Cardiac Conduction and Rhythm Disorders

Introduction

Cardiac conduction and rhythm disorders encompass the study of the heart's electrical system, the mechanisms underlying normal and abnormal rhythms, and the clinical implications of arrhythmias. Understanding these concepts is essential for recognizing, diagnosing, and managing cardiac rhythm disturbances.

Electrical Anatomy of the Heart

Normal Conduction Pathway

• Sinoatrial (SA) Node: The primary pacemaker of the heart, located in the right atrium. It initiates electrical impulses that set the heart rate.

• Atrioventricular (AV) Node: Receives impulses from the atria and delays them, allowing for atrial contraction before ventricular contraction.

• Bundle of His: Conducts impulses from the AV node to the ventricles.

• Right and Left Bundle Branches: Carry impulses through the interventricular septum to the respective ventricles.

• Purkinje Fibers: Distribute the electrical impulse throughout the ventricles, ensuring coordinated contraction.

Key Point: Synchronized contractions are vital for effective cardiac output and tissue perfusion.

Myocardial Cells and Action Potentials

Types of Myocardial Cells

• Nodal Tissue: Specialized for automaticity; depolarization is calcium-mediated (e.g., SA and AV nodes).

• Myocardial Tissue: Responsible for contraction; depolarization is sodium-mediated.

Phases of the Myocardial Action Potential

• Phase 0 (Depolarization): Rapid influx of Na+ through voltage-gated channels.

• Phase 1 (Initial Repolarization): Transient K+ efflux.

• Phase 2 (Plateau): Ca2+ influx balances K+ efflux, leading to a plateau; crucial for contraction.

• Phase 3 (Repolarization): K+ efflux predominates, restoring resting membrane potential.

• Phase 4 (Resting Potential): Na+/K+-ATPase maintains ionic gradients.

Example: The action potential phases correspond to specific EKG components (e.g., Phase 0 = QRS complex).

Key Terms and Concepts

Depolarization and Repolarization

• Depolarization: The process by which the cell membrane potential becomes less negative, leading to muscle contraction.

• Repolarization: Restoration of the resting membrane potential after depolarization.

Automaticity, Conduction Velocity, and Refractory Period

• Automaticity: The ability of cardiac cells (especially nodal cells) to spontaneously depolarize and generate action potentials.

• Conduction Velocity: The speed at which electrical impulses travel through cardiac tissue; affected by tissue health and medications.

• Refractory Period: The time during which cells cannot be re-excited. Includes:

  • Absolute Refractory Period (ARP): No new action potential can be initiated.

  • Relative Refractory Period (RRP): A stronger-than-normal stimulus may initiate another action potential.

Mechanisms of Arrhythmia

Impulse Generation Disorders

• Automatic: Abnormal pacemaker activity (e.g., sinus tachycardia).

• Triggered Activity: Early or delayed afterdepolarizations (EADs/DADs) can lead to arrhythmias.

Impulse Conduction Disorders

• Reentry: An electrical impulse re-excites a region of the heart, leading to tachyarrhythmias (e.g., atrial fibrillation, PSVT).

Electrocardiogram (EKG) Interpretation

Basic EKG Components

• P wave: Atrial depolarization (contraction).

• PR interval: Time from atrial to ventricular depolarization (normal: 0.12–0.20 sec).

• QRS complex: Ventricular depolarization (normal: <0.12 sec).

• QT interval: Total time for ventricular depolarization and repolarization (normal: 0.40–0.44 sec).

• T wave: Ventricular repolarization.

Example: Prolonged QT interval increases risk for Torsades de Pointes.

Determining Heart Rate

• Bradycardia: <60 bpm

• Normal sinus rhythm: 60–100 bpm

• Tachycardia: >100 bpm

• Rate calculation:

Classification of Arrhythmias

By Location

• Supraventricular: Originates above the ventricles (e.g., atrial fibrillation, atrial flutter, PSVT).

• Ventricular: Originates in the ventricles (e.g., ventricular tachycardia, ventricular fibrillation).

By Rate

• Bradycardias: Slow heart rhythms (e.g., sinus bradycardia, AV block).

• Tachycardias: Fast heart rhythms (e.g., sinus tachycardia, atrial fibrillation).

Common Arrhythmias and Their Features

Bradyarrhythmias

• Sinus Bradycardia: Heart rate <60 bpm; may be asymptomatic or cause dizziness, syncope, or fatigue.

• Sinus Node Dysfunction: Often due to age-related degeneration; may require pacemaker if symptomatic.

• AV Conduction Block: Impaired conduction through AV node or Bundle of His; classified as first, second (Mobitz I and II), or third degree.

Tachyarrhythmias

• Sinus Tachycardia: Heart rate >100 bpm; normal PQRST; often a physiologic response to stress, fever, or stimulants.

• Atrial Fibrillation (AF): Irregularly irregular rhythm, no discernible P waves, atrial rate 400–600 bpm; risk of stroke due to emboli.

• Atrial Flutter: Regular, saw-tooth pattern; atrial rate 240–340 bpm.

• Paroxysmal Supraventricular Tachycardia (PSVT): Sudden onset/termination; often due to reentry mechanisms (AVNRT, AVRT).

• Ventricular Tachycardia (VT): Three or more consecutive PVCs at >100 bpm; can be monomorphic or polymorphic (e.g., Torsades de Pointes).

• Ventricular Fibrillation (VF): Chaotic, disorganized ventricular activity; no effective cardiac output; medical emergency.

Mechanisms and Clinical Implications

Reentry Circuits

• Reentry requires a circuit, unidirectional block, and slowed conduction.

• Common in atrial fibrillation, atrial flutter, PSVT, and some ventricular arrhythmias.

Stroke Risk in Atrial Fibrillation

• AF increases risk of thromboembolic stroke due to stasis of blood in the atria.

• Anticoagulation is often indicated to reduce stroke risk.

Signs and Symptoms of Arrhythmias

• Palpitations

• Dizziness, syncope

• Chest pain, dyspnea

• EKG changes (irregular or abnormal rhythms)

• Hemodynamic compromise (hypotension, decreased perfusion)

Summary Table: Common Arrhythmias

Key Formulas and Equations

• Heart Rate Calculation:

• Corrected QT Interval (QTc):

QT and RR in seconds; QTc > 450 ms increases risk for Torsades de Pointes.

Summary

Understanding the cardiac conduction system, action potentials, and mechanisms of arrhythmias is essential for interpreting EKGs and managing rhythm disorders. Recognition of clinical signs, EKG features, and appropriate interventions can prevent complications such as stroke and sudden cardiac death.