Excitation-Contraction Coupling in Cardiac Muscle

Excitation-Contraction Coupling in Cardiac Muscle

• Cardiac muscle has a less developed sarcoplasmic reticulum compared to skeletal muscle.
• The sarcoplasmic reticulum in cardiac muscle forms a network of tubules surrounding myofibrils.
• It contains dilated terminals called cisternae that are located near the cell membrane and T tubules.
• Both the sarcoplasmic reticulum and cisternae store a high concentration of calcium ions.
• T tubules are invaginations of the cell membrane that conduct action potentials to the interior of the cell.
• They are present at the Z line of each sarcomere.
• Cardiac muscle contains one T tubule per sarcomere.
• T tubules are well developed in ventricles but poorly developed in atria.
• They form dyads with the sarcoplasmic reticulum.
• Action potentials travel through T tubules into the interior of the cardiac muscle cells.
• This triggers the release of calcium ions from the sarcoplasmic reticulum.
• Calcium ions diffuse into the myofibrils and initiate the sliding of actin and myosin filaments, leading to muscle contraction.
• Unlike skeletal muscle, cardiac muscle relies on extra calcium ions from the extracellular fluid, which enter the sarcoplasm through T tubules.
• T tubules in cardiac muscle contain mucopolysaccharides that bind calcium ions.
• This makes the strength of cardiac muscle contraction highly dependent on the extracellular calcium concentration.
• Skeletal muscle contraction is minimally affected by calcium concentration.

Cardiac Muscle Structure

• The sarcomere, the contractile unit of the myocardial cell, extends from Z line to Z line.
• It contains thick filaments (myosin) and thin filaments (actin, troponin, tropomyosin).
• Muscle contraction occurs when thin filaments slide along thick filaments, pulled by the myosin heads.

Sinoatrial (SA) Node and Pacemaker Potential

• The SA node is the heart's primary pacemaker, characterized by an unstable resting potential.
• It exhibits phase 4 depolarization, also known as automaticity.
• The AV node and His-Purkinje system are latent pacemakers that can take over if the SA node is suppressed.
• The SA node's intrinsic depolarization rate is the fastest, followed by the AV node and then the His-Purkinje system.
• This spontaneous depolarization is caused by the leakiness of the SA node fibers to calcium ions.
• The pacemaker potential gradually depolarizes from -60mV to -40mV, which is the threshold for initiating an action potential.
• This depolarization is driven by the influx of calcium ions through slow calcium channels.
• At the threshold level, fast calcium channels open, allowing a rapid influx of calcium ions.

Repolarization of the SA Node

• Repolarization is achieved by the opening of potassium gates and the efflux of potassium ions.
• Once repolarization reaches -60mV, a new pacemaker potential begins, leading to another action potential at the end of diastole.
• Three pairs of internodal tracts carry impulses from the SA node to the AV node.
• The impulse reaches the AV node within 0.03 seconds.
• There is a delay of 0.09 seconds at the AV node and an additional 0.04 seconds in the bundle of His.

Causes of AV Nodal Delay

• The transitional fibers connecting the internodal tract and the AV node are very small, slowing impulse conduction.
• Conduction velocity is also slow within the AV nodal fibers.
• Gap junctions connecting fibers in this pathway are limited.
• The bundle of His carries impulses from the AV node to its left and right branches.
• Under normal conditions, impulse transmission is unidirectional from atria to ventricles.
• A fibrous barrier between the atrial and ventricular muscles prevents retrograde conduction.
• The bundle of His descends through the ventricular septum and divides into left and right branches.
• These branches further divide into Purkinje fibers, which connect with cardiac muscle fibers.
• Impulse conduction from the bundle branches to Purkinje fibers takes 0.03 seconds.
• Purkinje fibers transmit impulses rapidly to ventricular muscle fibers.
• Impulse conduction velocity is 0.3 to 0.5 m/s in ventricular muscle fibers.
• The impulse spreads from the endocardium to the epicardium, taking about 0.03 seconds.
• The total time for impulse transmission from the bundle branches to the ventricles is 0.06 seconds.

Sympathetic and Parasympathetic Influences on SA Node

• Vagal stimulation hyperpolarizes the membrane, reducing the slope of the prepotentials and slowing down the depolarization rate.
• Acetylcholine released by vagal fibers increases potassium conductance in nodal tissue.
• This effect is mediated by M2 muscarinic receptors, which activate potassium channels.
• M2 receptor activation also lowers cAMP levels, slowing down the opening of calcium channels.
• This overall effect reduces firing rate and can even temporarily abolish spontaneous discharge.
• Sympathetic stimulation speeds up the depolarization process, accelerating the discharge rate.
• Norepinephrine released by sympathetic nerve endings binds to β1 receptors, raising intracellular cAMP levels.
• This facilitates the opening of calcium channels, accelerating the depolarization phase.

Duration of Contraction

• Atrial muscle contraction lasts 0.1 seconds, while ventricular muscle contraction lasts 0.3 seconds.

Ectopic Pacemakers

• Ectopic pacemakers occur when a site other than the SA node becomes the pacemaker.
• The AV node or Purkinje fibers can act as pacemakers, resulting in an abnormal sequence of cardiac contractions.

Shift of Pacemaker from SA Node

• A shift in pacemaker can occur if the discharge rate of another site exceeds that of the SA node.
• A blockage in the transmission of impulses from the SA node to the AV node can cause the pacemaker to shift.

Importance of AV Nodal Delay

• The AV nodal delay allows for a sequential contraction of the atria and ventricles.
• This separation in timing ensures efficient blood flow from the atria to the ventricles.

Resting Membrane Potential of Cardiac Muscle

• Cardiac muscle's resting membrane potential is between -85 to -95 mV.

Ventricular Cardiac Muscle Action Potential

• The action potential in ventricular cardiac muscle fiber cells is characterized by five phases:
  • Phase 0 (Upstroke): Rapid initial depolarization driven by sodium ion influx through voltage-gated sodium channels.
  • Phase 1 (Partial Repolarization): Rapid repolarization caused by potassium ion efflux and closure of sodium channels.
  • Phase 2 (Plateau): Prolonged plateau phase maintained by slower and prolonged calcium ion influx through voltage-gated calcium channels.
  • Phase 3 (Rapid Repolarization): Final repolarization caused by potassium ion efflux through voltage-gated potassium channels and closure of calcium channels.
  • Phase 4 (Complete Repolarization): Restoration of resting potential by the Na+/K+ pump, which moves excess sodium out and excess potassium in.

Plateau in Cardiac Muscle Action Potential

• The plateau is due to two factors:
  • Opening of slow voltage-gated calcium-sodium channels, allowing continuous influx of calcium and sodium ions.
  • Reduction in membrane permeability to potassium ions, decreasing outward potassium ion flux.
• The plateau ends when the slow calcium-sodium channels close, increasing potassium permeability and allowing rapid potassium efflux.

Sodium Ion Current and Cardiac Action Potentials

• Inward sodium ion current is responsible for the upstroke of the action potential in both the SA node and Purkinje fibers, but not the plateau phase in ventricular muscle.

Refractory Periods

• Absolute Refractory Period (ARP): During this period, no action potential can be generated, irrespective of stimulus intensity.
  • It lasts from the upstroke phase to the initial repolarization phase, covering about 0.25 to 0.30 seconds.
  • It prevents wave summation and tetanus in cardiac muscle.
• Relative Refractory Period (RRP): During this period, a very strong stimulus can generate an action potential.
  • It lasts from the end of the ARP to shortly before complete repolarization, covering about 0.05 seconds.

This quiz focuses on the mechanisms of excitation-contraction coupling specifically within cardiac muscle. Explore the role of the sarcoplasmic reticulum, T tubules, and calcium ions in initiating contraction. Understand how these structures differ between cardiac and skeletal muscle.