The Ventricle As A Muscle

For convenience, it is useful to consider contraction (systolic performance) as distinct from relaxation and filling (diastolic performance). This distinction is arbitrary, however. The two aspects of function overlap and interact.

Systolic Function

Systolic performance of the ventricle traditionally is characterized in terms of loading conditions (preload, afterload) and contractility.112 Although contractility is a term that is employed frequently and often perfectly reasonably, it is difficult to define. We use it here as a comparative concept to connote differences in the intrinsic level of contractile performance either before or after some intervention in the same heart or between different hearts that cannot be accounted for by differences in loading conditions. Thus one way to define a change or difference in contractility is as a change or difference in contractile performance when loading conditions are unchanged or can be accounted for, e.g., increased shortening despite increased afterload. Unfortunately, this is often impossible in the intact heart, especially in the clinical setting. Further, any definition of contractility that attempts to neatly separate it from loading conditions inevitably encounters the fundamental problem that the two are not really separable. A good example of this problem is the Frank-Starling relation, in which preload influences intrinsic contractile performance by modulating myofilament Ca sensitivity. Similarly, afterload, by influencing shortening, determines instantaneous length and myofilament Ca sensitivity during the course of contraction. Thus, while contractility is a useful concept, the notion that it is possible to define load-independent contractility indices is not entirely realistic.

Loading Conditions and Contractile Performance

In classic, isolated muscle experiments,58,60 a force in the form of a weight is applied to one end of a quiescent, quasi-linear muscle (e.g., a cardiac papillary muscle) whose other end is tethered (Fig. 3-17). This force is the preload, which stretches the muscle to some initial length preceding contraction. The muscle is then simulated electronically to contract and lift an additional weight, the afterload. Once stimulated, the muscle develops tension or force until it just meets and then slightly exceeds the opposing force of the afterload. At this point in time, the muscle can begin to lift the afterload, and shortening commences. In this system, once shortening begins, the developed force and afterload are constant (isotonic contraction). Force or afterload is reciprocally related to the magnitude and velocity of shortening; muscle performance is often characterized as the force-velocity or force-shortening relation (see Fig. 3-12), with upward or downward shifts reflecting changes in contractility. If both ends of the muscle are tethered, or if the afterload simply exceeds the force-generating capacity of the muscle, an isometric contraction ensues, in which tension is generated, but no shortening occurs. By varying the preload, the Frank-Starling effect (see Fig. 3-13) can be delineated by relating the initial length to shortening (isotonic contraction) or developed tension or force (isometric contraction).

Muscle Tension Starling

Figure 3-17: Schematic illustrating concept of preload and afterload during isotonic contraction. (Left) Linear muscle is depicted as consisting of contractile element (CE) (i.e., thick and thin filaments) and spring in series (SE). (Right) Shortening and force are depicted. A. Muscle is at rest, with one end tethered and the other connected to a weight (P). P is supported, however, so that muscle is only subjected to a fraction of weight (or load). This relatively small load is the preload, which stretches the muscle to the initial, resting length. B. Muscle begins to contract. In order to shorten, it must lift the entire weight P, which is the afterload. Initially, force increases but is insufficient to lift the weight. During this period, the CE shortens and reciprocally lengthens the SE, while total muscle length remains constant. Eventually, the developed force just exceeds the afterload, and the muscle begins to shorten (C). Once shortening begins, force is constant and essentially equal to the afterload. In an isometric contraction, the muscle cannot lift the load and therefore does not shorten (although the CE shortens and SE lengthens by the same amount).

Figure 3-17: Schematic illustrating concept of preload and afterload during isotonic contraction. (Left) Linear muscle is depicted as consisting of contractile element (CE) (i.e., thick and thin filaments) and spring in series (SE). (Right) Shortening and force are depicted. A. Muscle is at rest, with one end tethered and the other connected to a weight (P). P is supported, however, so that muscle is only subjected to a fraction of weight (or load). This relatively small load is the preload, which stretches the muscle to the initial, resting length. B. Muscle begins to contract. In order to shorten, it must lift the entire weight P, which is the afterload. Initially, force increases but is insufficient to lift the weight. During this period, the CE shortens and reciprocally lengthens the SE, while total muscle length remains constant. Eventually, the developed force just exceeds the afterload, and the muscle begins to shorten (C). Once shortening begins, force is constant and essentially equal to the afterload. In an isometric contraction, the muscle cannot lift the load and therefore does not shorten (although the CE shortens and SE lengthens by the same amount).

In isolated muscle, load also can be expressed as stress (force normalized to cross-sectional area). Normalization allows comparison of muscles of different size. Normalization for stress can be transferred to the ventricle, most easily the LV because of its relatively symmetrical shape. Estimation of LV wall stress can be accomplished by using the LaPlace relation.113 For a relatively thick-walled sphere, the LaPlace relation states that the average wall stress equals (pressure x internal radius) divided by twice the wall thickness. Variants of this equation can be employed to account for the actual shape of the LV, fiber orientation, and other geometric and structural features. Thus, for an ellipsoid, the ratio of the long to short axis (a measure of how ellipsoidal the shape is) modifies the stress; as shape changes from less to more spherical, wall stress increases.

Use of the LaPlace relation allows an estimate of the stress "seen" by the myofibers as the ventricle fills and then contracts against its afterload. In diastole, the stress applied to the myofibers constitutes their preload and determines initial length at the beginning of the next contraction. During contraction, the stress resulting from both the preload and the afterload (or systolic load) determines the velocity and extent of ejection. Total systolic load presented to the LV by the vascular system has two components, a resistive load determined at the level of small systemic arteries and arterioles by microvascular tone and a smaller capacitive load determined by the properties of the large arteries, which absorb a certain amount of blood pumped via expansion of their walls.ii4 As mentioned earlier, a component of vascular load is caused by reflection of pressure waves back to the heart from the periphery. In contrast to classic, isolated muscle experiments, during ventricular contraction, both afterload and developed wall stress vary.

Estimates of systolic stress using the LaPlace relation are helpful clinically in assessing and comparing contractile performance.!!-5 This can accomplished by relating some measure of shortening [e.g., ejection fraction (EF), defined as SV/ED volume] or shortening velocity [e.g., mean velocity of circumferential fiber shortening (Vcf); see discussion below] to a measure of systolic stress [e.g., peak, end-systolic (ES), or mean]. The ventricle behaves in a qualitatively similar fashion as isolated muscle; i.e., afterload (wall stress) is reciprocally related to shortening. As shown in Fig. 3-18, the stress-shortening relation can be characterized in a normal population with single data points obtained invasively or using noninvasive techniques such as echocardiography and cuff sphygmomanometry. If the value in a given patient falls above or below the normal range, this may indicate an alteration in intrinsic contractile performance.

Clinically, the most commonly employed index of ventricular contractile function is the EF (from angiography, echocardiography, or radionuclide ventriculography). Fractional shortening (minor axis diameter shortening/ED minor axis diameter) is calculated routinely from the echocardiogram and is interchangeable with EF, provided there are no regional wall motion abnormalities. Both these shortening measurements are sensitive to alterations in preload and afterload.!!2 Thus normal values are indicative of normal intrinsic contractile function only if loading conditions are also normal.

Elastance Concepts in the Assessment of Ventricular Contractile Function

As an alternative to characterization of systolic function in terms of stress and shortening, Suga and Sagawa proposed an elastance approach.116-118 This is based on the empirical observation that during systole the ventricle behaves like a spring with a time-varying elastance (or stiffness) that increases from a minimum at ED to a maximum at ES Fig. 3-19). The elastance of a spring is the slope of the linear relation between the stress or force applied to stretch it and its length normalized to its unstressed or rest length. A "stiffer" spring requires a larger stress to extend it by a given length. By analogy, ventricular elastance is the relation between pressure and volume at any time during systole normalized to a volume at which the pressure is zero (dead volume, Vq or Vd).

At any time during contraction, elastance can be estimated by varying loading conditions and generating a series of pressure-volume loops with varying ES volumes. In their original studies, Suga and Sagawa used isolated, perfused canine ventricles with controlled loading conditions and volumes.116,117 Analysis of such a series of pressure-volume loops (see Fig. 3-19) reveals that at any time t during each of the series of variably loaded contractions (e.g., 100 ms after the start of contraction), the relation between pressure and volume is linear, and its slope reaches a maximum (maximal elastance) at ES, or tmax. (The volume axis intercept can be measured directly or extrapolated from the linear pressure-volume relation at any time t.) Elastance then decreases as the ventricle relaxes. The slope (Emax) of the end-systolic pressure-volume relationship (ESPVR) changes with acute positive and negative inotropic interventions. Specifically, Emax increases with positive inotropic interventions and decreases with negative inotropic interventions, whereas Vq usually does not change. Based on these observations and initial studies suggesting that ED volume did not influence the ESPVR, it was thought initially that Emax offered the possibility of an index of contractility that was "load independent." Subsequent studies, especially those performed in the in situ heart and circulation, have modified these original conclusions.!!^ Thus the ESPVR is often significantly curvilinear, especially with augmented or depressed contractility. Furthermore, as expected based on the concept of length-dependent activation, it is influenced to some extent by preload (ED volume) and also can be modified by the way in which afterload is varied (e.g., resistive versus capacitive load change).

Systolic interaction also can modify the ESPVR.H9 Emax must be used with caution in comparing different hearts because of difficulties in normalizing ES relationships for size and variable curvilinearity. To overcome these problems, the ESPVR has been modified by calculating ES myocardial stiffness based on wall stress estimates, and comparative analyses have been devised that take curvilinearity into account.115,120-123 Last, the pressure-volume approach does not include rate of change of these parameters and therefore does not capture power output,58,112 an important aspect of performance.

Despite the aforementioned cautions, the ESPVR has proven to be a useful conceptual approach to assessment of contractile function in the experimental laboratory and the clinic. Measurements have been made in hearts as small as that of the mouse,124 whereas estimation of ES pressure and/or stress-volume relations can be obtained in patients.115,125 Although it corresponds to only a single point on the ESPVR, the ratio of systolic arterial pressure (as a surrogate for ES pressure) to ES volume determined noninvasively using cuff sphygmomanometry and echocardiography also has been used as an index of ventricular function. Moreover, despite the empirical nature of the original observations, the elastance approach has been shown to be very consistent with the molecular physiology of ECC and crossbridge cycling.126

Two extensions of elastance theory have proven valuable in understanding ventricular function. The first is its application to ventricular mechanoenergetics.i27 The main determinants of VO2 traditionally have been considered HR, afterload, and contractility (basal metabolism accounts for a significant fraction of VO2 but is not subject to much variability). HR is obviously a critical determinant of energy consumption per unit time. However, the difficulty in even defining contractility was discussed earlier. Moreover, it is not obvious how contractility or afterload is related quantitatively to the two major energy-consuming processes in heart, ECC and crossbridge cycling.

As proposed by Suga,127 use of elastance theory to quantify mechanoenergetics is based on quantification of the total mechanical energy of contraction. Total mechanical energy consists of two components (Fig. 320, top), external work (EW), which can be quantified as the area enclosed within the pressure-volume loop of a contraction, and potential energy (PE), which is dissipated as heat during relaxation and possibly also converted to kinetic energy used for filling the ventricle by suction (see below). To understand PE in this context, consider an isovolumic contraction, which can be produced experimentally. Such a contraction obviously generates mechanical energy, but none of it is EW; i.e., it is all PE. As afterload is reduced and shortening and work increase, the ratio of EW to PE increases. The novelty of elastance theory in quantifying total mechanical energy is that it provides a basis for quantifying PE. In elastance theory, the PE stored in a spring is the area under its elastance relationship between its rest length and its actual length. Correspondingly, in the ventricle, PE for any beat can be considered the area under the ESPVR between its ES point and Vq (see Q+S; Figs. 3-19 and 3-20). The sum of EW and PE is total mechanical energy and is termed pressure-volume area (PVA). The relation between PVA and VO2 requires knowledge of the ESPVR and can be delineated by widely varying loading conditions while measuring LV VO2. This is done most easily in isolated, perfused heart preparations.123,127,128 PVA has a remarkably high linear correlation with VO2 in several species, under a variety of loading conditions, and in both normal and abnormal hearts123,124,127,128 (see Fig. 3-20, bottom).

Schematic Pva
Figure 3-20: (Top) Schematic of VO2-PVA concept (see text). In ejecting contraction, PVA = EW + PE; in isovolumic contraction, PVA = PE only. (Bottom) Correlation of PVA with VO2. (From Goto et al.128 Reproduced with permission of publisher.)

The linear VO2-PVA relation has a positive VO2 axis intercept (see Fig. 3-20), unloaded VO2, or O2 consumption at zero PVA, when virtually no mechanical energy is produced. Unloaded VO2 is largely accounted for by basal metabolism and Ca pumping by SERCA2, which continue under unloaded conditions. Subtraction of unloaded VO2 from total VO2 provides an estimate of VO2 used by the contractile machinery, or PVA-dependent VO2. Since VO2 can be converted to units of energy, the ratio of PVA to PVA-dependent VO2 (total mechanical energy output divided by total chemical energy input), or simply the inverse slope of the linear VO2-PVA relation, is an estimate of the efficiency of conversion of O2 to mechanical energy by the contractile machinery. Variations in myosin ATPase activity modulate efficiency assessed in this fashion.124,129

Based on the preceding analyses, it can be understood how changes in afterload and contractility as well as preload can alter myocardial energy demands and consumption (see Fig. 3-20). Assuming no change in ED volume or afterload, increased contractility increases £max, resulting in a smaller ES volume and increased

EW at any preload. Even though ES volume is smaller, which in and of itself decreases PE, this is at least partially compensated by increased Emax, which serves to increase the area under the ESPVR. The net result is increased PVA in association with more energy used for crossbridge cycling by the contractile machinery. Most positive inotropic interventions increase the amount of Ca cycled per beat and, in turn, energy consumption by SERCA2, resulting in increased unloaded VO2. Increased afterload increases the level of pressure at which the pressure-volume loop intersects the ESPVR, increasing PE with variable effects on EW but a net increase in PVA. In the whole LV, increases in preload have not been considered to markedly alter myocardial energy demands. Assuming constant contractility (ESPVR) and afterload, it is evident that changes in ED volume (preload) should modify EW and therefore PVA and VO2 in direct proportion to the magnitude of the change. However, it is likely that under basal conditions the LV operates at an ED volume not too far from the point at which the diastolic pressure-volume relation becomes relatively steep. Thus there is not a great deal of room for the LV to acutely increase its preload (although its FP certainly may increase considerably). This may explain the modest effect of preload on VO2.

A second application of elastance theory is ventricular-vascular coupling.130,131 Just as the ventricle can be considered in terms of an elastance relationship, systemic arteries also can be characterized by an elastance relationship. Arterial elastance is largely a function of the properties of the large arteries. There exists an optimal relationship between ventricular and arterial elastance at ES such that energy transfer from the heart to the periphery is most efficient; i.e., the largest possible proportion of total mechanical VO2 is converted to EW. In essence, this merely states that arterial loading influences the point at which the pressure-volume loop intersects the ESPVR and therefore the proportion of PVA converted to EW. The normal heart and vascular system operate at nearly optimal ventricular-vascular coupling. Vasoactive drugs can influence ventricular-vascular coupling. Moreover, in heart failure, coupling is adversely affected, resulting in less efficient transfer of energy from the heart to the vascular system.132

Other Approaches to Assessment of Systolic Ventricular Performance

Following is a sampling of a number of indexes that have been proposed to assess systolic function. Maximal rate of pressure rise (max dP/dt) is very sensitive to changes in intrinsic contractile performance but also varies somewhat with preload.133 134 It is not markedly influenced by changes in afterload. Max dP/dt is especially useful in quantifying acute changes in contractility. Its use for comparisons between different patients is limited by large interindividual variations. Mean circumferential fiber shortening velocity (Vc/)135-136 is LV internal minor axis shortening + (ejection time x ED minor axis dimension). It is readily calculated from echocardiograms. Although quite sensitive to changes in afterload (as is any shortening measurement), it is a useful measure of intrinsic contractile performance if afterload is normal or can be accounted for. Maximal ventricular power index137 is attractive because of its physiologic importance; i.e., it takes into account both the work done by the ventricle and the time over which it is generated. This index has been normalized to minimize effects of loading and has the potential for noninvasive determination. Two empirical indexes have been devised that appear to be relatively afterload-insensitive. One of these is preload recruitable stroke work,138 the relationship between ED volume (or strain) and stroke work. The other is the relationship between ED volume and max dP/dt.139-140 Both are linear and in essence representations of the Frank-Starling relation; by incorporating ED volume, length-dependent activation is an intrinsic component of these indexes.

Diastolic Function

In addition to meeting widely varying physiologic demands for blood flow, the heart must do so at levels of FP that do not result in circulatory congestion. This requires a normal sequence of relaxation and filling. Ventricular relaxation begins at about ES (defined as the time of maximal elastance, slightly before Ao valve closure), continues through isovolumic relaxation, and does not reach completion until after AV valve opening. Before filling commences, several factors combine to determine relaxation rate, represented by isovolumic pressure decline Fig. 3-21). After filling begins, but before relaxation is complete, other factors related to the level of ventricular volume and/or the rate of ventricular volume change also influence ventricular diastolic pressure. Once relaxation is complete, the so-called passive properties of the ventricle dominate the relation between pressure and volume as filling continues through ED.

During isovolumic relaxation, pressure falls exponentially. The rate of isovolumic pressure fall (a measure of relaxation rate) therefore has been quantified as a time constant (x)141,142 or simply the time to reach one-half of some starting value (71/2, typically measured beginning at peak negative dP/dtPeak negative dP/dt, maximal rate of pressure fall, also has been used but is less accurate. The determinants of the rate of isovolumic pressure fall are as follows:65!41!42!44 First, as discussed earlier, myocyte relaxation rate is determined by the balance between the avidity of the contractile proteins for Ca and the rate at which SERCA2 and other uptake and extrusion mechanisms remove Ca from the contractile proteins and restore the cytoplasmic concentration to normal diastolic levels. In some pathologic conditions, e.g., certain types of ischemia, diastolic Ca may not be restored to normal.145 Relaxation is therefore incomplete, and crossbridge cycling continues during diastole, resulting in increased diastolic tension. Isovolumic relaxation is also modulated by the load on the myocardium. 141,142,144,146150 Increased afterload through all of systole or beginning early in systole (a contraction load) results in delayed relaxation. Changes in load occurring late during systole (a relaxation load) cause opposite effects. Although changes in relaxation load may be considered to be of theoretical interest only, this may not be the case. Normal arterial waves reflected from the periphery return to the ventricle at about ES and may function to accelerate relaxation. When arteries become noncompliant, e.g., with aging, reflected waves return earlier and therefore may be converted to a contraction load, with delay of relaxation. Last, a normal temporal and spatial activation sequence results in the most rapid relaxation rate.151

As soon as ventricular pressure falls below atrial pressure, filling commences. As noted earlier, the magnitude and rate of ventricular filling are determined by the instantaneous AV pressure gradient (see Fig. 3-2). It is self-evident that the gradient is determined by properties of both ventricle and atrium. Immediately after AV valve opening, the rapid period of filling begins in association with a gradient of several millimeters of mercury (see Fig. 3-2). This corresponds to the E wave of mitral inflow measured with echocardiographic-Doppler techniques. During rapid filling, both ventricular and atrial pressures initially fall, but ventricular pressure falls faster than atrial pressure. Ventricular pressure soon reaches a minimum and then increases throughout the rest of diastole. The peak AV gradient occurs at or near the time of minimum ventricular pressure. (As noted earlier, it is common to observe a brief period of gradient reversal during the latter portion of rapid filling. Due to inertial effects, there is no retrograde mitral flow.) Rapid filling is succeeded by the variable slow filling phase during which the AV gradient is small to negligible. During this phase, a small, secondary increase in inflow (the L wave) is observed occasionally. The length of the slow filling phase is markedly dependent on HR, being maximal at slow rates and disappearing at rapid rates. Atrial contraction increases the AV gradient once again and injects an additional volume of blood into the ventricle.

The ventricular properties that determine pressure and the AV gradient during filling are as follows: As indicated earlier, relaxation continues past the time of AV valve opening. Therefore, the same factors (Ca reuptake, load) that modulate isovolumic pressure fall also influence pressure after filling begins. However, effects of load on relaxation rate may differ somewhat once filling begins.144,148,150

In addition to the ongoing process of relaxation, restoring forces generated during contraction also influence ventricular pressure during the early, rapid filling phase.152,154 By a restoring force, we mean PE generated during contraction in the form of a deformation(s) of the myocyte and/or the ventricle that can be converted into kinetic energy during diastole, accelerating flow of blood from atrium to ventricle. Restoring forces are caused by functional springs whose compression during contraction is converted to elastic recoil during diastole and filling by suction. When present, this active, energy-requiring driving force for filling results in lowering of ventricular pressure relative to atrial pressure and a larger AV gradient. Restoring forces are probably generated by two interrelated mechanisms. One is contraction of the ventricle to an ES volume below equilibrium volume (Ve?), the volume at which, in the fully relaxed state, the pressure inside and outside the chamber is equal (transmural pressure = 0). With contraction below Veq, the fully relaxed intracavitary pressure is negative with respect to the outside, and the chamber may be considered to be under compression. If allowed to fill, the PE stored in the walls results in elastic recoil and filling until Veq is reached. As noted earlier, titin appears to be the site of a restoring force in the myocyte. The second mechanism involves complex, contraction-dependent three-dimensional deformations that are normally dissipated (by elastic recoil) during isovolumic relaxation and the early phase of ventricular filling. One of these is torsional rotation. The magnitude of these deformations increases as ES volume decreases;1^3 105,155 hence they parallel compressive forces related simply to contraction below Veq. As a corollary, whether and how much of a restoring force is present are critically dependent on the ES volume in relation to Veq. The sine qua non of suction is a negative transmural pressure early during diastole, but this is rarely observed because filling is occurring rapidly and is driven simultaneously by the atrial pressure. Thus the presence of suction is ordinarily obscured. However, suction appears to be important at diastolic volumes within the physiologic range and especially during the stress of exercise, when ES volume decreases.103'104 A second myocardial property that theoretically influences ventricular pressure during rapid filling is viscous resistance to stretch, i.e., intrinsically greater stiffness at high lengthening rates due to elements that behave like dashpots.156 This property does not appear to be significant under normal physiologic conditions, however.

Relaxation and the generation of restoring forces are dynamic aspects of filling whose influence varies with time. Underlying these time varying properties is the passive ventricular pressure-volume relationship, the exponential relation between pressure and volume in the fully relaxed state.157 We will refer to this as the end diastolic pressure volume relationship (EDPVR) Fig. 3-22). (Although usually considered only at positive transmural pressures, as discussed earlier and as shown in Fig. 3-21, the EDPVR has a negative-pressure portion. The volume at zero transmural pressure is once again Veq.) Passive chamber compliance is the ratio of change in volume to change in pressure at any point on the EDPVR. Because the EDPVR is exponential, passive compliance is inversely related to volume. The inverse of chamber compliance is passive chamber stiffness. The EDPVR is determined mainly by the geometry of the ventricular chamber, especially the chamber volume to wall thickness ratio, and the intrinsic stiffness of the myocardial tissue itself. Thus, all else being equal, increases in wall thickness or myocardial stiffness increase its slope. Intrinsic stiffness is the change in stress (force normalized to cross-sectional area) occurring in association with a given change in strain (extension of the tissue above some initial length or area). Passive myocardial stiffness is largely accounted for by the properties of titin4344 at relatively low volumes and by connective tissue at larger volumes. Throughout all of relaxation and filling, a portion of the pressure in the ventricle is dictated by its position on its EDPVR. Early during filling, the relation between ventricular pressure and volume is determined by relaxation and elastic recoil (when present), superimposed on the EDPVR; the EDPVR alone is the prime determinant of ventricular pressure once relaxation is complete.

The EDPVR is modified by external restraints. The most important is the parietal pericardium.158 The pericardial sac has a relatively small reserve volume; at total heart volumes in the physiologic range, the pressure in the sac is very low in relation to left-side FPs. However, with relatively modest increments in volume above the physiologic range, the pericardial pressure-volume relation becomes quite steep (noncompliant), and the pressure rises rapidly. This external pressure acting on the surface of the heart is transmitted to the chambers and serves to restrain further filling; i.e., it decreases chamber compliance. Even under physiologic conditions, however, pericardial pressure is significant in relation to right-side FPs, which are normally lower than left-side FPs. Thus effective pericardial pressure is normally responsible for a significant fraction of right-side FP. Restraint to filling by the pericardium becomes quite important when the heart dilates rapidly, e.g., after RV myocardial infarction. The interventricular septum constitutes about one-third of the LV wall; diastolic pressure in the RV is therefore also an external restraint to filling of the LV (and vice versa). That is, a component of LV diastolic pressure is transmitted from the RV, an effect termed diastolic interaction.158 Diastolic interaction is normally modest but can become important when RV diastolic pressure is elevated, often in conjunction with augmented pericardial restraint.

An additional factor that influences the EDPVR is the volume of blood in the myocardial vascular bed, or myocardial turgor.159 A significant component of pressure in the fully relaxed ventricle is accounted for by turgor. This component is almost certainly reasonably constant under normal physiologic conditions because coronary blood volume is more or less constant. The significance of turgor is evident from the substantial drop in diastolic pressure that occurs when coronary flow is terminated abruptly.159

Following rapid filling and the variable period of slow filling, atrial contraction injects additional blood into the ventricle (typically one-quarter to one-third of the SV). During atrial systole, ventricular pressure and volume track the EDPVR.157

Atrial properties are also a key determinant of the AV gradient that drives filling.160 During ventricular systole, the atria fill continuously. Therefore, atrial pressure at the instant of AV valve opening is determined directly by atrial compliance; the lower the compliance, the higher is the pressure and the larger is the gradient. The relationship between ventricular pressure and volume as diastolic filling proceeds is also influenced by the properties of the atrium, as well as the pulmonary veins (for the LV). This is so because the ventricle, atrium, and pulmonary veins are an open system when the mitral valve is open. The ventricles, being much stiffer, are much more important determinants of the ventricular diastolic pressure-volume relation than the atria. Last, the contractile strength of the atrium is obviously a determinant of the gradient during atrial systole.

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