One-dimensional wall motion analysis, or M-mode echocardiography, has traditionally been one of the most commonly utilized methods to measure the extent of LV shortening. Shortening fraction (SF) represents the change in LV short axis diameter that occurs during systole (Fig. 5.1):
LVEDD = LV end-diastolic dimension; LVESD = LV end-systolic dimension

Normal values for shortening fraction range between 28 and 44 %. The LV TG Mid SAX plane is the TEE view most frequently used to make these measurements. Similar to fractional shortening, fractional area change (FAC) can also be measured in this view by determining the change in LV area that occurs during the cardiac cycle:

Normal values have been reported to be >36 % for fractional area change in adults. LVSF and FAC have been reported to be independent of changes in heart rate and age but are significantly impacted by changes in ventricular preload and afterload [52–56].

A concern regarding this evaluation was raised in a retrospective blinded analysis comparing TTE from TEE-derived FAC measured from LV TG Mid SAX images in pediatric patients with CHD [57]. Potential errors in this measurement were reported as well as significant interobserver variability. In spite of these findings the authors were not able to exclude echocardiographic experience and training of the investigators as potential factors accounting for the variability observed. In this study, TEE-derived FAC measurement was not possible in a significant number of patients due to inability to trace endocardial borders at end-systole. Technological advances since the publication of this work may facilitate this assessment in the current era.

Left ventricular ejection fraction (LVEF) is the most commonly measured parameter of ventricular systolic function. Global estimation of LVEF is often determined in a qualitative fashion; however, utilizing TTE or TEE, 2D imaging allows quantitative measurement of LVEF by assessing changes in ventricular volume during the cardiac cycle. The geometric model most commonly used for this measurement is the modified Simpson’s biplane method (Fig. 5.2e) [16, 58–60]. By utilizing orthogonal four chamber and two chamber views of the LV (from an apical window during TTE), this geometric model calculates LV end-diastolic volume (LVEDV) and LV end-systolic volume (LVESV) by summing equal sequential slices of LV area from each of these scan planes. LVEF can then be calculated as:

Normal values for LVEF range between 56 and 78 %. Similar to LVSF, LVEF has been shown to be dependent on changes in ventricular loading conditions [52, 54–56, 61].

Accurate calculation of LV volume by TEE can be challenging due to foreshortening of the LV cavity. To circumvent this limitation, an area-length method to derive LVEF can also be used [24]. This method utilizes the short axis area of the LV and the long axis LV length and can be obtained by imaging the LV in the TG mid SAX and ME 4 Ch views. Determination of ventricular volume and EF by these TEE methods has been shown to correlate reasonably well with invasively measured parameters of ventricular function.

New echocardiographic technology and advancements in image processing have allowed improved acquisition of ventricular volumes. Studies have validated the ability of 3D echocardiography to obtain accurate and reproducible estimates of LV and RV volumes and EF [32–35, 62–64]. While initially limited by the time-consuming reconstruction of acquired images, advances in 3D TEE now allow for real time data display, significantly enhancing the quantitative assessment of ventricular volume and function (Chap.​ 19) [63, 65, 66].

Automated border detection (ABD) is another approach in imaging technology that utilizes acoustic quantification to differentiate the myocardium from the blood pool and thereby allows enhanced visualization of the endocardial border. End-diastolic and end-systolic LV area can be continuously displayed with this modality enabling determination of ventricular volume, FAC, and even pressure-volume or pressure-area loops. Excellent correlation of ABD with other noninvasive and invasive measurements of ventricular function has been reported in a few adult studies but data is lacking in patients with CHD and altered ventricular geometry [44, 46, 67–73].

The rate of LV fiber shortening can be noninvasively assessed by M-mode echocardiography (a graphic display of distance over time). This measurement, termed the mean velocity of circumferential fiber shortening (V_cf), is normalized for LV end-diastolic dimension and can be obtained from the following equation:
LVET = LV ejection time.

Reported normal values for mean V_cf are 1.5 ± 0.04 circumferences (circ)/sec (s) for neonates and 1.3 ± 0.03 circ/s for children between 2 and 10 years of age [54, 74, 75]. This index not only assesses the degree of fractional shortening but the rate at which this shortening occurs. To normalize V_cf for variation in heart rate, LVET is divided by the square root of the R-R interval to derive a rate-corrected mean velocity of circumferential fiber shortening (V_cfc). Normal V_cfc has been reported to be 1.28 ± 0.22 and 1.08 ± 0.14 circ/s in neonates and children, respectively [54, 74–79]. Because V_cfc values are corrected for heart rate, a significant decrease in V_cfc between the neonatal and childhood age groups has been attributed to increased systemic afterload with advancing age. V_cf is sensitive to changes in contractility and afterload but relatively insensitive to changes in preload. Similar to fractional shortening, this parameter relies on the elliptical shape of the LV and is invalid with altered LV geometry.

Because the majority of ejection phase indices, including SF, EF, and V_cfc are dependent upon the underlying loading state of the LV, measures of wall tension, namely circumferential and meridional end-systolic wall stress, have been proposed to assess myocardial systolic performance in a relatively load-independent fashion [80]. Colan and colleagues have previously described a stress-velocity index that is an inverse linear relationship between V_cfc and end-systolic wall stress (Fig. 5.3). This stress-velocity index is independent of preload, normalized for heart rate, and incorporates afterload resulting in a noninvasive measure of LV contractility that is independent of ventricular loading conditions [81]. This index can therefore provide a more accurate characterization of LV myocardial systolic performance, by differentiating states of increased ventricular afterload from decreased myocardial contractility. While both conditions can affect cardiac output, the former represents increased resistance to myocardial output despite normal myocardial contractility, while the latter represents a true impairment of myocardial contractile performance. While the stress-velocity index is appealing, the clinical application of this index has been limited by its cumbersome acquisition and the need for time-consuming offline processing which are often not suitable for rapid assessment of ventricular performance such as is typically required during TEE. This index is also limited in patients with altered ventricular geometry and wall thickness, features that are hallmarks of CHD.

Echocardiographic evaluation of systolic function has primarily relied upon one-dimensional measures of LV shortening or on 2D measures of LV volume changes that are often difficult to assess in patients with distorted ventricular geometry. Doppler measures of global ventricular function have been reported to be a potentially more reproducible and sensitive measure of ventricular function overcoming the limitations of other approaches.

Regional ventricular function can be assessed by examining wall motion and systolic wall thickening. TEE, particularly in the intraoperative setting, is ideally suited for this purpose. Changes in ventricular wall motion typically occur during periods of decreased coronary perfusion, as can be the case during surgical interventions. These wall motion alterations are characterized by reduced systolic thickening and decreased inward endocardial excursion.

In order to facilitate regional wall function assessment several schemes have been proposed that include specific nomenclature, a variable number of LV segmental divisions, and different methods of wall motion analysis. Two models of LV segmental division have been favored as follows: (1) the 16-segment LV model and (2) the 17-segment LV model. The former, established in 1989 [16], represents an effort by the American Society of Echocardiography Committee on Standards and forms the basis for the recommendations in the original guidelines for performing a comprehensive intraoperative multiplane TEE examination established by the American Society of Echocardiography and the Society of Cardiovascular Anesthesiologists [95]. The latter, proposed by the American Heart Association in 2002, aimed to standardize myocardial segmentation and nomenclature for all types of cardiac imaging modalities [96]. These two models as applicable to TEE imaging are illustrated in Figs. 5.6 and 5.7.

The 16-segment model divides the LV into three levels from base to apex: basal, mid, and apical. The basal and mid levels are each divided circumferentially into six segments, and the apical level into four. The 17-segment model added the apical cap or myocardial apex at the extreme tip of the LV beyond the chamber cavity. It was also suggested that the term ‘inferior’ might be more suitable than ‘posterior’ in reference to the ventricular walls. In the most recent recommendations for chamber quantification it is pointed out that the 16-segment model is more suitable for assessing wall motion abnormalities (as the apical segment does not move), while the 17-segment model is more appropriate for myocardial perfusion evaluation and comparison among various imaging modalities [97].

The TG Mid SAX view at the level of the papillary muscles is the suggested starting point to facilitate the qualitative evaluation of regional ventricular systolic function. Although there is significant variability in the myocardial blood supply by the coronary arteries, this cross-section allows for a prompt assessment of segmental wall function since all coronary artery territories are represented in this view (Fig. 5.8). Additional TEE cross-sections are needed to evaluate all myocardial segments as allowed by multiplanar imaging, including the ME 4 Ch, ME 2 Ch, and ME LAX views (Fig. 5.8). The visual assessment of wall motion should be graded as normal/hyperkinetic, hypokinetic (reduced systolic thickening), akinetic (absent systolic thickening), dyskinetic (paradoxical systolic motion), or aneurysmal (diastolic deformation).

The feasibility of this segmental functional analysis and its utility has been reported in infants with CHD. In a prospective study of neonates undergoing an arterial switch operation for transposition of the great arteries, segmental wall motion was examined in the TG Mid SAX and ME 4 Ch views [98]. The presence of severe wall motion abnormalities that persisted at the completion of surgery and were present in multiple segments was found to correlate with myocardial ischemia in this cohort. This highlights the importance of regional functional analysis in patients undergoing interventions that involve the coronary arteries, aortic root or any other procedures that can potentially impact coronary perfusion.

Obviously, the two segmental models discussed apply principally to the LV in an anatomically “normal” heart—one with situs solitus, normal segments, and atrioventricular and ventriculoarterial connections (Chap.​ 4). As such, there will be limited direct application of these models for a number of congenital heart defects. Nonetheless the principles embodied in this segmental wall motion analysis—in particular, the evaluation of segmental wall kinetic motion—can be more generally applied to all forms of CHD. It facilitates a semi-quantitative, analytic assessment of wall motion and function even in hearts with very abnormal ventricular shape and morphology.

The assessment of regional systolic LV function, as detailed above, has centered upon the evaluation of segmental endocardial excursion and LV wall thickening. These semi-quantitative methods often fail to discriminate between active and passive myocardial motion. Newer echocardiographic modalities, including tissue Doppler imaging and strain rate imaging, offer a potentially more quantitative and accurate approach to the assessment of regional myocardial contraction and relaxation.

Tissue Doppler imaging (TDI, also known as Doppler tissue imaging or DTI) has been an addition to the armamentarium of the echocardiographer in recent years. By incorporating a high pass filter, tissue Doppler allows the display and quantitation of the low velocity high amplitude Doppler shifts present within the myocardium as opposed to the higher velocity lower amplitude Doppler signals more commonly measured within the blood pool (Fig. 5.9). Tissue Doppler echocardiography is less load-dependent than corresponding Doppler velocities from the blood pool and has systolic and diastolic components. These systolic velocities are heterogenous depending on ventricular wall and position.

Measurement of myocardial wall velocities by TDI has been shown to be a promising modality for assessment of longitudinal systolic performance [49, 51, 100]. Recent studies have demonstrated significant changes in mitral annular systolic TDI velocities in adult patients with LV dysfunction and elevated filling pressures [101, 102]. These indices have also been used to identify subclinical systolic ventricular dysfunction in pediatric patients [103]. Data in children following cardiac transplantation have also been found to correlate with hemodynamic parameters [104].

Tissue Doppler velocities, however, cannot differentiate between active contraction and passive motion, representing a major limitation when assessing regional myocardial function. Regional strain rate corresponds to the rate of regional myocardial deformation and can be calculated from the spatial gradient in myocardial velocity between two neighbouring points within the myocardium. Regional strain represents the amount of deformation (expressed as a percentage) or the fractional change in length caused by an applied force and is calculated by integrating the strain rate curve over time during the cardiac cycle. Strain measures the total amount of deformation in either the radial or longitudinal direction while strain rate calculates the velocity of shortening (Fig. 5.10). These two measurements reflect different aspects of myocardial function and therefore provide complementary information. In contrast to tissue Doppler velocities, these indices of myocardial deformation are not influenced by global heart motion or tethering of adjacent segments and therefore represent better indices of true regional myocardial function.

Studies have demonstrated regional differences in strain rate in adult patients after myocardial infarction [50, 105]. Measurements of radial and longitudinal strain rate have also been reported in normal children [106]. In addition, quantification of regional RV and LV function by strain rate and strain indexes after surgical repair of tetralogy of Fallot in children demonstrated that RV deformation abnormalities are associated with electrical depolarization abnormalities or chronic pulmonary regurgitation [107–110]. Further studies are needed to identify potential applications of strain rate imaging and related newer modalities (speckle-tracking and vector velocity imaging) in the evaluation of ventricular mechanics and regional assessment of myocardial function of both right and left ventricles in children [111]. It is hoped that future investigations can address the suitability of these approaches in the perioperative setting.

Mitral inflow Doppler is readily obtained from the ME 4 Ch view and represents the diastolic pressure gradient between the left atrium (LA) and LV (Fig. 5.11). The early diastolic filling wave, or E-wave, is the dominant diastolic wave in children and young adults and represents the peak LA to LV pressure gradient at the onset of diastole. The deceleration time of the mitral E-wave reflects the time period needed for equalization of LA and LV pressures. The late diastolic filling wave, or A-wave, represents the peak pressure gradient between the LA and LV in late diastole at the onset of atrial contraction. Normal mitral inflow Doppler is characterized by a dominant E-wave, a smaller A-wave, and a ratio of E- and A-waves (E:A ratio) between 1.0 and 3.0. Normal duration of mitral deceleration time as well as isovolumic relaxation time vary with age and have been reported in both pediatric and adult populations [113, 115–118]. Mitral inflow Doppler velocities are not only impacted by changes in LV diastolic function but also by a variety of additional hemodynamic factors including age, altered loading conditions, heart rate, and changes in atrial and ventricular compliance. Interpretation of characteristic patterns of mitral inflow must be carefully evaluated with particular attention paid to the potential impact of each of these hemodynamic factors on the Doppler velocities.

The earliest stage of LV diastolic dysfunction demonstrated by mitral inflow Doppler is abnormal relaxation (Fig. 5.11). This Doppler pattern is characteristic of normal aging in adults and represents a mild decrease in the rate of LV relaxation with continued normal LA pressure. It is characterized by a reduced E-wave velocity, increased A-wave velocity, decreased E:A ratio <1.0, and a prolonged mitral deceleration time and isovolumic relaxation time (IVRT).

As diastolic dysfunction progresses, further changes in ventricular relaxation and compliance occur leading to an increase in LA pressure. Increased LA pressure normalizes the initial transmitral gradient between the LA and LV producing a “pseudo-normalized” mitral inflow Doppler pattern with increased E-wave velocity and E:A ratio, and normalized mitral deceleration and isovolumic relaxation time intervals (Fig. 5.11). This pseudo-normal Doppler pattern may be difficult to distinguish from normal mitral inflow Doppler; however, maneuvers that decrease ventricular preload, like the Valsalva maneuver, will uncover the underlying abnormalities of mitral inflow Doppler. In addition, evaluation of pulmonary venous inflow Doppler can help unmask this advanced degree of LV diastolic dysfunction (see below).

Further deterioration of LV diastolic function results in restrictive ventricular filling with an additional increase in LA pressure and a concomitant decrease in ventricular compliance. The Doppler pattern of restrictive LV filling is characterized by additional increases in E-wave velocity, reduction in A-wave velocity, an increased E:A ratio >3.0, and significant shortening of both mitral deceleration time and IVRT (Fig. 5.11) [115]. This pattern is typically seen in patients with restrictive cardiomyopathy and may also be seen in other conditions associated with restrictive physiology (i.e., acute post-transplant setting).

Pulmonary venous Doppler, combined with mitral inflow Doppler, provides a more comprehensive assessment of LA and LV filling pressures (Fig. 5.11) [119–121]. TEE is ideally suited to the acquisition and quantitation of pulmonary venous flows, particularly in patients with poor transthoracic windows [19, 20, 27, 122]. Pulmonary venous inflow consists of three distinct Doppler waves: a systolic wave (S-wave), a diastolic wave (D-wave), and a reversal wave that occurs with atrial contraction (Ar-wave). In normal adolescents and adults, the characteristic pattern of pulmonary venous inflow consists of a dominant S-wave, a smaller D-wave, and a small Ar-wave of low velocity and brief duration. In neonates and younger children, a dominant D-wave is often present with a similar brief low velocity, or even absent, Ar-wave.

With worsening LV diastolic dysfunction, LA pressure increases leading to diminished systolic forward flow into the LA from the pulmonary veins with relatively increased diastolic forward flow resulting in a diastolic dominance of pulmonary venous inflow (Fig. 5.11). More importantly, both the velocity and duration of the pulmonary venous atrial reversal wave are increased. Pediatric and adult studies have demonstrated that an Ar-wave duration >30 ms longer than the corresponding mitral A-wave duration or a ratio of pulmonary venous Ar-wave to mitral A-wave duration >1.2 is predictive of elevated LV filling pressure (Fig. 5.12) [113, 120]. Pulmonary venous flow variables as measured by TEE have been correlated with estimations of mean LA pressure in adults undergoing cardiovascular surgery [19].

Tissue Doppler imaging is particularly well suited to the quantitative evaluation of LV diastolic function and can be easily obtained by either a transthoracic or transesophageal approach. Both early (Ea) and late (Aa) annular diastolic velocities can be readily obtained by tissue Doppler echocardiography (Fig. 5.9). Similar to systolic tissue Doppler velocities, differences in diastolic velocities exist between (1) the subendocardium and subepicardium, (2) from cardiac base to apex, and (3) between various myocardial wall segments. Previous studies have reported an excellent correlation between the early annular diastolic mitral velocity and simultaneous invasive measures of diastolic function at cardiac catheterization [123]. Early annular diastolic velocities also appear to be less sensitive to changes in ventricular preload compared to the corresponding early transmitral Doppler inflow velocity [101, 123, 124]. These diastolic tissue Doppler velocities, however, are impacted by significant alterations in preload. The influence of afterload on tissue Doppler velocities is less controversial with many studies documenting significant changes in systolic and diastolic annular velocities with changes in ventricular afterload [125–127]. Therefore, the clinical use of tissue Doppler velocities in patients with valvar stenoses or other etiologies of altered ventricular afterload need to be interpreted carefully in light of this limitation.