Figure 18-1 illustrates the measurement of the RMP through the placement of one microelectrode inside the cell and another outside the cell. A wire from each microelectrode is connected to a voltmeter, which measures the electrical potential difference across the membrane at about −90 mV.

Figure 18-1 Measurement of the RMP. The recording electrode is inside and the reference electrode is outside of the cell, measuring a potential difference (voltage) of −90 mV.

The main ions involved in generating the RMP are sodium (Na⁺), potassium (K⁺), calcium (Ca⁺⁺), and large protein anions (negatively charged ions). As with all other cells in the body, K⁺ ion concentration inside the cardiac cell is much greater than outside the cell (about 151 mEq/L vs. 4 mEq/L).² The opposite is true for Na⁺ and Ca⁺⁺ ions; [Na⁺] is about 144 mEq/L outside the cell and about 7 mEq/L inside the cell, and [Ca⁺⁺] is 5 mEq/L outside the cell and less than 1 mEq/L inside the cell.

The resting cardiac cell membrane is fairly permeable to K⁺ ions but only slightly permeable to Na⁺ and Ca⁺⁺ ions. The permeability of the membrane to K⁺ allows potassium to diffuse out of the cell, down its high concentration gradient (Figure 18-2). Large, negatively charged protein ions and molecules cannot diffuse outward with K⁺ because the cell membrane is completely impermeable to them. Thus, as potassium leaves, an increasingly negative intracellular charge develops; this represents an electrostatic force that slows and eventually stops the outward diffusion of K⁺. The equilibrium between the outward diffusion force of K⁺ and the cell’s electrostatic attractive force is largely responsible for the cardiac cell RMP, altered only slightly by Na⁺ ion diffusion dynamics, as explained next.

Figure 18-2 Potassium equilibrium potential. The outward diffusion force of potassium is in equilibrium with the inward electrostatic attraction exerted by nondiffusible protein anions.

Although the cardiac cell membrane is highly impermeable to Na⁺, small amounts of this ion diffuse through leak channels into the cell because of its extremely high diffusion gradient (Figure 18-3).¹ This diffusion alters the potassium-driven membrane potential, causing it to be slightly less negative (closer to 0) than it would be otherwise. The Na⁺-K⁺ exchange pump in the cell membrane counteracts Na⁺ leakage into the cell by actively pumping it out while pumping potassium back in. Three Na⁺ ions are pumped out of the cell for every two K⁺ ions pumped back in, adding to the electronegativity of the intracellular environment (see Figure 18-3). In the end, the RMP is the result of the complex interactions between (1) chemical diffusion forces, (2) electrostatic attractive forces, and (3) the Na⁺-K⁺ exchange pump.

Figure 18-3 Generation of the RMP. The potassium equilibrium potential is altered by a small influx of Na⁺ ions through leak channels and the unequal pumping of Na⁺ and K⁺ ions.

CONCEPT QUESTION 18-1

Explain how high extracellular K⁺ concentration affects the RMP and heart muscle excitability.

Ion Channels and Gates

Sodium and Potassium Channels

The permeability of the myocardial cell membrane to Na⁺ and K⁺ ions is mainly controlled by voltage-gated ion channels in the membrane (Figure 18-4). These channels are formed by large protein molecules and are specific for each ion. Gatelike structures called gating proteins control these channels. Gating proteins are voltage sensitive, opening and closing in response to changes in the membrane potential. Changes in membrane potential alter the shape of the protein molecule, which opens or closes the channel gates² (i.e., the membrane’s permeability to K⁺ and Na⁺ is voltage dependent).

As shown in Figure 18-4, K⁺ and Na⁺ channel activation gates are closed at the cardiac cell’s RMP of −90 mV. Although both of these channels are closed, some K⁺ and Na⁺ ions diffuse across the membrane through leak channels because of their high diffusion gradients.

Calcium Channels

In addition to the Na⁺ and K⁺ channels, cardiac fibers have numerous calcium ion channels. These channels are similar to Na⁺ channels in that they have activation and inactivation gates. However, calcium channel gates respond 10 to 20 times more slowly than sodium channel gates to changes in membrane potential.¹ Calcium channels are therefore called slow channels, whereas sodium channels are called fast channels. Although they mainly transmit Ca⁺⁺ ions, calcium channels also permit the passage of some Na⁺ ions. The responses of sodium, potassium, and calcium channels to changes in their membrane potentials bring about an event known as the action potential. The action potential is an electrical event ultimately leading to the mechanical event of muscle fiber contraction.

Action Potential

Cardiac muscle fiber depolarization occurs when the fiber RMP of −90 mV abruptly changes to 0 mV. Repolarization occurs when the RMP is again established at −90 mV. The action potential is a real-time recording of the moment-to-moment changes in the membrane potential as the cardiac fiber depolarizes and repolarizes. This recording plots voltage against time on specially designed graph paper or a monitoring screen. Figure 18-5 illustrates the action potential of a single ventricular muscle fiber. The different phases of the action potential (0 to 4) are created by Na⁺, K⁺, and Ca⁺⁺ movement in and out of the cell.

Depolarization: Phase 0

The action potential of a ventricular muscle fiber (see Figure 18-5) is normally initiated by an electrical impulse originating from the sinoatrial (SA) node in the right atrium. The impulse changes the RMP to a less negative value that begins to open some of the fast sodium channel activation gates. Increased influx of sodium makes the fiber’s membrane potential even less negative, causing more activation gates to swing open. When the membrane potential reaches a critical level called the threshold potential (TP), all activation gates open instantaneously; this brings about an explosive influx of Na⁺, which instantaneously depolarizes the cell membrane and generates the upstroke (phase 0) of the action potential (see Figure 18-5).

Two forces cause Na⁺ ions to enter the cell during phase 0 of the action potential: (1) an electrostatic attraction created by the negative intracellular environment and (2) a high chemical diffusion force favoring movement of sodium into the cell (Figure 18-6, A). When the membrane potential reaches 0 mV, Na⁺

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