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Source: Adapted from A.M. Katz (ed.), Physiology of the Heart, 3rd Ed., 2001.

Fig. 6. Typical cardiac action potentials (slow on top and fast below). The resting membrane potential, threshold potential, and phases of depolarization (0-4) are shown.

Fig. 8. Ion flow during the phases of a cardiac action potential.

Fig. 7. A cardiac cell at rest. The intracellular space is dominated by potassium ions; the extracellular space has a higher concentration of sodium and calcium ions.

Fig. 8. Ion flow during the phases of a cardiac action potential.

with the interventricular septum. The skeleton can be thought to: (1) form the foundation to which the valves attach; (2) prevent overstretching of the valves; (3) serve as points of insertion for cardiac muscle bundles; and (4) act as an electrical insulator that prevents the direct spread of action potentials from the atria to the ventricles. Refer to Chapter 4 for further details on the cardiac skeleton.

A healthy myocardial cell has a resting membrane potential of approx -90 mV. The resting potential is described by the Goldman-Hodgkin-Katz equation, which takes into account the permeabilities Ps as well as the intracellular and extracellular concentrations of ions [X], where X is the ion.

In the cardiac myocyte, the membrane potential is dominated by the K+ equilibrium potential. An action potential is initiated when this resting potential becomes shifted toward a more positive value of approx -60 to -70 mV (Fig. 6). At this threshold potential, the voltage-gated Na+ channels of the cell open and begin a cascade of events involving other ion channels. In artificial electrical stimulation, this shift of the resting potential and subsequent depolarization is produced by the pacing system. The typical ion concentrations for a mammalian cardiac myocyte are summarized in Table 1 and graphically depicted in Fig. 7.

When a myocyte is brought to a threshold potential, normally via a neighboring cell, voltage-gated fast Na+ channels actively open (activation gates); the permeability of the sarco-lemma (plasma membrane) to sodium ions PNa+ then increases. Because the cytosol is electrically more negative than extracellular fluid and the Na+ concentration is higher in the extracellular fluid, Na+ rapidly crosses the cell membrane. Importantly, within a few milliseconds, these fast Na+ channels automatically inactivate (inactivation gates), and PNa+ decreases.

The membrane depolarization caused by the activation of the Na+ induces the opening of the voltage-gated slow Ca2+ channels located within both the sarcolemma and sarcoplasmic reticulum (internal storage site for Ca2+) membranes. Thus, there is an increase in the Ca2+ permeability PCa2+, which allows the concentration to dramatically increase intracellularly (Fig. 8). At the same time, the membrane permeability to K+ ions decreases because of closing of K+ channels. For approx 200250 ms, the membrane potential stays close to 0 mV as a small outflow of K+just balances the inflow of Ca2+. After this fairly long delay, voltage-gated K+ channels open, and repolarization is initiated. The opening of these K+ channels (increased membrane permeability) allows K+ to diffuse out of the cell because of their concentration gradient. At this same time, Ca2+ channels begin to close, and net charge movement is dominated by the outward flux of the positively charged K+, restoring the negative resting membrane potential (-90 mV; Figs. 8 and 9).

As mentioned, not all action potentials that are elicited in the cardiac myocardium have the same time-courses; slow-and fast-response cells have different shape action potentials with different electrical properties in each phase. Recall that

Fig. 9. A typical action potential of a ventricular myocyte and the underlying ion currents. The resting membrane potential is approx -90 mV (phase 4). The rapid depolarization is primarily because of the voltage-gated Na+ current (phase 0), which results in a relatively sharp peak (phase 1) and transitions into the plateau (phase 2) until repolarization (phase 3). Also indicated are the refractory period and the timing of the ventricular contraction. Modified from G.J. Tortora and S.R. Grabowski (eds.), Principles of Anatomy and Physiology, 9th Ed., 2000.

Fig. 9. A typical action potential of a ventricular myocyte and the underlying ion currents. The resting membrane potential is approx -90 mV (phase 4). The rapid depolarization is primarily because of the voltage-gated Na+ current (phase 0), which results in a relatively sharp peak (phase 1) and transitions into the plateau (phase 2) until repolarization (phase 3). Also indicated are the refractory period and the timing of the ventricular contraction. Modified from G.J. Tortora and S.R. Grabowski (eds.), Principles of Anatomy and Physiology, 9th Ed., 2000.

the pacemaker cells (slow-response type) have the ability to depolarize spontaneously until they elicit action potentials.

Action potentials from such cells are also characterized by a slower initial depolarization phase, a lower amplitude overshoot, a shorter and less-stable plateau phase, and a repolar-ization to an unstable, slowly depolarizing resting potential (Fig. 10). In the pacemaker cells, at least three mechanisms are thought to underlie the slow depolarization that occurs during phase 4 (diastolic interval): (1) a progressive decrease in PK+; (2) a slight increase in PNa+; and (3) an increase in PCa2+.

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Essentials of Human Physiology

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