Modified with permission from Lang RM, Bierig M, Devereux RB, et al; Chamber Quantification Writing Group; American Society of Echocardiography’s Guidelines and Standards Committee; European Association of Echocardiography. Recommendations for chamber quantification: A report from the American Society of Echocardiography’s Guidelines and Standards Committee and the Chamber Quantification Writing Group, developed in conjunction with the European Association of Echocardiography, a branch of the European Society of Cardiology. J Am Soc Echocardiogr. 2005;18:1440-1463.

Figure 6-2 Display, on a circumferential polar plot, of the 17 myocardial segments and the recommended nomenclature for tomographic imaging of the heart.

Modified from American Society of Nuclear Cardiology. Imaging guidelines for nuclear cardiology procedures, part 2. J Nucl Cardiol. 1999;6:G47–G84.

Overview of Echocardiographic Approach

Table 6-1 presents an evaluation of LV systolic function.

TABLE 6-1 EVALUATION OF LEFT VENTRICULAR SYSTOLIC FUNCTION

Anatomic Imaging

An orderly sequence of image acquisition ensures that all views will be obtained. A suggested approach is to start with the midesophageal (ME) views, progress to the transgastric (TG) views, and conclude with three-dimensional (3D) image acquisition.

Acquisition

• ME four-chamber (ME 4C) (Figure 6-7).

• ME two-chamber (ME 2C) (Figure 6-8).

• ME long axis (ME LAX) (Figure 6-9).

• TG short axis (TG SAX) at the apex, midpapillary, and basal levels (Figure 6-10).

• TG long axis (TG LAX 2C) (Figure 6-11).

• Deep TG (TG DEEP) (Figure 6-12).

• 3D ME 4C, focusing on the left side (Figure 6-13).

Figure 6-7 ME 4C view of the LV with the multiplane scan angle at 0 degrees.

Figure 6-8 ME 2C view of the LV with the multiplane scan angle at approximately 90 degrees.

Figure 6-9 ME LAX view of the LV with the multiplane scan angle at approximately 120 degrees.

Figure 6-10 TG SAX views of the LV with the multiplane scan angle at 0 degrees at the apical (A), mid (B), and basal (C) levels.

Figure 6-11 TG 2C view of the LV with the scan angle rotated to 90 degrees.

Figure 6-12 Deep TG LAX view of the LV with the scan angle at 0 degrees and the probe tip anteflexed.

Figure 6-13 3D image of the LV acquired using the ME 4C view as the reference 2D image.

Analysis

Ejection Fraction Linear Measurement

• Fractional shortening (FS) (%) = [(left ventricular end-diastolic dimension [LVEDd] − left ventricular end-systolic dimension [LVESd])/LVEDd] × 100.

• LV internal dimensions at end-diastole and end-systole are measured from endocardial border to endocardial border with M-mode at a TG SAX view just above the papillary muscles (Figure 6-15).

• Superior temporal resolution of M-mode allows for more accurate identification of endocardial borders.

• FS is not accurate in patients with marked regional differences such as WMA or aneurysms.

• Normal FS is defined as 27% to 45% in women and 25% to 43% in men.

Figure 6-15 TG mid SAX of the LV with the M-mode cursor directed perpendicularly across the image. Measurements are shown of the LVEDd and LVESd, respectively, from one endocardial border to the other.

Ejection Fraction Area Measurement

• Fractional area of change FAC (%) = [(left ventricular area in end-diastole [LVAd] − LV area in end-systole [LVAs])/LVAd] × 100

• LV cavity area is measured via manual tracing of the endocardial border to assess area at end-diastole and end-systole in the TG SAX or TG LAX views.

• The papillary muscles should be ignored when estimating the chamber area.

• FAS provides an improved estimate over linear measurements, because information regarding septal and lateral ventricular walls is taken into account.

• Normal FAC is 59% to 65% in women and 56% to 62% in men.

Ejection Fraction Volumetric Measurements

• LVEF = [(left ventricular end-diastolic volume [LVEDV] − left ventricular end-systolic volume [LVESV])/LVEDV] × 100%

• Biplane: LV systolic and diastolic volume estimation utilizing the endocardial border.

• Volume is calculated from the manually traced endocardial border in the ME 4C and ME 2C views (Figure 6-16).

• Assumes a symmetrically shaped LV.

• Simpson’s method of disks calculates diastolic and systolic volume from a summation of stacked elliptical disks.

• Measured in the ME 4C and ME 2C views (Figure 6-17).

• Endocardial border detection may be improved using automated software, enhanced tissue harmonics, or contrast-based LV opacification.

Figure 6-16 ME 2C view of the LV with the endocardial border traced during systole (A) and diastole (B).

Figure 6-17 ME 2C view of the LV with internal volume measured using Simpson’s method of disks during systole (A) and diastole (B).

Ejection Fraction Three-Dimensional Measurement

• Involves construction of a ventricular model based upon endocardial border detection.

• Typically a 3D data set is best obtained from an ME 4C view (Figure 6-18).

• 3D modeling may be performed using specific 3D software at the time of acquisition or off-line when the images are reviewed (Figure 6-19).

• 3D imaging accounts for regional abnormalities, yielding more accurate stroke volumes (SVs) than two-dimensional (2D) analysis (see Videos 6-6 and 6-7 on the Expert Consult website).

• Problems associated with foreshortening in 2D can be avoided with 3D imaging.

Figure 6-18 Image of a 3D full-volume data set of the LV acquired using the ME 4C view as the reference 2D image. The default setting ensures that the 3D image displayed reflects the reference 2D image.

Figure 6-19 Image of a 3D full-volume analysis of the LV using 3D advanced quantification software. Detailed segmental analysis is obtained for wall motion, volume, and timing of contractility.

Key Points Pitfalls

• Identification of the LV endocardial borders can be difficult, particularly with shadowing of the ventricular walls secondary to calcification, prosthetic valve artifact, air, and other factors. This can make estimates of LVEF inaccurate.

• Linear LV measurements may be inaccurate if there are regional WMAs because they evaluate only two opposing walls in one imaging plane.

• Volumetric calculations involve geometric assumptions of the shape of the LV. This may be inaccurate with regional WMAs and aneurysms.

• Foreshortening of the LV apex is common in 2D imaging, which may result in underestimations of LV dimensions, volume, and EF.

• High-quality 2D images are necessary to generate a usable 3D data set. Suboptimal 2D imaging can lead to inaccurate 3D calculations.

• Ventricular function may be more difficult to interpret in the patient with dysrhythmias that cause variability in SV, such as atrial fibrillation.

• Acquisition of full-volume 3D data sets requires minimal translational motion, electrocautery interference, or irregular rhythms. These can be difficult to avoid in the perioperative setting.

Physiologic Data

Acquisition

• ME 4C continuous wave (CW) Doppler of MR jet for dP/dT. (Figure 6-20).

• TG DEEP or TG LAX pulsed wave (PW) Doppler of the LVOT velocity time integral (VTI) for cardiac output (CO; Figure 6-21).

• ME 4C tissue Doppler imaging (TDI) PW Doppler of lateral mitral annulus peak systolic velocity (Figure 6-22).

Figure 6-20 Top, ME 4C view with color flow Doppler across the MV shows a regurgitant jet. Bottom, CW spectral Doppler tracing across the MV shows high-velocity systolic waveforms consistent with MR.

Figure 6-21 PW spectral Doppler across the LVOT shows a tracing (VTI) for calculating the LV SV.

Figure 6-22 Spectral recording of tissue velocity of the lateral mitral annulus using TDI in the ME 4C view. Diastolic velocities (E′ and A′) and timings (deceleration time and slope) measurements are shown.

Analysis

Rate of Rise in Left Ventricle Pressure (dP/dT)

• The rate of rise in LV pressure is well correlated with systolic function and can be measured using the rate of rise in velocity of the MR jet (Figure 6-23).

• The MR jet is interrogated using CW Doppler and the time interval between velocities of 1 and 3 m/s is measured (Figure 6-24).

• The pressure differential can be calculated by converting the measured velocities into pressures using the simplified Bernoulli equation.

Figure 6-23 Pressure tracing diagram.

From Pai RG, Bansal RC, Shah PM. Doppler-derived rate of left ventricular pressure rise. Its correlation with the postoperative left ventricular function in mitral regurgitation. Circulation. 1990;82:514-520.

Figure 6-24 Spectral recording of CW Doppler interrogation of an MR jet in the ME 4C view shows the measurement of dP/dT on the MR jet waveform from 1 to 3 m/s.

• Normal dP/dT values are greater than 1000 mm Hg/s.

Cardiac Output

• SV (in mL or cm³) can be calculated by measuring flow through a known cross-sectional area (CSA).

• Although SV can be theoretically measured anywhere, the most common site for measurement is the relatively cylindrical LVOT, just below the aortic valve (Figure 6-25).

• CSA (in cm²) is measured utilizing LVOT diameter obtained in the ME LAX view, assuming that the CSA is a circle.

Figure 6-25 ME aortic LAX view shows the location of measurement of the LVOT.

• Flow through the LVOT is measured using range-specific PW Doppler, obtaining a sample velocity over time. The distance traveled by blood through the cylindrical LVOT in a single beat is measured in centimeters and known as the VTI (Figure 6-26):

Figure 6-26 Deep TG LAX view with a PW Doppler sample volume shown located in the LVOT for measurement of the VTI at the level of the LVOT.

• CO can be calculated by multiplying the SV by the heart rate (HR).

• Cardiac index (CI) can be calculated by factoring in the patient’s body surface area (BSA in m²). A normal cardiac index is greater than 2 L/min/m².

Tissue Doppler Imaging of the Mitral Annulus

• Lateral mitral annular motion is measured using PW Doppler.

• Myocardial velocities are much lower than the velocities of blood flow, and adjustments to the sector width may be necessary to achieve high frame rates.

• Measurement is less dependent of loading conditions.

• Velocities are measured in the ME 4C and ME 2C views (see Figure 6-22).

• Velocities are age- and gender-dependent, but globally normal LV systolic function is associated with velocities greater than 7.5 cm/s. Velocities less than 5.5 cm/s are seen in LV impairment.

Strain/Strain Rate and Speckle Tracking

• Strain (ε) is the change of length of an object divided by its original length.

• Positive strain indicates lengthening and negative strain indicates shortening.

• Myocardial strain occurs in three dimensions: longitudinal, circumferential, and radial.

• During systole, there is negative strain in the longitudinal and circumferential dimensions and positive strain in the radial dimension.

• Strain rate is the change of strain over time (Δε/Δt).

• TDI of the mitral annulus in the ME 4C view can be used to assess strain and strain rate. Specialized software is necessary to calculate strain and strain rate.

• 2D speckle tracking can be used in place of TDI as a means of assessing strain and is not dependent upon the angle of interrogation like tissue Doppler. Specialized software is necessary for speckle tracking and may not be available on all ultrasound machines.

Key Points Pitfalls

• CO and dP/dT are load-dependent and can vary widely as a result.

• Measurements of velocities will be underestimated if the angle of Doppler interrogation is not parallel to motion/flow, giving falsely low estimations of ventricular function.

• Inaccurate 2D measurements of LVOT diameter will grossly impair the ability to calculate an accurate CO, particularly because this measurement is squared.

• dP/dT can be performed only if there is MR.

• TDI of the mitral annulus is difficult in the presence of mitral annular calcification or prosthetic valve.

Alternate Approaches—When Transesophageal Echocardiography Is Insufficient

• Visual estimation of LVEF and WMA using 2D images can be a quick method to roughly assess ventricular function. The reliability of this method may improve with observer experience, although it is still subject to interobserver variability.

• Echocardiographic assessment of LV systolic function can always be correlated with other modalities (cardiac magnetic resonance imaging [MRI], cardiac catheterization, left ventriculogram, or pulmonary artery [PA] catheterization).

Key Points

• Changes in preload and afterload can affect LVEF.

• Regional WMA must be assessed in multiple planes.

• Avoid foreshortening of the LV when assessing systolic function.

• Ventricular pacing can cause abnormal septal motion. Consequently, WMAs may be difficult to assess in the perioperative period.

• When the endocardial borders are difficult to determine in 2D, echo contrast can be used to better identify the borders and assist with volume measurements.

• High-quality 2D images are necessary to generate a usable 3D data set.

Figure 6-27 presents an LV assessment flow chart.

Figure 6-27 LV assessment flow chart.

Right Ventricular Systolic Function

Background

Coronary Anatomy and Right Ventricular Wall Motion

• The RV is primarily supplied by the right coronary artery (RCA). A small portion of the anterior free wall may be supplied by a branch of the LAD (see Figure 6-1).

• The posterior descending artery (PDA) supplies the RV, the inferior wall and the posterior third of the septum.

• In the majority of the population, the PDA arises from the RCA and the coronary circulation is termed right dominant coronary circulation.

• If the PDA extends off the LCX artery, the circulation is known as left dominant coronary circulation.

• The RV medial wall is composed of the ventricular septum, and its function is evaluated as part of the LV.

• The RV free wall can be divided into basal, mid, and apical segments.

• Systolic function is assessed solely by endocardial excursion. The typical RV wall is too thin to evaluate wall thickening.

• Normal wall motion is defined as greater than 30% excursion of the endocardial border (see Video 6-8 on the Expert Consult website).

Right Ventricular Ejection Fraction

• Right ventricular ejection fraction (RVEF) is a measure of contractility and can be calculated using RV systolic and diastolic volumes.

• RVEF depends upon preload and afterload.

• RV systolic function is typically graded qualitatively as normal, mildly reduced, moderately reduced, or severely reduced.

• Typically, RV systolic function is graded in comparison with LV systolic function.

• Normal RVEF is equal to or greater than 55%.

Pathophysiology

Wall Motion

• WMAs can be either segmental or global and are most often caused by decreased perfusion in the corresponding arterial distribution.

• Wall motion is graded as normal, hypokinetic, akinetic, dyskinetic (paradoxical systolic motion), or aneurysmal (diastolic deformation) (see Video 6-9 on the Expert Consult website).

• RV wall motion is more afterload dependent than LV wall motion and prone to dysfunction with elevated PA pressures.

• The RV is particularly prone to perioperative ischemia for the following reasons:

• Retrograde cardioplegia delivery intraoperatively may be inadequate to protect the RV.

• Intracardiac air will preferentially enter the RCA given the anterior position of the right coronary ostium in the supine patient (see Video 6-4 on the companion website).

• The anterior position of the RV makes it more susceptible to warming intraoperatively from surgical lights and ambient air.

• Significant RV infarction may be accompanied by inferior LV wall infarction as well, given the shared coronary perfusion.

• Other signs of RV infarction include right atrium (RA) enlargement, increased central venous pressure (CVP), RV dilation, tricuspid regurgitation (TR), paradoxical ventricular septal motion, and right-to-left shunting in the presence of a patent foramen ovale.

• RV function can also be affected by the long-term effects of pulmonary and valvular disease, particularly lesions that result in RV volume or pressure overload, such as pulmonic stenosis, pulmonary hypertension, pulmonary valve insufficiency, and TR.

Right Ventricular Dilatation

• The RV is a thin-walled volume-pumping chamber that is extremely sensitive to increases in afterload, which frequently result in systolic dysfunction.

• RV dilation typically is the result of volume overload but can also occur with pressure overload.

• RV CSA is typically 60% of LV cross-sectional area at end-diastole.

• RV dilation can be quantified as mild (60-100% LV size), moderate (equal to LV size), and severe (>LV size) (Figure 6-30).

• The LV typically forms the apex of the heart. However, with RV dilation, the apex includes the RV (Figure 6-31).

Figure 6-30 TG mid SAX view of a dilated and severely hypokinetic RV. The LV is seen to the right of the image and is smaller in comparison.

Figure 6-31 ME 4C view of a dilated RV that forms a part of the cardiac apex. The LV is seen to the right of the image.

Right Ventricular Hypertrophy

• Right ventricular hypertrophy (RVH) may indicate pulmonic stenosis (PS) or elevated PA pressures. Trabeculae are more prominent when RVH is present.

• RV free wall hypertrophy occurs before septal hypertrophy (Figure 6-32).

Figure 6-32 TG mid SAX view demonstrates a normal-sized RV (A) and a severely hypertrophied RV (B). The thickness of the RV is indicated by the double-sided arrow. The LV can be seen adjacent to the RV in each panel.

Interventricular Septum

• Flattening of the septum is a characteristic feature of RV dysfunction. The septum normally functions as part of the LV and has a convex curvature in regards to the RV chamber.

• Conduction abnormalities, ventricular pacing, previous surgery, and pericardial disease can also cause abnormal ventricular septal motion.

Figure 6-33 TG mid SAX view in a patient with high RV systolic pressures demonstrates flattening of the septum at systole.

Overview of Echocardiographic Approach

Table 6-2 presents an evaluation of RV systolic function.

TABLE 6-2 EVALUATION OF RIGHT VENTRICULAR SYSTOLIC FUNCTION

Anatomic Imaging

As with the LV images, it is important to maintain an orderly acquisition sequence. A suggested approach is to start with the ME views, progress to the TG views, and conclude with 3D image acquisition.

Acquisition

• ME 4C (Figure 6-34).

• ME LAX (Figure 6-35).

• ME RV inflow-outflow (Figure 6-36).

• ME bicaval (Figure 6-37).

• TG SAX at the midpapillary and basal levels (Figure 6-38).

• TG LAX (Figure 6-39).

• TG DEEP (Figure 6-40).

• Upper esophageal aortic arch short axis (UE aortic arch SAX) (Figure 6-41).

• 3D ME 4C focusing on right side (Figure 6-42).

Figure 6-34 ME 4C view obtained with the scan plane at 0 degrees.

Figure 6-35 ME LAX view obtained with the scan angle rotated to 120 degrees.

Figure 6-36 ME RV inflow-outflow view with the scan angle rotated to 61 degrees.

Figure 6-37 ME bicaval view with the scan plane rotated to 102 degrees.

Figure 6-38 TG SAX views at the basal (A) and midpapillary (B) levels obtained with the probe in the stomach and the scan angle at 0 degrees.

Figure 6-39 TG RV inflow view obtained with the probe in the stomach at the midpapillary level with the scan angle rotated to 90 degrees and manually turned to the right.

Figure 6-40 Deep TG view with the probe deep in the stomach at 12 degrees, anteflexed and manually turned to the right to obtain a view of the RV. The RA is seen in the lower part of the image.

Figure 6-41 UE aortic arch SAX view with the scan angle rotated to 97 degrees.

Figure 6-42 A, ME 4C view focusing on right side, obtained with the probe at the midesophagus at 0 degrees, manually turned toward the right. B, 3D acquisition data set in the ME 4C view, focusing on the right side.

Analysis

Chamber Dimensions

• The RV chamber can be quantified by measuring the RV major and minor diameters in ME 4C. Normal dimensions are 3.5 cm ± 0.2 and 2.8 cm ± 0.2, respectively (see Figure 6-28).

• Normal RV diastolic area ranges from 11 to 28 cm³ and normal RV systolic area ranges from 7.5 to 16 cm³.

Wall Thickness

• Normal RV wall thickness is less than 0.5 cm.

• Measurement is best made of the free wall at end diastole.

• Free wall thickness greater than 1 cm may be present with severe pulmonary hypertension.

• Trabeculae carnae will also be more prominent if RVH is present.

Ejection Fraction

• Area measurement

• RV cavity area is measured via manual tracing of the endocardial border to assess area at end-diastole and end-systole in the TG SAX or TG RV inflow views.

• Papillary muscles should be ignored when estimating the chamber area.

• Volumetric measurements

• Biplane

• RV systolic and diastolic volume estimation utilizing the endocardial border. Volume is calculated from the manually traced endocardial border in the ME 4C view.

• Simpson’s method of disks may be used, although this technique has not been validated.

• As with the LV, endocardial border detection of the RV may be improved using automated software, tissue harmonic imaging, or contrast-based RV opacification.

• Tricuspid annular plane systolic excursion (TAPSE)

• Apical to basal shortening of the lateral annulus of the tricuspid valve (TV) is measured as an assessment of global RV function (Figure 6-43; see Videos 6-11 and 6-12 on the Expert Consult website)

• Normal TAPSE is 1.5 to 2 cm.

• TDI may be used to quantify TAPSE.

• 3D estimation of EF

• 3D EF analysis involves construction of a ventricular model based upon endocardial border detection. Typically, a 3D data set is best obtained from an ME 4C view (see Figure 6-42B).

• 3D modeling may be performed using specific 3D software at the time of acquisition or off-line when the images are reviewed (see Videos 6-13 and 6-14 on the Expert Consult website).

• 3D imaging accounts for regional abnormalities, yielding more accurate SVs than 2D analysis.

• Problems associated with foreshortening in 2D can be avoided with 3D imaging.

Figure 6-43 ME 4C view of the RV with the tricuspid annulus (arrow) indicated in diastole (A) and systole (B).

Key Points Pitfalls

• The irregular shape of the RV makes quantification of RVEF difficult. Therefore, qualitative methods are more commonly used.

• Ventricular function may be more difficult to interpret in the patient with dysrhythmias that cause variability in SV, such as atrial fibrillation.

• Identification of the RV endocardial borders can be difficult, particularly with shadowing of the ventricular walls secondary to calcification, prosthetic valve artifact, intracardiac catheters, air, and other factors. This can make estimates of RVEF inaccurate.

• High-quality 2D images are necessary to generate a usable 3D data set. Suboptimal 2D imaging can lead to inaccurate 3D calculations.

• Acquisition of full-volume 3D data sets require minimal translational motion, electrocautery interference, or irregular rhythms. These can be difficult to avoid in the perioperative setting.

Physiologic Data

Acquisition

• ME 4C or ME RV inflow-outflow views for CW Doppler of TR jet for dP/dT (Figures 6-44 and 6-45).

• ME RV inflow-outflow or UE aortic arch SAX for PW Doppler of RVOT flow to calculate right-sided CO (Figure 6-46).

• TG of the liver for PW Doppler of hepatic venous flow (Figure 6-47).

Figure 6-44 ME 4C view shows a TR jet with CW Doppler.

Figure 6-45 A, Modified ME bicaval view with color flow Doppler shows a TR jet. B, CW Doppler interrogation of the TR jet.

Figure 6-46 ME RV inflow-outflow view with the scan plane at 77 degrees shows RVOT.

Figure 6-47 View of the hepatic vein adjacent to the IVC with the probe in the lower esophageal position, rotated toward the right, following the path of the IVC from the right atrial-IVC junction in the 4C view. The PW Doppler sample volume is shown placed in the hepatic vein. Color flow Doppler is helpful in identifying flow within the hepatic vein.

Analysis

• Rate of rise in RV pressure (dP/dT)

• The rate of rise in RV pressure is well correlated with systolic function and can be measured using the rate of rise in velocity of the TR jet.

• The TR jet is interrogated using CW Doppler and the time interval between velocities of 1 and 2 m/s is measured (in contrast to the 1–3 m/s time interval used with LV dP/dT assessment from the MR jet).

• The pressure differential can be calculated by converting the measured velocities into pressures using the simplified Bernoulli equation.

• Normal dP/dT values are greater than 1000 mm Hg/s.

• CO

• As with the LV, SV (in mL or cm³) of the RV can be calculated by measuring flow through a known CSA.

• Although SV can be theoretically measured anywhere, the most common site for measurement is the relatively cylindrical RVOT.

• CSA (in cm²) can be measured utilizing RVOT diameter obtained in the ME RV inflow-outflow or the UE aortic arch SAX views, assuming that the CSA is circular.

• Flow through the RVOT is measured using PW Doppler, obtaining a sample velocity over time. The distance traveled by blood in a single beat is measured in centimeters and known as the VTI (Figure 6-48).

Figure 6-48 TG deep view with RVOT PW Doppler.

• Right-sided CO can be calculated by multiplying the SV by the HR:

• Right-sided CI can be calculated by factoring in the patient’s BSA (in m²). A normal CI is greater than 2 L/min/m².

• Calculation of right-sided CO may be particularly beneficial when intracardiac shunts are present and pulmonary flow is greater than systemic flow (Qp/Qs > 1).

• Right ventricular systolic pressure (RVSP)

• The pressure gradient between the RV and the RA is first calculated using the simplified Bernoulli equation and the maximum velocity of the TR jet (see Figure 6-45).

• The RSVP can be calculated if right atrial (RA) pressure is known.

• In absence of PS or RVOT obstruction, RVSP and PA systolic pressure are equivalent.

• Hepatic venous flow may be used to assess global RV function

• Impaired RV systolic function can result in blunting of systolic inflow and augmentation of diastolic inflow, but this must be differentiated from elevated RA pressures for other reasons.

• Severe TR results in reversal of systolic hepatic venous flow, and this may be seen with severe RV systolic dysfunction (Figure 6-49).

Figure 6-49 PW spectral Doppler image of hepatic venous flow shows systolic flow reversal.

Key Points Pitfalls

• The RV is particularly load dependent, and wide variation in CO and dP/dT can be seen with differences in afterload.

• dP/dT and RVSP can be calculated only if there is TR.

• Measurements of velocities will be underestimated if the angle of Doppler interrogation is not parallel to motion/flow, giving falsely low estimations of ventricular function.

• Inaccurate 2D measurements of RVOT diameter will grossly impair the ability to calculate an accurate right-sided CO, particularly because this measurement is squared in the equation.

Alternate Approaches

• Visual estimation of RVEF and WMA using 2D images can be a quick method to roughly assess systolic function. The reliability of this method may improve with observer experience, although it is still subject to interobserver variability.

• Echocardiographic assessment of RV systolic function can always be correlated with other modalities, and this may be valuable when echocardiographic images are unavailable or of insufficient quality.

• Cardiac MRI estimation of RVEF and right-sided cardiac catheterization estimation of RVEF.

• RV function can also be assessed with central venous catheters and measured pressures.

• Filling pressures (right ventricular end-diastolic pressures [RVEDPs]) as measured with CVPs. Elevated filling pressures are indicative of impaired RV systolic function.

Key Points

• RV dilatation is present when the apex is formed by the RV.

• The RV is more sensitive to increases in afterload than the LV.

• The RV is generally assessed qualitatively and compared with LV function.

• Abnormal ventricular septal motion can be seen with either volume or pressure overload, and the bowing of the septum during the cardiac cycle can offer clues to the etiology.

• TR may be an indicator of systolic RV dysfunction, particularly with hepatic venous flow reversal.

Figure 6-50 is a flow chart for the RV.

Figure 6-50 RV assessment flow chart. HTN, hypertension.

Left Ventricular Diastolic Function

Background

• The pump performance of the LV depends on its ability not only to eject and empty (systolic performance) but also to relax and fill (diastolic performance).

• Diastolic dysfunction is common and often severe, even when silent.

• When symptomatic, its clinical presentation may be attributed to other conditions; therefore, diastolic dysfunction may remain undiagnosed or ignored because symptoms may mimic other conditions.

• Diastolic heart failure may occur in isolation with a normal EF and is also known as heart failure with a normal ejection fraction (HFNEF).

• Concentric left ventricular hypertrophy (LVH) frequently coexists with diastolic dysfunction.

• Echocardiography has emerged over the past two decades as a reliable and relatively noninvasive method of evaluating LV diastolic function and filling pressures.

• The treatment of intraoperative diastolic heart failure per se is limited to rate reduction, which can be challenging in the immediate postoperative period.

Physiology of Diastole

• The classic approach is to divide diastole into four phases (Figure 6-51):

• Isovolumetric relaxation extends from aortic valve (AV) closure to MV opening. During this phase, LV pressure steadily declines without a change in volume.

• Early filling begins with the opening of the MV. Most of the diastolic filling occurs during this phase in healthy subjects and is the result of the pressure gradient between the left atrium (LA) and the LV at the opening of the MV.

• Diastasis or slow filling occurs during the midportion of diastole when the pressures between the LA and the LV equilibrate and the flow across the MV ceases.

• Atrial contraction results in a second pressure gradient between the LA and the LV, leading to late LV filling. In young healthy individuals, atrial contraction may usually contribute up to 20% of the LV filling.

• A simplified approach divides the cardiac cycle into three phases: contraction, relaxation, and diastolic filling. Of note is that LV relaxation begins before the closure of the AV and continues into the early filling phase of diastole.

Figure 6-51 In the classic system, the diastole is divided in four phases: isovolumic relaxation (IVR), rapid filling (RF), diastasis or slow filling (SF), and atrial contraction (AC). A more simplified approach divides cardiac cycle in three phases: contraction, relaxation, and filling. The schematic also represents the pressure tracings in the aorta (Ao), LV, and LA.

Physiologic Determinants of Diastolic Function

Left Ventricle Relaxation

• The process during which the myocardium returns to its initial resting length and tension.

• This begins during midsystole and continues throughout the first third of diastole.

• It is dependent on the reuptake of the cytosolic calcium into the sarcoplasmic reticulum (SR), which is an active process, requiring energy accomplished by the SR calcium pump.

Left Ventricle Compliance

• Described as the passive properties of the LV during diastolic filling.

• It is defined as the change in pressure over the change in volume (ΔP/ΔV) (Table 6-3)

TABLE 6-3 DIASTOLIC DETERMINANTS *

Diastolic Function Determinant	Intrinsic Factors	Extrinsic Factors
LV relaxation	Synchrony of cardiac contraction Velocity of cardiac contraction Duration of systole Stored energy during systole (elastic recoil) Calcium homeostasis Cytoskeleton alterations Neurohormonal activation (sympathetic nervous system, renin-angiotensin-aldosterone)

Arterial impedance

Preload

LV compliance

Fibrillar collagen (amount, geometry, distribution, type)

Myocardial fibrosis, scar, or hypertrophy

Chamber geometry

Neurohormonal activation

Hemodynamic load (preload and afterload)

Pericardium (effusions, constriction)

Ventricular interdependence (e.g., RV dilatation)

LA, left atrial; LV, left ventricular; RV, right ventricular.

* Other determinants of diastolic function are heart rate, mitral valve area, LA function.

Pathophysiology

The pathophysiology of diastolic dysfunction is primarily described in terms of LV filling patterns (Table 6-4).

TABLE 6-4 GRADING OF LEFT VENTRICULAR DIASTOLIC FUNCTION

Grade of Diastolic Dysfunction	Underlying Mechanism	Pathophysiology
Grade I (impaired relaxation)	Impaired LV relaxation	Decreased early transmitral pressure gradient Decreased LV filling during early filling phase Compensatory increased LV filling during atrial contraction

Grade II (pseudonormal) Impaired LV relaxation
Elevated LA pressure

“Pseudonormal” early transmitral pressure gradient

Improved LV filling during early filling phase

“Pseudonormalization” of diastolic filling pattern

Elevated LA pressure

Grade III (restrictive) Impaired LV relaxation
Decreased LV compliance
Highly elevated LV filling pressures

Elevated early transmitral pressure gradient

Limited LV filling at high blood velocities

Elevated LV filling pressures

LA, left atrial; LV, left ventricular.

Overview of Echocardiographic Approach (Table 6-5)

Anatomic Imaging

• Anatomic imaging is an integral part of diastolic function evaluation by providing information on LA size, LV size and wall thickness, LV systolic function, and valvular and pericardial pathology.

• LVH is a common reason for impaired diastolic function

• Concentric LVH occurs in situations of pressure overload (hypertension, aortic valve stenosis).

• Eccentric LVH occurs in situations of volume overload (regurgitant valvular lesions, depressed systolic function).

• In the absence of primary atrial pathology or valvular disease, LA enlargement may be a marker of the chronicity and severity of diastolic dysfunction and a sign of chronic elevation of atrial pressure.

TABLE 6-5 EVALUATION OF LEFT VENTRICULAR DIASTOLIC FUNCTION

Echocardiographic Method	Measurements	Comments
Transmitral flow (TMF) (Figure 6-52)	IVRT	Depends on LV relaxation, LA pressure
	Early filling peak velocity (E wave)	Reflects LV-LA pressure gradient in early diastole
	Early filling peak velocity (E wave)	Depends on LV relaxation, LV compliance
	E wave DT	Depends on LV compliance
	Late filling deceleration time (A-wave)	Depends on LV compliance, LA function
	A-wave duration	Useful in assessment of filling pressures
Pulmonary vein flow (PVF) (Figure 6-53)	Peak systolic flow velocity (S-wave)	May have two components S1 and S2
Pulmonary vein flow (PVF) (Figure 6-53)	Peak systolic flow velocity (S-wave)	Depends on LA relaxation, pulmonary vein flow
	Peak diastolic flow velocity (D-wave)	Depends on LV relaxation, LV compliance
	Peak atrial reversal flow velocity (AR wave)	Depends on LA function, LA compliance, LV compliance
	AR wave duration (ARdur)	Useful in assessing filling pressures
Tissue Doppler imaging (TDI) (Figure 6-54)	Early diastolic velocity (E’ wave)	Corresponds to the E-wave of TMF
Tissue Doppler imaging (TDI) (Figure 6-54)	Early diastolic velocity (E’ wave)	Measures myocardial velocities at lateral or septal mitral annulus
	Late diastolic velocity (A’ wave)	Corresponds to the A-wave of the TMF
	Systolic velocity (S’ wave)	Due to mitral annulus descent during LV systole
Propagation velocity (Vp) (Figure 6-55)	Vp	Measures velocities along a scan line from the mitral annulus to LV apex
Propagation velocity (Vp) (Figure 6-55)	Vp	Correlates well with LV relaxation

DT, deceleration time; IVRT, isovolumic relaxation time; LA, left atrial; LV, left ventricular.

Figure 6-52 Transmitral inflow. The PW Doppler TMF velocity profile shows two distinct waveforms below the baseline-early filling peak velocity (E-wave) and late filling peak velocity (A-wave).

Figure 6-53 Pulmonary vein (PV) flow. The PW Doppler PV velocity profile shows three distinct waveforms. There is a forward flow in systole (S-wave) followed by an early forward diastolic flow (D-wave) into the LA. In late diastole, atrial contraction results in a reversed flow (AR) into the PV.

Figure 6-54 Myocardial velocity. The spectral Doppler tissue velocity profile shows an upward motion in early diastole, marking the E’ wave, followed by a late diastolic A’ wave due to atrial contraction.

Figure 6-55 Myocardial propagation velocity (Vp), normal profile.

Physiologic Data

Acquisition

• Transmitral inflow (TMF) is obtained by employing PW Doppler in the ME 4C view (Figure 6-56).

• Isovolumic relaxation time (IVRT) is obtained by employing CW Doppler in the TG deep LAX view (Figure 6-57).

• Pulmonary venous flow is obtained by employing PW Doppler in the left or right upper pulmonary veins (PVs; Figure 6-58).

• Myocardial velocity TDI is obtained by employing PW Doppler in the ME 4C view with the TDI function of the TEE machine activated (Figure 6-59).

• Propagation velocity (Vp) is obtained by employing M-mode and CF Doppler in the ME 4C view (Figure 6-60).

Figure 6-56 TMF velocities are obtained in the ME 4C view by employing PW Doppler and placing the sample volume at the level of the tips of the MV leaflets. Color flow Doppler of the blood flow through the MV may be helpful in better aligning the ultrasound beam with the blood flow.

Figure 6-57 IVRT is the time interval between aortic valve closure and MV opening. It is usually recorded in the deep TG LAX view by employing CW Doppler (top panel). The ultrasound beam aligned with the blood flow across the aortic valve will also intercept the blood flow across the MV resulting in the spectral Doppler velocity display shown in the bottom panel.

Figure 6-58 The PV Doppler flow velocity profile can be obtained by PW Doppler interrogation of the blood flow in the PVs with the sample volume placed 1 to 2 cm from the opening of the PV in the LA. Both the left upper (top) and the right upper (bottom) PVs can be interrogated, because they lie almost parallel with the ultrasound beam.

Figure 6-59 The myocardial velocities of the mitral annulus can be recorded with TDI by placing the PW Doppler sample gate at the level of the lateral or septal mitral annulus in the ME 4C view. Minimal angulation should be present between the ultrasound beam and the plane of cardiac motion.

Figure 6-60 Myocardial propagation velocity is obtained in the ME 4C view. A narrow color sector map extending from the mitral annulus to the LV apex is selected and the M-mode cursor is aligned with the mitral inflow. The color scale baseline is reduced to about 20 cm/s in order to enable visualization of the first aliasing velocity. Vp is measured by drawing a line from the mitral annulus at the first aliasing velocity during early filling to 4 cm distally toward the LV apex.

Pitfalls

• TMF velocities are highly dependent on age, HR, and loading conditions.

• With aging, there is a gradual decline in the rate of myocardial relaxation resulting in reduced early LV filling and increased contribution of the atrial contraction to LV filling (E < A).

• Tachycardia results in an increase in the A-wave velocity and fusion of the E- and A-waves, because atrial contraction occurs before early filling is complete.

• Associated valvular lesions can affect measurements of diastolic function.

• Severe MR may result in a restrictive TMF pattern in the absence of diastolic dysfunction and in the blunting or reversal of the PV S-wave.

• Severe acute aortic insufficiency may lead to a restrictive TMF pattern due to a rapid increase in LV pressure.

• Mitral stenosis increases TMF velocities and causes a fusion of the E- and A-waves, with an increase in deceleration time (DT).

• E′ velocity is reduced in patients with mitral annular calcifications, mitral stenosis, mitral annuloplasty, or prosthetic MVs.

• E′ may not reflect accurately LV relaxation when there are WMAs in the basal segments of the septal and lateral LV walls.

Right Ventricular Diastolic Function

Background

• There is still little information regarding RV diastolic function and numerous gaps remain in our understanding.

• RV diastolic filling time is slightly shorter than LV diastolic filling time and the larger tricuspid annulus results in lower maximal velocities.

• RV diastolic function patterns have been investigated in various diseases including heart failure, chronic obstructive pulmonary disease with pulmonary hypertension, and restrictive cardiomyopathy.

• RV and LV diastolic dysfunction are associated with difficult separation from cardiopulmonary bypass.

Overview of Echocardiographic Approach (Table 6-8)

Anatomic Imaging

• 2D imaging is useful in the evaluation of pathology associated with diastolic dysfunction: RV volume and mass, RVH, and cardiomyopathy.

• During normal breathing, the inferior vena cava (IVC) diameter and diameter variation (collapsibility index) can be used to estimate CVP. A reduction in IVC diameter of more than 50% is consistent with a CVP less than 10 mm Hg. A dilated IVC without collapse with inspiration suggests a CVP greater than 15 mm Hg.

• In mechanically ventilated patients, the IVC diameter has also been shown to correlate well with CVP. The IVC diameter is measured at the cavoatrial junction in the ME bicaval view at the end of the T-wave on the electrocardiogram.

TABLE 6-8 EVALUATION OF RIGHT VENTRICULAR DIASTOLIC FUNCTION

Echocardiographic Method	Measurements	Comments
TTF (Figure 6-61)	Early filling peak velocity (E-wave)	Flow velocities may vary during spontaneous respiration by 20%. They increase during inspiration and decrease during expiration. Positive-pressure ventilation may have the opposite effect in comparison with spontaneous ventilation
	E-wave DT
	Late filling peak velocity (A-wave)
	A-wave duration
HVF (Figure 6-62)	Antegrade systolic flow (S-wave)	Influenced by TV annular motion, RA relaxation, and TR
	Retrograde end-systolic flow (V-wave)	Influenced by RV and RA compliance
	Antegrade diastolic flow (D-wave)	Occurs after TV opening
	Retrograde end-diastolic flow (A-wave)	Occurs during atrial contraction
	Retrograde end-diastolic flow (A-wave)	Influenced by RV and RA compliance
Myocardial velocities TDI (Figure 6-63)	Early diastolic velocity (E’ wave)	E/E’ correlates with RV filling pressures
	E/E’ ratio

DT, deceleration time; HVF, hepatic venous flow; RA, right atrial; RV, right ventricular; TDI, tissue Doppler imaging; TR, tricuspid regurgitation; TTF, transtricuspid flow; TV, tricuspid valve.