Ventricular Diastolic Filling and Function

Phases of Diastole

Diastole is the interval from aortic valve closure (end-systole) to mitral valve closure (end-diastole) ( Fig. 7.1 ). The isovolumic contraction period, from mitral valve closure to aortic valve opening, is part of systole.

Diastole can be divided into four phases:

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  Isovolumic relaxation

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  Early rapid diastolic filling

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  Diastasis

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  Late diastolic filling caused by atrial contraction

Isovolumic relaxation starts with aortic valve closure, followed by a rapid decline in LV pressure. When LV pressure falls below LA pressure, the mitral valve opens, ending the isovolumic relaxation period. Maximal opening of the mitral leaflets occurs rapidly, within 100 ± 10 ms of valve opening, in normal individuals. Mitral valve opening is followed by rapid early diastolic filling , with the rate and time course of LA to LV flow determined by several factors, including the pressure difference along the flow stream, ventricular relaxation, and the relative compliances of the two chambers.

As the ventricle fills, pressures in the atrium and ventricle equalize, resulting in a period of diastasis, during which little movement of blood between the chambers occurs, and the mitral leaflets remain in a semiopen position. The duration of diastasis depends on heart rate; it is longer at slow heart rates and entirely absent at faster heart rates. With atrial contraction , LA pressure again exceeds LV pressure, thus resulting in further mitral leaflet opening and a second pulse of LV filling. In normal individuals this atrial contribution accounts for only about 20% of total ventricular filling ( Fig. 7.2 ).

The phases of diastole for the RV are analogous to those described for the LV, with the difference that the total duration of diastole is slightly shorter in normal individuals because of a slightly longer RV systolic ejection period.

Parameters of Diastolic Function

Several physiologic parameters can be used to describe different aspects of diastolic function, but no single measure of overall diastolic function exists. The most clinically relevant parameters of diastolic function are:

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  Ventricular relaxation

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  Myocardial or chamber compliance

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  Filling pressures

Additional parameters of interest include elastic recoil of the ventricle and the effect of pericardial constraint, but the importance of these factors in normal diastolic ventricular function remains controversial.

Ventricular Relaxation

LV relaxation, occurring during isovolumic relaxation and the early diastolic filling period, is an active process involving the use of energy by the myocardium. Factors affecting isovolumic relaxation include internal loading forces (cardiac fiber length), external loading conditions (wall stress, arterial impedance), inactivation of myocardial contraction (metabolic, neurohumoral, and pharmacologic), and nonuniformity in the spatial and temporal patterns of these factors. Abnormal relaxation results in prolongation of the isovolumic relaxation time, a slower rate of decline in ventricular pressure, and a consequent reduction in the early peak filling rate (due to a smaller pressure difference between the atrium and the ventricle when the atrioventricular valve opens). Measures of LV relaxation include the isovolumic relaxation time (IVRT), the maximum rate of pressure decline ( − dP/dt), and the time constant of relaxation (tau or τ). Several different mathematical approaches to the calculation of τ are available, but basically it reflects the rate of pressure decline from the point of maximum − dP/dt to mitral valve opening. Although peak rapid filling rate is affected by ventricular relaxation, it is only an indirect measure of this physiologic parameter because several other factors also affect peak filling ( Fig. 7.3 ).

Ventricular Compliance

Compliance is the ratio of change in volume to change in pressure (dV/dP). Stiffness is the inverse of compliance: the ratio of change in pressure to change in volume (dP/dV). Conceptually, compliance can be divided into myocardial (the characteristics of the isolated myocardium) and chamber (the characteristics of the entire ventricle) components. Chamber compliance is influenced by ventricular size and shape, in addition to the characteristics of the myocardium. Extrinsic factors also affect measurement of compliance, including the pericardium, RV volume, and pleural pressure. Evaluation of ventricular compliance is based on diastolic passive pressure-volume curves showing the degree to which pressure and volume change in relation to each other over the physiologic range ( Fig. 7.4 ).

Atrial Pressures and Filling Curves

Another component in the evaluation of ventricular diastolic function is the measurement of atrial filling patterns and pressures. The atrium serves as a “conduit” for flow from the venous circulation to the ventricle, especially in early diastole, when the atrium is not contracting. In addition, elevations in ventricular diastolic pressures are reflected in elevated pressures in the atrium ( Fig. 7.5 ).

RA pressures normally are quite low (0 to 5 mmHg), with only small increases in pressure following atrial ( a -wave) and ventricular ( v -wave) contraction.

Right atrial filling is characterized by:

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  A small reversal of flow following atrial contraction ( a -wave)

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  A systolic phase (which is effectively “diastole” for the atrium) when blood flows from the superior and inferior vena cavae into the atrium

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  A small reversal of flow at end-systole ( v -wave)

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  A diastolic filling phase when the atrium serves as a conduit for flow from the systemic venous return to the RV

These filling phases are reflected in the patterns of jugular venous pulsation familiar to the clinician: the a -wave following atrial contraction, the x -descent corresponding to atrial filling during ventricular systole, the v -wave at end-systole, and the y -descent corresponding to atrial filling during ventricular diastole. Disease processes affect the jugular venous pulsations and the Doppler pattern of RA filling in similar ways.

LA filling from the pulmonary veins also is characterized by:

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  A small reversal of flow following atrial contraction ( a -wave)

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  A systolic filling phase

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  A blunting of flow or brief reversal at end-systole ( v -wave)

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  A diastolic filling phase

In normal individuals, the systolic and diastolic filling phases are approximately equal in volume. Normal LA pressure is low (5 to 10 mmHg), corresponding to the normal LV end-diastolic pressure, with slight increases in pressure following atrial ( a -wave) and ventricular ( v -wave) contraction.

Normal Respiratory Changes

Normal LV and RV diastolic filling shows respiratory variation. With inspiration, negative intrapleural pressure results in an increase in systemic venous return into the thorax and thus into the RA. This increase in RA volume and pressure results in a transient increase in RV diastolic filling volumes and velocities, with a normal magnitude of increase of up to 20% compared with end-expiratory values.

LA filling does not increase with inspiration because pulmonary venous return is entirely intrathoracic and thus not affected significantly by respiratory changes in intrathoracic pressure. In fact, LA and, consequently, LV diastolic filling is slightly higher at end-expiration than during inspiration. The mechanism of this observation remains controversial. Some investigators postulate a delay in transit of the increased RV filling to the left side of the heart. Others suggest a decrease in LA filling during inspiration because of an increased volume (or “pooling”) in the pulmonary venous bed. Less likely in normal individuals is impaired LV diastolic filling due to an increase in RV diastolic volume within a fixed-volume pericardium. This last mechanism becomes important in patients with pericardial disease (e.g., constriction, tamponade) and partly accounts for the exaggerated respiratory changes in RV and LV diastolic filling seen in these conditions.

Causes of Diastolic Dysfunction

Although diastolic dysfunction can be seen with a wide range of cardiac disorders, the four basic mechanisms of disease ( Table 7.1 ) that lead to diastolic dysfunction are:

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  Primary myocardial disease

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  Secondary LV hypertrophy

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  Coronary artery disease

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  Extrinsic constraint

Left Ventricular Changes

Evaluation of ventricular chamber dimensions and wall thickness is an integral part of the echocardiographic evaluation of diastolic function. The relative degree of systolic and diastolic dysfunction in patients with heart failure ranges from severe diastolic dysfunction with a normal ejection fraction to severe systolic dysfunction with normal filling pressures. However, most patients with systolic dysfunction have some degree of diastolic dysfunction, and most patients with diastolic dysfunction have anatomic cardiac changes evident on echocardiographic imaging. Typically, diastolic heart failure (HFpEF) occurs in patients with a thick-walled, small ventricle due to either restrictive cardiomyopathy or hypertensive heart disease. The presence and severity of LA enlargement reflect chronically elevated filling pressures, so that measurement of LA size or volume is integral to evaluation of diastolic function (see Fig. 2.16 ).

In patients with heart failure due primarily to systolic ventricular dysfunction (heart failure with reduced ejection fraction), typical imaging findings include a dilated LV with global or regional dysfunction and a reduced ejection fraction. Diastolic dysfunction usually accompanies systolic dysfunction, and measures of diastolic function and LV filling pressures are important for patient management and prognosis.

Left Atrial Volumes

LA volume is a key element in the evaluation of diastolic dysfunction. Measurement of LA volumes by two-dimensional (2D) or 3D imaging is feasible and accurate and is a strong predictor of clinical outcome. However, LA volume is nonspecific because, in addition to diastolic dysfunction, LA volume increases with age, athletic conditioning, cardiac arrhythmias, high-output states (e.g., anemia), and mitral valve disease.

Other Imaging Parameters

Other imaging findings that raise the question of diastolic dysfunction include pericardial thickening (as in constrictive pericarditis), the pattern of ventricular septal motion with respiration (especially with tamponade physiology), and dilation of the inferior vena cava and hepatic veins (consistent with elevated RA pressures). Elevated pulmonary artery systolic pressures, in the absence of another cause such as mitral valve disease or primary pulmonary disease, also raise the concern for LV diastolic dysfunction.

Nomenclature and Measurements

Doppler recordings of LV diastolic filling velocities correspond closely with ventricular filling parameters measured by other techniques. The normal Doppler ventricular inflow pattern is characterized by a brief time interval between aortic valve closure and the onset of ventricular filling (the isovolumic relaxation time). Immediately following mitral valve opening rapid acceleration of blood flow from the LA to the ventricle occurs with an early peak filling velocity of 0.6 to 0.8 m/s 90 to 110 ms after the onset of flow in young, healthy individuals ( Table 7.2 ). This early maximum filling velocity ( E velocity) occurs simultaneously with the maximum pressure gradient between the atrium and the ventricle. After this maximum velocity, flow decelerates rapidly (i.e., with a steep slope) in normal individuals with a normal deceleration slope of 4.3 to 6.7 m/s ² ( Table 7.3 ). Deceleration time, defined as the time interval from the E peak to where a line following the deceleration slope intersects with the zero baseline, ranges from 140 to 200 ms. Early diastolic filling is followed by a variable period of minimal flow (diastasis), depending on the total duration of diastole. With atrial contraction, LA pressure again exceeds ventricular pressure, with a resulting second velocity peak (late diastolic or atrial velocity), which typically ranges from 0.19 to 0.35 m/s in young, normal individuals ( Fig. 7.6 ).

Quantitative measurements that can be made from the Doppler velocity curve include ( Fig. 7.7 ):

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  Maximum velocities: The E velocity, the A velocity, and their ratio ( E/A ratio)

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  Velocity-time integrals: Total, early diastolic, atrial contribution, first third or half of diastole, and their ratios

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  Time intervals: The isovolumic relaxation time, the total duration of diastole, the deceleration time, and the atrial filling period

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  Measures of acceleration and deceleration: The time from onset of flow to the E velocity, the maximum rate of rise in velocity, and the slope of early diastolic deceleration