6 Ventricular Function

Wendy L. Pabich, Alina Nicoara, Madhav Swaminathan

Left Ventricular Systolic Function

Background

Coronary Anatomy and Left Ventricular Wall Segmentation

• The left anterior descending (LAD) artery arises from the left main coronary artery and supplies the anterior wall and anterior septum.

• The left circumflex (LCX) artery arises from the left main coronary artery and supplies the lateral wall (Figure 6-1).

• The LV is divided into 17 segments for better characterization of wall motion and thickening. There are 6 segments at the basal and midpapillary levels, 4 segments each at the apex and the apical cap (Figure 6-2).

• Normal wall motion is defined as greater than 30% excursion of the endocardial border and 30% to 50% thickening (see Video 6-1 on the Expert Consult website).

Figure 6-1 Typical distributions of the RCA, the LAD, and the LCX coronary arteries.

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.

Pathophysiology

• Wall motion and thickening are graded as normal, hypokinetic, akinetic (negligible thickening), dyskinetic (paradoxical systolic motion), or aneurysmal (diastolic deformation).

• Wall motion abnormalities (WMAs) can be either segmental or global and are most often due to decreased perfusion in the corresponding arterial distribution.

• Ventricular pacing can cause abnormal septal motion and WMAs may be difficult to assess, particularly in the perioperative period (see Videos 6-2, 6-3, and 6-4 on the Expert Consult website).

• LV function can also be affected by the long-term effects of valvular disease, particularly lesions that result in LV volume or pressure overload, such as aortic stenosis, aortic regurgitation (AR), and mitral regurgitation (MR; Figure 6-4).

Figure 6-4 TG mid SAX view of the LV in a patient with severe aortic insufficiency and dilatation of the LV cavity. A reasonable estimate of LV cavity dimensions can be made in this view considering the depth of view (15 cm) and the 1-cm markings on the cursor to the left of the display.

Cardiomyopathies

• Cardiomyopathies can affect ventricular function and can result from chronic ischemic, valvular, or intrinsic myocardial disease.

• Dilated cardiomyopathy may be ischemic or nonischemic in nature (Figure 6-5).

• Tako-Tsubo cardiomyopathy is associated with specific septal ballooning.

• Peripartum cardiomyopathy.

• Restrictive cardiomyopathy

1 Restrictive cardiomyopathy can be difficult to distinguish from constrictive pericardial disease (see “Left Ventricular Diastolic Function”).

2 Infiltrative disorders such as amyloidosis, sarcoidosis, and carcinoid disease frequently lead to restrictive cardiomyopathy.

Figure 6-5 ME 2C view of the LV in a patient with dilatation of the LV cavity. A reasonable estimate of LV cavity dimensions can be made in this view considering the depth of view (22 cm) and the 1-cm markings on the cursor to the right of the display.

Figure 6-6 ME LAX view of the LV shows SAM of the anterior mitral leaflet (circle) in a patient with HOCM.

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

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.