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Summary Cardiovascular System Physiology
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A summarised version of Guyton's physiology for Medical, Dental and Nursing Students. Hope you all find it useful.
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19. Physiology of cardiac muscle. Action potentials in cardiac muscle.Contraction of cardiac muscle. Specialized excitatory and conductive system of
the heart. Ionic basis of automaticity.
Physiology of cardiac muscle
● The heart is composed of:
○ atrial muscle
○ ventricular muscle
■ The atrial and ventricular muscles contract in much the same way
as skeletal muscle
■ The duration of contraction is much longer
● Specialized excitatory and conductive fiber
○ generate rhythmical electrical impulses to cause rhythmical contraction of
the heart muscle
○ conduct these impulses rapidly through the heart
● Cardiac muscle works as a functional syncytium which means that gap junctions
allow action potentials to move from one cell to the next.
● The heart is composed of 2 separate functional syncytiums, the atrial and the
ventricular syncytium.
○ They are separated by fibrous tissue surrounding the valvular rings
○ Action potentials can be conducted from the atrial into the ventricular
syncytium by the A-V bundle - part of the specialized conduction system.
● All or nothing principle
○ If the strength of the stimulus is below the threshold , it will be ineffective.
○ If the stimulus strength reaches the threshold, heart will respond with a
maximum excitation and contraction for the moment.
Action Potentials in the Cardiac Muscle
● The resting membrane potential of cardiac muscle is about 85 to 95 millivolts,
and the action potential is 105 millivolts.
● In cardiac muscle, the fast sodium channels are open at the initiation of the
action potential, but cardiac muscle has unique slow calcium channels, or
calcium-sodium channels. Calcium and sodium ions flow through the slow
channels into the cell after the initial spike of the action potential, and they
maintain the plateau. Calcium that enters the cell through these channels also
promotes cardiac muscle contraction.
● The decrease in cardiac potassium permeability also prevents return of the
membrane potential in cardiac muscle. When the slow calcium-sodium channels
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