Electrophysiology

Key Concepts

• Automaticity: The heart's intrinsic capability to spontaneously depolarize and generate action potentials, enabling muscle contraction without relying on the nervous system.
• Myocardium Components:
  • Nodal Cells: Non-contractile cells responsible for generating automaticity and action potentials (e.g., SA node, AV node, AV bundle, bundle branches, Purkinje fibers).
  • Contractile Cells: Cells that contain contractile proteins (actin, myosin, troponin, tropomyosin) and the sarcoplasmic reticulum, responsible for muscle contraction.

Conduction System

• Sinoatrial (SA) Node: Pacemaker located in the right atrium, setting the sinus rhythm (60-80 bpm).
• Bachman's Bundle: Pathway for action potentials from the right atrium to the left atrium.
• Internodal Pathway: Routes action potentials from the SA node to the AV node.
• Atrioventricular (AV) Node: Delays action potential by 0.1 seconds, allowing atrial contraction before ventricular contraction.
• AV Bundle (Bundle of His): Transmits action potentials from the AV node to the bundle branches.
• Bundle Branches: Divide into left and right branches, conducting impulses to the left and right sides of the heart.
• Purkinje Fibers: Transmit action potentials to contractile cells across the myocardium, initiating muscle contraction.

Cellular Mechanisms

Nodal Cells

• Resting membrane potential: ~ -60 mV
• Funny Sodium Channels: Slowly let sodium into the cell.
• T-Type Calcium Channels: Open around -55 mV, allowing calcium influx.
• L-Type Calcium Channels: Open at -40 mV, leading to rapid calcium influx and quick depolarization to +40 mV.
• Gap Junctions: Allow ions to pass between nodal cells and contractile cells.

Contractile Cells

• Resting membrane potential: ~ -85 to -90 mV
• Voltage-Gated Sodium Channels: Open at threshold (-70 mV), causing rapid depolarization.
• Potassium Channels: Initially open to bring potential to ~ 0 mV.
• Calcium Channels: L-Type channels keep membrane potential stable during the plateau phase (~ 0 mV).
• Phases:
  • Phase 0: Depolarization (sodium influx)
  • Phase 1: Initial repolarization (potassium efflux)
  • Phase 2: Plateau (calcium influx, potassium efflux)
  • Phase 3: Repolarization (potassium efflux)
  • Phase 4: Resting potential (maintenance phase)
• Calcium-Induced Calcium Release: Calcium triggers further calcium release from the sarcoplasmic reticulum.
• Troponin Complex: Calcium binds to troponin, moving tropomyosin, allowing actin-myosin interaction, leading to contraction.
• Desmosomes and Gap Junctions: Intercalated discs that provide structural stability and ion movement, ensuring coordinated contraction.

Importance of AV Node Delay

• Ensures atrial contraction completes before ventricular contraction, ensuring efficient blood flow.
• AV node's delay is due to fewer gap junctions and smaller diameter fibers.

Functional Syncytium

• Cardiac cells are interconnected and synchronize their contractions via gap junctions, ensuring the heart functions as a cohesive unit.

Relaxation Mechanisms

• Calcium Removal: Calcium is pumped back into the sarcoplasmic reticulum and out of the cell via calcium ATPases and sodium-calcium exchangers.
• Potassium Channels: Facilitate repolarization by expelling potassium ions, bringing the cell back to resting membrane potential.

Upcoming Topic

• Extrinsic Regulation: How the autonomic nervous system (sympathetic and parasympathetic) modulates heart rate (Tachycardia and Bradycardia).