducted supraventricular).

By Origin

Supraventricular arrhythmias originate in the atria or AV node (above the ventricles). Ventricular arrhythmias originate in the ventricles. This distinction critically affects treatment and prognosis.

By Mechanism

Re-entry (the most common mechanism): an electrical impulse travels in a circular loop rather than extinguishing after normal activation. Abnormal automaticity: an ectopic focus fires spontaneously at an inappropriate rate. Triggered activity: afterdepolarizations in damaged or stressed heart muscle trigger premature beats.

By Clinical Significance

Benign arrhythmias: occasional extra beats in structurally normal hearts. Clinically significant arrhythmias: those causing symptoms or haemodynamic compromise. Life-threatening arrhythmias: ventricular fibrillation and sustained ventricular tachycardia with haemodynamic collapse.

Types of Arrhythmia

Supraventricular Tachycardias (SVT)

Fast heart rhythms originating above the ventricles. Generally associated with a better prognosis than ventricular arrhythmias but can cause significant symptoms and haemodynamic compromise.

Atrial Fibrillation (AFib)

The most common sustained arrhythmia. Chaotic electrical activity in the atria causes an irregular ventricular response. Associated with significant stroke risk. Covered in detail on our dedicated AFib page.

Atrial Flutter

A rapid, organized re-entry circuit in the right atrium causes atrial rates of 250 to 300 per minute, with the ventricles typically responding at half that rate (150 beats per minute in 2:1 flutter). Causes palpitations and breathlessness. Highly amenable to curative radiofrequency ablation.

AVNRT (AV Nodal Re-entry Tachycardia)

The most common paroxysmal SVT. A re-entry circuit within or adjacent to the AV node causes sudden-onset, sudden-termination rapid heart rate (150 to 220 beats per minute). Causes palpitations, dizziness, and chest tightness. Cured in over 95% of cases with radiofrequency ablation.

AVRT (AV Re-entry Tachycardia)

An accessory electrical pathway connecting atria and ventricles (bypass tract) creates a re-entry circuit involving the AV node and the accessory pathway. Includes WPW syndrome when the accessory pathway is capable of fast conduction during AFib, which can be life-threatening.

Atrial Tachycardia

A focal ectopic focus in the atria fires repetitively at a rate of 120 to 250 beats per minute. Can cause tachycardia-induced cardiomyopathy if persistent. Amenable to ablation when the focus is mapped precisely.

Sinus Tachycardia

Appropriate elevation of heart rate by the normal sinus node. Usually a physiological response to exercise, fever, pain, anxiety, or dehydration. Treatment addresses the underlying cause rather than the heart rate itself.

Ventricular Arrhythmias

Arrhythmias originating in the ventricles. Severity ranges from benign extra beats to immediately life-threatening ventricular fibrillation.

Premature Ventricular Contractions (PVCs)

Extra beats arising from an ectopic ventricular focus. Extremely common, present in most people at some time. Occasional PVCs in a structurally normal heart are benign. Frequent PVCs (more than 10,000 per 24 hours) can cause symptoms and, over time, reduce cardiac function through tachycardia-induced cardiomyopathy.

Ventricular Tachycardia (VT)

A rapid, regular ventricular rhythm above 100 beats per minute arising from the ventricles. Sustained VT can cause haemodynamic compromise, syncope, and degenerate into ventricular fibrillation. Most commonly occurs in the context of coronary artery disease with scarred heart muscle or cardiomyopathy.

Ventricular Fibrillation (VF)

Completely disorganized electrical activity in the ventricles causing no effective contraction. Results in cardiac arrest within seconds. The most common cause of sudden cardiac death. Requires immediate defibrillation. Survivors of VF require ICD implantation.

Torsades de Pointes

A specific form of polymorphic VT associated with prolongation of the QT interval on ECG, either congenital (long QT syndrome) or acquired (from medications, electrolyte abnormalities). Can degenerate into VF.

Bradyarrhythmias

Abnormally slow heart rhythms from failure of the sinus node or the electrical conduction pathways between the atria and ventricles.

Sick Sinus Syndrome

The sinus node fails to maintain an adequate rate, causing bradycardia, pauses, or alternating bradycardia and tachycardia (tachy-brady syndrome). A common indication for pacemaker implantation.

Heart Block

Failure of electrical conduction from the atria to the ventricles at the AV node or below. First-degree block is benign. Second-degree Mobitz type II and third-degree (complete) heart block are clinically significant and usually require pacemaker implantation.

Symptoms of Arrhythmia

Symptoms vary widely depending on the arrhythmia type, heart rate, duration, and the presence of underlying heart disease.

Palpitations:

An awareness of the heartbeat, often described as fluttering, racing, pounding, or an irregular thumping sensation. The most common symptom of arrhythmia.

Breathlessness:

Fast arrhythmias reduce the time for ventricular filling, lowering cardiac output and causing breathlessness, particularly during episodes.

Dizziness or lightheadedness:

From reduced cerebral blood flow during a fast or slow arrhythmia episode.

Syncope (fainting):

Sudden loss of consciousness from profound haemodynamic compromise. Ventricular arrhythmias causing syncope are a medical emergency. Syncope during exercise or in a young person demands urgent cardiac evaluation.

Chest discomfort:

A vague pressure or tightness during tachycardia episodes, from increased myocardial oxygen demand or reduced coronary filling time.

Fatigue:

Particularly in persistent arrhythmias such as long-standing AFib or frequent PVCs, where cardiac efficiency is chronically reduced.

Sudden cardiac arrest:

The most severe presentation of ventricular arrhythmias. Requires immediate CPR and defibrillation.

Fainting during exercise, in a young person, or associated with palpitations requires urgent cardiological evaluation. These symptoms can indicate a potentially life-threatening ventricular arrhythmia or structural heart condition.

Diagnosing Arrhythmias at Germanten

The key to arrhythmia diagnosis is capturing the rhythm during a symptomatic episode. Our diagnostic suite covers the full range of monitoring durations, from a resting ECG to extended event recording.

12-Lead Resting ECG:

The first investigation. Diagnoses arrhythmias present at the time of recording. Also identifies pre-existing ECG abnormalities such as WPW pattern, long QT, or Brugada pattern that indicate arrhythmia risk.

Holter Monitor (24 to 48 hours):

Continuous ECG recording worn for one to two days. Captures arrhythmias occurring during daily activities, sleep, and exercise. Quantifies PVC burden and detects asymptomatic episodes.

Event Monitor (30 days):

Extended recording for symptoms occurring infrequently. The patient activates the recorder when symptoms occur. Results are transmitted wirelessly for review.

Exercise Stress Test (TMT):

Identifies exercise-triggered arrhythmias, including CPVT (catecholaminergic polymorphic ventricular tachycardia) and rate-dependent conduction abnormalities.

2D Echocardiography:

Assesses structural heart disease underlying arrhythmias: reduced ejection fraction, hypertrophy, valve disease, and wall motion abnormalities.

Electrophysiology Study (EP Study):

An invasive catheter-based investigation that maps the heart's electrical system, identifies re-entry circuits and accessory pathways, and induces arrhythmias under controlled conditions to guide ablation therapy.

Cardiac MRI:

Identifies myocardial fibrosis (scar) in cardiomyopathy and ARVC, which is the substrate for ventricular arrhythmias. Late gadolinium enhancement on MRI directly influences ICD and ablation decisions.

Arrhythmia Treatment at Germanten

Medications

Antiarrhythmic drugs modify the heart's electrical properties to suppress ectopic firing, slow conduction, or alter the refractory period of cardiac tissue. Rate-controlling drugs (beta-blockers, calcium channel blockers, digoxin) slow the ventricular response in fast arrhythmias without necessarily restoring sinus rhythm. Rhythm-controlling drugs (flecainide, amiodarone, sotalol, propafenone) aim to restore and maintain normal sinus rhythm. All antiarrhythmic medications require careful monitoring as they can also cause proarrhythmia in some patients.

Radiofrequency Ablation

Radiofrequency ablation is the preferred curative treatment for SVT, atrial flutter, WPW syndrome, and AFib. It targets and permanently eliminates the abnormal electrical tissue driving the arrhythmia. Success rates are above 95% for SVT and atrial flutter, and 70 to 80% for paroxysmal AFib in a single procedure.

Cardioversion

Electrical cardioversion delivers a synchronized electrical shock under brief sedation to reset the heart's rhythm from AFib or flutter back to normal sinus rhythm. It is used for acute arrhythmias causing haemodynamic compromise and for elective rhythm restoration in persistent AFib. It treats the current episode but does not prevent future recurrence.

Pacemaker Implantation

Pacemaker implantation is the treatment of choice for symptomatic bradycardia, sick sinus syndrome, and significant heart block. A small device implanted under the skin near the collarbone delivers gentle electrical impulses to maintain an adequate heart rate.

ICD Implantation

For patients at significant risk of life-threatening ventricular arrhythmias, an implantable cardioverter defibrillator (ICD) provides protection. The device continuously monitors heart rhythm and delivers a high-energy shock to terminate VF or sustained VT if detected. ICDs are implanted in survivors of cardiac arrest, patients with significantly reduced ejection fraction, and high-risk patients with HCM, ARVC, or channelopathies such as long QT syndrome and Brugada syndrome.