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
Propagation of Action Potentials:
In cardiac muscle, action potentials propagate from cell to cell; in skeletal muscle, they are electrically isolated.
Spontaneity in Action Potentials:
Cardiac pacemaker cells generated spontaneous action potentials; skeletal muscle cells require motor neuron stimulation to depolarize.
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^+.
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.