Membrane potential in cardiac muscle
Resting membrane potential in cardiac muscle
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Conduction system = - 90 to -100 mV
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Ventricle muscle = -100 to -105 mV
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S.A. node = - 50 to - 55 mV
Action potential in cardiac muscle
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Cardiac muscle has an inherent property of generating its own action potentials rhythmically, independent of nerve stimulation. This occurs in the peacemaker cells of the S.A. node, which depolarises faster than any other parts of the heart.
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The onset of action potential in cardiac muscle is slower but prolonged than skeletal muscle which lasts for 150msec. in atria and 300 m.sec. in ventricle. In cardiac muscle, repolarisation does not occur immediately after depolarisation The positivity generated as the spike potential by the depolarisation remains as a plateau near the peak. This plateau lasts for a few-hundred m.sec prolongs the contraction of the cardiac muscle.
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The reason for the prolonged action potential in cardiac muscle cells is due to the presence of two separate channel systems
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Activation of the fast Na channels causes the spike potential of the action potential, whereas the slow channel prolongs the passage of Ca ++ and Na+ into the interior of the cell, thus establishes the plateau in the action potential.
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The inflow of Ca++ in to the cardiac muscle cells decreases K+ permeability by about 5 fold. This delays the K+ permeability to outside which in turn delays the re-polarisation process of the action potential in cardiac muscle. This prolonged action potential (250 – 300 m.sec) provides longer contraction period in the cardiac muscle cells than the skeletal muscles. Hence cardiac muscle is not functionally tetanized.
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Last modified: Saturday, 3 December 2011, 5:42 AM