1. Introduction to Heart Rhythm

Introduction to Heart Rhythm

• Instructor: Dr. Declan McKernan

• Course: PM309 Cardiovascular Drugs

• Contact: declan.mckernan@universityofgalway.ie

Learning Outcomes

• Cardiac Electrophysiology: Describe the mechanisms and cell types involved.

• Action Potentials: Differentiate between nodal and myocardial cell action potentials.

• Dysrhythmias: Explain the origin of dysrhythmias and identify their various types.

Cardiac Electrophysiology

Normal Heartbeat

• Components:

  • P Wave: Atrial depolarization.

  • QRS Complex: Ventricular depolarization.

  • T Wave: Ventricular repolarization.

• Patterns:

  • Fast Heartbeat: Tachycardia.

  • Slow Heartbeat: Bradycardia.

  • Irregular Heartbeat: Dysrhythmia.

Cell Types

• Structure of Cardiac Muscle:

  • Branched structure with intercalated disks.

  • Essential for synchronized contraction.

Membrane Potential of Cardiac Cells

• Autorhythmic Cells:

  • Membrane potentials facilitate the generation of electrical impulses.

• Contractile Cells:

  • Coordinated contraction through intercalated disks and gap junctions.

Cardiac Cell Excitability

• Resting Membrane Potential: Approximately -85 mV

  • Higher concentrations of Na+, Cl-, and Ca2+ outside; Higher K+ inside.

  • Maintained by Na+/K+ ATPase pump.

  • More permeable to K+ than other ions.

Nodal Cell Action Potentials

• SA Node Action Potential Phases:

  • Phase 4 (Resting): Pacemaker current; Na+ influx, K+ efflux affecting membrane potential.

  • Phase 0: Rapid depolarization due to Ca2+ influx.

  • Phase 3: Repolarization via K+ efflux.

Myocardial Cell Action Potential

Phases of Ventricular Action Potential

• Phase 4: Stable potential at -90mV.

• Phase 0: Rapid Na+ influx leads to depolarization.

• Phase 1: Transient K+ channel opening leads to slight repolarization.

• Phase 2: Ca2+ influx balances K+ efflux, sustaining plateau phase.

• Phase 3: K+ channels open; repolarization back to resting potential.

Cardiac Conduction

• Initiation: Starts at SA node, spreading to atria, then to AV node.

• Conduction Through AV Node: Delayed (~0.15s) to allow atrial contraction.

• Propagation: Rapid spread through His-Purkinje system into ventricles ( < 0.1s).

Autonomic Control

• Role of CNS: Innervates SA and AV nodes; influences heart rate.

• Noradrenaline's Effect:

  • Binds to β1-adrenergic receptors, increasing pacemaker current and conduction velocity.

Dysrhythmias

• Types:

  • Supraventricular: Arises from the SA node or atrial region.

  • Ventricular: Often leads to sudden cardiac death; includes fibrillation and asystole.

• Bradycardia: Decreased heart rate.

• Tachycardia: Increased heart rate.

Mechanisms of Dysrhythmias

• Impulse Formation: Abnormal automaticity may occur due to:

  • Ischemia with pH shifts and electrolyte imbalances.

  • Injury and ischemia-induced stretch of myocardial fibers.

• Triggered Activity: Existence of early or delayed after depolarizations (EAD, DAD) that can provoke dysrhythmias.

Impulse Conduction Disorders

• AV Block: Characterized by bradycardia; impairs normal conduction.

• Re-entry Phenomena: Responsible for tachycardia, examples include Atrial flutter or Wolff-Parkinson-White syndrome.

• Drug Therapy: Used to manage re-entry through conduction slowing and increasing refractory periods.

Summary

• Cardiac Cell Properties: Electrically excitable due to specific ion channels.

• Role of Action Potentials: Essential for cardiac conduction and heart rate regulation.

• Dysrhythmias: Can arise from either abnormal automaticity or conduction issues, necessitating appropriate intervention.