Overview of Heart Electrophysiology

Sep 19, 2024

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Electrophysiology Lecture Notes

Introduction to Electrophysiology

  • The heart can intrinsically depolarize, independent of the nervous system.
  • Automaticity: Heart's ability to spontaneously depolarize and generate action potentials to trigger contraction.

Structure of the Myocardium

  • Two types of cells:
    1. Nodal cells (non-contractile):
      • Generate automaticity.
      • Include SA node, AV node, AV bundle (His), bundle branches, and Purkinje fibers.
    2. Contractile cells:
      • Contain contractile proteins like actin, myosin, troponin, and tropomyosin.
      • Sarcoplasmic reticulum for calcium storage.

Function of Nodal Cells

  • SA Node:
    • Located in the right atrium beneath the superior vena cava.
    • Sets the heart's pace at 60-80 beats/minute (sinus rhythm).
  • AV Node:
    • Delays impulse by 0.1 seconds to allow atria to contract before ventricles.
  • Conduction Pathway:
    • SA node → Bachman's bundle (left atrium) & internodal pathways → AV node → Bundle of His → Right & left bundle branches → Purkinje fibers.

Generation of Action Potentials

  • Nodal Cell Action Potentials:

    • Funny sodium channels: Cause slow Na+ influx.
    • T-type calcium channels: Open at -55 mV.
    • L-type calcium channels: Open at -40 mV, causing rapid depolarization to +40 mV.
    • Repolarization: Potassium exits; returns to -60 mV, cycle repeats.

  • Contractile Cell Action Potentials:

    • Resting potential ~-85 to -90 mV.
    • Depolarization due to Na+ influx at threshold (-70 mV).
    • Phase 0: Rapid Na+ influx.
    • Phase 1: K+ exits causing slight repolarization.
    • Phase 2: Plateau, Ca2+ influx balances K+ efflux.
    • Phase 3: K+ efflux leads to repolarization.
    • Phase 4: Resting potential maintained until next impulse.

Contractile Mechanism

  • Calcium-induced calcium release: Ca2+ entry triggers further Ca2+ release from sarcoplasmic reticulum.
  • Troponin Complex:
    • Ca2+ binds troponin C, causes tropomyosin shift, allowing actin-myosin interaction.
  • Functional Syncytium: Muscle cells contract as a unit due to synchronized depolarization via gap junctions.

Relaxation Mechanism

  • Calcium removal:
    • Pumped back into sarcoplasmic reticulum.
    • Extruded out of the cell.
  • Repolarization completes with K+ efflux.

The contractile mechanism in heart muscle cells is a complex process involving calcium ions, troponin, and tropomyosin. Here's a breakdown:

Calcium-Induced Calcium Release

  1. Calcium Enters the Cell: The initial calcium ions that trigger contraction enter the cell through L-type calcium channels during the plateau phase of the action potential.
  2. T-Tubules: These calcium ions then travel through tiny invaginations in the cell membrane called T-tubules. These T-tubules extend deep into the cell, bringing the calcium close to the sarcoplasmic reticulum (SR).
  3. Ryanodine Receptor Activation: The calcium ions bind to a special protein called the ryanodine receptor type 2 (RyR2), which is located on the SR. This binding activates the RyR2, causing it to open up a channel.
  4. Calcium Release from SR: The opening of the RyR2 allows a massive amount of calcium stored within the SR to flood out into the cytoplasm of the muscle cell. This process is called calcium-induced calcium release because the initial calcium entry from the extracellular environment triggers the release of a much larger amount of calcium from the SR.

Troponin Complex Activation

  1. Calcium Binding: The calcium ions that have been released from the SR now bind to a protein called troponin C (TnC) within the troponin complex.
  2. Troponin Conformational Change: This binding causes a conformational change (shape change) in the troponin complex.
  3. Tropomyosin Movement: This change in troponin pulls on another protein called tropomyosin, which is wrapped around the actin filament. Tropomyosin moves away from the myosin-binding sites on the actin filament.

Actin-Myosin Interaction and Contraction

  1. Myosin Binding Sites Exposed: When tropomyosin moves away, it exposes the myosin-binding sites on the actin filament.
  2. Cross-Bridge Formation: The myosin heads can now bind to these exposed sites, forming cross-bridges between the actin and myosin filaments.
  3. Power Stroke: The myosin heads then use energy from ATP to pull on the actin filaments, causing them to slide past each other. This sliding action is what shortens the muscle cell and produces contraction.

Relaxation Mechanism

  1. Calcium Removal: For the muscle cell to relax, the calcium ions must be removed from the cytoplasm.
  2. Calcium Pumped Back into SR: Calcium ions are actively pumped back into the SR by the calcium ATPase pump (SERCA pump), which uses ATP to move calcium against its concentration gradient.
  3. Calcium Extruded Out of Cell: Some calcium ions are also pumped out of the cell through sodium-calcium exchangers (NCX), which use the energy of sodium moving down its concentration gradient to move calcium out.
  4. Tropomyosin Returns: As calcium levels in the cytoplasm decrease, troponin changes shape again, and tropomyosin moves back to cover the myosin-binding sites on actin.
  5. Cross-Bridges Break: With the myosin-binding sites blocked, the cross-bridges between actin and myosin break, and the muscle cell relaxes.

Important Points

  • Calcium is Key: The entire contractile process hinges on the precise control of calcium levels within the muscle cell.
  • ATP Required: The relaxation process also requires energy (ATP) to pump calcium back into the SR.
  • Functional Syncytium: The synchronized contraction of cardiac muscle cells is possible because they are connected by gap junctions. This creates a functional syncytium, where the cells act as a single unit.

Let me know if you have any more questions or if you'd like to delve deeper into specific aspects of this process!

Conclusion

  • Intrinsic conduction system detailed; extrinsic effects (sympathetic and parasympathetic) to be discussed in part two.