Part 2

 

 

20–3  The Heartbeat

  Objectives

 Describe the events of an action potential in cardiac muscle, and explain the importance of calcium ions to the contractile process.

 Discuss the differences between nodal cells and conducting cells, and describe the components and functions of the conducting system of the heart.

 Identify the electrical events associated with a normal electrocardiogram.

Explain the events of the cardiac cycle, including atrial and ventricular systole and diastole, and relate the heart sounds to specific events in the cycle.

Cardiac Physiology
In a single heartbeat, the entire heart contracts in series–first the atria and then the ventricles. Two types of cardiac muscle cells are involved in a normal heartbeat: (1) specialized muscle cells of the conducting system , which control and coordinate the heartbeat, and (2) contractile cells , which produce the powerful contractions that propel blood. Each heartbeat BEGINS with an action potential generated at a pacemaker called the SA node , which is part of the conducting system. This electrical impulse is then propagated by the conducting system and distributed so that the stimulated contractile cells will push blood in the right direction at the proper time. The electrical events can be monitored from the surface of the body through an electrocardiogram ( ECG or EKG).

 

The arrival of an impulse at a cardiac muscle cell membrane produces an action potential that is comparable to an action potential in a skeletal muscle fiber. Thanks to the coordination provided by the conducting system, the atria contract first, driving blood into the ventricles through the AV valves, and the ventricles contract next, driving blood out of the heart through the semilunar valves.

 

 After each heartbeat there is a brief pause–less than half a second–before the next heartbeat begins. The period between the start of one heartbeat and the start of the next is called the cardiac cycle .

A heartbeat lasts only about 370 msec. We begin our analysis of cardiac function by following the steps that produce a single heartbeat, from the generation of an action potential at the SA node through the contractions of the atria and ventricles:

 

 

 

The Conducting System
In contrast to skeletal muscle, cardiac muscle tissue contracts on its own in the absence of neural or hormonal stimulation. This property is called automaticity , or autorhythmicity . The cells responsible for initiating and distributing the stimulus to contract are part of the heart's conducting system , also known as the cardiac conduction system or the nodal system . This system is a network of specialized cardiac muscle cells that initiates and distributes electrical impulses

.
The conducting system includes the following elements:

 

1.The sinoatrial (SA) node , located in the wall of the right atrium.

 

2.The atrioventricular (AV) node , located at the junction between the atria and ventricles.

 

3. Conducting cells , which interconnect the two nodes and distribute the contractile stimulus throughout the myocardium. The impulse travels from the SA node to the AV node. The ventricular conducting cells include those in the AV bundle and the bundle branches , as well as the Purkinje fibers , which distribute the stimulus to the ventricular myocardium.

 

 (a) Components of the conducting system. (b) The spontaneous changes in the membrane potential of a pacemaker cell in the SA node that is establishing a heart rate of 72 beats per minute

 

 

Most of the cells of the conducting system are smaller than the contractile cells of the myocardium and contain very few myofibrils. Conducting cells of the SA and AV nodes share another important characteristic: Their excitable membranes cannot maintain a stable resting potential. Each time repolarization occurs, the membrane gradually drifts toward threshold. This gradual depolarization is called a prepotential.

The rate of spontaneous depolarization varies in different portions of the conducting system. It is fastest at the SA node, which in the absence of neural or hormonal stimulation will generate action potentials at a rate of 80–100 per minute. Isolated cells of the AV node depolarize more slowly, generating 40–60 action potentials per minute. Because the SA node reaches threshold first, it establishes the heart rate; the impulse generated by the SA node brings the AV nodal cells to threshold faster than does the prepotential of the AV nodal cells. The normal resting heart rate is somewhat slower than 80–100 per minute, however, due to the effects of parasympathetic (inhibitory) innervation.

 

If any of the atrial pathways or the SA node becomes damaged, the heart will continue to beat, but it will do so at a slower rate, usually 40–60 beats per minute, as dictated by the AV node. Certain cells in the Purkinje fiber network depolarize spontaneously at an even slower rate, and if the rest of the conducting system is damaged, they can stimulate a heart rate of 20–40 beats per minute. Under normal conditions, cells of the AV bundle, the bundle branches, and most Purkinje fibers do not depolarize spontaneously. If, due to damage or disease, these cells do begin depolarizing spontaneously, the heart may no longer pump blood effectively, and death can occur if the problem persists.

Trace the path of an impulse from its initiation at the SA node, examining its effects on the surrounding myocardium as we proceed:

1.The sinoatrial node (SA node) is embedded in the posterior wall of the right atrium, near the entrance of the superior vena cava  [STEP 1] . The SA node contains pacemaker cells , which establish the heart rate. As a result, the SA node is also known as the cardiac pacemaker or the natural pacemaker .

 

 

The SA node is connected to the larger AV node by the internodal pathways in the atrial walls. It takes roughly 50 msec for an action potential to travel from the SA node to the AV node along these pathways. Along the way, the conducting cells pass the stimulus to contractile cells of both atria. The action potential then spreads across the atrial surfaces by cell–to–cell contact  [STEP 2] . The stimulus affects only the atria, because the fibrous skeleton isolates the atrial myocardium from the ventricular myocardium.

 

2.The relatively large atrioventricular (AV) node sits within the floor of the right atrium near the opening of the coronary sinus. The rate of propagation of the impulse slows as it leaves the internodal pathways and enters the AV node, because the nodal cells are smaller in diameter than the conducting cells. In addition, the connections between nodal cells are less efficient than those between conducting cells at relaying the impulse from one cell to another. As a result, it takes about 100 msec for the impulse to pass through the AV node and enter the AV bundle [STEP 3] .

 

 

The delay at the AV node is important, because the atria must contract before the ventricles do. Otherwise, the contraction of the powerful ventricles would close the AV valves and prevent blood flow from the atria into the ventricles. Because there is a delay at the AV node, the atrial myocardium completes its contraction before ventricular contraction begins.

The cells of the AV node can conduct impulses at a maximum rate of 230 per minute. Since each impulse will result in a ventricular contraction, this value is the maximum normal heart rate. Even if the SA node generates impulses at a faster rate, the ventricles will still contract at 230 beats per minute (bpm). This limitation is important, because mechanical factors, discussed later, begin to decrease the pumping efficiency of the heart at rates above approximately 180 bpm. Rates above 230 bpm occur only when the heart or the conducting system has been damaged or stimulated by drugs. As ventricular rates increase toward their theoretical maximum limit of 300–400 bpm, pumping efficiency becomes dangerously, if not fatally, reduced.

A number of clinical problems are the result of abnormal pacemaker function. Bradycardia  is a condition in which the heart rate is slower than normal, whereas tachycardia indicates a faster–than–normal heart rate.

 

3.The AV Bundle, Bundle Branches, and Purkinje Fibers
The connection between the AV node and the AV bundle , also called the bundle of His , is the only electrical connection between the atria and the ventricles. Once an impulse enters the AV bundle, it travels to the interventricular septum and enters the right and left bundle branches . The left bundle branch, which supplies the massive left ventricle, is much larger than the right bundle branch. Both branches extend toward the apex of the heart, turn, and fan out deep to the endocardial surface. As the branches diverge, they conduct the impulse to Purkinje fibers and, through the moderator band, to the papillary muscles of the right ventricle.

Purkinje fibers conduct action potentials very rapidly–as fast as small myelinated axons. Within about 75 msec, the signal to begin a contraction has reached all the ventricular cardiac muscle cells. The entire process, from the generation of an impulse at the SA node to the complete depolarization of the ventricular myocardium, normally takes around 225 msec. By this time, the atria have completed their contractions and ventricular contraction can safely occur.

Contraction of the papillary muscles applies tension to the chordae tendineae, bracing the AV valves. By limiting the movement of the cusps, tension in the chordae tendineae prevents the backflow of blood into the atria when the ventricles contract. The Purkinje fibers radiate from the apex toward the base of the heart. As a result, ventricular contraction proceeds in a wave that begins at the apex and spreads toward the base. Blood is therefore pushed toward the base of the heart, into the aorta and pulmonary trunk.

 

If the conducting pathways are damaged, the normal rhythm of the heart will be disturbed. The resulting problems are called conduction deficits . If the SA node or internodal pathways are damaged, the AV node will assume command. The heart will continue beating normally, although at a slower rate. If an abnormal conducting cell or ventricular muscle cell begins generating action potentials at a more rapid rate, the impulses can override those of the SA or AV node. The origin of these abnormal signals is called an ectopic pacemaker . The activity of an ectopic pacemaker partially or completely bypasses the conducting system, disrupting the timing of ventricular contraction. The result is a dangerous reduction in the efficiency of the heart. Such conditions are commonly diagnosed with the aid of an Electrocardiogram.

 

Each time the heart beats, a wave of depolarization radiates through the atria, reaches the AV node, travels down the interventricular septum to the apex, turns, and spreads through the ventricular myocardium toward the base.

 

 

By comparing the information obtained from electrodes placed at different locations, a clinician can monitor the electrical activity of the heart, which is directly related to the performance of specific nodal, conducting, and contractile components. For example, when a portion of the heart has been damaged, the affected muscle cells will no longer conduct action potentials. An ECG will reveal an abnormal pattern of impulse conduction.

The appearance of the ECG varies with the placement of the monitoring electrodes, or leads .

 

 

 

(b) An ECG printout is a strip of graph paper containing a record of the electrical events monitored by the electrodes. The placement of electrodes on the body surface affects the size and shape of the waves recorded. This example is a normal ECG; the enlarged section indicates the major components of the ECG and the measurements most often taken during clinical analysis.

 

 

 

 

1.The small P wave accompanies the depolarization of the atria. The atria begin contracting about 100 msec after the start of the P wave.

 

2.The QRS complex appears as the ventricles depolarize. This is a relatively strong electrical signal, because the ventricular muscle is much more massive than that of the atria. It is also a complex signal, in part because it incorporates atrial repolarization as well as ventricular depolarization. The ventricles begin contracting shortly after the peak of the R wave .

 

3.The smaller T wave indicates ventricular repolarization. You do not see a deflection corresponding to atrial repolarization, because it occurs while the ventricles are depolarizing and the electrical events are masked by the QRS complex

 

To analyze an ECG, you must measure the size of the voltage changes and determine the durations and temporal relationships of the various components. Attention usually is focused on the amount of depolarization occurring during the P wave and the QRS complex. For example, an excessively large QRS complex often indicates that the heart has become enlarged. A smaller–than–normal electrical signal may mean that the mass of the heart muscle has decreased.

 

The size and shape of the T wave may also be affected by any condition that slows ventricular repolarization. For example, starvation and low cardiac energy reserves, coronary ischemia, or abnormal ion concentrations will reduce the size of the T wave.
You must also measure the time between waves. The values are reported as segments or intervals . Segments generally extend from the end of one wave to the start of another; intervals are more variable, but always include at least one entire wave.

 

4.The P–R interval extends from the start of atrial depolarization to the start of the QRS complex (ventricular depolarization) rather than to R, because in abnormal ECGs the peak can be difficult to determine. Extension of the P–R interval to more than 0.2 second can indicate damage to the conducting pathways or AV node.

 

5.The Q–T interval indicates the time required for the ventricles to undergo a single cycle of depolarization and repolarization. It is usually measured from the end of the P–R interval rather than from the bottom of the Q wave. The Q–T interval can be lengthened by conduction problems, coronary ischemia, or myocardial damage. A congenital heart defect that can cause sudden death without warning may be detectable as a prolonged Q–T interval.

 

 

Despite the variety of sophisticated equipment available to assess or visualize cardiac function, in the majority of cases the ECG provides the most important diagnostic information. ECG analysis is especially useful in detecting and diagnosing cardiac arrhythmias –abnormal patterns of cardiac electrical activity. Momentary arrhythmias are not inherently dangerous; about 5 percent of the healthy population experiences a few abnormal heartbeats each day. Clinical problems appear when the arrhythmias reduce the pumping efficiency of the heart. Serious arrhythmias may indicate damage to the myocardium, injuries to the pacemakers or conduction pathways, exposure to drugs, or variations in the electrolyte composition of extracellular fluids.

 

Contractile Cells
The Purkinje fibers distribute the stimulus to the contractile cells , which form the bulk of the atrial and ventricular walls. In the discussions of cardiac muscle tissue in earlier chapters, we considered only the structure of contractile cells, which account for roughly 99 percent of the muscle cells in the heart. In both cardiac muscle cells and skeletal muscle fibers, (1) an action potential leads to the appearance of calcium among the myofibrils, and (2) the binding of calcium to troponin on the thin filaments initiates the contraction. But skeletal and cardiac muscle cells differ in terms of the nature of the action potential, the source of the calcium and the duration of the resulting contraction.

The Action Potential in Cardiac Muscle Cells
Take a closer look at the origin and conduction of an action potential in a contractile cell:

 
The resting potential of a ventricular contractile cell is approximately comparable to that of a resting skeletal muscle fiber.

 

Threshold is normally reached in a portion of the membrane next to an intercalated disc. The typical stimulus is the excitation of an adjacent muscle cell. Once threshold has been reached, the action potential proceeds in three basic steps:

 

 

1. Rapid Depolarization. At threshold, voltage–regulated sodium channels open and the membrane suddenly becomes permeable to sodium. The result is a massive influx of sodium ions and the rapid depolarization of the sarcolemma. The channels involved are called fast channels , because they open quickly and remain open for only a few milliseconds.

2.The Plateau. As the transmembrane potential approaches +30mv  the voltage–regulated sodium channels close. They will remain closed and inactivated until the membrane potential reaches The cell now begins actively pumping sodium out of the cell. However, a net loss of positive charges does not continue, because as the sodium channels are closing, voltage–regulated calcium channels are opening.

 

These channels are called slow calcium channels , because they open slowly and remain open for a relatively long period–roughly 175 msec. While the slow calcium channels are open, calcium ions enter the sarcoplasm. The entry of positive charges through the calcium channels balances the loss of positive ions through the active transport of sodium and the transmembrane potential remains near 0 mV for an extended period. This portion of the action potential curve is called the plateau . The presence of a plateau is the major difference between action potentials in cardiac muscle cells and in skeletal muscle fibers. In a skeletal muscle fiber, rapid depolarization is immediately followed by rapid repolarization.

3.Repolarization. As the plateau continues, slow calcium channels begin closing and slow potassium channels begin opening. As the channels open, potassium ions rush out of the cell, and the net result is a period of rapid repolarization that restores the resting potential.

 


The Refractory Period

 As with skeletal muscle contractions, for some time after an action potential begins, the membrane will not respond normally to a second stimulus. This time is called the refractory period. In the absolute refractory period, the membrane cannot respond at all, because the sodium channels either are already open or are closed and inactivated. In a ventricular muscle cell, the absolute refractory period lasts approximately 200 msec, spanning the duration of the plateau and the initial period of rapid repolarization.

The absolute refractory period is followed by a shorter (50 msec) relative refractory period. During this period, the voltage–regulated sodium channels are closed, but can open. The membrane will respond to a stronger–than–normal stimulus by initiating another action potential. In total, an action potential in a ventricular contractile cell lasts 250–300 msec, roughly 30 times as long as a typical action potential in a skeletal muscle fiber.

Calcium Ions and Cardiac Contractions
The appearance of an action potential in the cardiac muscle cell membrane produces a contraction by causing an increase in the concentration of Calcium Ions around the myofibrils. This process occurs in two steps:

Calcium ions entering the cell membrane during the plateau phase of the action potential provide roughly 20 percent of the required for a contraction.

The arrival of extracellular Calcium is the trigger for the release of additional Calcium from reserves in the sarcoplasmic reticulum (SR).

 

Extracellular calcium ions thus have both direct and indirect effects on cardiac muscle cell contraction. For this reason, cardiac muscle tissue is highly sensitive to changes in the concentration of the extracellular fluid.

In a skeletal muscle fiber, the action potential is relatively brief and ends as the related twitch contraction begins. The twitch contraction is short and ends as the SR reclaims the Calcium  it released. In a cardiac muscle cell, as we have seen, the action potential is prolonged and calcium ions continue to enter the cell throughout the plateau. As a result, the period of active muscle cell contraction continues until the plateau ends. As the slow calcium channels close, the intracellular calcium ions are absorbed by the SR or are pumped out of the cell, and the muscle cell relaxes.

In skeletal muscle fibers, the refractory period ends before peak tension develops. As a result, twitches can summate and tetanus can occur. In cardiac muscle cells, the absolute refractory period continues until relaxation is under way. Because summation is not possible, tetanic contractions cannot occur in a normal cardiac muscle cell, regardless of the frequency or intensity of stimulation. This feature is vital: A heart in tetany could not pump blood. With a single twitch lasting 250 msec or longer, a normal cardiac muscle cell can reach 300–400 contractions per minute under maximum stimulation. This rate is not reached in a normal heart, due to limitations imposed by the conducting system.

The Cardiac Cycle
Each heartbeat is followed by a brief resting phase, allowing time for the chambers to relax and prepare for the next heartbeat. The period between the start of one heartbeat and the beginning of the next is a single cardiac cycle . The cardiac cycle, therefore, includes alternating periods of contraction and relaxation. For any one chamber in the heart, the cardiac cycle can be divided into two phases: (1) systole and (2) diastole. During systole, or contraction, the chamber contracts and pushes blood into an adjacent chamber or into an arterial trunk. Systole is followed by diastole, or relaxation. During diastole, the chamber fills with blood and prepares for the next cardiac cycle.

In the course of the cardiac cycle, pressure within each chamber rises during systole and falls during diastole. Valves between adjacent chambers help ensure that blood flows in the desired direction, but blood will flow from one chamber to another only if the pressure in the first chamber exceeds that in the second chamber.

 

This basic principle governs the movement of blood between atria and ventricles, between ventricles and arterial trunks, and between major veins and arteries.

The elaborate pacemaking and conducting systems normally provide the required spacing between atrial and ventricular systoles. At a representative heart rate of 75 bpm, a sequence of systole and diastole in either the atria or the ventricles lasts 800 msec. For convenience, we shall assume that the cardiac cycle is determined by the atria and that it includes one cycle of atrial systole and atrial diastole.

Phases of the Cardiac Cycle
As the cardiac cycle begins, all four chambers are relaxed and the ventricles are partially filled with blood. During atrial systole, the atria contract, filling the ventricles completely with blood. Atrial systole lasts 100 msec.

 

 

Over this period, blood cannot flow into the atria because atrial pressure exceeds venous pressure. Yet there is very little backflow into the veins, even though the connections with the venous system lack valves, because blood takes the path of least resistance. Resistance to blood flow through the broad AV connections and into the ventricles is less than that through the smaller, angled openings of the large veins, which are connected to miles of smaller vessels–many of which do have valves.

The atria next enter atrial diastole, which continues until the start of the next cardiac cycle. Atrial diastole and ventricular systole begin at the same time. Ventricular systole lasts 270 msec. During this period, blood is pushed through the systemic and pulmonary circuits and toward the atria. The heart then enters ventricular diastole, which lasts 530 msec (the 430 msec remaining in this cardiac cycle, plus the first 100 msec of the next). For the rest of this cycle, filling occurs passively and both the atria and the ventricles are relaxed. The next cardiac cycle begins with atrial systole and the completion of ventricular filling.

When the heart rate increases, all the phases of the cardiac cycle are shortened. The greatest reduction occurs in the length of time spent in diastole. When the heart rate climbs from 75 bpm to 200 bpm, the time spent in systole drops by less than 40 percent, but the duration of diastole is reduced by almost 75 percent.

 

 

Pressure and Volume Changes in the Cardiac Cycle

Although pressures are lower in the right atrium and right ventricle, both sides of the heart contract at the same time, and they eject equal volumes of blood.

At the start of atrial systole, the ventricles are already filled to about 70 percent of their normal capacity, due to passive blood flow toward the end of the previous cardiac cycle. As the atria contract, rising atrial pressures provide the missing 30 percent by pushing blood through the open AV valves. Atrial systole essentially "tops off" the ventricles.

 

At the end of atrial systole, each ventricle contains the maximum amount of blood that it will hold in this cardiac cycle. That quantity is called the end–diastolic volume (EDV). In an adult who is standing at rest, the end–diastolic volume is typically about 130 ml.

 

 

Ventricular Systole As atrial systole ends, ventricular systole begins. This period lasts approximately 270 msec in a resting adult. As the pressures in the ventricles rise above those in the atria, the AV valves swing shut.

During this stage of ventricular systole, the ventricles are contracting. Blood flow has yet to occur, however, because ventricular pressures are not high enough to force open the semilunar valves and push blood into the pulmonary or aortic trunk. Over this period, the ventricles contract isometrically. The ventricles are now in the period of isovolumetric contraction : All the heart valves are closed, the volumes of the ventricles remain constant, and ventricular pressures rise.

 

Once pressure in the ventricles exceeds that in the arterial trunks, the semilunar valves open and blood flows into the pulmonary and aortic trunks. This point marks the beginning of the period of ventricular ejection . The ventricles now contract isotonically: The muscle cells shorten, and tension production remains relatively constant.

 

After reaching a peak, ventricular pressures gradually decline near the end of ventricular systole.

 

 Although pressures in the right ventricle and pulmonary trunk are much lower, the right ventricle also goes through periods of isovolumetric contraction and ventricular ejection. During ventricular ejection, each ventricle will eject 70–80 ml of blood, the stroke volume (SV) of the heart. The stroke volume at rest is roughly 60 percent of the end–diastolic volume. This percentage, known as the ejection fraction , can vary in response to changing demands on the heart.

 

As the end of ventricular systole approaches, ventricular pressures fall rapidly. Blood in the aorta and pulmonary trunk now starts to flow back toward the ventricles, and this movement closes the semilunar valves. As the backflow begins, pressure decreases in the aorta. When the semilunar valves close, pressure rises again as the elastic arterial walls recoil. This small, temporary rise produces a valley in the pressure tracing that is called a dicrotic notch. The amount of blood remaining in the ventricle when the semilunar valve closes is the end–systolic volume (ESV) . At rest, the end–systolic volume is 50 ml, about 40 percent of the end–diastolic volume.

 

Ventricular Diastole The period of ventricular diastole lasts for the 430 msec remaining in the current cardiac cycle and continues through atrial systole in the next cycle.

 

All the heart valves are now closed, and the ventricular myocardium is relaxing. Because ventricular pressures are still higher than atrial pressures, blood cannot flow into the ventricles. This is the period of isovolumetric relaxation . Ventricular pressures drop rapidly over this period, because the elasticity of the connective tissues of the heart and fibrous skeleton helps reexpand the ventricles toward their resting dimensions.

 

When ventricular pressures fall below those of the atria, the atrial pressures force the AV valves open. Blood now flows from the atria into the ventricles. Both the atria and the ventricles are in diastole, but the ventricular pressures continue to fall as the ventricular chambers expand. Throughout this period, pressures in the ventricles are so far below those in the major veins, that blood pours through the relaxed atria and on through the open AV valves into the ventricles. This passive mechanism is the primary method of ventricular filling. The ventricles will be nearly three–quarters full before the cardiac cycle ends.

 

The relatively minor contribution that atrial systole makes to ventricular volume explains why individuals can survive quite normally when their atria have been so severely damaged that they can no longer function. In contrast, damage to one or both ventricles can leave the heart unable to maintain adequate blood flow through peripheral tissues and organs. A condition of heart failure then exists.

Heart Sounds
Listening to the heart, a technique called auscultation, is a simple and effective method of cardiac diagnosis. Physicians use a stethoscope to listen to normal and abnormal heart sounds. Where to place the stethoscope depends on which valve is under examination.

 

 

 Valve sounds must pass through the pericardium, surrounding tissues, and the chest wall, and some tissues muffle sounds more than others. As a result, the placement of the stethoscope does not always correspond to the position of the valve under review.

There are four heart sounds. When you listen to your own heart, you usually hear the first and second heart sounds . These sounds accompany the closing of your heart valves. The first heart sound, known as "lubb" lasts a little longer than the second, called "dupp". Lubb which marks the start of ventricular contraction, is produced as the AV valves close; Dupp occurs at the beginning of ventricular filling, when the semilunar valves close.

Third and fourth heart sounds may be audible, but they are usually very faint and seldom are detectable in healthy adults. These sounds are associated with blood flowing into the ventricles and atrial contractions, rather than with valve action.

 

 

Minor valve abnormalities are relatively common. For example, 5 to 10 percent of healthy individuals have some degree of mitral valve prolapse , a condition in which the mitral valve cusps do not close properly. The problem may involve abnormally long (or short) chordae tendineae or malfunctioning papillary muscles. Because the valve does not work perfectly, some regurgitation may occur during left ventricular systole. The surges, swirls, and eddies that accompany regurgitation create a rushing, gurgling sound known as a heart murmur .

 

Minor heart murmurs are very common. Most individuals with this condition are completely asymptomatic and live normal lives, unaware of any circulatory malfunction. Extreme prolapse and valve failure, which may be caused by breakage of the chordae tendineae, can be life threatening. This condition is known as a mitral valve flail .

 

 

The Energy for Cardiac Contractions
When a normal heart is beating, the energy required is obtained by the mitochondrial breakdown of fatty acids (stored as lipid droplets) and glucose (stored as glycogen). These aerobic reactions can occur only when oxygen is readily available.

In addition to obtaining oxygen from the coronary circulation, cardiac muscle cells maintain their own sizable reserves of oxygen. In these cells, oxygen molecules are bound to the heme units of myoglobin molecules. Normally, the combination of circulatory oxygen supplies plus myoglobin reserves is enough to meet the oxygen demands of your heart, even when it is working at maximum capacity.

Heart Attacks

In a myocardial  infarction (MI) , or heart attack , part of the coronary circulation becomes blocked and cardiac muscle cells die from lack of oxygen. The affected tissue then degenerates, creating a nonfunctional area known as an infarct . Heart attacks most commonly result from severe coronary artery disease (CAD). The consequences depend on the site and nature of the circulatory blockage. If it occurs near the start of one of the coronary arteries, the damage will be widespread and the heart may stop beating. If the blockage involves one of the smaller arterial branches, the individual may survive the immediate crisis but may have many complications, all unpleasant. As scar tissue forms in the damaged area, the heartbeat may become irregular and other vessels can become constricted, creating additional circulatory problems.

 

Myocardial infarctions are generally associated with fixed blockages, such as those seen in CAD. When the crisis develops as a result of thrombus (clot) formation at a plaque, the condition is called coronary thrombosis . A vessel already narrowed by plaque formation may also become blocked by a sudden spasm in the smooth muscles of the vascular wall. The individual then may experience intense pain, similar to that felt in an angina attack, but persisting even at rest. However, pain does not always accompany a heart attack, and silent heart attacks may be even more dangerous than more apparent, because the condition may go undiagnosed and may not be treated before a fatal MI occurs. Roughly 25 percent of heart attacks are not recognized when they occur.

 

The cytoplasm of a damaged cardiac muscle cell differs from that of a normal muscle cell. As the supply of oxygen decreases, the cells become more dependent on anaerobic metabolism to meet their energy needs. Over time, the cytoplasm accumulates large numbers of enzymes involved with anaerobic energy production. As the membranes of the cardiac muscle cells deteriorate, these enzymes enter the surrounding intercellular fluids. The appearance of such enzymes in the circulation thus indicates that an infarct has occurred. The enzymes that are tested for in a diagnostic blood test include lactate dehydrogenase (LDH) , serum glutamic oxaloacetic transaminase ( SGOT , also called aspartate aminotransferase ), creatine phosphokinase ( CPK or CK ), and a special form of creatine phosphokinase that occurs only in cardiac muscle ( CK–MB ).

 

About 25 percent of MI patients die before obtaining medical assistance, and 65 percent of MI deaths among those under age 50 occur within an hour after the initial infarct. Anticoagulants (even aspirin chewed and swallowed at the start of an MI) may help prevent the formation of additional thrombi, and clot–dissolving enzymes may reduce the extent of the damage if they are administered within six hours after the MI occurred.

 

Follow–up treatment with heparin, aspirin, or both is recommended; without further treatment, the circulatory blockages will reappear in about 20 percent of patients.

 

Roughly 1.3 million MIs occur in the United States each year, and half the victims die within a year of the incident. The following factors appear to increase the risk of a heart attack:

 

(1) smoking, (2) high blood pressure, (3) high blood cholesterol levels, (4) high circulating levels of low–density lipoproteins (LDLs), (5) diabetes, (6) male gender (below age 70), (7) severe emotional stress, (8) obesity, (9) genetic predisposition, and (10) a sedentary lifestyle.

 

Although the heart attack rate of women under age 70 is lower than that of men, the mortality rate for women is higher–perhaps because heart disease in women is neither diagnosed as early nor treated as aggressively as that in men.

 

The presence of two risk factors more than doubles the risk of heart attack, so eliminating as many risk factors as possible will improve the chances of preventing or surviving a heart attack. Changing the diet to limit cholesterol, exercising to lower weight, and seeking treatment for high blood pressure are steps in the right direction. It has been estimated that a reduction in coronary risk factors could prevent 150,000 deaths each year in the United States alone.

 

 

 Cardiodynamics The term cardiodynamics refers to the movements and forces generated during cardiac contractions. Each time the heart beats, the two ventricles eject equal amounts of blood.

 

Define cardiac output, and describe the factors that influence this variable.

Describe the variables that influence heart rate.
Describe the variables that influence stroke volume.
Explain how adjustments in stroke volume and cardiac output are coordinated at different levels of activity.

Earlier we introduced these terms:

 

End–Diastolic Volume (EDV). The amount of blood in each ventricle at the end of ventricular diastole (the start of ventricular systole).

 

End–Systolic Volume (ESV). The amount of blood remaining in each ventricle at the end of ventricular systole (the start of ventricular diastole).

 

Stroke Volume (SV). The amount of blood pumped out of each ventricle during a single beat, which can be expressed as

 

Ejection Fraction. The percentage of the EDV represented by the SV.

 

Stroke volume is the most important factor in an examination of a single cardiac cycle. If the heart were an old–fashioned bicycle pump, the stroke volume would be the amount of air pumped in one up–down cycle of the handle.

 

 

Where you stop when you lift the handle determines the end–diastolic volume–how much air the pump contains. How far down you push the handle determines the end–systolic volume–how much air remains in the pump at the end of the cycle. You can increase the amount of air pumped in each cycle by increasing the range of movement of the handle. You pump the maximum amount when the handle moves all the way from the top to the bottom. In other words, you get the largest stroke volume when the EDV is as great as it can be and the ESV is as small as it can be.

When considering cardiac function over time, physicians generally are most interested in the cardiac output (CO), the amount of blood pumped by each ventricle in one minute. In essence, cardiac output is an indication of the blood flow through peripheral tissues–without adequate blood flow, homeostasis cannot be maintained.

 

The cardiac output provides a useful indication of ventricular efficiency over time. We can calculate it by multiplying the heart rate (HR) by the average stroke volume (SV):
For example, if the heart rate is 75 bpm and the stroke volume is 80 ml per beat, the cardiac output will be 75x80=600 ml or 6L per minute.

Cardiac output is precisely adjusted such that peripheral tissues receive an adequate circulatory supply under a variety of conditions. When necessary, the heart rate can increase by 250 percent, and stroke volume in a normal heart can almost double.

 

Overview: The Control of Cardiac Output
Cardiac output can be adjusted by changes in either heart rate or stroke volume. For convenience, we can consider these independently as we discuss the individual factors involved. However, changes in cardiac output generally reflect changes in both heart rate and stroke volume.

The heart rate can be adjusted by the activities of the autonomic nervous system or by circulating hormones. The stroke volume can be adjusted by changing the end–diastolic volume (how full the ventricles are when they start to contract), the end–systolic volume (how much blood remains in the ventricle after it contracts), or both. Stroke volume peaks when EDV is high and ESV is low.

 

Factors Affecting The Heart Rate
Under normal circumstances, autonomic activity and circulating hormones are responsible for making delicate adjustments to the heart rate as circulatory demands change. These factors act by modifying the natural rhythm of the heart. Even a heart removed for a heart transplant will continue to beat unless steps are taken to prevent it from doing so.

Autonomic Innervation
The sympathetic and parasympathetic divisions of the autonomic nervous system innervate the heart by means of the cardiac plexus.

 

 

 

Postganglionic sympathetic neurons are located in the cervical and upper thoracic ganglia. The vagus nerves (X) carry parasympathetic preganglionic fibers to small ganglia in the cardiac plexus. Both ANS divisions innervate the SA and AV nodes and the atrial muscle cells. Although ventricular muscle cells are also innervated by both divisions, sympathetic fibers far outnumber parasympathetic fibers there.

The cardiac centers of the medulla oblongata contain the autonomic headquarters for cardiac control. The cardioacceleratory center controls sympathetic neurons that increase the heart rate; the adjacent cardioinhibitory center controls the parasympathetic neurons that slow the heart rate. The activities of the cardiac centers are regulated by reflex pathways and through input from higher centers, especially from the parasympathetic and sympathetic headquarters in the hypothalamus.

Cardiac Reflexes

 Information about the status of the cardiovascular system arrives over visceral sensory fibers accompanying the vagus nerve and the sympathetic nerves of the cardiac plexus. The cardiac centers monitor baroreceptors and chemoreceptors innervated by the glossopharyngeal (IX) and vagus (X) nerves. On the basis of the information received, the centers adjust cardiac performance to maintain adequate circulation to vital organs, such as the brain. The centers respond to changes in blood pressure and in arterial concentrations of dissolved oxygen and carbon dioxide. For example, a decline in blood pressure or oxygen concentrations or an increase in carbon dioxide levels generally indicates that the heart must work harder to meet the demands of peripheral tissues. The cardiac centers then call for an increase in cardiac activity. We will detail these reflexes and their effects on the heart and peripheral vessels in Chapter 21 .

Autonomic Tone As is the case in other organs with dual innervation, the heart has a resting autonomic tone. Both autonomic divisions are normally active at a steady background level, releasing ACh and NE at the nodes and into the myocardium. Thus, cutting the vagus nerves increases the heart rate, and sympathetic blocking agents slow the heart rate.

In a healthy, resting individual, parasympathetic effects dominate. In the absence of autonomic innervation, the heart rate is established by the pacemaker cells of the SA node. Such a heart beats at a rate of 80–100 bpm (too fast). At rest, a typical adult heart with normal innervation beats at 70–80 bpm due to inhibitory activity in the parasympathetic nerves innervating the SA node. If parasympathetic activity increases, the heart rate declines further. Conversely, the heart rate will increase if either parasympathetic activity decreases or sympathetic activation occurs. Through dual innervation and adjustments in autonomic tone, the ANS can make very delicate adjustments in cardiovascular function to meet the demands of other systems.

Effects on the SA Node The sympathetic and parasympathetic divisions alter the heart rate by changing the permeabilities of cells in the conducting system. The most dramatic effects are seen at the SA node, where changes in the rate of which impulses are generated affect the heart rate.

 
Consider the SA node of a resting individual whose heart is beating at 75 bpm .

 

 

Any factor that changes the rate of spontaneous depolarization or the duration of repolarization will alter the heart rate by changing the time required to reach threshold.

 

Acetylcholine released by parasympathetic neurons opens chemically regulated channels in the cell membrane, thereby dramatically slowing the rate of spontaneous depolarization and also slightly extending the duration of repolarization. The result is a decline in heart rate.

The NE (norepinephrine) released by sympathetic neurons binds to beta–1 receptors, leading to the opening of calcium ion channels. The subsequent influx of increases the rate of depolarization and shortens the period of repolarization. The nodal cells reach threshold more quickly, and the heart rate increases.

 

 

 

Pacemaker Function.
Pacemaker cells have membrane potentials closer to threshold than those of other cardiac muscle cells.

 

The Atrial Reflex The atrial reflex , or Bainbridge reflex , involves adjustments in heart rate in response to an increase in the venous return. When the walls of the right atrium are stretched, the stimulation of stretch receptors in the atrial walls triggers a reflexive increase in heart rate caused by increased sympathetic activity. Thus, when the rate of venous return to the heart increases, the heart rate, and hence the cardiac output, rises as well. Thus, Venous Return return has an indirect effect on heart rate by way of the atrial reflex. It also has direct effects on nodal cells. When venous return increases, the atria receive more blood and the walls are stretched. Stretching of the cells of the SA node leads to more rapid depolarization and an increase in the heart rate.

 

Hormones
Epinephrine, norepinephrine, and thyroid hormone increase the heartrate by their effect on the SA node. The effects of epinephrine on the SA node are similar to those of norepinephrine. Epinephrine also affects the contractile cells; after massive sympathetic stimulation of the adrenal medullae, the myocardium may become so excitable that abnormal contractions occur.

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AT THE END OF THE CHAPTER:

 

Selected Clinical Terminology

 

Terms Discussed in This Chapter

 

Chapter Review

 

Study Outline