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Unformatted text preview: Cardiac Cycle Cardiac Anatomy
The detailed anatomy of the heart can be found in anatomy textbooks. The following presents only a brief description of cardiac anatomy so that the physiology of the cardiac cycle can be understood. Venous blood enters the right atrium (RA) of the heart through the superior vena cava (SVC) and inferior vena cava (IVC). The right atrium has a relatively thin muscular wall and easily expands with blood as it fills (i.e., it is highly compliant). Because of its high compliance, the RA pressure is normally very low (0-3 mmHg). It also undergoes spontaneous contractions (see cardiac cycle) to aid in the filling of the right ventricle (RV). Blood passes from the RA to the RV through the tricuspid valve. The free wall of the right ventricle is not as thick as the left ventricle, and anatomically it wraps itself around part of the larger, and thicker, left ventricle. The RV wall, however, is thicker and more muscular than the RA, so that when it contracts, it can develop considerably more pressure (~25 mmHg) than the RA. As the RV contracts and generates pressure, blood leaves the RV, flows across an open semilunar pulmonic valve, and enters the pulmonary artery that distributes the output of the right ventricle to the lungs where exchange of oxygen and carbon dioxide occur. The pulmonic valve, like all healthy heart valves, permits blood to flow in only one direction. Blood returns to the heart from the lungs through four pulmonary veins that enter the left atrium (LA). This chamber is similar to the RA in that it is very distensible, although the blood pressure within the LA is several mmHg higher than the RA (6-10 mmHg in the LA compared to 0-3 mmHg in the RA). Blood flows from the LA, across the mitral valve, and into the left ventricle (LV). The LV wall is very thick so that it can generate high pressures when it contracts (normally ~120 mmHg at rest ). When the LV 1 Cardiac Cycle contracts, blood is expelled through the semilunar aortic valve and into the aorta, which then distributes blood to the arterial system. The tricuspid and mitral valves (also called atrioventricular, or AV valves) have fibrous strands (chordae tendineae) on their leaflets that attach to papillary muscles located on the respective ventricular walls. The papillary muscles contract during ventricular contraction and generate tension on the valve leaflets via the chordae tendineae to prevent the AV valves from bulging back into the atria and becoming incompetent. The semilunar valves (pulmonic and aortic) do not have analogous attachments. 2 Cardiac Cycle Cardiac Cycle The cardiac cycle diagram shown to the right depicts changes in aortic pressure (AP), left ventricular pressure (LVP), left atrial pressure (LAP), left ventricular volume (LV Vol), 3 Cardiac Cycle and heart sounds during a single cycle of cardiac contraction and relaxation. These changes are related in time to the electrocardiogram. Aortic pressure is measured by inserting a pressure catheter into the aorta from a peripheral artery, and the left ventricular pressure is obtained by placing a pressure catheter inside the left ventricle and measuring changes in intraventricular pressure as the heart beats. Left atrial pressure is not usually measured directly, except in investigational procedures. Ventricular volume changes can be assessed in real time using echocardiography or radionuclide imaging, or by using a special volume conductance catheter placed within the ventricle. A single cycle of cardiac activity can be divided into two basic stages. The first stage is diastole, which represents ventricular filling and a brief period just prior to filling at which time the ventricles are relaxing. The second stage is systole, which represents the time of contraction and ejection of blood from the ventricles. To analyze these two stages in more detail, the cardiac cycle is usually divided into seven phases. The first phase begins with the P wave of the electrocardiogram, which represents atrial depolarization. The last phase of the cardiac cycle ends with the appearance of the next P wave. In order to understand the events of the cardiac cycle, the reader should first review basic cardiac anatomy. The entire cardiac cycle diagram, which contains information on aortic, left ventricular and left atrial pressures, along with ventricular volume, heart sounds and the electrocardiogram, is shown above. Detailed descriptions of each phase can be obtained by clicking on each of the seven phases listed below. Phase 1 - Atrial Contraction Phase 2 - Isovolumetric Contraction Phase 3 - Rapid Ejection Phase 4 - Reduced Ejection Phase 5 - Isovolumetric Relaxation Phase 6 - Rapid Filling Phase 7 - Reduced Filling 4 Cardiac Cycle Cardiac Cycle - Atrial Contraction (Phase 1)
A-V Valves Open; Semilunar Valves Closed This is the first phase of the cardiac cycle because it is initiated by the p wave of the electrocardiogram (ECG), which represents electrical depolarization of the atria. Atrial depolarization then causes contraction of the atrial musculature. As the atria contract, the pressure within the atrial chambers increases, which forces more blood flow across the open atrioventricular (AV) valves, leading to a rapid flow of blood into the ventricles. Blood does not flow back into the vena cava because of inertial effects of the venous return and because the wave of contraction through the atria moves toward the AV valve thereby having a "milking effect." However, atrial contraction does produce a small increase in venous pressure that can be noted as the "a-wave" of the left atrial pressure (LAP). Just following the peak of the a wave is the x-descent. Atrial contraction normally accounts for about 10% of left ventricular filling when a person is at rest because most of ventricular filling occurs prior to atrial contraction as blood passively flows from the pulmonary veins, into the left atrium, then into the left ventricle through the open mitral valve. At high heart rates, however, the atrial contraction may account for up to 40% of ventricular filling. This is sometimes referred to as the "atrial kick." The atrial contribution to ventricular filling varies inversely with duration of ventricular diastole and directly with atrial contractility. 5 Cardiac Cycle After atrial contraction is complete, the atrial pressure begins to fall causing a pressure gradient reversal across the AV valves. This causes the valves to float upward (preposition) before closure. At this time, the ventricular volumes are maximal, which is termed the end-diastolic volume (EDV). The left ventricular EDV (LVEDV), which is typically about 120 ml, represents the ventricular preload and is associated with enddiastolic pressures of 8-12 mmHg and 3-6 mmHg in the left and right ventricles, respectively. A heart sound is sometimes noted during atrial contraction (fourth heart sound, S4). This sound is caused by vibration of the ventricular wall during atrial contraction. Generally, it is noted when the ventricle compliance is reduced ("stiff" ventricle) as occurs in ventricular hypertrophy and in many older individuals. 6 Cardiac Cycle Cardiac Cycle - Isovolumetric Contraction (Phase 2)
All Valves Closed This phase of the cardiac cycle begins with the appearance of the QRS complex of the ECG, which represents ventricular depolarization. This triggers excitation-contraction coupling, myocyte contraction and a rapid increase in intraventricular pressure. Early in this phase, the rate of pressure development becomes maximal. This is referred to as maximal dP/dt. The AV valves to close as intraventricular pressure exceeds atrial pressure. Ventricular contraction also triggers contraction of the papillary muscles with their attached chordae tendineae that prevent the AV valve leaflets from bulging back into the atria and becoming incompetent (i.e., "leaky"). Closure of the AV valves results in the first heart sound (S1). This sound is normally split (~0.04 sec) because mitral valve closure precedes tricuspid closure. During the time period between the closure of the AV valves and the opening of the aortic and pulmonic valves, ventricular pressure rises rapidly without a change in ventricular volume (i.e., no ejection occurs). Ventricular volume does not change because all valves are closed during this phase. Contraction, therefore, is said to be "isovolumic" or "isovolumetric." Individual myocyte contraction, however, is not necessarily isometric because individual myocyte are undergoing length changes. 7 Cardiac Cycle Individual fibers contract isotonically (i.e., concentric, shortening contraction), while others contract isometrically (i.e., no change in length) or eccentrically (i.e., lengthening contraction). Therefore, ventricular chamber geometry changes considerably as the heart becomes more spheroid in shape; circumference increases and atrial base-to-apex length decreases. The rate of pressure increase in the ventricles is determined by the rate of contraction of the muscle fibers, which is determine by mechanisms governing excitationcontraction coupling. The "c-wave" noted in the LAP may be due to bulging of mitral valve leaflets back into left atrium. Just after the peak of the c wave is the x'-descent. 8 Cardiac Cycle Cardiac Cycle - Rapid Ejection (Phase 3)
Aortic and Pulmonic Valves Open; AV Valves Remain Closed This phase represents the initial and rapid ejection of blood into the aorta and pulmonary arteries from the left and right ventricles, respectively. Ejection begins when the intraventricular pressures exceed the pressures within the aorta and pulmonary artery, which causes the aortic and pulmonic valves to open. Blood is ejected because the total energy of the blood within the ventricle exceeds the total energy of blood within the aorta. In other words, there is an energy gradient to propel blood into the aorta and pulmonary artery from their respective ventricles. During this phase, ventricular pressure normally exceeds outflow tract pressure by a few mmHg. This pressure gradient across the valve is ordinarily low because of the relatively large valve opening (i.e., low resistance). Maximal outflow velocity is reached early in the ejection phase, and maximal (systolic) aortic and pulmonary artery pressures are achieved. No heart sounds are ordinarily noted during ejection because the opening of healthy valves is silent. The presence of sounds during ejection (i.e., ejection murmurs) indicate valve disease or intracardiac shunts. Left atrial pressure initially decreases as the atrial base is pulled downward, expanding the atrial chamber. Blood continues to flow into the atria from their respective venous inflow tracts and the atrial pressures begin to rise, and continue to rise until the AV valves open at the end of phase 5. 9 Cardiac Cycle Cardiac Cycle - Reduced Ejection (Phase 4)
Aortic and Pulmonic Valves Open; AV Valves Remain Closed Approximately 200 msec after the QRS and the beginning of ventricular contraction, ventricular repolarization occurs as shown by the T-wave of the electrocardiogram. Repolarization leads to a decline in ventricular active tension and therefore the rate of ejection (ventricular emptying) falls. Ventricular pressure falls slightly below outflow tract pressure; however, outward flow still occurs due to kinetic (or inertial) energy of the blood. Left atrial and right atrial pressures gradually rise due to continued venous return from the lungs and from the systemic circulation, respectively. 10 Cardiac Cycle Cardiac Cycle - Isovolumetric Relaxation (Phase 5)
All Valves Closed When the intraventricular pressures fall sufficiently at the end of phase 4, the aortic and pulmonic valves abruptly close (aortic precedes pulmonic) causing the second heart sound (S2) and the beginning of isovolumetric relaxation. Valve closure is associated with a small backflow of blood into the ventricles and a characteristic notch (incisura or dicrotic notch) in the aortic and pulmonary artery pressure tracings. After valve closure, the aortic and pulmonary artery pressures rise slightly (dicrotic wave) following by a slow decline in pressure. The rate of pressure decline in the ventricles is determined by the rate of relaxation of the muscle fibers, which is termed lusitropy. This relaxation is regulated largely by the sarcoplasmic reticulum that are responsible for rapidly re-sequestering calcium following contraction (see excitation-contraction coupling). Although ventricular pressures decrease during this phase, volumes remain constant because all valves are closed. The volume of blood that remains in a ventricle is called the end-systolic volume and is ~50 ml in the left ventricle. The difference between the end-diastolic volume and the end-systolic volume is ~70 ml and represents the stroke volume. Left atrial pressure (LAP) continues to rise because of venous return from the lungs. The peak LAP at the end of this phase is termed the v-wave. 11 Cardiac Cycle Cardiac Cycle - Rapid Filling (Phase 6)
A-V Valves Open As the ventricles continue to relax at the end of phase 5, the intraventricular pressures will at some point fall below their respective atrial pressures. When this occurs, the AV valves rapidly open and ventricular filling begins. Despite the inflow of blood from the atria, intraventricular pressure continues to briefly fall because the ventricles are still undergoing relaxation. Once the ventricles are completely relaxed, their pressures will slowly rise as they fill with blood from the atria. The opening of the mitral valve causes a rapid fall in LAP. The peak of the LAP just before the valve opens is the "v-wave." This is followed by the y-descent of the LAP. A similar wave and descent are found in the right atrium and in the jugular vein. Ventricular filling is normally silent. When a third heart sound (S3) is audible, it may represent tensing of chordae tendineae and AV ring during ventricular relaxation and filling. This heart sound is normal in children; but is often pathological in adults and caused by ventricular dilation. 12 Cardiac Cycle Cardiac Cycle - Reduced Filling (Phase 7)
A-V Valves Open As the ventricles continue to fill with blood and expand, they become less compliant and the intraventricular pressures rise. This reduces the pressure gradient across the AV valves so that the rate of filling falls. In normal, resting hearts, the ventricle is about 90% filled by the end of this phase. In other words, about 90% of ventricular filling occurs before atrial contraction (phase 1). Aortic pressure and pulmonary arterial pressures continue to fall during this period. 13 Cardiac Cycle Cardiac Valve Disease
What are heart valves and what is their function?
Valves within the heart separate the right atrium and ventricle (tricuspid valve), the left atrium and ventricle (mitral valve), the right ventricle and the pulmonary artery (pulmonic valve), and the left ventricle and aorta (aortic valve) (click here to see cardiac anatomy diagram). The valves ensure that blood flows in a single pathway through the heart by opening and closing in a particular time sequence during the cardiac cycle. Normal valves permit blood to flow in only one direction, for example, from the right atrium into the right ventricle. When heart valves become diseased or damaged, they may not fully open or close. This can seriously impair cardiac function by causing blood to leak back into cardiac chambers or by requiring heart chambers to contract more forcefully to move blood across a narrowed valve. What causes valve defects?
A chronic disease process is responsible for defective valves in most older individuals. Sometimes, the disease results from a triggering event many years earlier, such as rheumatic fever. Bacterial infection, viral infection and inflammation of valves can trigger changes in valve structure and function. Normally, valve leaflets are very thin and flexible, but they can become thickened and rigid in response to a disease processes. When this occurs to a valve, it may not be able to fully open or to completely close. Valve disease found in younger individuals is usually due to a congenital defect in the embryologic development of the heart. Valve dysfunction can occur secondarily to other cardiac diseases, such as coronary artery disease, cardiac hypertrophy and cardiac dilation. If coronary artery disease progresses to the point where papillary muscles become hypoxic or infarcted, then the impaired contractile function of these muscles can lead to a leaky tricuspid or mitral valve. Cardiac hypertrophy or dilation, by altering cardiac chamber structure and dimensions, can lead to valve dysfunction. Finally, valve dysfunction can also occur if the chordae tendineae that connect the valve leaflet to the papillary muscle ruptures. There are two general types of cardiac valve defects: stenosis and insufficiency. Some patients, however, may have a combination of stenosis and insufficiency. Valvular stenosis results from a narrowing of the valve orifice that is usually caused by a thickening and increased rigidity of the valve leaflets, often accompanied by calcification. When this occurs, the valve does not open completely as blood flows across it, thereby resulting in a high resistance to flow and the development of a large pressure gradient across the valve when blood is flowing through the valve. Valvular insufficiency results from the valve leaflets not completely sealing when the valve is closed so that regurgitation of blood occurs (backward flow of blood) into the proximal chamber. What are the clinical symptoms of defective valves? 14 Cardiac Cycle Valvular stenosis and insufficiency can have serious cardiac consequences, and produce the following clinical symptoms: Shortness of breath (dyspnea) Fatigue Reduced exercise capacity Light headedness or fainting (syncope) Heart failure Pulmonary hypertension Pulmonary/systemic edema Chest pain (angina) Arrhythmias Blood clots (thromboembolism) which can cause stroke 15 Cardiac Cycle Valvular Stenosis
Stenosis of either atrioventricular valves (tricuspid, mitral) or outflow tract valves (pulmonic, aortic) leads to a pressure gradient across the valve during the time blood is flowing through the valve opening. This increased pressure gradient is expressed as an increase in the pressure proximal to the valve and a small fall in pressure distal to the valve. The magnitude of the pressure gradient depends on the severity of the stenosis and the flow rate across the valve. Mitral valve stenosis results from a narrowing of the mitral valve orifice when the valve is open. The high resistance across the stenotic mitral valve causes blood to back up into the left atrium thereby increasing LA pressure. This results in the left atrial (LA) pressure being much greater than left ventricular (LV) pressure during diastolic filling (shaded gray in figure). The gradient is highest during early diastole when the the flow across the valve is highest. Normally, the pressure gradient across the valve is very small (a few mmHg); however, the pressure gradient can become quite high during severe stenosis (10-30 mmHg). Despite this elevated LA pressure, filling (end-diastolic volume) of the left ventricle may be significantly reduced. (The effects of mitral stenosis on ventricular filling can be appreciated better by examining the changes in the LV pressure-volume loop). The reduced ventricular filling (decreased preload) decreases ventricular stroke volume by the Frank-Starling mechanism. If stroke volume falls significantly, the reduced cardiac output may result in a reduction in aortic pressure. The increase in LA pressure can cause pulmonary congestion and edema because of increased pulmonary capillary hydrostatic pressure. Mitral valve stenosis is associated with a diastolic murmur because of turbulence that occurs as blood flows across the stenotic valve. Tricuspid valve stenosis is similar to mitral valve stenosis except that the pressure and volume changes occur on the right side of the heart. 16 Cardiac Cycle Aortic valve stenosis is characterized by the left ventricular pressure being much greater than aortic pressure during left ventricular ejection (shaded gray in figure). LV pressure is greatly elevated and the aortic pressure is slightly reduced in this example. Normally, the pressure gradient across the aortic valve is very small (a few mmHg); however, the pressure gradient can become quite high during severe stenosis (>100 mmHg). The pressure gradient across the stenotic lesion results from both increased resistance (related to narrowing of the valve opening) and turbulence distal to the valve. The magnitude of the pressure gradient is determined by the severity of the stenosis and the flow rate across the valve. Severe aortic stenosis results in 1) reduced ventricular stroke volume due to increased afterload (which decreases ejection velocity), 2) increased end-systolic volume, and 3) a compensatory increase in end-diastolic volume and pressure. (These changes in ventricular pressures and volumes are best depicted using pressure-volume loops). Long-term consequences include left ventricular hypertrophy and heart failure. Aortic valve stenosis is associated with a midsystolic systolic murmur because of turbulence that occurs as blood flows across the stenotic valve. Pulmonic valve stenosis is analogous to aortic valve stenosis except that the changes in pressure are on the right side of the heart. A pressure gradient occurs across the pulmonic valve during right ventricular ejection. Compensatory increases in right ventricular end-diastolic pressure as well as right atrial pressure and volume occur. 17 Cardiac Cycle Valvular Insufficiency (Regurgitation)
Valvular insufficiency results from the valve leaflets not completely sealing when the valve is closed so that regurgitation of blood occurs (backward flow of blood) into the proximal chamber. Aortic regurgitation occurs when the aortic valve fails to close completely and blood flows back into the left ventricle after ejection into the aorta is complete (after S2). Normally, there is a brief period of time after the aortic valve closes when the ventricle relaxes isovolumetrically (the mitral valve is also closed during this phase). But when the aortic valve is leaky, the ventricle begins to fill from the aorta after the incomplete closure of the aortic valve. This leads to an increase in ventricular volume prior to the opening of the mitral valve and normal ventricular filling. Because blood is leaving the aorta in two directions (back into the heart as well as down the arterial network), the aortic diastolic pressure falls more rapidly thereby leading to a decrease in arterial diastolic pressure. Because the ventricle fills from both the aorta and the left atrium, there is a large increase in left ventricular volume and pressure (increased preload), which is best depicted by pressure-volume loops for this condition. The increased preload causes the left ventricle to contract more forcefully (FrankStarling mechanism), thereby increasing ventricular (and aortic) systolic pressure and increasing stroke volume to help compensate for the regurgitation. The increase in ventricular end-diastolic pressure, however, also leads to an increase in left atrial pressure, which can result in pulmonary congestion and edema. Regurgitation, coupled with enhanced left ventricular stroke volume, results in a characteristic widening of the aortic pulse pressure. The backward flow of blood into the ventricular chamber during diastole results in a diastolic murmur between S2 and S1. Early in the course of regurgitant aortic valve disease, there is a large increase in left ventricular end-diastolic pressure and left atrial pressure. The ventricle and atria function on a stiffer portion of their compliance curves so that the increased volume results in a large rise in pressure. With long-standing regurgitation, the ventricles and atria dilate so that the increased volume does not result in an exceptionally large 18 Cardiac Cycle increase in pressure. In other words, remodeling of the chambers results in increased compliance and more normal filling pressures. Pulmonary valve regurgitation has a similar hemodynamic basis as aortic regurgitation except that the changes in pressures and volumes are noted on the right side of the heart (pulmonary artery, right ventricle, and right atrium). Mitral valve regurgitation occurs when the mitral valve fails to close completely, which causes blood to flow back (regurgitate) into the left atrium during ventricular systole (between S1 and S2). The backward flow results in a holosystolic murmur. Because the left atrium now receives blood from the ventricle as well as from the pulmonary veins, there is a large increase in the v-wave as the left atrium fills. The regurgitation reduces the net stroke volume of the ventricle into the aorta, although total ventricular stroke volume defined as the enddiastolic minus the end-systolic volume increases. Changes in ventricular pressures and volume are best depicted using pressure-volume loops. Increased blood volume in the left atrium enlarges the atrial chamber and increases the atrial pressure. The left atrium compensates by increasing its force of contraction through the Frank-Starling mechanism in order to enhance ventricular filling. However, the increased atrial pressure can lead to pulmonary congestion and edema. In in the course of chronic mitral regurgitation (or after sudden regurgitation caused by rupture of the chordae tendineae or papillary muscle dysfunction), the atrial pressure can become very elevated. In long-standing mitral regurgitation, the left atrium adapts to the larger volume by dilating, which increases its compliance. This remodeling can help to normalize the left atrial pressure. Tricuspid valve regurgitation has a similar hemodynamic basis as mitral regurgitation except that the changes in pressures and volumes are noted on the right side of the heart (pulmonary artery, right ventricle, and right atrium). 19 Cardiac Cycle Mitral Stenosis
The following describes changes that occur in the left ventricular pressure-volume loop when there is mitral stenosis. Mitral stenosis (red pressure-volume loop in figure) impairs left ventricular filling so that there is a decrease in end-diastolic volume (preload). This leads to a decrease in stroke volume by the Frank-Starling mechanism and a fall in cardiac output and aortic pressure. This reduction in afterload (particularly aortic diastolic pressure) enables the end-systolic volume to decrease slightly, but not enough to overcome the decline in end-diastolic volume. Therefore, because enddiastolic volume decreases more than end-systolic volume decreases, the stroke volume (shown as the width of the loop) decreases. The changes described above and shown in the figure do not include cardiac and systemic compensatory mechanisms (e.g., systemic vasoconstriction, increased blood volume, and increased heart rate and inotropy) that attempt to maintain cardiac output and arterial pressure. 20 Cardiac Cycle Aortic Stenosis
The following describes changes that occur in the left ventricular pressure-volume loop when there is aortic stenosis. In aortic stenosis (red loop in figure), left ventricular emptying is impaired because of high outflow resistance caused by a reduction in the valve orifice area when it opens. This high outflow resistance causes a large pressure gradient to occur across the aortic valve during ejection, such that the peak systolic pressure within the ventricle is greatly increased. This leads to an increase in ventricular afterload, a decrease in stroke volume, and an increase in end-systolic volume. Stroke volume (width of pressure-volume loop) decreases because the velocity of fiber shortening is decreased by the increased afterload (see force-velocity relationship). Because end-systolic volume is elevated, the excess residual volume added to the incoming venous return causes the end-diastolic volume to increase. This increases preload and activates the Frank-Starling mechanism to increase the force of contraction to help the ventricle overcome, in part, the increased outflow resistance. In mild aortic stenosis, this can be adequate to maintain normal stroke volume, but in moderate stenosis (as shown in the figure) or severe stenosis, the stroke volume may fall considerably because the end-systolic volume increases substantially more than the end-diastolic volume increases. The fall in stroke volume can lead to a reduction in arterial pressure. Stroke volume falls even further if the ventricle begins to exhibit systolic and diastolic dysfunction. Compensatory increases in end-diastolic volume will be limited by ventricular hypertrophy that occurs due to the chronic increase in afterload. This hypertrophy can lead to large increases in enddiastolic pressure. The changes described above and shown in the figure do not include cardiac and systemic compensatory mechanisms (e.g., systemic vasoconstriction, increased blood volume, and increased heart rate and inotropy) that attempt to maintain cardiac output and arterial pressure, nor do they include the ventricular hypertrophy (remodeling) that decreases ventricular compliance. 21 Cardiac Cycle Mitral Regurgitation
The following describes changes that occur in the left ventricular pressure-volume loop when there is mitral regurgitation. In mitral valve regurgitation (red pressure-volume loop in figure), as the left ventricle contracts, blood is not only ejected into the aorta but also back up into the left atrium. This causes left atrial volume and pressure to increase during ventricular systole. Note in the pressure-volume loop that there is no true isovolumetric contraction phase because blood begins to flow across the mitral valve and back into the atrium before the aortic valve opens as soon as ventricular pressure exceeds left atrial pressure. Because of mitral regurgitation, the afterload on the ventricle is reduced (total outflow resistance is reduced) so that end-systolic volume can be smaller than normal; however, end-systolic volume can increase if the heart also goes into systolic failure. There is no true isovolumetric relaxation because when the aortic valve closes and the ventricle begins to relax, the mitral valve is not completely close so blood flows back into the left atrium (therefore further decreasing ventricular volume) as long as intraventricular pressure is greater than left atrial pressure. During ventricular diastolic filling, the elevated pressure within the left atrium is transmitted to the left ventricle during filling so that left ventricular end-diastolic volume (and pressure) increases. This would cause wall stress (afterload) to increase if it were not for the reduced outflow resistance because of mitral regurgitation that tends to decrease afterload during ejection because of reduced pressure development by the ventricle. The net effect of these changes is that the width of the pressure-volume loop is increased (i.e., ventricular stroke volume is increased); however, ejection into the aorta (forward flow) is reduced. The increased ventricular "stroke volume" (measured as the end-diastolic minus the end-systolic volume) in this case includes the volume of blood ejected into the aorta as well as the volume ejected back into the left atrium. These changes just described do not include cardiac and systemic compensatory mechanisms (e.g., systemic vasoconstriction, increased blood volume, and increased heart rate and inotropy) that attempt to maintain cardiac output and arterial pressure, nor do they include the ventricular dilation (remodeling) that increases ventricular compliance. 22 Cardiac Cycle Aortic Regurgitation
The following describes changes that occur in the left ventricular pressure-volume loop when there is aortic regurgitation. In aortic valve regurgitation (red loop in figure), the aortic valve does not close completely at the end of systolic ejection. As the ventricle relaxes during diastole, blood flows from the aorta back into the ventricle so the ventricle immediately begins to fill from the aorta. Therefore, there is no true phase of isovolumetric relaxation because as the ventricle relaxes, even before the mitral valve opens, blood is entering the ventricle from the aorta thereby increasing ventricular volume. Once the mitral valve opens, filling occurs from the left atrium; however, blood continues to flow from the aorta into the ventricle throughout diastole because aortic pressure is higher than ventricular pressure during diastole. This greatly enhances ventricular filling so that end-diastolic volume is increased as shown in the pressurevolume loop. When the ventricle begins to contract and develop pressure, blood is still entering the ventricle from the aorta because aortic pressure is higher than ventricular pressure; therefore, there is no true isovolumetric contraction because volume continues to increase. Once the ventricular pressure exceeds the aortic diastolic pressure, the ventricle then begins to eject blood into the aorta. The increased enddiastolic volume (increased preload) activates the Frank-Starling mechanism to increase the force of contraction, ventricular peak (systolic) pressure, and stroke volume (as shown by the increased width of the pressure-volume loop). As long as the ventricle is not in failure, end-systolic volume may only be increased a small amount (as shown in figure) due to the increased afterload (ventricular wall stress). If the ventricle goes into systolic failure, then endsystolic volume will increase by a large amount and the peak systolic pressure and stroke volume (net forward flow into aorta) will fall. These changes just described do not include cardiac and systemic compensatory mechanisms (e.g., systemic vasoconstriction, increased blood volume, and increased heart rate and inotropy) that attempt to maintain cardiac output and arterial pressure, nor do they include the ventricular dilation (remodeling) that increases ventricular compliance. 23 Cardiac Cycle Heart Sounds
When a stethoscope is placed over different regions of the heart, there are four basic heart sounds that can be heard (listening to heart sounds is called cardiac auscultation). The sounds waves responsible for heart sounds (including abnormal sounds such as murmurs) are generated by vibrations induced by valve closure, abnormal valve opening, vibrations in the ventricular chambers, tensing of the chordae tendineae, and by turbulent or abnormal blood flow across valves or between cardiac chambers (see heart anatomy). The most fundamental heart sounds are the first and second sounds, usually abbreviated as S1 and S2. S1 is caused by closure of the mitral and tricuspid valves at the beginning of isovolumetric ventricular contraction. S1 is normally slightly split (~0.04 sec) because mitral valve closure precedes tricuspid valve closure; however, this very short time interval cannot normally be heard with a stethoscope so only a single sound is perceived. S2 is caused by closure of the aortic and pulmonic valves at the beginning of isovolumetric ventricular relaxation. S2 is physiologically split because aortic valve closure normally precedes pulmonic valve closure. This splitting is not of fixed duration. S2 splitting changes depending on respiration, body posture and certain pathological conditions. The third heart sound (S3), when audible, occurs early in ventricular filling, and may represent tensing of the chordae tendineae and the atrioventricular ring, which is the connective tissue supporting the AV valve leaflets. This sound is normal in children, but when heard in adults it is often associated with ventricular dilation as occurs in systolic ventricular failure. The fourth heart sound (S4), when audible, is caused by vibration of the ventricular wall during atrial contraction. This sound is usually associated with a stiffened ventricle (low ventricular compliance), and therefore is heard in patients with ventricular hypertrophy, myocardial ischemia, or in older adults. 24 Cardiac Cycle Heart Sound Occurs during: S1 Isovolumetric contraction S2 Isovolumetric relaxation S3 Early ventricular filling Associated with: Closure of mitral and tricuspid valves Closure of aortic and pulmonic valves Normal in children; in adults, associated with ventricular dilation (e.g. ventricular systolic failure) Associated with stiff, low compliant ventricle (e.g., ventricular hypertrophy S4 Atrial contraction 25 ...
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This note was uploaded on 04/18/2008 for the course BIOC 1010 taught by Professor Zhang during the Fall '07 term at New York Medical College.
- Fall '07