Fig. 16.1 demonstrates the action potentials observed in various cardiac cells. The heart experiences two main types of action potentials. The first type, known as the fast response, is found in normal atrial and ventricular myocytes as well as in the specialized conducting fibers (Purkinje fibers of the heart). This type consists of five phases. Phase 0 represents the rapid upstroke of the action potential, followed by a brief period of partial early repolarization (phase 1). This is succeeded by a plateau phase (phase 2) that lasts for approximately 0.1 to 0.2 second. Phase 3 represents the repolarization of the membrane until the resting state of polarization (phase 4) is reached. Final repolarization (phase 3) occurs at a slower pace than depolarization (phase 0). The second type of action potential, the slow response, occurs in the sinoatrial (SA) node (the natural pacemaker region of the heart) and the atrioventricular (AV) node (the specialized tissue responsible for conducting the cardiac impulse from the atria to the ventricles). Unlike fast-response cells, slow-response cells lack the early repolarization phase (phase 1).

There are several differences between the electrical properties of fast-response and slow-response cells. The resting membrane potential (phase 4) of fast-response cells is considerably more negative than that of slow-response cells. Additionally, the fast-response cells exhibit a steeper slope of the upstroke (phase 0), greater action potential amplitude, and a larger overshoot (membrane voltage positive to 0 mV) compared to slow-response cells. These differences in action potential characteristics and steepness play a crucial role in determining the propagation velocity along the myocardial fibers. Slow-response cardiac tissue experiences slower action potential propagation and a higher likelihood of conduction block compared to fast-response cardiac tissue. These factors contribute to an increased risk of rhythm disturbances.

The action potential initiates the contraction of the myocyte. Fig. 16.2 illustrates the relationship between the action potential and contraction of a cardiac myocyte. Rapid depolarization (phase 0) precedes cell shortening, and repolarization is completed just before peak shortening. The relaxation of the muscle primarily occurs during phase 4 of the action potential. The duration of contraction typically mirrors the duration of the action potential.

The various phases of the cardiac action potential correspond to changes in cell membrane permeability, primarily involving Na+, K+, and Ca++ ions. Alterations in cell membrane permeability modify the movement rate of these ions across the membrane, subsequently influencing the membrane voltage (Vm). These changes in permeability are facilitated by the opening and closing of ion channels specific to each ion.

Similar to other cells in the body, the concentration of K+ inside a cardiac muscle cell (intracellular [K+]) is higher than the concentration outside the cell (extracellular [K+]). The concentration gradient is reversed for Na+ and Ca++. Estimates of the extracellular and intracellular concentrations of Na+, K+, and Ca++ and the Nernst equilibrium potentials are provided in Table 16.1.

At the resting cell membrane potential, there is relatively high permeability for K+ and much lower permeability for Na+ and Ca++. Due to the existing chemical gradient for K+ and Vm, K+ tends to diffuse from the inside to the outside of the cell. During phase 4 (resting membrane potential), any diffusion of K+ primarily occurs through four specific potassium channels. Multiple types of potassium channels exist in cardiac cell membranes, some of which are regulated by Vm, while others are controlled by chemical signals (e.g., extracellular acetylcholine concentration). One specific voltage-regulated channel is responsible for conducting the inward rectifying K+ current (iK1), which will be further discussed later.
Fig. 16.1 illustrates action potentials found in different cardiac cells. Two main types of action potentials occur in the heart and are depicted. One type, the fast response, occurs in normal atrial and ventricular myocytes and in the specialized conducting fibers (Purkinje fibers of the heart) and is divided into five phases. The rapid upstroke of the action potential is designated phase 0. The upstroke is followed by a brief period of partial, early repolarization (phase 1) and then by a plateau (phase 2) that persists for approximately 0.1 to 0.2 second. The membrane then repolarizes (phase 3) until the resting state of polarization (phase 4) is again attained. Final repolarization (phase 3) develops more slowly than depolarization (phase 0). The other type of action potential, the slow response, occurs in the sinoatrial (SA) node, which is the natural pacemaker region of the heart, and in the atrioventricular (AV) node, which is the specialized tissue that conducts the cardiac impulse from the atria to the ventricles. The slow-response cells lack the early repolarization phase (phase 1).
Other differences between the electrical properties of the fast-response and slow-response cells include the following: The resting membrane potential (phase 4) of the fast-response cells is considerably more negative than that of the slow-response cells. Moreover, the slope of the upstroke (phase 0), the amplitude of the action potential, and the overshoot (membrane voltage positive to 0 mV) are greater in the fast-response cells than in the slow-response cells. The action potential amplitude and the steepness of the upstroke are important determinants of propagation velocity along the myocardial fibers. In slow-response cardiac tissue, the action potential is propagated more slowly and conduction is more likely to be blocked than in fast-response cardiac tissue. Slow conduction and a tendency toward conduction block increase the likelihood of some rhythm disturbances (see the section “
The action potential initiates contraction of the myocyte. The relationship between the action potential and contraction of a cardiac myocyte is shown in
Fig. 16.2 . Rapid depolarization (phase 0) precedes cell shortening, and completion of repolarization occurs just before peak shortening. Relaxation of the muscle takes place mainly during phase 4 of the action potential. The duration of contraction usually parallels the duration of the action potential.
The various phases of the cardiac action potential are associated with changes in cell membrane permeability, mainly by Na+, K+, and Ca++ ions. Changes in cell membrane permeability alter the rate of movement of these ions across the membrane and thereby change the membrane voltage (Vm). These changes in permeability are accomplished by the opening and closing of ion channels that are specific for individual ions (see
As with all other cells in the body, the concentration of K+ inside a cardiac muscle cell (intracellular [K+]) exceeds the concentration outside the cell (extracellular [K+]). The concentration gradient is reversed for Na+ and Ca++ . Estimates of the extracellular and intracellular concentrations of Na+, K+, and Ca++ and the Nernst equilibrium potentials (see
Eq. 1.5b ) for these ions are compiled in
Table 16.1
The resting cell membrane has a relatively high permeability for K+; permeability for Na+ and Ca++ is much less. Because of the existing chemical gradient for K+ and Vm, K+ tends to diffuse from the inside to the outside of the cell.
3 Any diffusion of K+ that occurs at the resting membrane potential (i.e., during phase 4) takes place mainly through 4 specific potassium channels. Several types of potassium channels exist in cardiac cell membranes. Opening and –120
ERP RRP closing of some of these channels are regulated by Vm, whereas others are controlled by a chemical signal (e.g., the extracellular acetylcholine concentration). The specific 4 is a voltage-regulated channel that conducts the inward rectifying K+ current (iK1), which is discussed in more detail later. For now, it is necessary only to know how this current is established.