What is the appropriate treatment plan for an adult patient with a history of heart disease and cardiac arrhythmias, considering normal impulse formation and basic cardiac electrophysiology?

Management of Adult Patients with Heart Disease and Cardiac Arrhythmias

For adult patients with heart disease and cardiac arrhythmias, treatment must be guided by comprehensive understanding of the underlying arrhythmia mechanism (automaticity, triggered activity, or reentry), followed by mechanism-specific therapy using antiarrhythmic medications, catheter ablation, or device implantation based on the specific arrhythmia type and hemodynamic consequences. 1

Understanding Normal Cardiac Electrophysiology

Normal impulse formation originates in the sinoatrial (SA) node and propagates sequentially through the atrial specialized conducting system, atrioventricular (AV) node, His-Purkinje system, and into the ventricles 2. The cardiac action potential consists of five distinct phases representing changing ionic fluxes and membrane potentials, with two types of conducting fibers (fast-current and slow-current) exhibiting different electrophysiologic properties 2.

Critical electrophysiologic parameters to assess:

• Intracardiac conduction velocities, particularly His-Purkinje system (H-V conduction) 3
• AV nodal conduction time and intra-atrial conduction times 3
• Ventricular refractory periods 3
• Sinus node recovery times, especially in patients with sinus node dysfunction 3

Arrhythmia Mechanisms and Diagnostic Approach

The three fundamental mechanisms responsible for cardiac arrhythmias are automaticity (abnormal impulse initiation), triggered activity, and reentry 1. Identifying the specific mechanism may require invasive electrophysiologic study but is critical for developing appropriate treatment strategies 1.

Diagnostic evaluation must include:

• In-hospital telemetry monitoring for continuous rhythm assessment 4
• Exercise testing to evaluate exercise-induced arrhythmias 4
• Ambulatory ECG monitoring (Holter) for paroxysmal events 4
• Signal-averaged electrocardiography for risk stratification 4
• Invasive electrophysiologic testing when noninvasive studies are insufficient 4

During electrophysiologic testing, clinicians must evaluate sinus node dysfunction, atrioventricular conduction disturbances, supraventricular tachycardias, ventricular tachycardias, and pre-excitation syndromes 4.

Treatment Algorithm Based on Arrhythmia Type

Bradyarrhythmias

Permanent pacemaker implantation is the definitive treatment for symptomatic bradyarrhythmias 5. The decision requires knowledge of device indications, contraindications, implantation methods, postoperative care, and long-term follow-up protocols 4.

Supraventricular Tachycardias (SVT)

Radiofrequency catheter ablation is the first-line curative therapy for recurrent paroxysmal SVT, including AV re-entrant tachycardia using accessory pathways, AV nodal re-entrant tachycardia, atrial tachycardia, and atrial flutter, with success rates of 98% 5. This approach eliminates recurrent symptoms, life-threatening attacks, tachycardia-induced cardiomyopathy, and the need for lifelong drug therapy 5.

For poorly controlled atrial fibrillation, options include AV nodal ablation followed by pacemaker insertion or AV nodal modification 5.

Ventricular Arrhythmias

For premature ventricular contractions (PVCs) and ventricular tachycardia:

• Plasma levels of 0.2 to 1 mcg/mL of antiarrhythmic agents (such as flecainide) may be needed for maximal therapeutic effect 3
• Trough plasma levels in successfully treated recurrent ventricular tachycardia patients range between 0.2 and 1 mcg/mL 3
• Caution: Plasma levels above 0.7 to 1 mcg/mL are associated with higher rates of cardiac adverse events including conduction defects and bradycardia 3

For idiopathic non-ischemic VT arising from the left ventricle or right ventricular outflow tract, radiofrequency ablation offers curative therapy with 94% success rates 5.

For resuscitated sudden cardiac death or high-risk patients, the implantable cardioverter defibrillator (ICD) is the only technique that significantly improves survival from sudden cardiac death 5. The ICD prevents sudden death but is limited by cost and is not suitable for patients with severe heart failure 5.

Pharmacologic Considerations

Antiarrhythmic drug selection must account for:

• Effects on cellular and whole organ electrophysiology 4
• Pharmacokinetics and pharmacodynamics principles 4
• Autonomic nervous system balance between parasympathetic and sympathetic activity 2
• Electrolyte concentrations (potassium, calcium, magnesium), which critically affect cardiac electrophysiology and can influence drug efficacy or toxicity 2

Flecainide produces dose-related decreases in intracardiac conduction with greatest effect on the His-Purkinje system, and can cause negative inotropic effects with decreases in ejection fraction 3. Dose reduction appears to reduce the frequency and severity of proarrhythmic events 3.

Critical Pitfalls to Avoid

• Do not ignore sinus node dysfunction: Flecainide and similar agents increase sinus node recovery times, which may become clinically significant 3
• Monitor for proarrhythmic effects: Dose reduction is essential when plasma levels exceed 0.7 mcg/mL 3
• Assess ventricular function: Negative inotropic effects can worsen heart failure 3
• Recognize device limitations: ICDs prevent sudden death but do not address underlying heart failure 5
• Consider ablation early: For recurrent SVT and non-ischemic VT, catheter ablation offers cure rather than chronic suppression 5

Emerging Therapeutic Targets

Ion channels, transporters, and their regulatory mechanisms—including accessory proteins, Ca2+ homeostasis, phosphorylation processes, autonomic signaling, and metabolic changes—represent potential therapeutic targets 6. Inflammatory and structural changes such as fibrotic and hypertrophic remodeling also influence arrhythmogenesis and may be modifiable 6.