19.2 Cardiac muscle and electrical activity  (Page 5/40)

Membrane potentials and ion movement in cardiac conductive cells

Action potentials are considerably different between cardiac conductive cells and cardiac contractive cells. While Na ⁺ and K ⁺ play essential roles, Ca ²⁺ is also critical for both types of cells. Unlike skeletal muscles and neurons, cardiac conductive cells do not have a stable resting potential. Conductive cells contain a series of sodium ion channels that allow a normal and slow influx of sodium ions that causes the membrane potential to rise slowly from an initial value of −60 mV up to about –40 mV. The resulting movement of sodium ions creates spontaneous depolarization    (or prepotential depolarization    ). At this point, calcium ion channels open and Ca ²⁺ enters the cell, further depolarizing it at a more rapid rate until it reaches a value of approximately +5 mV. At this point, the calcium ion channels close and K ⁺ channels open, allowing outflux of K ⁺ and resulting in repolarization. When the membrane potential reaches approximately −60 mV, the K ⁺ channels close and Na ⁺ channels open, and the prepotential phase begins again. This phenomenon explains the autorhythmicity properties of cardiac muscle ( [link] ).

Action potential at the sa node

Membrane potentials and ion movement in cardiac contractile cells

There is a distinctly different electrical pattern involving the contractile cells. In this case, there is a rapid depolarization, followed by a plateau phase and then repolarization. This phenomenon accounts for the long refractory periods required for the cardiac muscle cells to pump blood effectively before they are capable of firing for a second time. These cardiac myocytes normally do not initiate their own electrical potential, although they are capable of doing so, but rather wait for an impulse to reach them.

Contractile cells demonstrate a much more stable resting phase than conductive cells at approximately −80 mV for cells in the atria and −90 mV for cells in the ventricles. Despite this initial difference, the other components of their action potentials are virtually identical. In both cases, when stimulated by an action potential, voltage-gated channels rapidly open, beginning the positive-feedback mechanism of depolarization. This rapid influx of positively charged ions raises the membrane potential to approximately +30 mV, at which point the sodium channels close. The rapid depolarization period typically lasts 3–5 ms. Depolarization is followed by the plateau phase, in which membrane potential declines relatively slowly. This is due in large part to the opening of the slow Ca ²⁺ channels, allowing Ca ²⁺ to enter the cell while few K ⁺ channels are open, allowing K ⁺ to exit the cell. The relatively long plateau phase lasts approximately 175 ms. Once the membrane potential reaches approximately zero, the Ca ²⁺ channels close and K ⁺ channels open, allowing K ⁺ to exit the cell. The repolarization lasts approximately 75 ms. At this point, membrane potential drops until it reaches resting levels once more and the cycle repeats. The entire event lasts between 250 and 300 ms ( [link] ).