Cardiac Muscle, Cardiac Cycle, and Function of Atria, Ventricles, and Valves (PDF)

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CEU Universidad Cardenal Herrera

Belén Merck MD PhD

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cardiac muscle physiology of heart heart anatomy cardiac cycle

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This document is an overview of cardiac muscle, its function, structure, and the cardiac cycle. It explains the physiology of cardiac muscle, including preload and afterload. It also presents the methods of heart rate and strength regulation of the heart, and regulation of cardiac pumping. The document presents an in-depth understanding of heart anatomy and functions. It also includes regulation of heart pumping and control by the sympathetic and parasympathetic nerves

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1. CARDIAC MUSCLE. CARDIAC CYCLE. FUNCTION OF ATRIA, VENTRICLES AND VALVES. REGULATION OF CARDIAC PUMPING Belén Merck MD PhD  The heart is actually two separate pumps: a right heart that pumps blood through the lungs, and a left heart that pumps blood through...

1. CARDIAC MUSCLE. CARDIAC CYCLE. FUNCTION OF ATRIA, VENTRICLES AND VALVES. REGULATION OF CARDIAC PUMPING Belén Merck MD PhD  The heart is actually two separate pumps: a right heart that pumps blood through the lungs, and a left heart that pumps blood through the peripheral organs.  Each of these hearts is a pulsatile two-chamber pump composed of an atrium and a ventricle.  Each atrium is a weak primer pump for the ventricle, helping to move blood into the ventricle.  The ventricles then supply the main pumping force that propels the blood either (1) through the pulmonary circulation by the right ventricle or (2) through the peripheral circulation by the left ventricle.  Special mechanisms in the heart cause a continuing succession of heart contractions called cardiac rhythmicity, transmitting action potentials throughout the cardiac muscle to cause the heart’s rhythmical beat PHYSIOLOGY OF CARDIAC MUSCLE  The heart is composed of three major types of cardiac muscle: atrial muscle, ventricular muscle, and specialized excitatory and conductive muscle fibers.  The atrial and ventricular types of muscle contract in much the same way as skeletal muscle, except that the duration of contraction is much longer.  The specialized excitatory and conductive fibers contract only feebly because they contain few contractile fibrils. They exhibit either automatic rhythmical electrical discharge in the form of action potentials or conduction of the action potentials through the heart. PHYSIOLOGY OF CARDIAC MUSCLE  Cardiac muscle fibers are arranged in a latticework, with the fibers dividing, recombining, and then spreading again.  Cardiac muscle is striated in the same manner as in skeletal muscle.  It has typical myofibrils that contain actin and myosin filaments almost identical to those found in skeletal muscle; these filaments lie side by side and slide along one another during contraction in the same manner as occurs in skeletal muscle PHYSIOLOGY OF CARDIAC MUSCLE  The dark areas crossing the cardiac muscle fibers are called intercalated discs; they are actually cell membranes that separate individual cardiac muscle cells from one another.  Cardiac muscle fibers are made up of many individual cells connected in series and in parallel with one another.  At each intercalated disc the cell membranes fuse with one another in such a way that they form permeable “communicating” junctions (gap junctions) that allow rapid diffusion of ions. PHYSIOLOGY OF CARDIAC MUSCLE  From a functional point of view, ions move with ease in the intracellular fluid along the longitudinal axes of the cardiac muscle fibers so that action potentials travel easily from one cardiac muscle cell to the next, past the intercalated discs.  Thus, cardiac muscle is a syncytium of many heart muscle cells in which the cardiac cells are so interconnected that when one of these cells becomes excited, the action potential spreads to all of them, from cell to cell throughout the latticework interconnections. PHYSIOLOGY OF CARDIAC MUSCLE  The heart actually is composed of two syncytiums: the atrial syncytium, which constitutes the walls of the two atria, and the ventricular syncytium, which constitutes the walls of the two ventricles.  The atria are separated from the ventricles by fibrous tissue that surrounds the atrioventricular (A-V) valvular openings between the atria and ventricles. PHYSIOLOGY OF CARDIAC MUSCLE  Potentials are not conducted from the atrial syncytium into the ventricular syncytium directly through this fibrous tissue. Instead, they are conducted only by way of a specialized conductive system called the A-V bundle, a bundle of conductive fibers.  This division of the muscle of the heart into two functional syncytiums allows the atria to contract a short time ahead of ventricular contraction, which is important for effectiveness of heart pumping. PHYSIOLOGY OF CARDIAC MUSCLE The action potential recorded in a ventricular muscle fiber, averages about 105 mV, which means that the intracellular potential rises from a very negative value, about -85 mV, between beats to a slightly positive value, about +20 mV, during each beat. After the initial spike, the membrane remains depolarized for about 0.2 s, exhibiting a plateau, followed at the end of the plateau by abrupt repolarization The presence of this plateau in the action potential causes ventricular contraction to last as much as 15 times as long in cardiac muscle as in skeletal muscle. WHAT CAUSES THE LONG ACTION POTENTIAL AND THE PLATEAU? At least two major differences between the membrane properties of cardiac and skeletal muscle account for the prolonged action potential and the plateau in cardiac muscle. First, the action potential of skeletal muscle is caused almost entirely by sudden opening of large numbers of so called fast sodium channels that allow tremendous numbers of sodium ions to enter the skeletal muscle fiber from the extracellular fluid. These channels are called “fast” channels because they remain open for only a few thousandths of a second and then abruptly close. At the end of this closure, repolarization occurs. WHAT CAUSES THE LONG ACTION POTENTIAL AND THE PLATEAU? In cardiac muscle, the action potential is caused by opening of two types of channels: (1) the same fast sodium channels as those in skeletal muscle and (2) another entirely different population of slow calcium channels, which are also called calcium-sodium channels. This second population of channels differs in that they are slower to open and, even more important, remain open for several tenths of a second. During this time, a large quantity of both calcium and sodium ions flows through these channels to the interior of the cardiac muscle fiber, and this maintains a prolonged period of depolarization, causing the plateau in the action potential. WHAT CAUSES THE LONG ACTION POTENTIAL AND THE PLATEAU? Further, the calcium ions that enter during this plateau phase activate the muscle contractile process, while the calcium ions that cause skeletal muscle contraction are derived from the intracellular sarcoplasmic reticulum. The second major functional difference between cardiac muscle and skeletal muscle that helps account for both the prolonged action potential and its plateau is the immediately decrease of the permeability of the cardiac muscle membrane for potassium ions after the onset of the action potential. WHAT CAUSES THE LONG ACTION POTENTIAL AND THE PLATEAU? The decreased potassium permeability greatly decreases the outflux of positively charged potassium ions during the action potential plateau and thereby prevents early return of the action potential voltage to its resting level. When the slow calcium-sodium channels do close at the end of 0.2 to 0.3 s and the influx of calcium and sodium ions ceases, the membrane permeability for potassium ions also increases rapidly; this rapid loss of potassium from the fiber immediately returns the membrane potential to its resting level, thus ending the action potential. PHYSIOLOGY OF CARDIAC MUSCLE Cardiac muscle, like all excitable tissue, is refractory to restimulation during the action potential. The refractory period of the heart is the interval of time during which a normal cardiac impulse cannot reexcite an already excited area. The normal refractory period of the ventricle is 0.25 to 0.30 s, which is about the duration of the prolonged plateau action potential. There is an additional relative refractory period of about 0.05 s during which the muscle is more difficult than normal to excite but nevertheless can be excited by a very strong excitatory signal. The refractory period of atrial muscle is much shorter than that for the ventricles READ Excitation-Contraction Coupling—Function of Calcium Ions and the Transverse Tubules in the book CARDIAC CYCLE The cardiac events that occur from the beginning of one heartbeat to the beginning of the next are called the cardiac cycle. Each cycle is initiated by spontaneous generation of an action potential in the sinus node. This node is located in the wall of the right atrium near the opening of the superior vena cava, and the action potential travels from here rapidly through both atria and then through the A-V bundle into the ventricles. CARDIAC CYCLE Because of this special arrangement of the conducting system from the atria into the ventricles, there is a delay of more than 0.1 second during passage of the cardiac impulse from the atria into the ventricles. This allows the atria to contract ahead of ventricular contraction, thereby pumping blood into the ventricles before the strong ventricular contraction begins. CARDIAC CYCLE The cardiac cycle consists of a period of relaxation called diastole, during which the heart fills with blood, followed by a period of contraction called systole. The total duration of the cardiac cycle, including systole and diastole, is the reciprocal of the heart rate. For example, if heart rate is 72 beats/min, the duration of the cardiac cycle is 1/72 beats/min—about 0.0139 minutes per beat, or 0.833 second per beat. CARDIAC CYCLE When heart rate increases, the duration of each cardiac cycle decreases. The duration of the action potential and the period of systole also decrease, but not by as great as does the diastole. At a normal heart rate of 72 beats/min, systole comprises about 0.4 of the entire cardiac cycle. At three times the normal heart rate, systole is about 0.65 of the entire cardiac cycle. This means that the heart beating at a very fast rate does not remain relaxed long enough to allow complete filling of the cardiac chambers before the next contraction. CARDIAC CYCLE: ATRIA Blood normally flows continually from the great veins into the atria; about 80% of the blood flows directly through the atria into the ventricles even before the atria contract. Atrial contraction usually causes an additional 20% filling of the ventricles. The heart can continue to operate under most conditions even without this extra 20% effectiveness because it normally has the capability of pumping 300 to 400% more blood than is required by the resting body. When the atria fail to function, the difference is unlikely to be noticed unless a person exercises. CARDIAC CYCLE: ATRIA In the atrial pressure curve three minor pressure elevations, called the a, c, and v atrial pressure waves, are noted. The a wave is caused by atrial contraction. The right atrial pressure increases 4 to 6 mm Hg during atrial contraction, and the left atrial pressure increases about 7 to 8 mm Hg. CARDIAC CYCLE: ATRIA The c wave occurs when the ventricles begin to contract; it is caused partly by slight backflow of blood into the atria at the onset of ventricular contraction but mainly by bulging of the A-V valves backward toward the atria because of increasing pressure in the ventricles. The v wave occurs toward the end of ventricular contraction; it results from slow flow of blood into the atria from the veins while the A-V valves are closed during ventricular contraction. CARDIAC CYCLE: VENTRICLES During ventricular systole, large amounts of blood accumulate in the right and left atria because of the closed A-V valves. As soon as systole is over and the ventricular pressures fall again to their low diastolic values, the moderately increased pressures that have developed in the atria during ventricular systole immediately push the A-V valves open and allow blood to flow rapidly into the ventricles. This is called the period of rapid filling of the ventricles. CARDIAC CYCLE: VENTRICLES The period of rapid filling lasts for about the first third of diastole. During the middle third of diastole, only a small amount of blood normally flows into the ventricles; this is blood that continues to empty into the atria from the veins and passes through the atria directly into the ventricles. During the last third of diastole, the atria contract and give an additional thrust to the inflow of blood into the ventricles; this accounts for about 20% of the filling of the ventricles during each heart cycle. CARDIAC CYCLE: VENTRICLES Immediately after ventricular contraction begins, the ventricular pressure rises abruptly causing the A-V valves to close. Then an additional 0.02 to 0.03 s is required for the ventricle to build up sufficient pressure to push the semilunar (aortic and pulmonary) valves open against the pressures in the aorta and pulmonary artery. During this period, contraction is occurring in the ventricles, but there is no emptying. This is called the period of isovolumic or isometric contraction, meaning that tension is increasing in the muscle but little or no shortening of the muscle fibers is occurring. CARDIAC CYCLE: VENTRICLES When the left ventricular pressure rises slightly above 80 mm Hg (and the right ventricular pressure slightly above 8 mm Hg), the ventricular pressures push the semilunar valves open. Immediately, blood begins to pour out of the ventricles, with about 70% of the blood emptying occurring during the first third of the period of ejection and the remaining 30% emptying during the next two thirds. Therefore, the first third is called the period of rapid ejection, and the last two thirds, the period of slow ejection. CARDIAC CYCLE: VENTRICLES At the end of systole, ventricular relaxation begins suddenly, allowing both the right and left intraventricular pressures to decrease rapidly. The elevated pressures in the distended large arteries that have just been filled with blood from the contracted ventricles immediately push blood back toward the ventricles, which snaps the aortic and pulmonary valves closed CARDIAC CYCLE: VENTRICLES For another 0.03 to 0.06 s, the ventricular muscle continues to relax, even though the ventricular volume does not change, giving rise to the period of isovolumic or isometric relaxation. During this period, the intraventricular pressures decrease rapidly back to their low diastolic levels. Then the A-V valves open to begin a new cycle of ventricular pumping. END-DIASTOLIC VOLUME, END-SYSTOLIC VOLUME, AND STROKE VOLUME OUTPUT. During diastole, normal filling of the ventricles increases the volume of each ventricle to about 110 to 120 ml. This volume is called the end-diastolic volume. Then, as the ventricles empty during systole, the volume decreases about 70 ml, which is called the stroke volume output. The remaining volume in each ventricle, about 40 to 50 ml, is called the end- systolic volume. The fraction of the end-diastolic volume that is ejected is called the ejection fraction—usually equal to about 60 percent. END-DIASTOLIC VOLUME, END-SYSTOLIC VOLUME, AND STROKE VOLUME OUTPUT. When the heart contracts strongly, the end-systolic volume can be decreased to as little as 10 to 20 ml. Conversely, when large amounts of blood flow into the ventricles during diastole, the ventricular end-diastolic volumes can become as great as 150 to 180 ml in the healthy heart. By both increasing the end-diastolic volume and decreasing the end- systolic volume, the stroke volume output can be increased to more than double normal. ATRIOVENTRICULAR VALVES. The A-V valves prevent backflow of blood from the ventricles to the atria during systole, and the semilunar valves prevent backflow from the aorta and pulmonary arteries into the ventricles during diastole. These valves close and open passively. They close when a backward pressure gradient pushes blood backward, and they open when a forward pressure gradient forces blood in the forward direction. ATRIOVENTRICULAR VALVES. For anatomical reasons, the thin, filmy A-V valves require almost no backflow to cause closure, whereas the much heavier semilunar valves require rather rapid backflow for a few milliseconds. The papillary muscles attach to the vanes of the A-V valves by the chordae tendineae. The papillary muscles contract when the ventricular walls contract, but contrary to what might be expected, they do not help the valves to close. ATRIOVENTRICULAR VALVES. Instead, they pull the vanes of the valves inward toward the ventricles to prevent their bulging too far backward toward the atria during ventricular contraction. If a chorda tendinea becomes ruptured or if one of the papillary muscles becomes paralyzed, the valve bulges far backward during ventricular contraction, sometimes so far that it leaks severely and results in severe or even lethal cardiac incapacity. AORTIC AND PULMONARY ARTERY VALVES. The aortic and pulmonary artery semilunar valves function quite differently from the A-V valves. The high pressures in the arteries at the end of systole cause the semilunar valves to snap to the closed position, in contrast to the much softer closure of the A-V valves. Because of smaller openings, the velocity of blood ejection through the aortic and pulmonary valves is far greater than that through the much larger A-V valves. AORTIC AND PULMONARY ARTERY VALVES. Because of the rapid closure and rapid ejection, the edges of the aortic and pulmonary valves are subjected to much greater mechanical abrasion than are the A-V valves. Finally, the A-V valves are supported by the chordae tendineae, which is not true for the semilunar valves. It is obvious from the anatomy of the aortic and pulmonary valves that they must be constructed with an especially strong yet very pliable fibrous tissue base to withstand the extra physical stresses. AORTIC PRESSURE CURVE When the left ventricle contracts, the ventricular pressure increases rapidly until the aortic valve opens. After the valve opens, the pressure in the ventricle rises much less rapidly, because blood immediately flows out of the ventricle into the aorta and then into the systemic distribution arteries. The entry of blood into the arteries causes the walls of these arteries to stretch and the pressure to increase to about 120 mm Hg. AORTIC PRESSURE CURVE At the end of systole, after the left ventricle stops ejecting blood and the aortic valve closes, the elastic walls of the arteries maintain a high pressure in the arteries, even during diastole. A so-called incisura occurs in the aortic pressure curve when the aortic valve closes. This is caused by a short period of backward flow of blood immediately before closure of the valve, followed by sudden cessation of the backflow. AORTIC PRESSURE CURVE After the aortic valve has closed, the pressure in the aorta decreases slowly throughout diastole because the blood stored in the distended elastic arteries flows continually through the peripheral vessels back to the veins. Before the ventricle contracts again, the aortic pressure usually has fallen to about 80 mm Hg (diastolic pressure), which is two thirds the maximal pressure of 120 mm Hg (systolic pressure) that occurs in the aorta during ventricular contraction. CONCEPTS OF PRELOAD AND AFTERLOAD. In assessing the contractile properties of muscle, it is important to specify the degree of tension on the muscle when it begins to contract, which is called the preload, and to specify the load against which the muscle exerts its contractile force, which is called the afterload. For cardiac contraction, the preload is usually considered to be the end- diastolic pressure when the ventricle has become filled. CONCEPTS OF PRELOAD AND AFTERLOAD. The afterload of the ventricle is the pressure in the aorta leading from the ventricle. The importance of the concepts of preload and afterload is that in many abnormal functional states of the heart or circulation, the pressure during filling of the ventricle (the preload), the arterial pressure against which the ventricle must contract (the afterload), or both are severely altered from normal. REGULATION OF HEART PUMPING At rest, the heart pumps only 4 to 6 liters each minute. During severe exercise, the heart may be required to pump four to seven times this amount. The basic means by which the volume pumped by the heart is regulated are (1) intrinsic cardiac regulation of pumping in response to changes in volume of blood flowing into the heart and (2) control of heart rate and strength of heart pumping by the autonomic nervous system. REGULATION OF HEART PUMPING Under most conditions, the amount of blood pumped by the heart each minute is normally determined almost entirely by the rate of blood flow into the heart from the veins, which is called venous return. Each peripheral tissue of the body controls its own local blood flow, and all the local tissue flows combine and return by way of the veins to the right atrium. The heart, in turn, automatically pumps this incoming blood into the arteries so that it can flow around the circuit again. REGULATION OF HEART PUMPING This intrinsic ability of the heart to adapt to increasing volumes of inflowing blood is called the Frank-Starling mechanism of the heart. The Frank-Starling mechanism means that the greater the heart muscle is stretched during filling, the greater is the force of contraction and the greater the quantity of blood pumped into the aorta. Within physiologic limits, the heart pumps all the blood that returns to it by the way of the veins. REGULATION OF HEART PUMPING When an extra amount of blood flows into the ventricles, the cardiac muscle itself is stretched to greater length. This in turn causes the muscle to contract with increased force because the actin and myosin filaments are brought to a more nearly optimal degree of overlap for force generation. Therefore, the ventricle, because of its increased pumping, automatically pumps the extra blood into the arteries. REGULATION OF HEART PUMPING This ability of stretched muscle, up to an optimal length, to contract with increased work output is characteristic of all striated muscle. In addition to the important effect of lengthening the heart muscle, still another factor increases heart pumping when its volume is increased. Stretch of the right atrial wall directly increases the heart rate by 10 to 20%; this, too, helps increase the amount of blood pumped each minute, although its contribution is much less than that of the Frank-Starling mechanism. CONTROL BY THE SYMPATHETIC & PARASYMPATHETIC NERVES The pumping effectiveness of the heart also is controlled by the sympathetic and parasympathetic nerves, which abundantly supply the heart. For given levels of atrial pressure, the amount of blood pumped each minute (cardiac output) often can be increased more than 100% by sympathetic stimulation. By contrast, the output can be decreased to as low as zero or almost zero by vagal (parasympathetic) stimulation. CONTROL BY THE SYMPATHETIC NERVES Strong sympathetic stimulation can increase the heart rate in young adult humans from the normal rate of 70 beats/min up to 180 to 200 and, even 250 beats/min. It also increases the force of heart contraction to as much as double normal, thereby increasing the volume of blood pumped and increasing the ejection pressure. Thus, sympathetic stimulation often can increase the maximum cardiac output as much as twofold to threefold, in addition to the increased output caused by the Frank-Starling. CONTROL BY THE SYMPATHETIC NERVES Inhibition of the sympathetic nerves to the heart can decrease cardiac pumping to a moderate extent: Under normal conditions, the sympathetic nerve fibers to the heart discharge continuously at a slow rate that maintains pumping at about 30% above that with no sympathetic stimulation. When the activity of the sympathetic nervous system is depressed below normal, this decreases both heart rate and strength of ventricular muscle contraction, thereby decreasing the level of cardiac pumping as much as 30% below normal. CONTROL BY THE PARASYMPATHETIC NERVES Strong stimulation of the parasympathetic nerve fibers in the vagus nerves to the heart can stop the heartbeat for a few seconds, but then the heart usually “escapes” and beats at a rate of 20 to 40 beats/min as long as the parasympathetic stimulation continues. Strong vagal stimulation can decrease the strength of heart muscle contraction by 20 to 30%. CONTROL BY THE PARASYMPATHETIC NERVES The vagal fibers are distributed mainly to the atria and not much to the ventricles, where the power contraction of the heart occurs. This explains the effect of vagal stimulation mainly to decrease heart rate rather than to decrease greatly the strength of heart contraction. The great decrease in heart rate combined with a slight decrease in heart contraction strength can decrease ventricular pumping 50% or more. EFFECT OF POTASSIUM IONS. Excess potassium in the extracellular fluids causes the heart to become dilated and flaccid and also slows the heart rate. Large quantities also can block conduction of the cardiac impulse from the atria to the ventricles through the A-V bundle. Elevation of potassium concentration to only 8 to 12 mEq/L—two to three times the normal value—can cause such weakness of the heart and abnormal rhythm that death occurs. EFFECT OF POTASSIUM IONS. These effects result partially from the fact that a high (K+) in the extracellular fluids decreases the resting membrane potential in the cardiac muscle fibers. High extracellular fluid (K+) partially depolarizes the cell membrane, causing the membrane potential to be less negative. As the membrane potential decreases, the intensity of the action potential also decreases, which makes contraction of the heart progressively weaker.. EFFECT OF CALCIUM IONS An excess of calcium ions causes effects almost exactly opposite to those of potassium ions, causing the heart to go toward spastic contraction. This is caused by a direct effect of calcium ions to initiate the cardiac contractile process. Deficiency of calcium ions causes cardiac flaccidity, similar to the effect of high potassium. Calcium ion levels in the blood normally are regulated within a very narrow range. Cardiac effects of abnormal calcium concentrations are seldom of clinical concern.

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