The assessment of ventricular systolic performance is one of the most important roles of perioperative echocardiography. Ventricular function is a key determinant of cardiac output, and global or regional dysfunction may be present before surgery or develop de novo perioperatively. Patients with coronary disease are particularly at risk. The ability of the echocardiographer to recognize such abnormalities is critical to optimal patient care.

In most clinical settings, the assessment of ventricular systolic function is performed qualitatively and relies heavily on the scanning ability and trained interpretive eye of the echocardiographer.1,2 The ability to accurately assess global and regional ventricular systolic function is one of the most difficult transesophageal echocardiographic (TEE) skills to acquire, and there is no shortcut to supervised training, ideally with access to an independent gold standard. Paradoxically, whereas quantitative methods may require more time for image acquisition and processing, interpretation of the results of such approaches may be relatively straightforward.

All the methods presented in this chapter were first described using transthoracic imaging methods and have been extrapolated to the transesophageal approach. However, it is worth noting that, in some situations, studies directly validating TEE-based applications have not been performed. Since right ventricular (RV) performance is arguably equally important, methods of assessing RV function are discussed in Chapter 13.

A basic understanding of ventricular physiology, in particular pressure-volume relations, is essential to appropriate utilization of available methods of assessing left ventricular (LV) systolic performance.

The cardiac cycle includes three basic phases: ventricular contraction, relaxation, and filling. LV contraction is initiated when, as a result of rising cytosol calcium levels, the actin and myosin filaments increase the degree to which they overlap, resulting in sarcomere shortening. As more and more cardiomyocytes are activated, the left ventricle begins to contract and LV pressure rises. The LV pressure continues to rise until it overcomes the left atrial pressure, at which point the mitral valve closes. During isovolumic contraction, the period between mitral closure and aortic opening, the LV pressure continues to rise. When it exceeds the aortic pressure, the aortic valve opens and blood is ejected. As ejection continues, LV pressure peaks and begins to decrease. When it decreases below the aortic pressure, the aortic valve closes and ejected blood continues to be propagated through the systemic circulation. On a cellular level, calcium is taken up by the sarcoplasmic reticulum, and the myofilaments enter a state of relaxation. Because the mitral and aortic valves are in a closed position, ventricular volume remains constant. This period is known as isovolumic relaxation. With continued relaxation, LV pressure decreases further and the mitral valve opens. LV filling occurs in response to the gradient between the left atrium and the ventricle. This first period of filling is known as the early diastolic filling period. A second, later component occurs after atrial contraction. One method of displaying the phases of the cardiac cycle is by plotting pressure versus volume, thus creating pressure-volume loops (Figure 6–1).

It might appear that indices of systolic performance should focus exclusively on isovolumic contraction and ejection. However, the diastolic filling portion of the pressure-volume loops is also relevant because it addresses the concept of preload, which, as described below, is an important determinant of many of the most commonly used indices of systolic function. A discussion of diastolic function itself may be found in Chapter 12.

Load Dependence

Overall cardiac performance is perhaps best measured by cardiac output or stroke volume (cardiac output/heart rate). These reflect not only ventricular systolic and diastolic function, but also function of the cardiac valves and pericardium. Ventricular systolic performance in turn is a function of intrinsic myocardial contractility and loading conditions. Thus, in discussing measures of ventricular systolic function, it is important to recognize that many of these are load dependent and that only a few are pure indices of myocardial contractility.

Preload is defined as the wall stress at end-diastole or the load the ventricle experiences before contraction is initiated. It is a function of venous return. Afterload is the wall stress during ventricular contraction or the load against which the ventricle ejects. In the absence of mechanical obstruction to ventricular emptying, such as aortic stenosis, it is a function of the systolic blood pressure.

An appreciation of the effect of loading conditions is particularly important in the intraoperative setting, where dynamic changes in loading typically occur. Preoperatively, preload may be reduced due to the patient’s fasting status or, perhaps, from aggressive diuresis as treatment for the patient’s underlying heart disease. In the noncardiac setting, an acute event associated with blood loss or fluid shifts may have led to hypovolemia. Induction of anesthesia typically is associated with vasodilation that may further reduce preload. In cardiac surgical patients, preload may be reduced after cardiopulmonary bypass if underlying shunts or regurgitant valve lesions have been corrected. This is compounded by the significant vasodilation that is typical of the period immediately after cardiopulmonary bypass.

Abrupt shifts in afterload also typically occur in the perioperative period. Anesthetic agents may reduce afterload, and surgical correction of outflow tract obstruction, such as aortic valve replacement for aortic stenosis, also may have a major effect. These changes do not invalidate the use of load-dependent indices of systolic function, but their effect must be understood if one is to use these measures appropriately.

In simple terms, load dependence refers to the fact that, for the same degree of intrinsic ventricular contractility, the index of systolic function will vary with the degree to which the ventricle is filled and/or the pressure against which it ejects. For example, in the presence of severe mitral regurgitation, a ventricle with normal contractility will have an LV ejection fraction (LVEF; a load-dependent index) that would be considered elevated in a normally loaded heart. Conversely, in the same setting, an LVEF that would be considered normal for a normally loaded heart would, in fact, indicate depressed function. Table 6–1 lists indices of ventricular systolic performance that can be derived with echocardiography.

Chamber Dimensions

The normal shape of the LV is symmetric with two relatively equal short axes and with the long axis running from the base through the mitral annulus to the apex. In the long-axis views, the apex is rounded, so the apical half of the ventricle resembles a hemiellipse. The basal half, however, is more cylindrical.

Initial evaluation of global systolic performance includes measurement of the linear dimensions of the LV cavity. Chamber dilation or hypertrophy often provides the first diagnostic clues of the underlying pathophysiology. The major long-axis measurement of ventricular dimension is made from the apical endocardium to the plane of the mitral valve by using a midesophageal four-chamber view (see Chapter 4). The minor short axis is measured perpendicular to a point one-third of the length of the long axis, moving from the base to the apex. Short-axis dimensions are often easier to obtain accurately with TEE and involve measurement of the end-diastolic anterior-posterior or medial-lateral diameter at the midpapillary level. A diameter larger than 5.4 cm is considered enlarged, but care must be taken to ensure that the papillary muscles are excluded from the line of measurement.

LV wall thickness is best determined from a transgastric long-axis or midpapillary short-axis view using M-mode or two-dimensional (2D) imaging. An end-diastolic wall thickness greater than 1.1 cm is considered increased. Although increased wall thickness is often viewed as being synonymous with left ventricular hypertrophy, this is incorrect, as left ventricular hypertrophy refers to increased left ventricular mass and LV mass may increase without an increase in thickness. LV mass is the total weight of the myocardium and is equal to the product of the volume of the myocardium and the specific density of cardiac muscle. LV mass can be derived from the transgastric midpapillary short-axis view by using a simple geometric cube formula:

LV Mass = {1.04 × [(LVID + PWT + IVST)3 − LVID3]} × 0.8 + 0.6 g

where LVID is the end-diastolic internal dimension (diameter), PWT is the inferolateral (posterior) wall thickness, IVST is the interventricular septal thickness, 1.04 is the specific density of the myocardium, and 0.8 and 0.6 are correction factors. Calculation of LV mass by TEE is comparable with transthoracic echocardiography (TTE); however, TEE measurements are higher by an average of 6 gm/m2 (see Table 4–2).3

Cardiac Output

Cardiac output is the product of stroke volume and heart rate. Whereas right heart catheterization using Swan-Ganz catheters is common in the perioperative period and provides the most widely used method for deriving cardiac output, the thermodilution method may be invalid in the setting of tricuspid regurgitation. Further, the devices are expensive, and placement may be risky in some patients, such as those with right-side cardiac masses. Echocardiographic methods are not used routinely for cardiac output determinations, in large part for logistic reasons. However, they are well validated and may provide an alternative or adjunct to thermodilution methods.

Echocardiographic measures of cardiac output are based on the continuity equation, which states that in the absence of valve dysfunction or shunting, blood flow is constant throughout the heart. Thus, cardiac output is equal to the forward flow across each of the cardiac valves. For a given valve, this assumption will be invalid if there is significant regurgitation or if valve flow reflects the augmented flow of a shunt lesion. Because of the circular and relatively fixed geometry of the ventricular outflow tracts and semilunar valves, and the relative ease of echocardiographic imaging of these sites, stroke volume calculations typically are derived by measuring forward flow across the LV outflow tract,4,5 aortic valve,6,7 or, less commonly, RV outflow tract.8 Although several methods have been proposed for measuring transmitral and transtricuspid flows, the complex dynamic geometry of the orifices of these valves makes them less desirable.

The measurement of the stroke volume starts with the velocity time integral, the integrated area under the curve of a pulsed Doppler spectrum. This represents the length of a column of blood moving through the targeted point in the heart per beat and has units of distance. Multiplying the velocity time integral by the cross-sectional area of the sampling site yields stroke volume. Cross-sectional area is calculated by using the formula for the area of a circle (πr2), where r is the cross-sectional diameter divided by 2. The product of stroke volume and heart rate is cardiac output. Although these methods were originally validated with transthoracic imaging, they have been successfully transposed to the transesophageal approach.

The most widely used method is shown in Figure 6–2. The velocity-time integral is recorded from a deep transgastric view of the LV outflow tract, and the LV outflow tract diameter is measured by using a midesophageal long-axis view.4,5 Ideally, the diameter should be measured at the same location as the velocity-time integral. Measurement of the LV outflow tract diameter from a transgastric view is less desirable because it relies on the lateral resolution of the image rather than on the superior axial resolution used when the measurement is taken from a midesophageal window. Once the stroke volume is calculated (cross-sectional area × velocity-time integral), multiplication by the heart rate yields cardiac output.

Commercially available echocardiographic systems have software packages designed to facilitate these calculations, typically included in the more extended analysis needed for Qp/Qs shunt calculations. However, it must be understood that, although shunts or valve regurgitation do not invalidate this calculation as a measure of flow at the site being interrogated, these flows may no longer simply reflect forward systemic cardiac output. For example, in the presence of aortic regurgitation, LV outflow tract flow will include the forward flow (cardiac output) and the regurgitant flow. Another caveat relates to the presence of valvular stenosis, where prestenotic accelerated flow signals and signals at or distal to the stenosis must be avoided.

A potential alternative to the Doppler imaging approach is to determine LV volumes at end-systole and end-diastole. The difference between the two measurements is the stroke volume (equal to LV end-diastolic volume minus LV end-systolic volume), which, when multiplied by heart rate, yields cardiac output. Echocardiographic methods for determining LV volume are described at greater length in subsequent sections dealing with LVEF.

Ejection Phase Indices

Echocardiographic images provide a series of methods for measuring the reduction in chamber dimension that occurs with systole, typically expressed as:

These ejection phase indices of systolic function include fractional shortening, fractional area change, and ejection fraction.

Fractional Shortening and Velocity of Circumferential Fiber Shortening

The simplest ejection phase index is fractional shortening, defined as:

This method dates back to the M-mode era of transthoracic echocardiography. Although theoretically of value in the symmetrically contracting heart, its ability to provide a sense of global ventricular function is limited when there is regional dysfunction. Thus, its use is waning. For reference, the lower limit of normal when using a transthoracic approach is 25% in men and 27% in women.3 Normal values using transesophageal views are reportedly similar but were derived from a smaller series of anesthetized patients.9

A variant of fractional shortening is the velocity of circumferential fiber shortening, defined as:

Fractional Shortening × Ejection Time

Ejection time can be measured on M-mode or LV outflow tract spectral Doppler. The lower limit of normal is 1.1 circumferences/second. Although it has been suggested that this is less preload dependent than ejection fraction,10 it is rarely used in the clinical setting.

Fractional area Change (area Ejection Fraction)

The tomographic slices of the left ventricle provided by 2D echocardiography provide another easily derived ejection phase index: fractional area change or area ejection fraction. This is defined as:

Originally described using transthoracic short-axis or apical views of the left ventricle, this index can be derived with transesophageal echocardiography by using transgastric short-axis views. Due to the apical foreshortening that is inherent in the TEE midesophageal four-chamber view, this parameter is not generally derived through this window. Although ventricular areas typically are outlined and measured by manual planimetry, systems with automatic boundary detection can automate the process and provide real-time displays of area and calculated fractional area change. Fractional area change derived from TEE and manual planimetry has been shown to correlate with ejection fraction when using nuclear methods in a variety of clinical settings,11–13 as has TEE-derived fractional area change assisted with automated boundary detection.14 Acceptable inter- and intra-observer variabilities also have been demonstrated,14 although Bailey and associates, in a study of pediatric patients with congenital heart disease, suggested an error of approximately 10% under optimal conditions.15 In symmetrically contracting ventricles, values were shown to be similar at multiple short-axis levels (60 ± 6%, mean ± standard deviation).16

It must be emphasized that although such approaches may be valid in patients with symmetric ventricular contraction, they have limited value in patients with regional wall motion abnormalities. Further, the presence of an excellent correlation between fractional area change and LVEF does not mean that the two values are identical. Thus, although it may be conceded that determinations of fractional area change are the most widely used means of quantitating ventricular function with TEE, the reader is encouraged to use the terms fractional area change or area ejection fraction rather than simply ejection fraction when referring to these calculations. The term ejection fraction should be reserved for calculations based on ventricular volumes (see below).

Volume Measurement and Ejection Fraction

The universal language for assessing LV systolic performance is ejection fraction (LVEF). Indeed, LVEF is measured routinely in invasive angiographic studies and with noninvasive echocardiographic, nuclear cardiologic, computed tomographic, and magnetic resonance methods. Although there are several quantitative echocardiographic approaches for calculating LVEF, a semiquantitative visual assessment is most widely applied in clinical transthoracic and transesophageal echocardiographic studies. This requires a trained eye. Although less desirable for research applications, this approach works well in the clinical setting in the hands of an operator with good scanning and interpretive skills.17

Quantitative Approaches