What is filling pressure

Contact Credits Site map. Other PIE sites. Feedback Send us your comments. Donate to PIE Donate today! If there is mitral valve disease, left ventricular disease or pulmonary hypertension the LVEDP cannot be estimated from right heart pressures. The problem of the ambiguity of "filling pressure s " is readily solved by the abandonment of this term and the use of either LVEDP or mean LAP as appropriate. Keywords: Left atrial pressure; Left ventricular end diastolic pressure; Left ventricular filling pressure; Left ventricular filling pressures.

The longitudinal vectors result in shortening of the LV long axis and descent of the mitral annulus toward the apex. The velocity of this motion can be readily obtained with tissue Doppler by placing the sample volume at a corner of the annulus; the recorded velocities reflect the longitudinal vector of contraction and relaxation of that particular wall at its base Fig.

Although one can obtain recordings from the septal, lateral, anterior, and inferior corners of the annulus, in routine clinical practice the septal and lateral corners provide most of the needed information. In addition, Ea declines gradually with aging, concordant with other indices of relaxation, and is inversely affected by increasing afterload.

In the normally contracting and relaxing heart, Ea is directly altered by changes in preload. However, this relation virtually disappears in abnormal hearts with impaired relaxation. This can be expressed mathematically as:. Evaluation of Intracardiac Filling Pressures. Two-Dimensional Echocardiography Echocardiography plays a pivotal role in the evaluation of patients presenting with dyspnea of suspected cardiac origin.

Example of a patient in whom the anteroposterior left atrial dimension LAd is mildly increased 4. No pseudonormal noted. Recording of left ventricular outflow and transmitral velocity. Both recordings provide a measurement of isovolumic relaxation time IVRT as the interval from the end of ejection to the onset of mitral inflow. Examples of normal transmitral velocity with the three stages of diastolic dysfunction patterns.

Range of values is listed under each pattern. Diagrammatic illustration of transmitral and pulmonary vein velocities in normal relaxation, impaired left ventricular LV relaxation with normal left atrial pressure LAP , and impaired relaxation with high LAP. Box Increased afterload Aging Systemic hypertension Pathologic secondary left ventricular hypertrophy Hypertrophic cardiomyopathy Ischemia Myocardial diseases Infiltrative cardiomyopathies. Modified from Nagueh SF et al: Feasibility and accuracy of Doppler echocardiographic estimation of pulmonary artery occlusive pressure in the intensive care unit.

Am J Cardiol ;— Transmitral and pulmonary vein velocity recorded in a patient with elevated left ventricular end diastolic pressure.

A, Color Doppler image obtained in an apical four-chamber view with the M-mode cursor positioned through the center of the mitral inflow. Because the Valsalva maneuver decreases preload during the strain phase, pseudonormal mitral inflow changes to a pattern of impaired relaxation. Furthermore, the lack of reversibility with Valsalva is imperfect as an indicator that the diastolic filling pattern is irreversible.

One major limitation of the Valsalva maneuver is that not everyone is able to perform this maneuver adequately, and it is not standardized. Its clinical value in distinguishing normal from pseudonormal mitral inflow has diminished since the introduction of tissue Doppler recordings of the mitral annulus to assess the status of LV relaxation and estimate filling pressures more quantitatively and easily.

In a busy clinical laboratory, the Valsalva maneuver can be reserved for patients in whom diastolic function assessment is not clear after mitral inflow and annular velocity measurements. PW Doppler of pulmonary venous flow is performed in the apical 4-chamber view and aids in the assessment of LV diastolic function. In most patients, the best Doppler recordings are obtained by angulating the transducer superiorly such that the aortic valve is seen. Wall filter settings must be low enough to display the onset and cessation of the atrial reversal Ar velocity waveform.

The major technical problem is LA wall motion artifacts, caused by atrial contraction, which interferes with the accurate display of Ar velocity. There are two systolic velocities S1 and S2 , mostly noticeable when there is a prolonged PR interval, because S1 is related to atrial relaxation.

S2 should be used to compute the ratio of peak systolic to peak diastolic velocity. S1 velocity is primarily influenced by changes in LA pressure and LA contraction and relaxation, 59 , 60 whereas S2 is related to stroke volume and pulse-wave propagation in the PA tree.

Recording of mitral inflow at the level of the annulus left and pulmonary venous flow right from a patient with increased LVEDP. Mitral A duration is best recorded at the level of the annulus. Pulmonary venous inflow velocities are influenced by age Table 1.

This isolated increase in LVEDP is the first hemodynamic abnormality seen with diastolic dysfunction. Other Doppler echocardiographic variables, such as maximal LA size, mitral DT, and pseudonormal filling, all indicate an increase in mean LA pressure and a more advanced stage of diastolic dysfunction. Unlike mitral inflow velocities, few studies have shown the prognostic role of pulmonary venous flow.

One of the important limitations in interpreting pulmonary venous flow is the difficulty in obtaining high-quality recordings suitable for measurements.

This is especially true for Ar velocity, for which atrial contraction can create low-velocity wall motion artifacts that obscure the pulmonary flow velocity signal. Sinus tachycardia and first-degree AV block often result in the start of atrial contraction occurring before diastolic mitral and pulmonary venous flow velocity has declined to the zero baseline. This increases the width of the mitral A-wave velocity and decreases that of the reversal in the pulmonary vein, making the Ar-A relationship difficult to interpret for assessing LV A-wave pressure increase.

With atrial fibrillation, the loss of atrial contraction and relaxation reduces pulmonary venous systolic flow regardless of filling pressures. The most widely used approach for measuring mitral-to-apical flow propagation is the slope method. The M-mode scan line is placed through the center of the LV inflow blood column from the mitral valve to the apex. Then the color flow baseline is shifted to lower the Nyquist limit so that the central highest velocity jet is blue.

Flow propagation velocity Vp is measured as the slope of the first aliasing velocity during early filling, measured from the mitral valve plane to 4 cm distally into the LV cavity.

Similar to transmitral filling, normal LV intracavitary filling is dominated by an early wave and an atrial-induced filling wave. Most of the attention has been on the early diastolic filling wave, because it changes markedly during delayed relaxation with myocardial ischemia and LV failure.

In the normal ventricle, the early filling wave propagates rapidly toward the apex and is driven by a pressure gradient between the LV base and the apex. During heart failure and during myocardial ischemia, there is slowing of mitral-to-apical flow propagation, consistent with a reduction of apical suction.

Not only driving pressure, inertial forces, and viscous friction but geometry, systolic function, and contractile dyssynchrony play major roles. The slow mitral-to-apical flow propagation in a failing ventricle is in part attributed to ring vortices that move slowly toward the apex. The complexity of intraventricular flow and the limitations of current imaging techniques make it difficult to relate intraventricular flow patterns to LV myocardial function in a quantitative manner.

There is a well-defined intraventricular flow disturbance that has proved to be a semiquantitative marker of LV diastolic dysfunction, that is, the slowing of mitral-to-apical flow propagation measured by color M-mode Doppler.

In addition, it is possible to use Vp in conjunction with mitral E to predict LV filling pressures. Acquisition is performed in the apical 4-chamber view, using color flow imaging. The M-mode scan line is placed through the center of the LV inflow blood column from the mitral valve to the apex, with baseline shift to lower the Nyquist limit so that the central highest velocity jet is blue. Vp is measured as the slope of the first aliasing velocity during early filling, measured from the mitral valve plane to 4 cm distally into the LV cavity, or the slope of the transition from no color to color.

Patients with normal LV volumes and EFs but elevated filling pressures can have misleadingly normal Vp. The sample volume should be positioned at or 1 cm within the septal and lateral insertion sites of the mitral leaflets and adjusted as necessary usually 5—10 mm to cover the longitudinal excursion of the mitral annulus in both systole and diastole.

Attention should be directed to Doppler spectral gain settings, because annular velocities have high signal amplitude. Most current ultrasound systems have tissue Doppler presets for the proper velocity scale and Doppler wall filter settings to display the annular velocities. Primary measurements include the systolic S , early diastolic, and late diastolic velocities.

For the assessment of global LV diastolic function, it is recommended to acquire and measure tissue Doppler signals at least at the septal and lateral sides of the mitral annulus and their average, given the influence of regional function on these velocities and time intervals. Once mitral flow, annular velocities, and time intervals are acquired, it is possible to compute additional time intervals and ratios.

Mitral inflow top , septal bottom left , and lateral bottom right tissue Doppler signals from a year-old patient with heart failure and normal EF. Normal values Table 1 of DTI-derived velocities are influenced by age, similar to other indices of LV diastolic function. Septal left and lateral right tissue Doppler recordings from a patient with an anteroseptal myocardial infarction. There are both technical and clinical limitations.

For technical limitations, proper attention to the location of the sample size, as well as gain, filter, and minimal angulation with annular motion, is essential for reliable velocity measurements. With experience, these are highly reproducible with low variability. Because time interval measurements are performed from different cardiac cycles, additional variability is introduced. This limits their application to selective clinical settings in which other Doppler measurements are not reliable.

It is increased in patients with moderate to severe primary MR and normal LV relaxation due to increased flow across the regurgitant valve. PW DTI is performed in the apical views to acquire mitral annular velocities.

The sample volume should be positioned at or 1 cm within the septal and lateral insertion sites of the mitral leaflets. For the assessment of global LV diastolic function, it is recommended to acquire and measure tissue Doppler signals at least at the septal and lateral sides of the mitral annulus and their average.

Strain means deformation and can be calculated using different formulas. In clinical cardiology, strain is most often expressed as a percentage or fractional strain Lagrangian strain. Systolic strain represents percentage shortening when measurements are done in the long axis and percentage radial thickening in the short axis. Systolic strain rate represents the rate or speed of myocardial shortening or thickening, respectively.

Myocardial strain and strain rate are excellent parameters for the quantification of regional contractility and may also provide important information in the evaluation of diastolic function.

During the heart cycle, the LV myocardium goes through a complex 3-dimensional deformation that leads to multiple shear strains, when one border is displaced relative to another. However, this comprehensive assessment is not currently possible by echocardiography.

By convention, lengthening and thickening strains are assigned positive values and shortening and thinning strains negative values. Until recently, the only clinical method to measure myocardial strain has been magnetic resonance imaging with tissue tagging, but complexity and cost limit this methodology to research protocols. Tissue Doppler—based myocardial strain has been introduced as a bedside clinical method and has undergone comprehensive evaluation for the assessment of regional systolic function.

The methodology is angle independent; therefore, measurements can be obtained simultaneously from multiple regions within an image plane. This is in contrast to tissue Doppler—based strain, which is very sensitive to misalignment between the cardiac axis and the ultrasound beam. Problems with tissue Doppler—based strain include significant signal noise and signal drifting. Speckle-tracking echocardiography is limited by relatively lower frame rates.

A number of studies suggest that myocardial strain and strain rate may provide unique information regarding diastolic function. This includes the quantification of postsystolic myocardial strain as a measure of postejection shortening in ischemic myocardium and regional diastolic strain rate, which can be used to evaluate diastolic stiffness during stunning and infarction.

Few studies have shown a significant relation between segmental and global early diastolic strain rate and the time constant of LV relaxation. Currently, Doppler flow velocity and myocardial velocity imaging are the preferred initial echocardiographic methodologies for assessing LV diastolic function. LV twisting motion torsion is due to contraction of obliquely oriented fibers in the subepicardium, which course toward the apex in a counterclockwise spiral.

The moments of the subepicardial fibers dominate over the subendocardial fibers, which form a spiral in opposite direction. Therefore, when viewed from apex toward the base, the LV apex shows systolic counterclockwise rotation and the LV base shows a net clockwise rotation.

Untwisting starts in late systole but mostly occurs during the isovolumetric relaxation period and is largely finished at the time of mitral valve opening. The rate of untwisting is often referred to as the recoil rate. LV twist appears to play an important role for normal systolic function, and diastolic untwisting contributes to LV filling through suction generation.

Because the measurement of LV twist has been possible only with tagged magnetic resonance imaging and other complex methodologies, there is currently limited insight into how the quantification of LV twist, untwist, and rotation can be applied in clinical practice. To measure basal rotation, the image plane is placed just distal to the mitral annulus and for apical rotation just proximal to the level with luminal closure at end-systole.

The clinical value of assessing LV untwisting rate is not defined. When LV twist and untwisting rate were assessed in patients with diastolic dysfunction or diastolic heart failure, both twist and untwisting rate were preserved, , and no significant relation was noted with the time constant of LV relaxation.

In an animal model, and in both groups of heart failure, the strongest association was observed with LV end-systolic volume and twist, suggesting that LV untwisting rate best reflects the link between systolic compression and early diastolic recoil. In conclusion, measurements of LV twist and untwisting rate, although not currently recommended for routine clinical use and although additional studies are needed to define their potential clinical application, may become an important element of diastolic function evaluation in the future.

The selection of image plane is a challenge, and further clinical testing of speckle-tracking echocardiography in patients is needed to determine whether reproducible measurements can be obtained from ventricles with different geometries.

Speckle tracking can be suboptimal at the LV base, thus introducing significant variability in the measurements. When myocardial relaxation is impaired, LV pressure falls slowly during the isovolumic relaxation period, which results in a longer time before it drops below LA pressure. Therefore, mitral valve opening is delayed, and IVRT is prolonged.

IVRT is easily measured by Doppler echocardiography, as discussed in previous sections. However, IVRT by itself has limited accuracy, given the confounding influence of preload on it, which opposes the effect of impaired LV relaxation. The instantaneous pressure gradient between the aorta and the left ventricle during diastole can be calculated from the CW Doppler aortic regurgitant velocity spectrum. Tau calculation was validated in an animal study, but clinical experience is limited to only a few patients.

Using the modified Bernoulli equation, the maximal and mean pressure gradients between the left ventricle and the left atrium can be determined by CW Doppler in patients with MR, which correlate well with simultaneously measured pressures by catheterization.

Given the presence of more simple methods to assess myocardial relaxation, both the aortic regurgitation and MR methods described above are rarely used in clinical practice. Aside from the above-described calculations, it is of value to examine the morphology of the jets by CW Doppler. On the other hand, a rounded signal with slow ascent and descent supports the presence of LV systolic dysfunction and impaired relaxation.

For aortic regurgitation, in the absence of significant aortic valve disease in patients with mild aortic regurgitation , a rapid rate of decline of peak velocity and a short pressure half time are usually indicative of a rapid rise in LV diastolic pressure due to increased LV stiffness.

In addition, in the presence of bradycardia, a characteristic low middiastolic after early filling mitral inflow velocity may be seen, due to a progressive fall in LV diastolic pressure related to slow LV relaxation.

However, increased filling pressure can mask these changes in mitral velocities. Because impaired relaxation is the earliest abnormality in most cardiac diseases, it is expected in most, if not all, patients with diastolic dysfunction.

However, this approach has more variability than a single velocity measurement and is needed in few select clinical scenarios see previous discussion. However, Vp can be increased in patients with normal LV volumes and EFs, despite impaired relaxation. Therefore, Vp is most reliable as an index of LV relaxation in patients with depressed EFs and dilated left ventricles. In the other patient groups, it is preferable to use other indices.

IVRT by itself has limited accuracy, given the confounding influence of preload on it, which opposes the effect of impaired LV relaxation. Vp is most reliable as an index of LV relaxation in patients with depressed EFs and dilated left ventricles.

Diastolic pressure-volume curves can be derived from simultaneous high-fidelity pressure recordings and mitral Doppler inflow, provided filling rates multiplying on a point-to-point basis the Doppler curve by the diastolic annular mitral area are integrated to obtain cumulative filling volumes and normalized to stroke volume by 2D imaging.

The estimation of end-diastolic compliance the reciprocal of LV stiffness from a single coordinate of pressure and volume is also feasible at end-diastole, using echocardiography to measure LV end-diastolic volume and to predict LVEDP, but this method can be misleading in patients with advanced diastolic dysfunction.

Patients with conditions associated with increased LV stiffness have more rapid rates of deceleration of early LV filling and shorter DTs. LA contraction generates a pressure-velocity wave that enters the left ventricle. The wave moves through the inflow tract of the ventricle and reflects off the apex in the direction of the aortic valve. The time taken for the pressure-velocity wave to propagate through the ventricle, referred to as A-wave transit time, may be measured using PW Doppler echocardiography.

Many patients with diastolic dysfunction have symptoms, mainly with exertion, because of the rise in filling pressures that is needed to maintain adequate LV filling and stroke volume. Therefore, it is useful to evaluate LV filling pressure with exercise as well, similar to the use of exercise to evaluate patients with coronary artery or mitral valve disease. Exercise Doppler recordings from a patient with reduced diastolic reserve.

Furthermore, the delayed recording of Doppler velocities avoids the merging of E and A velocities that occurs at faster heart rates. Exercise is usually performed using a supine bicycle protocol, and TR signals by CW Doppler are recorded as well to allow for the estimation of PA systolic pressure at rest and during exercise and recovery. Diastolic stress echocardiography has been also performed with dobutamine infusion, and restrictive filling with dobutamine was shown to provide prognostic information.

The test is most useful in patients with unexplained exertional dyspnea who have mild diastolic dysfunction and normal filling pressures at rest. However, the paucity of clinical data and the potential limitations in patients with regional LV dysfunction, mitral valve disease, and atrial fibrillation preclude recommendations for its routine clinical use at this time.

It is important to consider the possibility of constrictive pericarditis when evaluating patients with the clinical diagnosis of heart failure with normal EFs, because it is potentially curable.

On the other hand, patients in respiratory distress, such as those with asthma, sleep apnea, chronic obstructive lung disease, and obesity, may show exaggerated respiratory variation in mitral E velocity due to increased swings in intrathoracic pressure.

Recording hepatic venous flow is essential for the differential diagnosis and in establishing the presence of constrictive pericarditis. Patients with restrictive cardiomyopathy exhibit diastolic flow reversal during inspiration, whereas patients with pulmonary disease overfill the right heart chambers with inspiration, as seen by large increases in superior vena cava and inferior vena cava velocities.

Patients with constrictive pericarditis and atrial fibrillation still have the typical 2D echocardiographic features, and a longer period of Doppler velocity observation is needed to detect velocity variation with respiration.

Mitral annular velocities by tissue Doppler are important to acquire and analyze. Lateral left and septal right TD velocities from a patient with constrictive pericarditis. Differentiation of constrictive pericarditis from restrictive cardiomyopathy. Key Point. Restrictive LV filling, prominent diastolic flow reversal during expiration in the hepatic veins, and normal or increased tissue Doppler annular velocities should raise suspicion of constrictive pericarditis in patients with heart failure and normal EFs, even when the respiratory variation in mitral inflow is absent or not diagnostic.

Typically, patients with mitral stenosis have normal or reduced LV diastolic pressures, except for the rare occurrence of coexisting myocardial disease. The same hemodynamic findings are present in patients with other etiologies of LV inflow obstruction, such as as LA tumors, cor triatriatum, and congenital mitral valve stenosis.

The transmitral gradient is influenced by the severity of stenosis, cardiac output, and the diastolic filling period. If atrial fibrillation occurs, LA pressure increases to maintain adequate LV filling.

Although the severity of valvular stenosis, patient symptoms, and secondary pulmonary hypertension are the focus of clinical management, a semiquantitative estimation of instantaneous LA pressure can be provided in early and late diastole by Doppler variables.

If LA compensation is incomplete, mean LA pressure and right-sided pressures increase, which is related not to LV dysfunction but to the regurgitant volume entering the left atrium and pulmonary veins.

With LV diastolic dysfunction, a myocardial component of increased filling pressures is added over time. The sequence is opposite to that seen in primary myocardial disease such as dilated cardiomyopathy, which leads to increased filling pressures earlier on and later to functional MR. Therefore, in patients with secondary MR, echocardiographic correlates of increased filling pressures reflect the combination of both myocardial and valvular disorders.

In severe MR, systolic pulmonary venous flow reversal can be seen in late systole. In patients with normal EFs, these parameters do not correlate with filling pressures. The Doppler estimation of LV filling pressures in atrial fibrillation is limited by the variability in cycle length, the absence of organized atrial activity, and the frequent occurrence of LA enlargement. The variability of mitral inflow velocity with the RR cycle length should be examined, because patients with increased filling pressures have less beat-to-beat variation.

A comprehensive approach is recommended in all of the above settings, and conclusions should not be based on single measurements. Importantly, this relation remained strong irrespective of mitral inflow pattern and LV EF, as well as in the presence of a single velocity due to complete merging of both mitral and annular E and A.