The Hemodynamics of Vascular Disease

John S. Pellerito MD, FACR, FSRU, FAIUM , in Introduction to Vascular Ultrasonography , 2020

Flow and pressure changes during the cardiac cycle

There are typical changes in pressure and blood flow during the cardiac cycle in large veins such as the vena cava ( Fig. 1.17). Such oscillations in pressure and flow may, at times, be transmitted to more peripheral vessels. There are three positive pressure waves (a, c, v) in the central veins corresponding to changes in pressure changes in the atria. Thea wave is caused by atrial contraction at end diastole. The upstroke of thec wave is related to the increase in pressure when the tricuspid valve is closed and bulges during isovolumetric ventricular contraction. The subsequent downstroke (x descent) results from the fall in pressure during atrial relaxation caused by pulling the tricuspid valve ring toward the apex of the heart during ventricular contraction, thus tending to increase right atrial volume. The upstroke of thev wave results from a passive rise in atrial pressure during late ventricular systole when the tricuspid valve is closed and the atrium fills with blood from the peripheral veins. The v wave downstroke is caused by the fall in pressure that occurs when the blood leaves the atria rapidly and fills the ventricles, soon after the opening of the tricuspid valve, early in ventricular diastole, the so-called y descent. Early ventricular filling starts at the y descent.

These venous pressure waves are associated with changes in blood flow. There are two periods of increased venous flow during each cardiac cycle (Fig. 1.18). The first occurs during ventricular systole, when shortening of the ventricular muscle pulls the tricuspid valve ring toward the apex of the heart. This movement of the valve ring tends to increase atrial volume and decrease atrial pressure, thus increasing flow from the extracardiac veins into the atrium. The second phase of increased venous flow occurs after the tricuspid valve opens and blood rushes into the ventricles from the atria. Venous flow is reduced in the intervening periods of the cardiac cycle as the atrial pressure rises during and soon after atrial contraction and in the later part of the ventricular systole. Because there are no valves at the junction of the right atrium and vena cava, blood flow transiently reverses in the large thoracic veins during atrial contraction.

The changes in pressure and blood flow in the large central veins that are associated with the events of the cardiac cycle are not usually evident in the peripheral veins of the extremities. This is probably the result of damping related to the high distensibility (compliance) of the veins, as well as compression of the veins by intra-abdominal pressure and mechanical compression in the thoracic inlet. Because the effects of right-sided heart contractions are more readily transmitted to the large veins of the arms, the pulsatile changes in venous blood flow velocity associated with the events of the cardiac cycle tend to be more obvious in the upper extremities than in the veins of the legs (Fig. 1.19).

DESIGN AND PHYSIOLOGY OF THE HEART | Physiology of Cardiac Pumping

A.P. Farrell , in Encyclopedia of Fish Physiology, 2011

The Flow Events: Cardiac Chamber Filling and Emptying

Figure 1 illustrates the sequential filling and emptying of the cardiac chambers during a cardiac cycle.

Figure 1. A schematic diagram of the three main phases of filling and emptying of four cardiac chambers of the fish heart. (a) Both the atrium and ventricle are filling due the venous blood pressure. (b) The atrium contracts (as shown by the small arrows), further expanding and completing the filling of the ventricle. (c) The ventricle contracts, ejecting fluid into the bulbus arteriosus. At the same time, the atrium begins to fill.

The cardiac cycle begins with the atrium and ventricle in a relaxed state. During diastole, blood flowing from central veins fills the atrium and partially fills the ventricle, passing through the sinus venosus, the sino-atrial (SA) canal and the atrio-ventricular (AV) canal. Atrial contraction (atrial systole) then ejects blood from the atrium and into the ventricle, which is still in diastole, and this completes ventricular filling. The contributions of these two phases of ventricular filling vary among species, with sometimes only ∼50% occurring via atrial contraction. In addition, the contribution of passive ventricular filling may decrease at high heart rates when the diastole is shorter.

Atrial relaxation (atrial diastole) occurs while the ventricle is contracting (ventricular systole). However, before ventricular contraction starts, the propagation of the action potential from the atrium is briefly delayed in the AV canal. This AV delay ensures that blood has sufficient time to move from the atrium and complete ventricular filling. Ventricular contraction ejects blood into the outflow tract past an opened bulbo-ventricular (BV) valve. The cardiac cycle is completed when the ventricle relaxes (ventricular diastole).

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Cardiac and Circulatory Function

Lee Goldman MD , in Goldman-Cecil Medicine , 2020

The Cardiac Cycle

In resting humans, the heart beats approximately once per second. With each beat, the heart cycles through a series of four hemodynamic events represented by changes in pressures and volumes (E-Fig. 47-4) as well as electrical activity as represented by the ECG. When the heart muscle is relaxed at end diastole, the ventricular pressure is at its resting level (end-diastolic pressure) and the ventricular volumes are at their maximal value (end-diastolic volume ). Aortic pressure declines as the blood ejected into the aorta during the previous ventricular contraction flows to the peripheral circulation. Atrial contraction provides a final boost to ventricular volume immediately before ventricular systole. Ventricular contraction increases the pressure in the ventricle; when this pressure exceeds the pressure in the atrium, the mitral valve closes. However, because ventricular pressure remains less than aortic pressure, the aortic valve remains closed, and no blood enters or leaves the ventricle during this first phase of the cardiac cycle, the isovolumic contraction phase. During systole, ventricular pressure eventually exceeds aortic pressure, at which time the aortic valve opens, blood is ejected into the aorta, and ventricular volume decreases during theejection phase of the cycle. At the end of systole when contraction is maximum, ejection ends, and the ventricular volumes are at their lowest (end-systolic volume). The volume of the ejected blood, which is termed the stroke volume (SV), is defined as the difference between the end-diastolic and end-systolic volumes. The ejection fraction (EF), defined as the percentage of end-diastolic volume (EDV) ejected during a contraction (EF = 100 × SV/EDV), is an index of heart function. The next phase in the cycle occurs when the heart muscle relaxes, ventricular pressures are less than the aorta pressure, and the aortic valve closes. During thisisovolumic relaxation phase, ventricular volumes remain constant because, once again, both the mitral and aortic valves are closed. When ventricular pressures fall below atrial pressures, the mitral and tricuspid valves open, and blood flows from the atria into the ventricles during thefilling phase.

E-FIGURE 47-4. Wiggers diagram.

Changes in aortic, left ventricular, and left atrial pressures represented graphically as a function of time, with the corresponding electrocardiogram signal for each. LVP = left ventricular pressure.

These four phases of the cardiac cycle can be represented by apressure-volume diagram (E-Fig. 47-5), which plots the instantaneous ventricular pressure versus volume to calculate thepressure-volume loop. Similar effects occur on the left and right sides of the heart, but with higher pressures on the left side (Table 47-1).

Murmurs

Andrew N. Pelech , in Nelson Pediatric Symptom-Based Diagnosis, 2018

Cardiac Cycle

Cardiac sounds and murmurs that arise from turbulence or vibrations within the heart and vascular system may be innocent or pathologic. It is important to understand the timing of events in the cardiac cycle as a prerequisite to understanding heart murmurs. The relationship between the normal heart cycle and that of the heart sounds is noted in Fig. 8.2.

The cardiac cycle begins with atrial systole, the sequential activation and contraction of the 2 thin-walled upper chambers. Atrial systole is followed by the delayed contraction of the more powerful lower chambers, termed ventricular systole. Ventricular systole has 3 phases:

1.

Isovolumic contraction: the short period of early contraction when the pressure builds within the ventricle but has yet to rise sufficiently to permit ejection

2.

Ventricular ejection: when the ventricles eject blood to the body (via the aorta) and to the lungs (via the pulmonary artery)

3.

Isovolumic relaxation: the period of ventricular relaxation when ejection ceases and pressure falls within the ventricles

During ventricular contraction, the atria relax (atrial diastole) and receive venous return from both the body and the lungs. Then, in ventricular diastole, the lower chambers relax, allowing initial passive filling of the thick-walled ventricles and emptying of the atria. Later, during the terminal period of ventricular relaxation, the atria contract. This atrial systole augments ventricular filling just before the onset of the next ventricular contraction.

The sequence of contractions generates pressure and blood flow through the heart. The relationship of blood volume, pressure, and flow determines opening and closing of heart valves and generates characteristic heart sounds and murmurs.

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Mechanisms of Cardiac Contraction and Relaxation

Douglas P. Zipes MD , in Braunwald's Heart Disease: A Textbook of Cardiovascular Medicine , 2019

The Cardiac Cycle

The cardiac cycle, fully assembled by Lewis 58 but first conceived by Wiggers, 59 yields important information on the temporal sequence of events ( Fig. 22.16 ). The three basic events with respect to the left ventricle are LV contraction, LV relaxation, and LV filling ( Table 22.3 ). Similar mechanical events occur in the right ventricle.

Left Ventricular Contraction

LV pressure increases as Ca2+ arrives at the contractile proteins after cellular depolarization triggers actin-myosin interaction. 4 This occurs shortly after the upstroke of the ventricular action potential, indicated by the QRS complex of the electrocardiogram (ECG; Fig. 22.16 ). When LV pressure exceeds that in the left atrium (normally 8 to 15 mm Hg), the mitral valve closes, causing the mitral component of the first sound, M1. Right ventricular (RV) pressure changes are usually slightly delayed because of electrical conduction, such that tricuspid valve closure (T1), follows M1. The phase of LV contraction after mitral closure and before aortic opening when the LV volume is fixed is referred to asisovolumic contraction. As more myofibers become activated, LV pressure proceeds to increase until it exceeds aortic pressure, causing the aortic valve to open (usually a clinically silent event). Opening of the aortic valve is followed by the phase ofrapid ejection. The rate of ejection is determined by the pressure gradient across the aortic valve, as well as the elastic properties of the aorta and the arterial tree, which undergo systolic expansion. LV pressure rises to a peak and then starts to fall.

Left Ventricular Relaxation

As myocyte [Ca2+]i starts to decline because of SR Ca2+ uptake, Ca2+ dissociates from troponin C, thereby preventing further cross-bridge formation. 4 As this state of relaxation progresses, the rate of LV ejection of blood into the aorta falls (phase of reduced ejection). During this phase, blood flow from the left ventricle to the aorta rapidly diminishes but is maintained by aortic recoil—the Windkessel effect. 4 When the pressure in the aorta significantly exceeds the falling LV pressure, the aortic valve closes, which creates the first component of the second sound, A2 (the second component, P2, results from closure of the pulmonic valve as pulmonary artery pressure exceeds RV pressure). Thereafter, the ventricle continues to relax. Because the mitral valve is still closed during this phase after aortic closure, LV volume cannot change (isovolumic relaxation). The rate of pressure decay during isovolumic relaxation is related to the magnitude of systolic shortening in the preceding contraction, similar to a spring compressed below its unstressed slack length. 60 When LV pressure falls to below that in the left atrium, the mitral valve opens (normally silent), and the filling phase of the cardiac cycle restarts ( Fig. 22.16 ).

Introduction

Lambros S. Athanasiou , ... Lampros K. Michalis , in Atherosclerotic Plaque Characterization Methods Based on Coronary Imaging, 2017

1.1.2 The Cardiac Cycle

The cardiac cycle includes two phases: diastole and systole ( Fig. 1.4). In the diastole phase, blood returns to the heart from the superior and interior vena cava and flows into the right atrium. The pressure in the right atrium increases as blood flows into it. When the pressure of the right atrium exceeds the pressure of the right ventricle, the tricuspid valve opens passively allowing blood to flow into the right ventricle. At the same time, the oxygenated blood returning from the lungs flows into the left atrium. As left atrial pressure increases, the mitral valve opens and blood flows into the left ventricle.

Figure 1.4. The cardiac cycle.

In the systole phase, blood is forced to flow from the two atria into their respective ventricles as the atrial muscles contract due to the depolarization of the atria. There is a period called isovolumetric contraction during which the ventricles contract but the pulmonary and aortic valves are closed as the ventricles do not have enough force to open them. The atrioventricular valves also remain closed during the isovolumetric contraction period. The semilunar valves open when the ventricular muscle contracts and generates blood pressure within the ventricle higher than within the arterial tree. When the heart muscle relaxes the diastole phase begins again.

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Overview of Cardiac Muscle Physiology

John W. Calvert , David J. Lefer , in Muscle, 2012

Ventricular Pumping during Systole and Diastole

The cardiac cycle refers to all of the events that occur from the beginning of one heartbeat to the beginning of the next and can be divided into two parts: a period of relaxation known as diastole and a period of contraction known as systole. The pressure and volume changes that occur during the cardiac cycle for the left ventricle are depicted in Figure 6.2 and will serve as a platform for describing key events. Importantly, these changes depicted here for the left ventricle also occur simultaneously in the right side of the heart in the right atrium, right ventricle, and pulmonary artery.

Figure 6.2. Pressure and volume changes that occur during the cardiac cycle for the left ventricle.

Events of the cardiac cycle for the left ventricle, showing changes in left atrial pressure, left ventricular pressure and volume, and aortic pressure. Point A, the opening of the AV valve. Point B, atrial contraction. Point C, closing of AV valve. Point D, opening of semilunar valve. Point E, closing of semilunar valve.

 (Adapted and redrawn from Guyton and Hall, Textbook of Medical Physiology (10th ed.), Philadelphia, PA, W.B. Saunders, 2000.)

Throughout the cardiac cycle the atria collect deoxygenated blood returning to the heart from the peripheral circulation and the coronary circulation (right atria) or from the pulmonary circulation (left atria). During diastole, the build up of blood in the atria creates a pressure gradient that forces open the AV valves allowing for about 75% of this blood to pass into the ventricle causing a gradual increase in ventricular diastolic pressure (point A). In late diastole, the contraction of the atria propels the remaining 25% of the blood into the ventricles, which produces a further increase in atrial and ventricle pressures (point B). Contraction of the ventricle then follows, signaling the onset of mechanical systole. As the ventricles contract, the pressures within them rapidly exceed atrial pressures. This pressure gradient pushes back on the leaflets of the AV valves and forces them closed (point C). The onset of the ventricular contraction also creates tension on the papillary muscles, which apply extra force to the edges of the leaflets ensuring the proper alignment of the valves, which aids in their closing. Further ventricular contraction causes ventricular pressure to exceed the diastolic pressures in the pulmonary artery and aorta, which forces the opening of the semilunar valves (point D). This allows the ventricles to empty their contents into the pulmonary and systemic circulations. Because the semilunar valves are open, the continued contraction of the ventricles increases the pressure in the pulmonary artery and aorta. The conclusion of ventricular ejection causes the pressure in the ventricles to fall below those of the pulmonary artery and aorta. This allows for the blood in the pulmonary artery and aorta to push back on the semilunar valves forcing them closed (point E). The cardiac cycle then begins once again with the ventricles filling with blood that has collected in the atria.

The relationship between left ventricular volume and intraventricular pressure during systole and diastole is represented by the pressure–volume curves depicted in Figure 6.3. The curve for diastolic pressure is determined by filling the heart with increasing amounts of blood and then measuring intraventricular pressure before the start of contraction. In other words, this curve represents the end-diastolic pressure for a given amount of blood volume. The curve for systolic pressure represents the measurement of the intraventricular pressure at the end of contraction for each volume of filling. It is important to note that the pressure volume curve for diastole is initially flat, indicating that increasing the volume of the blood only minimally increases ventricular pressure. This holds true up to about 150   ml. Above this volume the pressure increases rapidly, partially because the fibrous tissue of the heart and the pericardium that surrounds the heart has reached its limits of stretching. In contrast, systolic pressure increases rapidly even at low ventricular volumes and continues to increase at a steady rate before reaching a maximum of roughly 250   mmHg at a volume of 150–170   ml. Above this volume, systolic pressure actually decreases because at these great volumes the actin and myosin filaments of the cardiac muscle are pulled apart in such a way that the strength of contraction becomes less than optimal.

Figure 6.3. Relationship between left ventricular volume and intraventricular pressure during systole and diastole.

The curve for diastolic pressure is determined by filling the heart with increasing amounts of blood and then measuring intraventricular pressure before the start of contraction. In other words, this curve represents the end-diastolic pressure for a given blood volume. The curve for systolic pressure is essentially the exact opposite for that of diastolic pressure, as it is a measurement of the intraventricular pressure at the end of contraction for each volume of filling.

 (Adapted and redrawn from Guyton and Hall, Textbook of Medical Physiology (10th ed.), Philadelphia, PA, W.B. Saunders, 2000.)

While the curves depicted in Figure 6.3 nicely represent the changes in left ventricular pressure in response to increasing amounts of blood volume, they do not really portray an acute picture of the normal changes that occur throughout a single cardiac cycle. This is depicted in Figure 6.4 as a standard pressure–volume loop, which is divided into four phases. Phase I is called the period of filling and begins at point A when diastolic filling begins. At this point, there is about 45   ml of blood in the ventricles and the pressure is about 0   mmHg. The 45   ml represents the amount of blood left in the ventricles after the previous heartbeat and is known as the end-systolic volume. The initial decrease in pressure from point A to point B that occurs despite an increase in volume is attributed to the progressive ventricular relaxation and distensibility. During the remainder of diastole (point B to C), the ventricle continues to fill with blood with only a minimal increase in pressure. The small increase in volume and pressure just to the left of point C is caused by the contribution of atrial contraction to ventricular filling. Phase I ends at point C, when diastole ends. At this point the ventricular volume has increased by about 70   ml to a total of 115   ml (end-diastolic volume) and the pressure has risen to 5   mmHg (end-diastolic pressure). Phase II is known as the period of isovolumic contraction and begins at point C. This phase is characterized by a large increase in pressure without a change in volume. The reason that the volume does not change during phase II is that all of the valves are closed, so blood can neither enter nor leave the ventricle. During phase II, the pressure in the ventricle increases to about 80   mmHg, which equals the pressure in the aorta. Point D represents the end of phase II and the beginning of phase III, which is known as the period of relaxation. During the initial phase of ejection (point D to point E), systolic pressure continues to rise even higher due to contraction of the heart. At the same time the volume of the ventricles starts to decrease because the aortic valve has opened and blood is flowing out of the ventricle and into the aorta (point E to point F). The closing of the aortic valve at point F marks the end of phase III and the beginning of phase IV, which is known as the period of isovolumic relaxation. A sharp drop in pressure back to the diastolic pressure level with no change in volume characterizes this phase. Thus, the ventricle returns to its starting point with about 45   ml of blood and a pressure of 0   mmHg. The mitral valve opens at this point and the entire cycle begins again.

Figure 6.4. Pressure–volume loop of the left ventricle for a single cardiac cycle.

The standard pressure–volume loop for a single cardiac cycle is divided into four phases. Phase I is called the period of filling and begins at point A when diastolic filling begins. Phase II is known as the period of isovolumic contraction and begins at point C. Phase III is known as the period of ejection and begins at point D. The closing of the aortic valve at point F marks the end of phase III and the beginning of phase IV, which is known as the period of isovolumic relaxation.

 (Adapted and redrawn from Berne and Levy, Cardiovascular Physiology (8th ed.), St Louis, MO, Mosby, 2001.)

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Normal Cardiac Physiology and Ventricular Function

B.D. Hoit , in Reference Module in Biomedical Sciences, 2014

The Cardiac Cycle

The cardiac cycle describes pressure, volume, and flow phenomena in the ventricles as a function of time. This cycle is similar for both the left and right ventricles, although there are differences in timing, which stem from differences in the depolarization sequence and the levels of pressure in the pulmonary and systemic circulations. For simplicity, the cardiac cycle for the left heart during one beat has been described ( Figure 10).

Figure 10. Pressure flow, volume, electrocardiographic, and phonocardiographic events constituting the cardiac cycle.

 Reproduced with permission from Berne, R.M., Levy, M.N., 1988. Physiology, second ed. Mosby, St Louis, p. 444.

The QRS complex on the surface ECG represents ventricular depolarization. Contraction (systole) begins after an approximately 50 ms delay and results in closure of the mitral valve. The left ventricle contracts isovolumetrically until the ventricular pressure exceeds the systemic pressure, which opens the aortic valve and results in ventricular ejection. Bulging of the mitral valve into the left atrium during isovolumetric contraction causes a slight increase in left atrial pressure (c wave). Shortly after ejection begins, the active state of ventricular myocardium declines and ventricular pressure begins to decrease. Left atrial pressure rises during ventricular systole (v wave) as blood returns to the left atrium by means of the pulmonary veins. The aortic valve closes when left ventricular pressure falls below aortic pressure, and momentum briefly maintains forward flow despite greater aortic than left ventricular pressure. Ventricular pressure then declines exponentially during isovolumetric relaxation, when both the aortic and mitral valves are closed. This begins the ventricular diastole. When ventricular pressure declines below left atrial pressure, the mitral valve opens and ventricular filling begins. Initially, ventricular filling is very rapid because of the relatively large pressure gradient between the atrium and ventricle. Ventricular pressure continues to decrease after mitral valve opening because of continued ventricular relaxation; its subsequent increase (and the decrease in atrial pressure) slows ventricular filling. Especially at low end-systolic volumes, early rapid ventricular filling can be facilitated by ventricular suction produced by elastic recoil. Ventricular filling slows during diastasis, when atrial and ventricular pressures and volumes increase vary gradually. Atrial depolarization is followed by atrial contraction, increased atrial pressure (a wave), and a second, late rapid-filling phase. A subsequent ventricular depolarization completes the cycle.

Valve closure and rapid-filling phases are audible with a stethoscope placed on the chest and can be recorded phonocardiographically after electronic amplification. The first heart sound, resulting from cardiohemic vibrations with closure of the AV (mitral, tricuspid) valves, heralds ventricular systole. The second heart sound, shorter and composed of higher frequencies than the first, is associated with closure of the semilunar valves (aortic and pulmonic) at the end of ventricular ejection. Third and fourth heart sounds are low-frequency vibrations caused by early rapid filling and late diastolic atrial contractile filling, respectively. These sounds can be heard in normal children, but in adults they usually indicate disease.

An alternative time-independent representation of the cardiac cycle is obtained by plotting instantaneous ventricular pressure and volume (Figure 11). During ventricular filling, pressure and volume increase nonlinearly (phase I). The instantaneous slope of the pressure–volume (P-V) curve during filling (dP/dV) is diastolic stiffness, and its inverse (dV/dP) is compliance. Thus, as chamber volume increases, the ventricle becomes stiffer. In a normal ventricle, operative compliance is high, because the ventricle operates on the flat portion of its diastolic P-V curve. During isovolumetric contraction (phase II) pressure increases and volume remains constant. During ejection (phase III) pressure rises and falls until the minimum ventricular size is attained. The maximum ratio of pressure to volume (maximal active chamber stiffness or elastance) usually occurs at the end of ejection. Isovolumetric relaxation follows (phase IV), and when left ventricular pressure falls below left atrial pressure, ventricular filling begins. Thus, end-diastole is at the lower right-hand corner of the loop, and end systole is at the upper left corner of the loop. Left ventricular P-V diagrams can illustrate the effects of changing preload, afterload, and inotropic state in the intact ventricle (see the following).

Figure 11. (a) Left ventricular pressure–volume (P-V) loop, the segments of which correspond to events of the cardiac cycle: diastolic ventricular filling along the passive P-V curve (phase I), isovolumetric contraction (phase II), ventricular ejection (phase III), and isovolumetric relaxation (phase IV). (b) The ventricle ejects to an end-systolic volume determined by the peak isovolumetric P-V line; an isovolumetric contraction (large arrowheads) from varying end-diastolic volumes (preload).

 Reproduced with permission from Hoit, B.D., Walsh, R.A., 1996. Determinants of left ventricular performance and cardiac output. In: Sperelakis, N., Banks, R.O. (Eds.), Essentials of Physiology, second ed. Little, Brown, and Company, Boston, p. 274.

A P-V loop can also be described for atrial events (Hoit et al., 1994). During ventricular ejection, descent of the ventricular base lowers atrial pressure and thus assists in atrial filling. Filling of the atria from the veins results in a v wave on the atrial and venous pressure tracing. When the mitral and tricuspid valves open, blood stored in the atria empties into the ventricles. Atrial contraction denoted by an a wave on the atrial pressure tracing actively assists ventricular filling. The resultant atrial P-V diagram has a figure-of-eight configuration with a clockwise V loop, representing passive filling and emptying of the atria and a counterclockwise A loop, representing active atrial contraction. Thus, the atria function as a reservoir and conduit for venous flow (during ventricular systole and diastole, respectively), and as a booster pump for ventricular filling late in diastole.

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Evaluation of Diastolic Function by Two-Dimensional and Doppler Assessment of Left Ventricular Filling Including Pulmonary Venous Flow

CHRISTOPHER P. APPLETON MD , in Diastology, 2008

INTRODUCTION

The cardiac cycle is continuous. The filling of the ventricle (diastole) is followed by ventricular contraction (systole) to provide an adequate cardiac output during both rest and exercise to meet the body's metabolic demands. Systole and diastole affect each other in an intimate manner to accomplish this goal. The normal elastic recoil after left ventricular (LV) contraction aids early filling of the ventricle, with the late diastolic atrial contraction ensuring that the myocardial sarcomeres are adequately stretched to optimize contractile force. Exercise tests the health of this integrated system by shortening the time for filling and myocardial perfusion, and a normally functioning cardiac electrical system is also needed for optimal performance.

The "new" epidemiology of LV diastolic dysfunction has been discussed in Chapter 6 of this volume. Diastolic heart failure is now recognized as a major national health problem, especially in the elderly, who have a high incidence of LV hypertrophy (LVH). These patients present with symptomatic heart failure despite a normal LV ejection fraction (LVEF) and have morbidity and mortality that is nearly equal to that of patients with reduced systolic function. Diastolic heart failure patients are also at risk for first-onset atrial fibrillation and a higher incidence of stroke. Although LVEF is normal in diastolic heart failure, ventricular contractile mechanics have been altered in a way that lengthens the isovolumic contraction and relaxation period so that the period for diastolic filling becomes shorter and may be inadequate. In both systolic and diastolic heart failure, the degree of diastolic dysfunction is a powerful predictor of prognosis.

Despite this new appreciation of the importance of both systole and diastole in maintaining normal cardiovascular physiology, the role of LV diastolic function in health and disease is incompletely understood and underappreciated by many primary care physicians and cardiologists. As discussed in Chapter 2, diastole is a complex phenomenon with many determinants that are difficult to study individually and several phases that encompass both the relaxation and the filling of the ventricle. Physical examination, echocardiography (ECG), chest radiographs, and laboratory studies are unreliable in diagnosing diastolic heart failure in most individuals, and invasive measurements of LV diastolic properties and pressures are impractical in clinical practice. Therefore, at present, assessing the type and degree of LV diastolic dysfunction relies on evaluating the pattern of LV filling. Although this can be accomplished by radionuclide and computed tomography (CT) angiographic and magnetic resonance imaging (MRI) techniques, cardiac ultrasound is currently the method of choice because of its noninvasive and portable nature. Evaluating LV filling by two-dimensional anatomic findings, Doppler flow, and tissue Doppler imaging (TDI) have emerged as powerful clinical techniques to predict adverse cardiovascular events such as new-onset atrial fibrillation and heart failure, as well as mortality regardless of LVEF. The purpose of this chapter will be to describe the various LV filling patterns encountered in clinical practice, and what these patterns and their measurable variables reveal about LV diastolic function. In cases of possible ambiguity, ancillary variables such as left atrial (LA) volume, pulmonary venous (PV) flow velocity, and TDI that help in interpreting mitral flow velocity patterns will be discussed.

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Coronary Microvascular Dysfunction

Paolo G. Camici , ... Filippo Crea , in Chronic Coronary Artery Disease, 2018

Extramural Compression

During the cardiac cycle the pulsatile pattern of CBF follows typical physiologic variations, which are influenced by the variations in intramyocardial and intracavitary pressures occurring during systole and diastole (see Fig. 5.1). 14,23 Approximately 90% of CBF occurs in diastole, and therefore diastolic abnormalities have a more significant impact on myocardial perfusion. Nevertheless, an increase in systolic intramyocardial and intracavitary pressures, for example in conditions of increased pressure overload, may negatively impact on myocardial perfusion. An increased microvascular compression during systole hinders subendocardial vessels' tone restoration in diastole, thus impairing diastolic microvascular CBF in the subendocardial layers. 62

Diastolic CBF is impaired whenever intracavitary diastolic pressure is increased. This is the case in the presence of either primary or secondary LV hypertrophy (LVH) 32 and also in the presence of diastolic dysfunction consequent to increased interstitial and perivascular fibrosis. 63 Diastolic impairment of CBF is enhanced when arteriolar driving pressure during diastole is significantly lower than intracavitary pressure, as in patients with severe aortic stenosis, critical coronary stenoses, prearteriolar constriction, or merely hypotension.

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