Cardiac Pacemaker Cells

Action potentials are considerably different between cardiac pacemaker cells and cardiac muscle cells. While Na⁺ and K⁺ play essential roles, Ca²⁺ is also critical for both types of cells. Unlike skeletal muscles and neurons, cardiac pacemaker cells do not have a stable resting potential. Pacemaker cells contain a series of Na⁺ channels that allow a normal and slow influx of Na⁺ 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 Na⁺ ions creates a spontaneous depolarization and brings the cell to threshold. At this point voltage-gated Ca²⁺ channels open and Ca²⁺ influx rapidly causes depolarization until it reaches a value of approximately +5 mV. At this point, the Ca²⁺ channels close and voltage-gated K⁺ channels open, allowing K⁺ efflux which causes repolarization. When the membrane potential reaches approximately −60 mV, the K⁺ channels close and voltage-gated slow Na⁺ channels open, and the drift phase begins again. This phenomenon explains the autorhythmicity properties of cardiac muscle (Figure 34.1).

Cardiac Muscle Cells

The cardiac muscle cells have a much different action potential. In this case, there is a rapid depolarization, followed by a brief repolarization and plateau phases, ending with a full 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, 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. Since the cells are connected by gap junctions, the action potential spreads from cell to cell by ion flow through the gap junctions. When stimulated by positive charge passing from neighboring cells, voltage-gated fast Na⁺ 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 Na⁺ channels close. The rapid depolarization period typically lasts 3–5 ms. Depolarization is followed by a brief repolarization phase due to the opening of some K⁺ channels which allows for K⁺ efflux. This 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 Ca²⁺ channels which allows Ca²⁺ influx, while open K⁺ channels allow K⁺ efflux. The relatively long plateau phase lasts approximately 175 ms. Once the membrane potential reaches approximately zero, the Ca²⁺ channels close and more K⁺ channels open, allowing more K⁺ efflux. 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 (Figure 34.2).

Cardiac muscle cells undergo twitch-type contractions with long refractory periods followed by brief relaxation periods. The relaxation is essential so the heart can fill with blood for the next cycle. The absolute refractory period for cardiac contractile muscle lasts approximately 200 ms, and the relative refractory period lasts approximately 50 ms, for a total of 250 ms. The refractory period is very long to prevent the possibility of tetany, a condition in which muscle remains involuntarily contracted. In the heart, tetany is not compatible with life, since it would prevent the heart from pumping blood.

Calcium Ions

Calcium ions play two critical roles in the physiology of cardiac muscle. Ca²⁺ influx accounts for the prolonged plateau phase and absolute refractory period that enable cardiac muscle to function properly. Calcium ions also combine with the regulatory protein troponin in the troponin-tropomyosin complex; this complex removes the inhibition that prevents the heads of the myosin molecules from forming cross bridges with the active sites on actin that provide the power stroke of contraction. Approximately 20 percent of the Ca²⁺ required for contraction is supplied by Ca²⁺ influx during the plateau phase. The remaining Ca²⁺ for contraction is released from storage in the sarcoplasmic reticulum.

Adapted from Anatomy & Physiology by Lindsay M. Biga et al, shared under a Creative Commons Attribution-ShareAlike 4.0 International License, chapter 19