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Myocardial Muscle Tissue Physiology

Myocardial Muscle Cells (Cardiac Myocytes)

• Shape and Structure:

  • Shorter than skeletal muscle cells.
  • Have branches.
  • Connect to one another, unlike skeletal muscle cells.

• Photomicrograph Observations:

  • Myocytes stain pink.
  • Nuclei stain dark purple due to densely packed DNA absorbing more dye.
  • White staining lines perpendicular to the cell length are junctions where cells connect.

Intercalated Discs

• Definition: Junctions where cardiac myocytes connect.
• Skeletal Muscle Contrast: Skeletal muscle cells do not touch due to the endomysium membrane.
• Components:
  • Desmosomes: Resist physical stress, prevent tearing, provide flexibility.
  • Gap junctions: Allow sharing of nutrients, wastes, and electric current (action potentials).

Striations and Myofilaments

• Striations:
  • Present in both cardiac and skeletal muscle due to the arrangement of myofilaments.
  • Myofilaments are muscle proteins arranged into myofibrils.
• Myofilaments:
  • Thick: Myosin
  • Thin: Actin, plus supporting proteins like Z discs, titin, and nebulin.

Intracellular Components

• Mitochondria:

  • Higher mitochondrial density in cardiac cells compared to skeletal cells.
  • Cardiac cells are always active and require more energy as they constantly contract and relax.

• T-Tubules and Sarcoplasmic Reticulum (SR):

  • Similar structures to skeletal muscle involved in stimulating contraction.
  • Transverse tubules (T tubules) connect to the sarcoplasmic reticulum (SR).

Detailed Intercalated Disc Structure

• Desmosomes: Maintain connection and resist physical stress while allowing flexibility.
• Gap Junctions: Facilitate communication by sharing electrocurrent.

Types of Cardiac Muscle Cells

• Contractile Cells:

  • Make up over 99% of myocardium.
  • Function: generate muscular force to push blood during the cardiac cycle.

• Conductive Cells:

  • Less than 1% of myocardium.
  • Not for contraction; develop from same embryonic precursor cells as contractile cells.
  • Similarities: have T tubules and SR.
  • Differences: relative or entire lack of muscle protein.
  • Function: rapidly conduct electric current from one point to another within the heart.

Electric Current Flow in the Heart

• Components:

  • Sinoatrial Node (SA node):
    • Cluster of connecting conductive cells in the right atrial wall.
    • Fires action potentials first, initiating current flow.
  • Atrioventricular Node (AV node):
    • Sits at the junction between atria and ventricles.
    • Receives current after it flows through contractile cells of the atrial myocardium.
  • Fibrous Skeleton:
    • Blocks electric signals between atria and ventricles.
    • The AV node sits in the only opening within this fibrous layer.

• Current Flow Sequence:

  1. SA node generates current.
  2. Current flows through atrial myocardium.
  3. Current reaches and stimulates AV node.
  4. AV node fires action potentials.
  5. Current flows down the interventricular septum via the AV bundle.
  6. Current flows through right and left bundle branches and Purkinje fibers, up the lateral edges of ventricular walls.

Cardiac Cycle Coordination

• First Event: Contraction of right and left atria, stimulated by the SA node firing action potentials.

• Excitation-Contraction Coupling: Cardiac myocytes maintain membrane potentials and fire action potentials when reaching threshold.

• AV Nodal Delay:

  • Brief pause after current reaches AV node.
  • Ensures atria contract and begin relaxing before ventricles receive the signal.
  • Prevents counterproductive simultaneous contraction of atria and ventricles.
  • Fibrous skeleton and AV node delay act as safety measures.

• Ventricular Contraction: Current passes through bundles and branches to Purkinje fibers, causing ventricles to contract simultaneously.

• Refilling Phase: Brief pause after contraction during which all four heart chambers relax and refill with blood.

Conductive Cell Alternate Names

• Autorhythmic Cells:

  • Generate current on their own without external stimulation.
  • Conductive cells in SA node, AV node, bundle branches, and Purkinje fibers have this ability.

• Pacemaker Cells:

  • Set the pace for heart contraction (heart rate).
  • SA node is the normal biological pacemaker because it fires action potentials first.
  • Artificial pacemakers replicate SA node activity.

SA Node as Pacemaker

• Reason: SA node fires action potentials fastest, reaching threshold sooner than other parts.

• Action Potential Firing Rates:

  • SA node: ~100 action potentials per minute.
  • AV node: 40-60 action potentials per minute.
  • Bundle branches/Purkinje fibers: 30-40 action potentials per minute.

• Backup Pacemaker:

  • AV node can take over if SA node is damaged, although it will result in problems.

Membrane Potentials of Conductive Myocytes

• Three Phases: Pacemaker potential, rapid depolarization, repolarization.

• Pacemaker Potential (Slow Depolarization):

  • Allows cells to self-depolarize and set the pace for heart contraction (autorhythmic nature).
  • Caused by the opening of voltage-gated sodium channels.
  • Sodium diffuses into the cell, making it less negative.

• Rapid Depolarization:

  • Occurs when the cell reaches threshold voltage of approximately -50 mV.
  • Triggers the opening of voltage-gated calcium channels.
  • Calcium flows into the cell, causing rapid depolarization.
  • Na^+ and Ca^{2+} influx.
  • This depolarization is the signal that flows through gap junctions to stimulate neighboring cells.

• Repolarization:

  • Represents the loss of positive charge.
  • Voltage-gated potassium channels open at the peak of the curve.
  • Potassium diffuses out of the cell, making it more negative.
  • K^+ eflux.

Membrane Potentials of Contractile Myocytes

• Resting Potential:

  • Maintained until stimulated by a neighboring cell through gap junctions.

• Rapid Depolarization:

  • Neighboring cell's depolarization rapidly pushes the cell to threshold.
  • Voltage-gated sodium channels open, causing rapid influx of sodium.
  • Na^+ influx.
  • Sodium channels close at the peak.

• Early Repolarization:

  • Voltage-gated potassium channels open, causing a slight repolarization.
  • K^+ eflux.
  • Small population of potassium channels.

• Plateau Phase:

  • Voltage-gated calcium channels open.
  • Calcium enters the cell, balancing the loss of potassium.
  • Maintains a relatively depolarized state for a prolonged amount of time.
  • Calcium channels close at the end of the plateau phase.
  • Ca^{2+} influx.

• Late Repolarization:

  • A second, larger population of voltage-gated potassium channels opens.
  • Potassium rushes out, causing rapid repolarization back to the resting potential.

Significance of the Plateau Phase

• Prolonged Action Potential:

  • Contractile cardiac myocytes have a much longer action potential than other cells.

• Prevention of Muscle Twitch Summation:

  • By the time the cell can fire a new action potential, it is nearly fully relaxed.
  • Prevents the heart muscle from locking up due to repeated contractions.

Comparison of Skeletal and Cardiac Muscle Action Potentials

• Skeletal Muscle:

  • Short action potential (20-30 milliseconds).
  • Can undergo twitch or wave summation, allowing for fine-tuned control of muscle tension.

• Cardiac Muscle:

  • Long action potential due to the plateau phase.
  • Refractory periods nearly completely overlap with muscle twitch.
  • Muscle twitch summation is essentially impossible, preventing the heart from locking up.

Excitation-Contraction Coupling in Contractile Cells

• Process:

  1. Action potential from a connecting cell depolarizes the contractile cell to threshold.
  2. Voltage-gated sodium channels open, leading to rapid depolarization.
  3. Action potential flows down T tubules.
  4. T tubules activate voltage-gated proteins that open calcium channels in the SR membrane.
  5. Calcium diffuses from the SR into the cytosol.

• Role of Calcium:

  • Calcium binds to troponin on the thin filament.
  • Troponin changes shape and moves tropomyosin away from myosin binding sites on actin.
  • Myosin heads attach to the binding sites, initiating cross-bridge cycling and contraction.

• Additional Calcium Source:

  • Contractile cardiac cells also use extracellular calcium, which enters during the plateau phase.
  • Extracellular calcium contributes to troponin binding and increases the strength of contraction.

Relaxation

• Process:

  • Return ion concentrations to resting values.
  • Calcium pumps actively transport calcium back into the SR and out of the cell, requiring ATP.
  • Potassium and sodium pumps redistribute those ions.

• Importance of Ion Pumps:

  • Active transport is necessary because calcium needs to be moved against its concentration gradient.

Lab Worksheet and Extrinsic Control

• Lab Worksheet: The first part of the electrical activity of the heart worksheet is pages one, two, and the upper half of page three.

• Extrinsic Control: The next lecture video will be on extrinsic control of the cardiac cycle, exploring how neural and hormonal signals can modify the activity of cardiac cells.