Instructor: Dr. Declan McKernan
Course: PM309 Cardiovascular Drugs
Contact: declan.mckernan@universityofgalway.ie
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.
Components:
P Wave: Atrial depolarization.
QRS Complex: Ventricular depolarization.
T Wave: Ventricular repolarization.
Patterns:
Fast Heartbeat: Tachycardia.
Slow Heartbeat: Bradycardia.
Irregular Heartbeat: Dysrhythmia.
Structure of Cardiac Muscle:
Branched structure with intercalated disks.
Essential for synchronized contraction.
Autorhythmic Cells:
Membrane potentials facilitate the generation of electrical impulses.
Contractile Cells:
Coordinated contraction through intercalated disks and gap junctions.
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.
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.
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.
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).
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.
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.
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.
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.
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.
1. Introduction to Heart Rhythm
Instructor: Dr. Declan McKernan
Course: PM309 Cardiovascular Drugs
Contact: declan.mckernan@universityofgalway.ie
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.
Components:
P Wave: Atrial depolarization.
QRS Complex: Ventricular depolarization.
T Wave: Ventricular repolarization.
Patterns:
Fast Heartbeat: Tachycardia.
Slow Heartbeat: Bradycardia.
Irregular Heartbeat: Dysrhythmia.
Structure of Cardiac Muscle:
Branched structure with intercalated disks.
Essential for synchronized contraction.
Autorhythmic Cells:
Membrane potentials facilitate the generation of electrical impulses.
Contractile Cells:
Coordinated contraction through intercalated disks and gap junctions.
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.
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.
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.
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).
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.
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.
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.
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.
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.