Physiology of Cardiac Conduction
A healthy heart is capable of altering cardiac output to meet the requirements of the body. The normal adult resting heart rate is between 60-100 beats per minute (bpm).
An individual may have a calm recumbent rate of 60 bpm. That rate may increase to 85 bpm when changing position to stand. When stressed or exercising the same heart may increase to a rate of 140 bpm or more. The change in rate (chronotropism), contractility (inotropism), and conduction (dromotropism) are regulated by the autonomic nervous system.
The supraventricular heart is innervated by both sympathetic and parasympathetic (vagal) fibers of the autonomic nervous system. The ventricular tissues are primarily modulated by sympathetic influence. Sympathetic stimulation of cardiac β1/β2 receptors by the neurotransmitter norepinehrine and circulating adrenal epinephrine increase cardiac chronotropy, inotropy and dromotropy. Parasympathetic (vagal) stimulation of muscarinic M2-receptors by the neurotransmitter acetlycholine (ACh) has an opposite effect.
The Sino-atrial node (SA) sets the heart rate by initiating each normal heart beat. The SA node is supraventricular and is sensitive to parasympathetic and sympathetic influence. Structurally the SA node is a heterogeneous collection of interwoven connective tissue, fibroblasts and roughly spindle shaped cardiomyocytes that "contain only a few poorly organised myofilaments".• It is believed that initial SA node electrical activity propagates from a small group of cells near the center of the SA node.
The SA node, AtrioVentricular node (AV) and the Bundle of His/Purkinje fibers are groups of specialized pacemaker cardiomyocytes that have the ability to self-depolarize. Of the three groups, the SA cardiomyocytes have the shortest time period between self-depolarizations. Because the SA node self-depolarizes faster then the other two, it sets the heart rate. If the SA node fails to initiate AV depolarization, the AV node takes over the role of ventricular pacer. The Bundle of His/Purkinje fibers are the slowest self-depolarizing pacemaker cells, they become the ventricular pacemaker of last resort.
Pacemakers depolarize in a series of electrical phases. Each phase reflects the staged movement of ions (principally Na+, Ca++ and K+) into or out of the pacemaker cell. The ions move through ion channels that are opened or closed depending upon the phase of the depolarization or repolarization cycle. When a channel is opened, ions specific to that ion channel move from high concentration to low concentration. Closure of ion channels decrease ion movement. As ions flow through open channels, they alter the distribution of charge across the membrane.
When a SA pacer cell depolarizes, the voltage change generates an action potential that depolarizes connected cells in a chain reaction that spreads throughout the cardiac conduction system, eventually causing atrial and then ventricular contraction. Retrograde conduction does not normally occur because a depolarized cell requires time (refractory period) to redistribute ions (repolarize) before it can be depolarized.
Cardiomyocytes, like those in the ventricles, work to acheive a stable resting hyperpolarized (-) internal charge known as Phase 4. They do this by pumping Na+and Ca++ ions out of the cytosol and K+ in. These cells maintain a relatively negative internal charge until they are depolarized by an external stimulus.
When the stimulus is sufficient:
In contrast to ordinary cardiomyocytes, pacemaker cells do not sustain a stable Phase 4 (-) internal charge. Instead, when a pacemaker cell reaches the hyperpolarized voltage:
Parasympathetic acetylcholine causes muscarinic receptors to