Cardiac Conduction and Rhythm Disorders

Introduction

Cardiac conduction and rhythm disorders encompass the study of the heart's electrical system, its normal function, and the pathological conditions that disrupt its rhythm. Understanding these concepts is essential for recognizing arrhythmias and their clinical implications.

Electrical Anatomy of the Heart

Main Components

• 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: The only electrical connection between atria and ventricles, responsible for delaying the impulse to allow atrial contraction before ventricular contraction.

• Bundle of His, Right and Left Bundle Branches, Purkinje Fibers: Specialized conduction pathways that rapidly transmit impulses to ventricular myocardium, ensuring coordinated contraction.

Example: The SA node generates impulses at 60-100 beats per minute under normal conditions.

Normal Cardiac Conduction Pathway

Sequence of Electrical Activation

1. Impulse originates in the SA node.

2. Spreads through atria causing atrial contraction (P wave on EKG).

3. Impulse reaches AV node, is delayed.

4. Travels down the Bundle of His and bundle branches.

5. Distributed via Purkinje fibers to ventricular myocardium, causing ventricular contraction (QRS complex).

Action Potentials in Cardiac Tissue

Phases of Myocardial Action Potential

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

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

• Phase 2 (Plateau): Influx of Ca2+ balances K+ efflux, leading to sustained depolarization. channels open$

• Phase 3 (Repolarization): K+ efflux restores negative membrane potential.

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

Example: The plateau phase (Phase 2) is crucial for the refractory period, preventing premature contractions.

Depolarization and Repolarization

Definitions

• Depolarization: The process by which cardiac cells become less negative, leading to contraction.

• Repolarization: Restoration of the resting negative membrane potential, allowing relaxation.

Application: On an EKG, depolarization corresponds to the P wave (atria) and QRS complex (ventricles), while repolarization is seen as the T wave.

Automaticity, Conduction Velocity, and Refractory Period

Key Terms

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

• Conduction Velocity: The speed at which electrical impulses travel through cardiac tissue.

• Refractory Period: The time during which cells cannot be re-excited. Includes absolute and relative refractory periods.

Example: The AV node has a slower conduction velocity, allowing time for ventricular filling.

Mechanisms of Arrhythmia

Types of Arrhythmogenic Mechanisms

• Abnormal Impulse Generation: Includes enhanced automaticity and triggered activity (early or delayed afterdepolarizations).

• Abnormal Impulse Conduction: Includes reentry circuits, conduction blocks, and accessory pathways.

Diagram: Reentry requires a circuit with areas of unidirectional block and slow conduction.

Electrocardiogram (EKG) Interpretation

Basic Components

• P wave: Atrial depolarization

• PR interval: Atrial to ventricular conduction (normal: 0.12-0.20 sec)

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

• QT interval: Ventricular depolarization and repolarization (normal: 0.40-0.44 sec)

• T wave: Ventricular repolarization

Formula for Rate Calculation:

Classification of Arrhythmias

By Location

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

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

By Rate

• Bradycardias: Heart rate < 60 bpm

• Tachycardias: Heart rate > 100 bpm

Bradyarrhythmias

Types and Causes

• Sinus Bradycardia: Slow heart rate due to decreased SA node activity.

• Sinus Node Dysfunction: Often age-related degeneration.

• AV Block: Impaired conduction through AV node or Bundle of His.

• Increased Vagal Tone: Seen in athletes or vasovagal episodes.

Symptoms: Dizziness, syncope, fatigue, chest pain.

AV Conduction Blocks

Degrees of Block

Tachyarrhythmias

Sinus Tachycardia

• Heart rate > 100 bpm, normal PQRST morphology

• Caused by increased sympathetic tone (e.g., fever, anxiety, exercise)

Supraventricular Arrhythmias

• Atrial Fibrillation (AF): Multiple reentry circuits, no discernible P waves, irregularly irregular rhythm. Associated with increased stroke risk.

• Atrial Flutter: Single reentry loop, saw-tooth pattern on EKG, regular rhythm.

• Paroxysmal Supraventricular Tachycardia (PSVT): Sudden onset/offset, reentry involving AV node or accessory pathways.

Ventricular Arrhythmias

Types

• Premature Ventricular Complexes (PVCs): Early ventricular depolarizations, wide QRS, usually benign if isolated.

• Ventricular Tachycardia (VT): Three or more consecutive PVCs, rate > 100 bpm, can be sustained or non-sustained.

• Torsades de Pointes: Polymorphic VT associated with prolonged QT interval, risk factors include hypokalemia, hypomagnesemia, and certain drugs.

• Ventricular Fibrillation (VF): Chaotic ventricular activity, no cardiac output, requires immediate defibrillation.

Signs and Symptoms of Arrhythmias

• Symptoms: Palpitations, dizziness, syncope, chest pain, fatigue.

• Signs: EKG changes, abnormal pulse, hypotension, irregular heart rhythm.

Stroke Risk in Atrial Fibrillation

Mechanism

• Loss of atrial contraction leads to stasis of blood, increasing risk of thrombus formation and embolic stroke.

• Most common arrhythmia associated with ischemic stroke is atrial fibrillation.

Treatment Overview

Arrhythmia Management

• Rate Control: Beta-blockers, non-dihydropyridine calcium channel blockers, digoxin.

• Rhythm Control: Antiarrhythmic drugs (Na+ and K+ channel blockers), electrical cardioversion.

• Stroke Prevention: Anticoagulants (warfarin, NOACs such as dabigatran, apixaban, rivaroxaban).

Summary Table: Arrhythmia Classification

Additional info: These notes expand on the provided slides with definitions, mechanisms, and clinical context for arrhythmias, suitable for Anatomy & Physiology students.