P4.20.6^20.6. Electrical Properties^689^693^,,^33085^33256%
20.6
Electrical Properties
    LEARNING OUTCOMES

    After reading this section, you should be able to:

  1. Summarize the characteristics of action potentials in cardiac muscle.
  2. Explain what is meant by the autorhythmicity of cardiac muscle and relate it to the pacemaker potential.
  3. Explain the importance of a long refractory period in cardiac muscle.
  4. Describe the waves and intervals of an electrocardiogram.

Cardiac muscle cells—like other electrically excitable cells, such as neurons and skeletal muscle fibers—have a resting membrane potential (RMP). The RMP depends on a low permeability of the plasma membrane to Na+ and Ca2+ and a higher permeability to K+. When neurons, skeletal muscle fibers, and cardiac muscle cells are depolarized to their threshold level, action potentials result (see Chapter 11).

Action Potentials

Like action potentials in skeletal muscle, those in cardiac muscle exhibit depolarization followed by repolarization of the RMP. Alterations in membrane channels are responsible for the changes in the permeability of the plasma membrane that produce the action potentials. Action potentials in cardiac muscle last longer than those in skeletal muscle, and the membrane channels differ somewhat from those in skeletal muscle. In contrast to action potentials in skeletal muscle, which take less than 2 milliseconds (ms) to complete, action potentials in cardiac muscle take approximately 200–500 ms to complete (figure 20.14).

 

FUNDAMENTAL Figure

PROCESS FIGURE 20.14
Comparison of Action Potentials in Skeletal and Cardiac Muscle(a) An action potential in skeletal muscle consists of depolarization and repolarization phases. (b) An action potential in cardiac muscle consists of depolarization, early repolarization, plateau, and final repolarization phases. Cardiac muscle does not repolarize as rapidly as skeletal muscle (indicated by the break in the curve) because of the plateau phase.

In cardiac muscle, the action potential consists of a rapid depolarization phase, followed by a rapid but partial early repolarization phase. Then a prolonged period of slow repolarization occurs, called the plateau phase. At the end of the plateau phase, a more rapid final repolarization phase takes place, during which the membrane potential returns to its resting level (figure 20.14).

Depolarization is the result of changes in membrane permeability to Na+, K+, and Ca2+. Membrane channels, called voltage-gated Na+ channels, open, bringing about the depolarization phase of the action potential. As the voltage-gated Na+ channels open, Na+ diffuse into the cell, causing rapid depolarization until the cell is depolarized to approximately +20 millivolts (mV).

The voltage change occurring during depolarization affects other ion channels in the plasma membrane. Several types of voltage-gated K+ channels exist, each of which opens and closes at different membrane potentials, causing changes in membrane permeability to K+. For example, at rest, the movement of K+ through open voltage-gated K+ channels is primarily responsible for establishing the resting membrane potential in cardiac muscle cells. Depolarization causes these voltage-gated K+ channels to close, thereby decreasing membrane permeability to K+. Depolarization also causes voltage-gated Ca2+ channels to begin to open. These changes contribute to depolarization. Compared with sodium channels, the calcium channels open and close slowly.

Repolarization is also the result of changes in membrane permeability to Na+, K+, and Ca2+. Early repolarization occurs when the voltage-gated Na+ channels and some voltage-gated Ca2+ channels close, and a small number of voltage-gated K+ channels open. Sodium ion movement into the cell slows, and some K+ move out of the cell. The plateau phase occurs as voltage-gated Ca2+ channels remain open, and the movement of Ca2+ and some Na+ through the voltage-gated Ca2+ channels into the cell counteracts the potential change produced by the movement of K+ out of the cell. The plateau phase ends, and final repolarization begins as the voltage-gated Ca2+ channels close and many more voltage-gated K+ channels open. Thus, Ca2+ and Na+ stop diffusing into the cell, and the tendency for K+ to diffuse out of the cell increases. These permeability changes cause the membrane potential to return to its resting level.

Action potential propagation in cardiac muscle differs from that in skeletal muscle. First, action potentials in cardiac muscle are conducted from cell to cell, whereas action potentials in skeletal muscle fibers are conducted along the length of a single muscle fiber, but not from fiber to fiber. Gap junctions of intercalated disks in cardiac muscle allow for the cell-to-cell conduction. Second, action potential propagation is slower in cardiac muscle than in skeletal muscle because cardiac muscle cells are smaller in diameter and much shorter than skeletal muscle fibers. Although the gap junctions allow the transfer of action potentials between cardiac muscle cells, they slow the rate of action potential conduction between the cardiac muscle cells.

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The movement of Ca2+ through the plasma membrane, including the membranes of the T tubules, into cardiac muscle cells stimulates the release of Ca2+ from the sarcoplasmic reticulum, a process called calcium-induced calcium release (CICR). When an action potential occurs in a cardiac muscle cell, Ca2+ enter the cell and bind to receptors in the membranes of the sarcoplasmic reticulum, resulting in the opening of Ca2+ channels. Calcium ions then move out of the sarcoplasmic reticulum and activate the interaction between actin and myosin to produce contraction of the cardiac muscle cells.

Autorhythmicity of Cardiac Muscle

The heart is said to be autorhythmic (aw'tō-rith'mik) because it stimulates itself (auto) to contract at regular intervals (rhythmic). If the heart is removed from the body and maintained under physiological conditions with the proper nutrients and temperature, it will continue to beat autorhythmically for a long time.

In the SA node, pacemaker cells generate action potentials spontaneously and at regular intervals. These action potentials spread through the conducting system of the heart to other cardiac muscle cells, causing voltage-gated Na+ channels to open. As a result, action potentials are produced and the cardiac muscle cells contract.

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The generation of action potentials in the SA node results when a spontaneously developing local potential, called the pacemaker potential, reaches threshold (figure 20.15). Changes in ion movement into and out of the pacemaker cells cause the pacemaker potential. Sodium ions cause depolarization by moving into the cells through specialized nongated Na+ channels. A decreasing permeability to K+ also causes depolarization as fewer K+ move out of the cells. The decreasing K+ permeability occurs due to the voltage changes at the end of the previous action potential. As a result of the depolarization, voltage-gated Ca2+ channels open, and the movement of Ca2+ into the pacemaker cells causes further depolarization. When the pacemaker potential reaches threshold, many voltage-gated Ca2+ channels open. In pacemaker cells, the movement of Ca2+ into the cells is primarily responsible for the depolarization phase of the action potential. This is different from other cardiac muscle cells, where the movement of Na+ into the cells is primarily responsible for depolarization. Repolarization occurs, as in other cardiac muscle cells, when the voltage-gated Ca2+ channels close and the voltage-gated K+ channels open. After the RMP is reestablished, production of another pacemaker potential starts the generation of the next action potential.

PROCESS FIGURE 20.15
SA Node Action PotentialThe production of action potentials by the SA node is responsible for the autorhythmicity of the heart.

Although most cardiac muscle cells respond to action potentials produced by the SA node, some cardiac muscle cells in the conducting system can also generate spontaneous action potentials. Normally, the SA node controls the rhythm of the heart because its pacemaker cells generate action potentials at a faster rate than other potential pacemaker cells, producing a heart rate of 70–80 beats per minute (bpm). An ectopic focus (eek-top'ik fō'kŭs; pl. foci, fō'sī) is any part of the heart other than the SA node that generates a heartbeat. For example, if the SA node does not function properly, the part of the heart that can produce action potentials at the next highest frequency is the AV node, which produces a heart rate of 40–60 bpm. Another cause of an ectopic focus is blockage of the conducting pathways between the SA node and other parts of the heart. For example, if action potentials do not pass through the AV node, an ectopic focus can develop in an AV bundle, resulting in a heart rate of only 30 bpm.

Drugs That Block Calcium Channels
V

arious chemical agents, such as manganese ions (Mn2+) and verapamil (ver-ap'ă-mil), block voltage-gated Ca2+ channels. Voltage-gated Ca2+ channel–blocking agents prevent the movement of Ca2+ through voltage-gated Ca2+ channels into the cell; for that reason, they are called calcium channel blockers. Some calcium channel blockers are widely used to treat various cardiac disorders, including tachycardia and certain arrhythmias (see table 20.1). Calcium channel blockers slow the development of the pacemaker potential and thus reduce the heart rate. If action potentials arise prematurely within the SA node or other areas of the heart, calcium channel blockers reduce that tendency. Calcium channel blockers also reduce the amount of work performed by the heart because less calcium enters cardiac muscle cells to activate the contractile mechanism. On the other hand, epinephrine and norepinephrine increase the heart rate and its force of contraction by opening voltage-gated Ca2+ channels.

 
TABLE 20.1
Major Cardiac Arrhythmias
Conditions Symptoms Possible Causes
Abnormal Heart Rhythms    
Tachycardia Heart rate in excess of 100 beats per minute (bpm) Elevated body temperature; excessive sympathetic stimulation; toxic conditions
Paroxysmal atrial tachycardia Sudden increase in heart rate to 95–150 bpm for a few seconds or even for several hours; P wave precedes every QRS complex; P wave inverted and superimposed on T wave Excessive sympathetic stimulation; abnormally elevated permeability of slow channels
Ventricular tachycardia Frequently causes fibrillation Often associated with damage to AV node or ventricular muscle
Abnormal Rhythms Resulting from Ectopic Action Potentials    
Atrial flutter 300 P waves/min; 125 QRS complexes/min, resulting in two or three P waves (atrial contraction) for every QRS complex (ventricular contraction) Ectopic action potentials in the atria
Atrial fibrillation No P waves; normal QRS complexes; irregular timing; ventricles constantly stimulated by atria; reduced pumping effectiveness and filling time Ectopic action potentials in the atria
Ventricular fibrillation No QRS complexes; no rhythmic contraction of the myocardium; many patches of asynchronously contracting ventricular muscle Ectopic action potentials in the ventricles
Bradycardia Heart rate less than 60 bpm Elevated stroke volume in athletes; excessive vagal stimulation; carotid sinus syndrome
Sinus Arrhythmia Heart rate varies 5% during respiratory cycle and up to 30% during deep respiration. Cause not always known; occasionally caused by ischemia or inflammation or associated with cardiac failure
SA Node Block Cessation of P wave; new low heart rate due to AV node acting as pacemaker; normal QRS complex and T wave Ischemia; tissue damage due to infarction; causes unknown
AV Node Block    
First-degree PR interval greater than 0.2 second Inflammation of AV bundle
Second-degree PR interval 0.25–0.45 second; some P waves trigger QRS complexes and others do not; 2:1, 3:1, and 3:2 P wave/QRS complex ratios may occur Excessive vagal stimulation
Third-degree (complete heart block) P wave dissociated from QRS complex; atrial rhythm approximately 100 bpm; ventricular rhythm less than 40 bpm Ischemia of AV nodal fibers or compression of AV bundle
Premature Atrial Contractions Occasional shortened intervals between contractions; frequently occurs in healthy people Excessive smoking; lack of sleep; too much caffeine; alcoholism
  P wave superimposed on QRS complex  
Premature Ventricular Contractions (PVCs) Prolonged QRS complex; exaggerated voltage because only one ventricle may depolarize; inverted T wave; increased probability of fibrillation Ectopic foci in ventricles; lack of sleep; too much caffeine, irritability; occasionally occurs with coronary thrombosis
Abbreviations: SA = sinoatrial; AV = atrioventricular.

Ectopic foci can also appear when the rate of action potential generation in cardiac muscle cells outside the SA node becomes enhanced. For example, when cells are injured, their plasma membranes become more permeable, resulting in depolarization. Inflammation or lack of adequate blood flow to cardiac muscle tissue can injure cardiac muscle cells. These injured cells can be the source of ectopic action potentials. Also, alterations in blood levels of K+ and Ca2+ can change the cardiac muscle membrane potential, and certain drugs, such as those that mimic the effect of epinephrine on the heart, can alter cardiac muscle membrane permeability. Changes in cardiac muscle cells' membrane potentials or permeability can produce ectopic foci.

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Refractory Periods of Cardiac Muscle

Cardiac muscle, like skeletal muscle, has refractory (rē-frak'tōr-ē) periods associated with its action potentials. During the absolute refractory period, the cardiac muscle cell is completely insensitive to further stimulation. During the relative refractory period, the cell is sensitive to stimulation, but a greater stimulation than normal is required to cause an action potential. Because the plateau phase of the action potential in cardiac muscle delays repolarization to the RMP, the refractory period is prolonged. The long refractory period ensures that contraction and most of relaxation are complete before another action potential can be initiated. This prevents tetanic contractions in cardiac muscle and is responsible for rhythmic contractions.

Predict 4

Predict the consequences if cardiac muscle could undergo tetanic contraction.

Predict 4
(Your score will be reported to your instructor)
Electrocardiogram

Action potentials conducted through the myocardium during the cardiac cycle produce electrical currents that can be measured at the body surface. Electrodes placed on the body surface and attached to an appropriate recording device can detect small voltage changes resulting from action potentials in the cardiac muscle. The electrodes do not detect individual action potentials; rather, they detect a summation of all the action potentials transmitted by the cardiac muscle cells through the heart at a given time. The summated record of the cardiac action potentials is an electrocardiogram (ECG or EKG) (figure 20.16).

FIGURE 20.16
ElectrocardiogramThe major waves and intervals of an electrocardiogram. Each thin, horizontal line on the ECG recording represents 1 mV, and each thin, vertical line represents 0.04 second.

The ECG is not a direct measurement of mechanical events in the heart, and neither the force of contraction nor blood pressure can be determined from it. However, each deflection in the ECG record indicates an electrical event within the heart that is correlated with a subsequent mechanical event. Consequently, electrocardiography is extremely valuable in diagnosing a number of abnormal cardiac rhythms (arrhythmias; table 20.1) and other abnormalities, particularly because it is painless, easy to record, and noninvasive (does not require surgery). In addition to abnormal heart rates and rhythms, ECG analysis can reveal abnormal conduction pathways, hypertrophy or atrophy of portions of the heart, and the approximate location of damaged cardiac muscle (table 20.1).

The normal ECG consists of a P wave, a QRS complex, and a T wave (figure 20.16). The P wave, which is the result of action potentials that cause depolarization of the atrial myocardium, signals the onset of atrial contraction. The QRS complex is composed of three individual waves: the Q, R, and S waves. The QRS complex results from ventricular depolarization and signals the onset of ventricular contraction. The T wave represents repolarization of the ventricles and precedes ventricular relaxation. A wave representing repolarization of the atria cannot be seen because it occurs during the QRS complex.

The time between the beginning of the P wave and the beginning of the QRS complex is the PQ interval, commonly called the PR interval because the Q wave is often very small. During the PR interval, which lasts approximately 0.16 second, the atria contract and begin to relax. The ventricles begin to depolarize at the end of the PR interval. The QT interval extends from the beginning of the QRS complex to the end of the T wave, lasting approximately 0.36 second. The QT interval represents the approximate length of time required for the ventricles to contract and begin to relax.

ASSESS YOUR PROGRESS
  1. For cardiac muscle action potentials, describe ion movement during the depolarization, early repolarization, plateau, and final repolarization phases.

  2. Why is cardiac muscle referred to as autorhythmic? What are ectopic foci?

  3. How does the depolarization of pacemaker cells differ from the depolarization of other cardiac cells? What is the pacemaker potential?

  4. How is the prolonged refractory period generated in cardiac muscle? What is the advantage of a prolonged refractory period?

  5. What does an ECG measure? Name the waves and intervals produced by an ECG, and state what events occur during each wave and interval.

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Alterations in the Electrocardiogram
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longation of the PR interval can result from three events: (1) a delay in action potential conduction through the atrial muscle because of damage, such as that caused by ischemia (is-kē'mē-ă), which is obstruction of the blood supply to the walls of the heart; (2) a delay in action potential conduction through atrial muscle because of a dilated atrium; or (3) a delay in action potential conduction through the AV node and bundle because of ischemia, compression, or necrosis of the AV node or bundle. These conditions result in slow conduction of action potentials through the bundle branches. An unusually long QT interval reflects the abnormal conduction of action potentials through the ventricles, which can result from myocardial infarctions or from an abnormally enlarged left or right ventricle.

Altered forms of the electrocardiogram due to cardiac abnormalities include complete heart block, premature ventricular contraction, bundle branch block, atrial fibrillation, and ventricular fibrillation (figure 20.17).

 
FIGURE 20.17
Alterations in an Electrocardiogram