From the *Division of Cardiac Anesthesiology, University of Ottawa Heart Institute; and †Department of Anesthesiology, University of Ottawa, Ottawa, Ontario, Canada.
Accepted for publication November 27, 2012.
Supported by the research funds of the Division of Cardiac Anesthesiology and Critical Care Medicine of the University of Ottawa Heart Institute, Ottawa, ON, Canada.
The authors declare no conflicts of interest.
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Address correspondence to Christopher C. C. Hudson, MD, FRCPC, Division of Cardiac Anesthesiology, University of Ottawa Heart Institute, H2410-40 Ruskin St., Ottawa, ON, Canada K1Y 4W7. Address e-mail to firstname.lastname@example.org.
A 78-year-old woman is undergoing an elective coronary bypass graft surgery via an open sternotomy. Upon disengagement from cardiopulmonary bypass, you notice on transesophageal echocardiography (TEE) that the interventricular septum (IVS) appears to have abnormal motion. You investigate further to determine the cause of this abnormal motion.
The IVS separates the left ventricle (LV) and right ventricle (RV), and it has an important role in the function of both ventricles. In this brief review, we discuss the basic anatomy, physiology, TEE examination, and common pathology of the IVS. Pathologic conditions arising in the IVS include hypertrophy, aneurysms, abnormal motion, and ventricular septal defects (beyond the scope of this document).
Anatomy and Blood Supply
The IVS is comprised of the thick muscular septum and the thin fibrous membranous septum and is concave toward the LV (Fig. 1).1 The muscular septum borders much of the LV and RV cavities. The membranous septum comprises the upper and posterior portion of the IVS, separates the LV outflow tract (LVOT) from the right atrium and RV, and is a common site for congenital LV–right atrium communications (Gerbode defect). The IVS is very important to the function of the RV by providing a structure against which the RV free wall contracts.
Important elements of the conduction system of the heart are found within the IVS.1 The bundle of His travels in the subendocardium, down the right side of the IVS for 1 cm before dividing into the right and left bundle branches. The right bundle branch continues down the right side of the IVS, while the left bundle branch crosses to the left side and splits into anterior and posterior divisions.
Echocardiographically, the IVS is divided into 5 segments: basal anteroseptal, basal inferoseptal, midanteroseptal, midinferoseptal, and apical septal. The blood supply of the IVS can be variable, but usually has contributions from branches of both the right coronary artery (RCA) and the left coronary artery (LCA).1 The RCA travels along the posterior interventricular groove, from base to apex, becoming the posterior descending artery (PDA) and supplying the posterior one-third of the IVS. The left anterior descending (LAD) branch of the LCA travels down the anterior interventricular groove, giving off septal perforators, and supplying the anterior two-thirds of the IVS. Figure 1 demonstrates a right dominant coronary circulation, where the PDA, perfusing the midinferoseptal segment of the LV, originates solely from the RCA (occurring in 70% of patients). However, in 10% of patients, the PDA originates solely from the LCA alone (left dominant circulation), whereas in 20% the PDA is supplied by both the RCA and the circumflex branch of the LCA (codominant circulation).
Normal Function of the IVS
In systole, the IVS both thickens and moves. The normal motion of the contracting IVS is away from the sternum and toward the inferior LV free wall, with shortening from base to apex. From a TEE perspective, there is clockwise rotation of the apex and counterclockwise rotation of the base. Normal motion is not uniform throughout the IVS. When the ventricles contract, the upper IVS acts as a hinge point between the aortic root and the remaining IVS.1 This motion is the result of the complex arrangement of the ventricular myocardial fibers.2 During ventricular contraction, myocardial fibers undergo longitudinal shortening, circumferential thinning, and radial thickening. The resulting deformation, also known as strain, cannot be fully appreciated using conventional 2-dimensional echocardiographic imaging: only radial thickening can be seen. Advanced imaging techniques such as Doppler tissue imaging, Doppler strain echocardiography, and 2-dimensional speckle tracking imaging allow for this analysis; information on these techniques can be found in a recent consensus statement by the American Society of Echocardiography.2
Basic TEE Views of the IVS
The IVS can be examined with 2 midesophageal (ME) views and 4 transgastric (TG) views: the ME 4-chamber view (0–10 degrees), the ME long-axis view (130–150 degrees), the TG basal short-axis view (0 degrees), the TG midpapillary short-axis view (0 degrees), the TG apical view (0 degrees), and the deep TG long-axis view (0 degrees).3 Figure 1 demonstrates these views, with the usual coronary supply of each myocardial segment. Note that in the ME 4-chamber view, anteflexion of the TEE probe reveals the anterior IVS, which is supplied by branches of the LAD, while retroflexion of the probe demonstrates the inferior IVS, which is usually supplied by the RCA-PDA. The ME long-axis and deep TG long-axis views allow further examination of the anterior IVS, whereas the TG midpapillary short-axis and basal views demonstrate anteroseptal and inferoseptal segments simultaneously. The TG apical view allows visualization of the apical septal segment.
The normal thickness of the LV myocardium is 6 to 9 mm in women and 6 to 10 mm in men.4 When performing TEE, the IVS thickness is measured in the TG midpapillary short-axis view at end diastole. This measurement should be compared with the thickness of the inferolateral (posterior) segment (Fig. 2). End diastole can be determined by the onset of the QRS, or the frame where the cardiac cavity is the largest.4 Measuring the IVS can be difficult: adjacent right-sided (tricuspid valve apparatus or moderator band) and left-sided (false tendon) structures can make it difficult to determine the endocardial borders for caliper placement. In addition, measurement of thickness and function depends on lateral resolution, which is less precise than main beam resolution: difficulty can arise when the epicardial border is not well delineated.
IVS hypertrophy can occur as part of generalized LV hypertrophy, or it can occur in isolation, such as in asymmetric septal hypertrophy (ASH).5 In ASH, the ratio of the IVS thickness to the inferolateral (posterior) wall thickness is >1.3. Although ASH is a characteristic feature of hypertrophic cardiomyopathy, it can also occur in the elderly due to hypertension or aortic stenosis. Excessive thickening can lead to LVOT obstruction in systole: this condition is termed hypertrophic obstructive cardiomyopathy.5 This obstruction can be further worsened with concomitant systolic anterior motion of the anterior leaflet of the mitral valve.
Surgical repair of hypertrophic cardiomyopathy with septal myectomy is generally performed for patients with severe LVOT obstruction: a gradient at rest >30 mm Hg, IVS thickness >18 mm, and evidence of systolic anterior motion.6 During septal myectomy, TEE can be used to evaluate the extent of resection required, determine the presence and severity of mitral regurgitation or papillary muscle abnormalities, assess the adequacy of surgical resection, and screen for iatrogenic septal defects postmyectomy.7 Measurements should be made in the ME long-axis view. To ensure adequate surgical resection, one must measure the thickness of the basal IVS and determine the extent of IVS hypertrophy toward the apex and anterolateral wall.7 In addition, it is important to determine the point of septal contact with the anterior mitral leaflet, and of subaortic obstruction, to ensure that the surgical resection extends beyond this point.8
Aneurysm of the IVS is rare. It is most often associated with congenital perimembranous ventricular septal defects, but can also be caused by increased atrial and ventricular pressure, endocarditis, or can occur after a transmural septal myocardial infarct.9 Echocardiographically, an aneurysm is characterized by myocardial thinning with dyskinetic motion toward the RV during systole. Thrombus is often present. Aneurysms are most frequently located in the anterior aspect of the IVS below the aortic valve and are best seen in the ME long-axis view or by anteflexing and/or withdrawing the probe in the ME 4-chamber view.
Abnormal Septal Motion
In addition to LV aneurysms, there are a number of pathologic conditions in which septal motion is abnormal.
Like every other segment of the LV, the normal IVS thickens during systole.1 Because the LV has a larger muscle mass than the RV, this thickening is usually associated with a relative movement of the IVS toward the LV cavity.
1. Right Ventricular Overload
In the setting of pressure and volume overload of the RV, the dynamics of the IVS change throughout the cardiac cycle, and result in characteristic patterns of IVS motion, better appreciated in the TG views. In RV pressure overload (i.e., after acute pulmonary embolism), the IVS flattens, causing the LV cavity to become “D” shaped throughout the cardiac cycle, but maximally in systole (Video 1, see Supplemental Digital Content 1, http://links.lww.com/AA/A512). In RV volume overload (i.e., tricuspid or pulmonary regurgitation), the LV cavity becomes “D” shaped only during diastole, shifting back to a round shape during ventricular systole as the RV empties (Video 2, see Supplemental Digital Content 2, http://links.lww.com/AA/A513).
The eccentricity index can be used to help distinguish between these 2 entities (Fig. 3).10 The eccentricity index is the ratio of the diameter of the LV cavity parallel to the IVS versus the diameter of the LV cavity perpendicular to the IVS, as measured in the TG mid short-axis view. In normal conditions, the LV cavity is round throughout the cardiac cycle, thus the eccentricity index should be approximately 1. In patients with RV pressure overload, the eccentricity index is >1 at both end systole and end diastole. In patients with RV volume overload, the eccentricity index is approximately 1 at end systole, but >1 in end diastole. Although the eccentricity index cannot be calculated in ME views, they can be useful to appreciate IVS motion.
2. Abnormal Conduction
The normal conduction system is very effective at disseminating electrical impulses, so that both ventricles contract in a synchronous manner. However, in certain conditions, electrical depolarization does not spread normally, resulting in dyssynchronous ventricular contraction. On echocardiographic examination, this manifests as abnormal motion of the IVS. In cardiac surgical patients, the most common causes of ventricular dyssynchrony are left bundle branch block and RV pacing. In both these conditions, the RV depolarizes before the LV. Echocardiographically, the IVS moves first toward the RV, subsequently moving back to the left along with the rest of the LV (aka septal bounce) (Video 3, see Supplemental Digital Content 3, http://links.lww.com/AA/A514). Visually, the apparent discordance can be confused with a segmental wall motion abnormality. However, myocardial thickening is normal. Note that atrial pacing preserves the normal sequence of depolarization, resulting in normal septal motion.
Improved temporal resolution can be obtained in M-mode, with frame rates exceeding 1000 samples per second: this can be particularly useful in the assessment of fast-moving structures such as the IVS.11 M-mode imaging of the IVS can be obtained in the TG midpapillary view; however, adequate alignment of the probe may be challenging.
In chronic constrictive pericarditis, the inability of the heart to expand due to a noncompliant pericardium leads to abnormal septal motion.12 The LV pressure-volume relationship is influenced by RV filling; this is referred to as ventricular interdependence. Septal bounce is characteristic of this condition. Because of ventricular interdependence, the RV fills during spontaneous inspiration at the expense of LV filling (with a corresponding IVS shift toward the LV), with the reverse occurring during spontaneous expiration. In patients receiving positive pressure ventilation, the opposite IVS motion is seen. Septal bounce can also be seen in cardiac tamponade; this motion is more pronounced and longer-lived than is seen with left bundle branch block.
4. Abnormal Motion After cardiopulmonary Bypass
Paradoxical septal motion, the abnormal systolic movement of the IVS toward the RV with preserved wall thickening, is a common phenomenon after cardiac surgery.13 This can be distinguished from dyskinetic septal motion due to ischemia, when wall thickening does not occur. The exact mechanism of paradoxical septal motion is not truly understood. Some explanations include loss of an intact pericardium, which limits excessive heart motion toward the sternum, restriction of the RV from closure of the pericardium or chest wall, and LV underfilling.13,14 This abnormal motion is of no pathologic significance and can persist for weeks after surgery.
* The 6 basic TEE views for assessing the IVS are (1) ME 4-chamber view, (2) ME long-axis view, (3) TG midpapillary short-axis view, (4) TG basal short-axis view, (5) TG apical view, and (6) deep TG view. In these views, the IVS can be divided into 5 segments.
* The PDA supplies the posterior one-third of the IVS, whereas the LAD supplies the anterior two-thirds of the IVS.
* Normal septal thickness is 6 to 9 mm in women and 6 to 10 mm in men. The measurement should be made from the TG midpapillary short-axis view (midventricular IVS) and the ME long-axis view (basal IVS), at end diastole.
* In RV pressure overload, the IVS is flattened throughout the cardiac cycle, causing the LV cavity to appear “D” shaped in the TG midpapillary short-axis view. In RV volume overload, the LV cavity appears “D” shaped only in diastole.
The IVS has a central role in the function of both ventricles and it is important for the echocardiographer to understand its structure and function, in normal and pathologic states.
Name: Christopher C. C. Hudson, MD, FRCPC.
Contribution: This author helped write the manuscript.
Name: Jordan K. C. Hudson, MD, FRCPC.
Contribution: This author helped write the manuscript.
This manuscript was handled by: Martin J. London, MD.
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