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1. Introduction to Heart Rhythm

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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.