Sino atrial node
The sinus node (also called sinoatrial node) is a small, flattened, ellipsoid strip of specialized cardiac muscle about 3 millimeters wide, 15 millimeters long, and 1 millimeter thick. It is located in the superior posterolateral wall of the right atrium immediately below and slightly lateral to the opening of the superior vena cava. The fibers of this node have almost no contractile muscle filaments and are each only 3 to 5 micrometers in diameter, in contrast to a diameter of 10 to 15 micrometers for the surrounding atrial muscle fibers
Automaticity
the "resting membrane potential" of the sinus nodal fiber between discharges has a negativity of about -55 to -60 millivolts, in comparison with -85 to -90 millivolts for the ventricular muscle fiber. The cause of this lesser negativity is that the cell membranes of the sinus fibers are naturally leaky to sodium and calcium ions, and positive charges of the entering sodium and calcium ions neutralize some of the intracellular negativity
cardiac muscle has three types of membrane ion channels (1) fast sodium channels, (2) slow sodium-calcium channels, and (3) potassium channels.
"Plateau" of the ventricular action potential is caused by slower opening of the slow sodium-calcium channels.
Finally, opening of potassium channels allows diffusion of large amounts of positive potassium ions in the outward direction through the fiber membrane and returns the membrane potential to its resting level.
Self-Excitation of Sinus Nodal Fibers
Because of the high sodium ion concentration in the extracellular fluid outside the nodal fiber, as well as a moderate number of already open sodium channels, positive sodium ions from outside the fibers normally tend to leak inside. Thus the "resting" potential gradually rises and becomes less negative between each two heartbeats.
When the potential reaches a threshold voltage of about -40 millivolts, the sodium-calcium channels become "activated," thus causing the action potential. Therefore, basically, the inherent leakiness of the sinus nodal fibers to sodium and calcium ions causes their self-excitation.
Repolarisation and Hyperpolarisation
First, the socdium-calcium channels become inactivated (i.e., they close) within about 100 to 150 milliseconds after opening, and second, at about the same time, greatly increased numbers of potassium channels open.
Furthermore, the potassium channels remain open for another few tenths of seconds, with resultant excess negativity inside the fiber; this is called hyperpolarization
Pathways
Anterior interatrial band, passes through the anterior walls of the atria to the left atrium.
The anterior, middle, and posterior internodal pathways are connected to the AV node.
The slow conduction in the transitional, nodal, and penetrating A-V bundle fibers is caused mainly by diminished numbers of gap junctions.
Purkinje fibers is believed to be caused by a very high level of permeability of the gap junctions, so conduction is 6 times faster than ventricular fibers.
The cardiac muscle wraps around the heart in a double spiral, with fibrous septa between the spiraling layers; therefore, the cardiac impulse does not necessarily travel directly outward toward the surface of the heart but instead angulates toward the surface along the directions of the spirals. Because of this, transmission from the endocardial surface to the epicardial surface of the ventricle requires as much as another 0.03 second, approximately equal to the time required for transmission through the entire ventricular portion of the Purkinje system. Thus, the total time for transmission of the cardiac impulse from the initial bundle branches to the last of the ventricular muscle fibers in the normal heart is about 0.06 second.
Purkinje System in Causing Synchronous Contraction of the Ventricular Muscle.
Nerve supply of heart
The parasympathetic nerves (the vagi) are distributed mainly to the S-A and A-V nodes.
The sympathetic nerves are distributed to all parts of the heart (ventricular muscle).
Effect of Parasympathetic stimulation
First, it decreases the rate of rhythm of the sinus node.
Second, it decreases the excitability of the A-V junctional fibers(ventricular escape).
Mechanism
Rapid leakage of potassium out of the conductive fibers -> increased negativity inside the fibers -> hyperpolarization -> less excitable -> inward sodium and calcium leakage requires much longer to reach the threshold potential for excitation.
Effect of Sympathetic Stimulation on Cardiac Rhythm and Conduction
First, it increases the rate of sinus nodal discharge.
Second, it increases the rate of conduction and level of excitability.
Third, it increases greatly the force of contraction of all the cardiac musculature.
Mechanism
Sympathetic stimulation - noradrenaline - beta 1 adrenergic receptors - Effect of Sympathetic Stimulation on Cardiac Rhythm and Conduction - increases the permeability of the fiber membrane to sodium and calcium ions.
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