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Rhythmical Excitation of the Heart
The human heart has a special system for rhythmic self-excitation and repetitive contraction approximately 100,000 times each day or 3 billion times in the average human lifetime. This impressive feat is performed by a system that does the following: (1) generates electrical impulses to initiate rhythmical contraction of the heart muscle; and (2) conducts these impulses rapidly through the heart. When this system functions normally, the atria contract about one-sixth of a second ahead of ventricular contraction, which allows filling of the ventricles before they pump blood through the lungs and peripheral circulation. Another especially important feature of the system is that it allows all portions of the ventricles to contract almost simultaneously, which is essential for the most effective pressure generation in the ventricular chambers.
This rhythmical and conductive system of the heart is susceptible to damage by heart disease, especially by ischemia resulting from inadequate coronary blood flow. The effect is often a bizarre heart rhythm or an abnormal sequence of contraction of the heart chambers, and the pumping effectiveness of the heart can be affected severely, even to the extent of causing death.
Specialized Excitatory and Conductive System of the Heart
Figure 10-1 shows the specialized excitatory and conductive system of the heart that controls cardiac contractions. The figure shows the sinus node (also called sinoatrial [S-A] node), in which the normal rhythmical impulses are generated; the internodal pathways that conduct impulses from the sinus node to the atrioventricular (A-V) node; the A-V node in which impulses from the atria are delayed before passing into the ventricles; the A-V bundle, which conducts impulses from the atria into the ventricles; and the left and right bundle branches of Purkinje fibers, which conduct the cardiac impulses to all parts of the ventricles.
Sinus (Sinoatrial) Node
The sinus node is a small, flattened, ellipsoid strip of specialized cardiac muscle about 3 mm wide, 15 mm long, and 1 mm thick. It is located in the superior posterolateral wall of the right atrium immediately below and slightly lateral to the opening of the superior vena cava. The fibers of this node have almost no contractile muscle filaments and are each only 3 to 5 micrometers (μm) in diameter, in contrast to a diameter of 10 to 15 μm for the surrounding atrial muscle fibers. However, the sinus nodal fibers connect directly with the atrial muscle fibers, so that any action potential that begins in the sinus node spreads immediately into the atrial muscle wall.
Automatic Electrical Rhythmicity of the Sinus Fibers
Some cardiac fibers have the capability of self-excitation , a process that can cause automatic rhythmical discharge and contraction. This capability is especially true of the heart’s specialized conducting system, including fibers of the sinus node. For this reason, the sinus node ordinarily controls the beat rate of the entire heart, as discussed in detail later in this chapter. First, let us describe this automatic rhythmicity.
Mechanism of Sinus Nodal Rhythmicity
Figure 10-2 shows action potentials recorded from inside a sinus nodal fiber for three heartbeats and, by comparison, a single ventricular muscle fiber action potential. Note that the resting membrane potential of the sinus nodal fiber between discharges is about –55 to –60 millivolts, in comparison with –85 to –90 millivolts for the ventricular muscle fiber. The cause of this lower negativity is that the cell membranes of the sinus fibers are naturally leaky to sodium and calcium ions, and positive charges of the entering sodium and calcium ions neutralize some of the intracellular negativity.
Before we explain the rhythmicity of the sinus nodal fibers, first recall from the discussions of Chapter 5, Chapter 9 that cardiac muscle has three main types of membrane ion channels that play important roles in causing the voltage changes of the action potential. They are (1) fast sodium channels , (2) calcium channels (particularly L-type or “slow” calcium channels) , and (3) potassium channels (see Figure 9-5).
Opening of the fast sodium channels for a few 10,000ths of a second is responsible for the rapid upstroke spike of the action potential observed in ventricular muscle because of rapid influx of positive sodium ions to the interior of the fiber. Then, the plateau of the ventricular action potential is caused primarily by slower opening of the slow sodium-calcium channels, which lasts for about 0.3 second. Finally, opening of potassium channels allows for the diffusion of large amounts of positive potassium ions in the outward direction through the fiber membrane and returns the membrane potential to its resting level.
However, there is a difference in the function of these channels in the sinus nodal fiber because the resting potential is much less negative—only –55 millivolts in the nodal fiber instead of the –90 millivolts in the ventricular muscle fiber. At this level of –55 millivolts, the fast sodium channels mainly have already become inactivated, or blocked. This is because any time the membrane potential remains less negative than about –55 millivolts for more than a few milliseconds, the inactivation gates on the inside of the cell membrane that close the fast sodium channels become closed and remain so. Therefore, only the slow sodium-calcium channels can open (i.e., can become activated) and thereby cause the action potential. As a result, the atrial nodal action potential is slower to develop than the action potential of the ventricular muscle. Also, after the action potential does occur, return of the potential to its negative state occurs slowly as well, rather than the abrupt return that occurs for the ventricular fiber.
Leakiness of Sinus Nodal Fibers to Sodium and Calcium Causes Self-Excitation
Because of the high sodium ion concentration in the extracellular fluid outside the nodal fiber, as well as a moderate number of already open sodium channels, positive sodium ions from outside the fibers normally tend to leak to the inside through inward, “funny” currents. Therefore, between heartbeats, the influx of positively charged sodium ions causes a slow rise in the resting membrane potential in the positive direction. Thus, as shown in Figure 10-2 , the resting potential gradually rises and becomes less negative between each two heartbeats. When the potential reaches a threshold voltage of about –40 millivolts, the L-type calcium channels become activated, thus causing the action potential. Therefore, basically, the inherent leakiness of the sinus nodal fibers to sodium and calcium ions causes their self-excitation.
Why does this leakiness to sodium and calcium ions not cause the sinus nodal fibers to remain depolarized all the time? Two events occur during the course of the action potential to prevent such a constant state of depolarization. First, the L-type calcium channels become inactivated (i.e., they close) within about 100 to 150 milliseconds after opening; and second, at about the same time, greatly increased numbers of potassium channels open. Therefore, influx of positive calcium and sodium ions through the L-type calcium channels ceases, while at the same time large quantities of positive potassium ions diffuse out of the fiber. Both these effects reduce the intracellular potential back to its negative resting level and therefore terminate the action potential. Furthermore, the potassium channels remain open for another few tenths of a second, temporarily continuing movement of positive charges out of the cell, with resultant excess negativity inside the fiber; this process is called hyperpolarization. The hyperpolarization state initially carries the resting membrane potential down to about –55 to –60 millivolts at the termination of the action potential.
Why is this new state of hyperpolarization not maintained forever? The reason is that during the next few tenths of a second after the action potential is over, progressively more and more potassium channels close. The inward-leaking sodium (“funny” current) and calcium ions once again overbalance the outward flux of potassium ions, which causes the resting potential to drift upward once more, finally reaching the threshold level for discharge at a potential of about –40 millivolts. Then, the entire process begins again: self-excitation to cause the action potential, recovery from the action potential, hyperpolarization after the action potential is over, drift of the resting potential to threshold, and finally re-excitation to elicit another cycle. This process continues throughout a person’s life.
Internodal and Interatrial Pathways Transmit Cardiac Impulses Through the Atria
The ends of the sinus nodal fibers connect directly with the surrounding atrial muscle fibers. Therefore, action potentials originating in the sinus node travel outward into these atrial muscle fibers. In this way, the action potential spreads through the entire atrial muscle mass and, eventually, to the A-V node. The velocity of conduction in most atrial muscle is about 0.3 m/sec, but conduction is more rapid, about 1 m/sec, in several small bands of atrial fibers. One of these bands, called the anterior interatrial band (also called Bachman’s bundle ), passes through the anterior walls of the atria to the left atrium. In addition, three other small bands curve through the anterior, lateral, and posterior atrial walls and terminate in the A-V node, shown in Figure 10-1 and Figure 10-3 ; these are called, respectively, the anterior, middle, and posterior internodal pathways . The cause of more rapid velocity of conduction in these bands is the presence of specialized conduction fibers. These fibers are similar to even more rapidly conducting Purkinje fibers of the ventricles, discussed below.
The Atrioventricular Node Delays Impulse Conduction From the Atria to the Ventricles
The atrial conductive system is organized so that the cardiac impulse does not travel from the atria into the ventricles too rapidly; this delay allows time for the atria to empty their blood into the ventricles before ventricular contraction begins. It is primarily the A-V node and its adjacent conductive fibers that delay this transmission into the ventricles.
The A-V node is located in the posterior wall of the right atrium, immediately behind the tricuspid valve, as shown in Figure 10-1 . Figure 10-3 diagrams the different parts of this node, plus its connections with the entering atrial internodal pathway fibers and the exiting A-V bundle. This figure also shows the approximate intervals of time (in fractions of a second) between the initial onset of the cardiac impulse in the sinus node and its subsequent appearance in the A-V nodal system. Note that the impulse, after traveling through the internodal pathways, reaches the A-V node about 0.03 second after its origin in the sinus node. Then, there is a delay of another 0.09 second in the A-V node itself before the impulse enters the penetrating portion of the A-V bundle, where it passes into the ventricles. A final delay of another 0.04 second occurs mainly in this penetrating A-V bundle, which is composed of multiple small fascicles passing through the fibrous tissue separating the atria from the ventricles.
Thus, the total delay in the A-V nodal and A-V bundle system is about 0.13 second. This delay, in addition to the initial conduction delay of 0.03 second from the sinus node to the A-V node, makes a total delay of 0.16 second before the excitatory signal finally reaches the contracting muscle of the ventricles.
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