Ninja nerd heart electrophysiology

Electrophysiology of the Heart

Introduction

  • Electrophysiology is a crucial area of study in understanding the heart's functioning.

  • The heart is unique because it can intrinsically depolarize itself, so its functioning is not solely reliant on the nervous system.

  • The nervous system can influence heart rate and contractility through extrinsic innervation.

Key Concept: Automaticity

  • Definition of Automaticity: The intrinsic ability of the heart to spontaneously depolarize and trigger action potentials, which spread throughout the myocardium to initiate contraction.

  • Automaticity is essential for the rhythmic activity of the heart.

Structure of the Heart

  • The myocardium consists of two types of cells:

    • Nodal Cells: Non-contractile cells responsible for generating automaticity (e.g., Sinoatrial node (SA node), Atrioventricular node (AV node), Bundle of His (AV bundle), bundle branches, Purkinje fibers).

    • Contractile Cells: These include contractile proteins (actin, myosin, troponin, tropomyosin) and sarcoplasmic reticulum, responsible for muscle contraction.

Detailed Breakdown of Components
  1. Nodal Cells

    • Generate automaticity and do not contract.

    • Examples include:

      • SA Node: The primary pacemaker of the heart located in the right atrium.

      • AV Node: Acts as a connection between atria and ventricles and introduces a delay.

      • Bundle of His: Conducts action potentials from the AV node to ventricles.

      • Bundle Branches: Right bundle branch and left bundle branch.

      • Purkinje Fibers: Spread action potentials throughout the myocardium.

  2. Contractile Cells

    • Make up the bulk of the myocardium and consist of contractile proteins, sarcoplasmic reticulum, and are responsible for generating force to pump blood.

Pacemaking Process

  • SA Node Function: Sets the heart rate at approximately 60 to 80 beats per minute, initiating the sinus rhythm independent of nervous system activity.

  • Conduction Pathway: Information from the SA node spreads through the following structures:

    • Bachmann's Bundle: Connects the right atrium to the left atrium, conducting electrical signals to depolarize both atria.

    • Internodal Pathway: Distributes signals throughout the right atrium.

    • Coupled with AV node to ensure coordinated contraction of atria before ventricles.

Conductivity and Action Potential Generation

  • The AV Node introduces a delay (approximately 0.1 seconds) allowing the atria to contract and fill ventricles before ventricular contraction.

  • The delay is due to the following:

    • Fewer gap junctions in the AV node compared to other nodal cells,

    • Smaller diameter of the AV node muscle fibers.

  • Bundle of His and Branches: Conduct action potentials from AV node into the ventricles:

    • Right bundle branch to the right myocardium.

    • Left bundle branch to the left myocardium.

    • Action potentials are further distributed through the Purkinje fibers.

Cell Types in Detail: Nodal and Contractile Cells

  • Nodal Cells:

    • Characterized by "funny" sodium channels that allow slow depolarization.

    • Nodal cells do not have a stable resting membrane potential, fluctuating around -60 mV.

    • Action potential generation process involves:

    1. Activation of funny sodium channels leading to a gradual depolarization from -60 mV to threshold (-40 mV).

    2. T-type calcium channels begin to open around -55 mV, further depolarizing the cell.

    3. At threshold, L-type calcium channels open allowing for rapid influx of calcium, causing a rapid depolarization to approximately +40 mV.

  • Contractile Cells:

    • Resting membrane potential significantly differs, generally around -85 to -90 mV.

    • Depolarization leads to:

    1. Action potentials begin as positive ions (sodium) enter via gap junctions from nodal cells.

    2. Threshold achieved around -70 mV opens voltage-gated sodium channels for rapid depolarization.

    3. Peaks at +10 mV, after which sodium channels inactivate while potassium channels open, resulting in a drop to 0 mV.

    4. Opening of L-type calcium channels leads to a plateau phase, maintaining depolarization for about 250 milliseconds.

    5. Phase transitions:

      • Phase 0: Rapid depolarization via sodium influx.

      • Phase 1: Initial repolarization as potassium exits.

      • Phase 2: Plateau where potassium appears balanced with slow calcium influx.

      • Phase 3: Repolarization primarily through potassium outflow.

      • Phase 4: Stable resting potential maintenance until the next nodal input.

Calcium Dynamics in Myocardial Contraction

  • Calcium influx during action potentials initiates contraction in cardiac muscle.

  • Calcium binds to troponin to initiate muscle contraction via cross-bridge formations with myosin and actin, effectively pumping blood.

  • Synchronization of contraction arises from the interconnectedness of muscle cells via gap junctions, forming a functional syncytium.

Resting Phase Mechanisms
  • Involves calcium active transport back into sarcoplasmic reticulum using ATP.

  • Reestablishes calcium levels across membranes and prepares the heart for the next contraction cycle.

  • Potassium channels are mainly responsible for returning the cell to resting potential after contraction.

Conclusion

  • Understanding the intrinsic ability of the heart to initiate and regulate its contractions through electrophysiology is key.

  • In the next part of this study, we will explore the extrinsic regulation mechanisms affecting heart function, including responses to autonomic nervous system activities (sympathetic and parasympathetic).