Electrophysiology of the Heart

Electrophysiology of the Heart

Overview of Heart Function

  • The heart operates as a muscular pump that circulates blood throughout the body.

    • Phases of Heart Function:

    • Diastole: Phase when the heart muscle relaxes and blood fills the atria and ventricles.

    • Systole: Atrial contraction phase helps to fill the ventricles with blood.

    • Ventricular Contraction: Ejects blood from the left ventricle into the aorta and from the right ventricle into the pulmonary artery.

  • Following contraction, both the atria and ventricles enter a relaxation phase and refill with blood.

  • The contractile sequence is initiated by an electrical signal called an action potential, which travels across the heart muscle cells.

Structure and Organization of Cardiac Muscle

  • Similarities to Skeletal Muscle: Cardiac muscle has a structure akin to skeletal muscle but includes key differences.

    • Presence of gap junctions: Promotes intercommunication between adjacent muscle fibers,

    • This property allows the action potential to spread quickly from one muscle fiber to neighboring fibers, enabling coordinated contractions.

  • Resting Membrane Potential: Most cardiac muscle cells maintain a stable resting membrane potential and do not form action potentials on their own.

  • Pacemaker Cells:

    • Specialized cardiac muscle cells capable of spontaneous depolarization and action potential formation, leading to heartbeat initiation.

Pacemaker Cells and Their Function

  • Located in the Sinoatrial (SA) Node at the right atrial wall, near where the venae cavae enter.

  • Functionality:

    • Pacemaker cells can autonomously initiate heartbeats without neural input.

    • Influence of Nervous System:

    • Sympathetic and parasympathetic nerves regulate the heart rate by affecting how quickly pacemaker cells reach the action potential threshold.

    • A heart can still beat after surgical transplantation due to the intrinsic functioning of pacemaker cells.

Conduction Pathway of the Heart

  • Each heartbeat starts with an action potential in pacemaker cells of the SA node.

  • The action potential spreads rapidly across right and left atria, causing simultaneous contraction of both atria.

  • Following atrial contraction, the action potential travels to the Atrioventricular (AV) Node through the specialized conduction pathway, known as the Bundle of His.

    • The AV node serves as the only conduction link between the atria and ventricles.

    • It introduces a delay between atrial and ventricular contraction.

Timing of Contraction and Relaxation

  • An action potential completes its propagation across both atria in approximately 0.1 seconds.

  • The action potential then moves through the AV node and the conduction path to reach the ventricular apex after about 0.17 seconds.

  • Final propagation through the ventricular walls triggers contraction, occurring by about 0.22 seconds post-initiation of the action potential.

  • After the ventricles contract, they undergo relaxation until the next heartbeat.

Differences in Action Potentials: Cardiac vs. Skeletal Muscle

  1. Propagation of Action Potentials:

    • In cardiac muscle, action potentials propagate from cell to cell; in skeletal muscle, they are electrically isolated.

  2. Spontaneity in Action Potentials:

    • Cardiac pacemaker cells generated spontaneous action potentials; skeletal muscle cells require motor neuron stimulation to depolarize.

  3. Duration:

    • Skeletal muscle action potential lasts 1-2 ms.

    • Cardiac action potential lasts between 100-250 ms, due to prolonged changes in membrane permeability to Na^+ and K^+.

  4. Presence of Ca Channels:

    • Cardiac muscle contains calcium channels not found in skeletal muscle, allowing calcium to mobilize, extending the action potential duration.

Mechanism of Action Potential Lengthening by Ca Channels

  • Calcium channels in cardiac muscle cells maintain a positive intracytoplasmic charge longer, delaying depolarization.

  • At the peak of the action potential, Na^+ channels become inactivated; they remain closed until the membrane potential approaches resting state, preventing overlap of action potentials.

  • This process allows for a period of relaxation and refilling of the heart between contractions.

Pacemaker Potential Initiation

  • Pacemaker cells utilize unique “funny Na+ channels”, which open spontaneously after an action potential ends.

  • As a result, intracellular Na^+ increases, and the cell gradually depolarizes toward threshold.

  • Concurrently, specialized potassium channels close, restricting K^+ efflux and making the interior less negatively charged.

  • Subsequently, calcium channels open, further increasing Ca^{2+} permeability and contributing to depolarization.

Influence of Autonomic Nervous System on Heart Rate

  • Sympathetic and Parasympathetic Regulation:

    • Sympathetic Nervous System:

    • Releases norepinephrine that stimulates beta-adrenergic receptors in pacemaker cells, boosting heart rate.

    • Parasympathetic Nervous System:

    • Releases acetylcholine acting on muscarinic cholinergic receptors in pacemaker cells to decrease contraction intervals.

  • Behavioral Influence on Heart Rate:

    • Different states (rest, activity, etc.) cause heart rates to vary significantly from 50 to 250 beats/min in a normal large dog due to the interaction of the intrinsic rate with sympathetic and parasympathetic activities.

    • The heart maintains an intrinsic rate of approximately 140 beats/min in the absence of neural influences.

Effects of Sympathetic vs. Parasympathetic Activation on Cardiac Function

  • Sympathetic Activation:

    • Increases heart rate via effects on SA node, enhances conduction velocity and shortens AV delay, and decreases refractory period for quicker, stronger heart contractions.

  • Parasympathetic Activation:

    • Decreases heart rate via effects on SA node, slows conduction at the AV node, increases ventricular cell refractory period, resulting in weaker contractions.

    • It can inhibit norepinephrine release at sympathetic terminals, further reducing heart contractility.