Eur J Cardiothorac Surg 2006;29:S126-S138
© 2006 Elsevier Science NL
The septal motor of biventricular function
Saleh Saleh
a
,
Oliver J. Liakopoulos
b
,
Gerald D. Buckberg
b
,
c
,
*
a Department of Medicine, David Geffen School of Medicine at UCLA, USA
b Option on Bioengineering, California Institute of Technology, Pasadena, CA, USA
c Department of Surgery, Division of Cardiothoracic Surgery, David Geffen School of Medicine at UCLA, 10833 Le Conte Avenue, 62-258 CHS, Los Angeles, CA 90095-1741, USA
Received 22 February 2006;
accepted 27 February 2006.
* Corresponding author. Tel.: +1 310 206 1027; fax: +1 310 825 5895. (Email: gbuckberg{at}mednet.ucla.edu).
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Abstract
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This paper describes the anatomic spiral arrangement of the cardiac interventricular septum that results in a twisting action that contributes to the forceful ejection of blood from both ventricles during systole. Right ventricular (RV) dysfunction seen in various clinical settings is discussed with reference to the septum and its mechanism of function. The role of the septum in the interdependence of ventricular function is described. The structure/function relationships of the septum are related to maintenance of its oblique fiber orientation and midline configuration; disruption of this spatial relationship is the lynchpin of the concept that ‘left heart failure begets right heart failure.’ The importance of recognizing how alterations in septal anatomy affect biventricular performance is related to improved understanding of the clinical manifestations of septal dysfunction, designing a management scheme, and determining how to prevent septal injury.
Key Words: Septum • Right ventricular failure • Helical ventricular myocardial band • Resynchronization • RV dysplasia • Ventricular interdependence
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1. Introduction
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Understanding of myocardial function must incorporate knowledge of underlying structure to allow a clear structure/function relationship to emerge. Without this framework, clinical decisions are made from patterns of behavior rather than from a stepwise breakdown of the architectural underpinning that produces a structural reason for the observed left or right ventricular (RV) activity. Dell’Italia [1] provided insight into this interaction in 1991 by observing that despite the markedly different muscle mass and chamber geometry, both ventricles are bound together by remarkable spiral muscle bundles that encircle them in a complex interlacing fashion that includes the septum to form a highly interdependent functional unit. The septum is the keynote to this ventricular interaction [2], and the report of Santamore [3] defines a broad spectrum of experimental and clinical adverse effects whereby septal dysfunction alters either left or right ventricular performance.
Understanding this interaction between ventricles requires knowledge of the anatomic components of the septum, and insight into how fiber orientation of the septum impacts right and left ventricular (LV) performance. The intent of this report is to (1) define the components of septal architecture and demonstrate that they are explained by the model of the helical ventricular myocardial band [4,5]; (2) demonstrate the structure function relationship that results from preservation of the normal anatomic framework; (3) describe how distortion of this anatomic framework by lesions of the left or right side of the heart can impair biventricular function; (4) define how stretch of the septum with bowing of its thick structure into either left or right ventricle can create an ‘architectural disadvantage’ that impairs septal contractile function; (5) indicate how restoration of normal anatomy will return septal function toward normal and thus improve biventricular performance, providing excitation contraction coupling is not impaired; (6) identify the importance of a sequential activation of the septum and its effect on cardiac dynamics, especially in regard to resynchronization; and (7) demonstrate why the septum is the ‘motor of biventricular function.’
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2. Septal anatomy and physiology
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The structure/function relationship is linked to the recent demonstration of how unfolding of the helical ventricular myocardial band demonstrated a septal architecture that mirrors the overlapping muscular configuration of the free wall of the left ventricular [6]. The septum is a midline structure between the two ventricles and is composed of oblique fibers from two layers of the myocardial band (the descending and ascending segments of the apical loop [4,7] that produces a septal thickness, whose weight is approximately 40% of ventricular myocardial mass.
Fig. 1
shows how the septum is composed of oblique fibers that are surrounded externally by the right segment of the basal loop that contains predominantly transverse fibers in the intact heart. The obliquity of septal fiber orientation is a central theme for subsequent function, since the ejection fraction is determined by the predominant orientation of fibers in the left and right sides of the circulation [8,9]. Although the septum anatomy contains two predominant muscle layers, it functions as a single unit. Therefore, there is no functional left- and right-sided septum.
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Fig. 1. Fiber orientation relationship of the septum, composed of oblique fibers that arise from the descending and ascending segments of the apical loop, surrounded by the transverse muscle orientation of the basal loop that composes the free right ventricular wall. Note the conical arrangement of the septum muscle and the basal loop wrap, forming the RV cavity.
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Fig. 2
shows an apical view of the septal fibers, and simultaneously demonstrates the crescent-shaped right ventricular cavity and conical left ventricular chamber. The unfolded heart is shown in Fig. 3
, as a schematic, and in Fig. 4
as a dissection. The septum is formed by the ascending and descending segments of the apical loop, and these same segments form the free wall of the left ventricle. An anisotropic shape is created as these muscle loops overlap at the apex to form a vortex or tip. The final shape of the left ventricle includes an inner ellipse that consists of the septum and free wall created by overlapping of oblique fibers of the descending and ascending segments, and surrounded by a wrap of the left segment of the basal loop, whose fibers are predominantly transverse.
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Fig. 2. Cross-sectional view of both ventricles demonstrating the crescent shape of the right ventricle and conical form of the left ventricle. The obliquity of the septal muscle structure and its spiral arrangement is clear. Note the thickened septum, and the wrap around basal loop.
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Fig. 3. Unfolding of the heart model to show (a) the intact ventricle; (b) detachment of the pulmonary artery to begin unfolding the basal segment (note underlying obliquely oriented descending and ascending segment of septum); (c) complete unfolding of basal loop of the right ventricle with the genu, posteriorly, separated from the left ventricular segment of the basal loop (note transverse fiber orientation of free wall); and (d) the entire basal loop with the entire genu in the midst of the transverse basal loop segment (left side right ventricle, right side left ventricle). Note the basal loop that surrounds the obliquely oriented fibers within the descending and ascending segments of the apical loop that is responsible for septal motion.
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Fig. 4. Posterior view of the right ventricle showing detachment of the pulmonary artery from the intact heart. This demonstrates the underlying obliquely oriented fibers of the apical loop that forms left and right ventricular sides of the septum, and how the transverse fibers of the basal loop wraps around the midwall septal structure.
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In contrast, the right ventricle is formed by the septum and free wall. The septum is comprised of the same oblique fibers that form the left ventricle, while its free wall is formed from the wrapping of the right segment of the basal loop. The fibers of the basal loop are oriented transversely with the exception of a small number of oblique fibers coming from the aberrant fibers of the ascending segment of the apical loop [10]. RV function is determined by the fiber orientation that underlies this architecture; the septum twists because of the oblique fiber orientation, and the wrapped transverse fibers of the basal loop cause constriction.
The criss-cross nature of septal fibers has been previously described from histological cross-sections [11,12], but structural segments that form these layers were not described until recent dissections of the helical ventricular myocardial band [4,6]. Fig. 5
shows that uncovering the right-sided septum requires detaching of the wrap around basal loop, which contains some oblique aberrant fibers that function similarly to oblique fibers that comprise the septum and free wall [13]. Septal fiber contraction was studied using sonomicrometer crystals, where maximal displacement of the crystals occurs when the crystals are aligned in the direction of fiber shortening. Septal fiber shortening was predominantly related to oblique fiber angulation, and mirrored the fibers found in the left ventricular free wall as shown in Fig. 6
. Conversely, Fig. 7
demonstrates the transverse orientation of the lateral or free wall fibers that is needed for understanding of right ventricular function.
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Fig. 5. Dissection specimens of the intact heart (left), and the unwrapped free wall that surrounds the underlying septum (right). The upper image shows the helical heart model, and mirrors the dissected ventricle are shown below. The ascending segment fibers (Asc) cover the right side of the septum. The basal loop is shown, and formed by a right segment (RS) and left segment (LS).
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Fig. 6. The relationships of the common stricture of the LV free wall and septum, in the dissected heart (A) and the intraoperative exposure (B). Note that the sonomicrometer crystals are placed in an oblique angular orientation in the ascending segment (solid lines) and in a criss-cross direction on the endocardium by transmural penetration into the descending segment of the apical loop (hatched lines).
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Fig. 7. Sonomicrometer crystal positions in RV free wall, demonstrating the improved systolic shortening (%SS), when the angulation is in transverse position (lower tracing at 120°). This is the predominant fiber orientation of the lateral wall of right ventricular basal loop.
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Sallin [8] and Ingels [9] furnished physiological studies that confirmed the importance of fiber orientation, by relating the effects of different angulations to expected ejection fraction. Basic science studies of myocyte function done on isolated fibers from muscle strips in a Petrie dish show that the maximal shortening of these fibers is 15%. The intact heart, however, has a continuum of muscle wrapped in a pattern that alters fiber orientation in different myocardial regions. Ejection fraction is 30% if the fibers are transverse, as occurs in the free wall of the right ventricle, and increases to 60% if there is predominant oblique fiber orientation, a pattern that comprises the septum and free wall of the left ventricle beneath the external wrapping of the left segment of the basal loop (Fig. 8
).
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Fig. 8. Comparison of ejection fraction in isolated ventricular muscle fibers. The changes in ejection fraction are shown with (a) transverse wrap, 30% ejection fraction, to simulate RV free wall transverse muscle, and (b) 60% in the septum, with spiral architecture (from helix formed by descending and ascending segments of apical loop, hatched and solid lines) to demonstrate how fiber angulation alters function, which was only 15% when muscle strips are in Petrie dish.
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The characteristic motion of twisting of the septum is linked to the anisotropic form created by this oblique fiber orientation (see Video 2 in http://ejcts.ctsnetjournals.org/content/vol27/issue2/images/data/202/DC1). Fiber orientation therefore accounts for both aspects of RV function that includes (a) bellows like action resulting in compression, caused by the transverse basal loop and (b) twisting due to oblique sequential septal contraction. The fundamental structure/function requirement is that underlying muscle maintains the natural structural configuration, together with simultaneous normal excitation contraction coupling, rather than the dyssynchrony seen with a wide QRS, or right- and left-sided bundle branch block.
The helical nature of the myocardial band with the appropriate folds [6,7] has shed a great deal of light upon the understanding of the structure and function of the septum. In contrast to prior concepts about the heart constricting and dilating during systole and diastole, the predominant movement is twisting to eject and reciprocal twisting to rapidly to fill, as shown by MRI technology [14,15] (see Video 2 in http://ejcts.ctsnetjournals.org/content/vol27/issue2/images/data/202/DC1). These actions are either accentuated or diminished by catecholamine infusion or by catecholamine blockers, respectively [14], and recent studies show that these actions are similar for the LV lateral wall and septum (Fig. 9
) in normal hearts [6].
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Fig. 9. (a) Sites of positioning of pairs of sonomicrometer crystals in the LV free wall and septum. Positioning sites are shown for the model of architecture (above) and whole heart intraoperatively (below). Note similarity of tracings from the descending segment of septum and free wall (upper 2) and ascending segment (lower 2). (b) Responsiveness of septum to control and positive and negative inotropic intervention. The changes by either dopamine or esmolol are similar to free wall findings reported by Castella et al. [13].
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The twisting action disappears when the cardiac chamber dilates and the septum gets bowed into the right ventricle by left-sided lesions such as aortic or mitral insufficiency, dilation from ischemic or non-ischemic congestive heart failure, or rhythm interruption from wide QRS (interval on electrocardiogram) or left bundle branch block (LBBB). Similarly, right-sided lesions like pulmonary insufficiency, atrial septal defect, or pulmonary outflow tract obstruction bow the septum toward the left side. The central theme [15,16] is that each event disrupts normal architecture by stretching the septum so that a more transverse, rather than oblique fiber orientation comprises its spatial configuration.
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3. Interventricular changes due to septal dynamics
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The concept of ventricular interdependence, used by Dell’Itaila [1] and Santamore and Dell’Itaila [3], exists by virtue of the normal folding of the myocardial band, and likely accounts for the fact that the septum is responsible for 
40% of left ventricular output [3]. During systole, the septum twists and shortens causing reduction in ventricular volume and forceful ejection of blood out of both ventricular cavities. In the case of the right ventricle, the septum seems to account for the major force of ejection, especially when there is pulmonary hypertension. In the absence of septal twisting due to septal damage, ventricular ejection is produced by circumferential constriction caused by contraction of the basal wall that contains predominantly transverse fibers. Such constriction may not allow delivery of enough contractile force to ensure adequate cardiac output when pulmonary vascular resistance is increased.
Septal dysfunction may underlie right ventricular dysfunction that can develop perioperatively when septal akinesia or hypokinesia follows many forms of cardioplegic myocardial protection [16] that damages the subendocardial muscle. Conversely, septal dysfunction does not normally cause severe left ventricular dysfunction, possibly because of the presence of undamaged oblique thick free wall epicardial fibers of the left ventricle that retain the capacity to twist and continue to contribute to ejection of blood out of the left ventricle into a vascular bed with higher resistance. In contrast, the right ventricle is bounded by its free wall with transverse fiber orientation and in the event of septal malfunction, the RV free wall can only generate the low pressure required to eject blood into a normal pulmonary circulation.
The fiber orientation in Figs. 1–3 defines the spatial reasons why the septum is the ‘ventricular motor,’ and clarifies major differences between septal contributions to left and right ventricular performance. The RV free wall fibers are oriented transversely and simply squeeze the contained blood by circumferential compression. Conversely, left ventricular free wall fiber orientation is oblique and can twist and shorten to eject blood more efficiently into a higher peripheral resistance vascular bed.
In contrast to the cardiac compromise resulting from a damaged septum, the septal contribution to cardiac function may be subtler. Geometric changes that follow elevation of right or left ventricular end diastolic pressure cause bowing and stretch of the septum, as it encroaches into the left or right ventricular cavities (Figs. 10 and 11
). The increased end diastolic pressure bows the septum as it stretches it, creating an ‘architectural septal disadvantage’ whereby the oblique orientation becomes more transverse, thereby impairing septal twist and shortening to decrease ventricular ejection of blood from either cavity.
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Fig. 10. Transesophageal echocardiogram showing bowing of septum to left side after right coronary artery occlusion with intact pericardium, as shown by Brooks et al. [50].
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Fig. 11. Comparison between healthy subject (left) and a patient with congestive heart failure with (a) left ventricular distension and (b) the stretched septum is bowed into the right ventricle, reducing its volume.
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4. Left heart failure begets right heart failure
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The aphorism ‘left heart failure begets right heart failure’ is well known to most clinicians and implies ventricular interdependence. The failure of one ventricle will in time lead to the failure of the other. This phenomenon can now be better understood with reference to the interventricular septum and the concept of septal disadvantage. Failure of one chamber will result in elevation of end diastolic pressure with diastolic bowing of the septum into the contra lateral chamber. This will result in encroachment of this chamber on the other, and will further compromise septal function due to stretch that changes fiber orientation, with resultant reduction of septal contribution to cardiac output of both ventricles.
When the initial event is left ventricular failure, then the septal contribution to right ventricular function is impaired and right ventricular ejection becomes dependent predominantly on the transverse fibers of the basal loop. Elevation of pulmonary artery pressure occurs because of increased left ventricular end diastolic pressure and results in right ventricular failure. Conversely, if the failure of the right ventricle is the primary event, then the septal dysfunction that results from stretch and alteration of fiber direction will not be as clinically obvious. Studies by Young et al. [17] show preferential septum stretching that precedes architectural changes of the lateral wall. The oblique muscle of the left ventricular free wall compensates initially and thereby maintains left ventricular cardiac output. Left heart failure in this setting will only become obvious when the function of the free wall of the left ventricle is impaired. This is why right ventricular failure as a consequence of left ventricular failure is more common than the converse.
Loss of septal function also has implications, since recognition that septal stretching is a geometric reason for impaired performance on the left or right side of the circulation. This finding allows changing septal fiber orientation to be incorporated into plans to improve biventricular performance. For example, knowledge that function returns after altering septal shape is linked to using recruitment of this septal reserve during planning for ventricular restoration for heart failure. The echocardiographic images before and after left ventricular rebuilding are shown in (see Appendix A, Supplementary data) and reinforce the importance of restoring the septal contribution to postoperative performance; septal function recovered after its return to midline position. This recovery is closely linked to avoidance of septal damage during left ventricular restoration, since septal injury from inadequate protection [16] will offset this benefit.
It naturally follows that any maneuver that favorably alters the ventricular pressures, and thereby results in reduction of septal bowing, will cause improvement in the ability of the septum to twist and eject, provided there is no electrical impairment of excitation contraction coupling. This could account for the acute improvement of ventricular function following clinical manipulation of filling pressures. With left ventricular failure, the dysfunction of the free wall unmasks the contribution of the septum to cardiac function.
A spectrum of clinical examples will now be summarized to employ this underlying physiologic concept and improve understanding of the septal role in biventricular performance. For example, when it is understood that the ‘motor’ of the right ventricle is the septum and not the right ventricular free wall, it becomes evident that a more logical explanation of RV failure can evolve, as well as better understanding of the septal contribution during resynchronization therapy for left heart failure.
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5. The right ventricle
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Historically, the right ventricle has been considered to be non-essential since cardiac output is not adversely affected in coagulation [18–20] or excision [21] experiments that rendered the right ventricular free wall non-functional. Furthermore, no significant hemodynamic consequences follow right coronary occlusion that damages only the RV free wall. Other evidence for its non-essential nature comes from the feasibility of doing the Fontan procedure, where the right ventricle was entirely bypassed without any immediate adverse consequences, provided the mean pulmonary arterial vascular resistance is low [22]. These observations emphasize that the right ventricle can only successfully function as a conduit with decreased pulmonary vascular resistance is low [23].
The importance of the septum becomes evident in other circumstances, such as in patients with inferior myocardial infarctions who sustain septal damage resulting in right ventricular failure. The consequent mortality exceeds 40% [24]. Septal dysfunction causes RV failure in postopen-heart surgery patients with pulmonary hypertension, especially after cardiac transplantation. These patients may require inotropic and sometimes mechanical assist devices yet the importance of the role of the septum in these situations is not widely appreciated.
Traditionally, little attention is paid to the septum, as evidenced by the fact that septal dysfunction postcardiac surgery is assumed to be a usual and inevitable event [16]. Right ventricular infarction with right-sided failure always involves occlusion of a posterior descending right coronary branch that causes septal damage with profound septal malfunction and hence right ventricular failure. The logic for this conclusion was established by studies of experimental RV infarction caused by ligation versus dye embolization of the RCA that resulted in divergent outcomes [25]. Occlusion did not result in marked RV dysfunction, while dye embolization caused RV failure [25]. The difference in outcome appears to be explainable by the resultant septal dysfunction when the RCA is embolized with interruption of collateral flow. Conversely occlusion itself does interfere with the capacity of collateral vessels to maintain some nourishment to the septum. Dye injection interferes with collateral flow to cause necrosis that becomes lethal when there is pulmonary hypertension. Each of these observations emphasizes the importance of septal contraction to right ventricular function, and implies that septum contraction is the most important factor in ejection of blood by the right ventricle. Infarction studies render the septum non-functional by necrosis, and it is easily understandable how such a specific septal lesion results in septal dysfunction.
On the other hand, septal stretch and impaired excitation contraction coupling from electrical causes (i.e. wide QRS and bundle branch block) are two alternate events that similarly impair the action of a viable and well-perfused septum. Thus, it is not only important for the septum to be contractile, but this contraction must sequentially and occur in the right time during the cardiac cycle to maximize the effective septal contribution to blood ejection. Stretch of the septum results in an architectural disadvantage that can also develop as a consequence of pressure or volume loading of either the left or right ventricles, or from conduction abnormalities leading to subsequent bowing into the contra lateral ventricular chamber with consequent septal bulge. The result is delayed thickening that causes late contraction.
The septum becomes the common culprit, whereby the architectural stretch causes dysfunction, characterized by impaired biventricular performance. With right-sided lesions, like pulmonary stenosis or insufficiency with RV dilation, the septum is stretched into the left side, usually displaying either hypokinesia or akinesia, and may compress the contra lateral chamber. Similar stretch follows atrial septal defects. Bernheim [26] in 1910 described right ventricular compression after left ventricular hypertrophy, and Dexter [27] in 1956 described a ‘reverse Bernheim effect’ after large atrial septal defects (ASD) and right-sided volume overload. The adverse hemodynamic changes are due to septal dysfunction which recovers after septal architecture is restored by correcting the hemodynamic lesion.
These changes in contra lateral ventricular function are now amended by adverse septal stretch following left-sided dilation from ischemic [28], valvular [17] and non-ischemic cardiomyopathy [29], or from right septal stretch following extensive left ventricular decompression following left ventricular assist devices (LVAD) insertion [30]. Young et al. [17] documented marked rightward septal shift, and dysfunction after chronic mitral insufficiency, with relatively little change in the LV free wall (Fig. 12
). The evolution of RV failure, following development of pulmonary hypertension is linked to this septal impairment.
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Fig. 12. LV end-diastolic epi- and endocardial surface displays of reconstructed MRI images before and 4 months after mitral insufficiency. Note the preferential bulging of the septum, compared to the lateral wall during this time frame, as shown by Young et al. [17].
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6. RV dysplasia
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The septum plays a central role in understanding and management of the RV failure seen in RV dysplasia. Only 20% of patients have septal involvement [31] in RV dysplasia, and gadolinium MRI scans can define septal viability (Fig. 13
). Right ventricular free wall is replaced by a fatty deposition that allows free wall to dilate and become aneurysmal. Right ventricular failure may exist because of this aneurysm, in spite of normal septal function, as some of the force of ejection is absorbed in the aneurysm wall, a condition that mirrors left-sided events with LV aneurysm. A similar capacity for global ventricular arrhythmias also occurs.
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Fig. 13. Right ventricular dysplasia observed by (a) MRI (upper) displaying whitish RV free wall, with anterior and inferior aneurysm, and normal septum; (b) cross-section of heart specimen showing free wall aneurysm; and (c) histology showing free wall thinning and fibrofatty replacement, and normal septum by Basso et al. [31].
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These right ventricular changes exist despite normal pulmonary artery pressure. Biplane ventriculograms or MRI (a) show normal septal function; (b) may demonstrate septal asynergy from stretch, despite existence of a viable muscle; and (c) show septal viability. Understanding septal function and its contribution to RV performance has allowed for a rational design of a procedure to treat this disease. The treatment goals are to limit free wall aneurysm, as reported experimentally [21] and restore the midline septal position [32].
RV restoration in a right ventricular dysplasia patient includes a surgical procedure to reduce free wall size by partial exclusion, together with outflow tract closure using an imbrication suture to rebuild a more normal free wall and septal size [2]. The heart was kept in the beating empty state, to avoid septal damage that may follow cardioplegia. This restoration excluded a non-contracting segment, limited RV volume and, raised RV ejection fraction since septal contraction force was no longer dissipated into the aneurysm; arrhythmias improved as ventricular volume was reduced [33].
This RV dysplasia study provided a better understanding of this surgical approach to RV failure. The importance of the septum, in dealing with RV failure is emphasized by the report of Sano et al. [34], who excluded the free wall by excision in pediatric patients with right heart failure, and showed that returning the bowed non-functional septum to a central position improved right-sided function. A similar result was recently reported by Frigiola et al. [32] using the same imbrication method to deal with the RV failure after right ventricular outflow tract obstruction during pulmonary valve implantation. These early concepts must be further tested, because mechanical exclusion of the aneurysmal right ventricular free wall and septal restoration may help patients with right ventricular dysplasia, and other pathologic RV states, provided the septum is found viable by MRI methods.
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7. Right ventricular failure after LVAD
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The importance of the oblique fiber orientation of the septum becomes emphasized in the cohort of patients that develop late RV failure after requiring left ventricular assist devices (LVAD) for perioperative global ventricular dysfunction. Biventricular support is not needed initially, because the thin right ventricular free wall is well preserved despite septal akinesia [35] so that the right ventricle empties readily into the lungs, where pulmonary vascular resistance is low due to satisfactory LVAD function. RV ejection is maintained by the unimpaired function of fibers of the basal loop with a transverse orientation that can readily produce a 30% ejection fraction.
Delayed right ventricular failure may occur several days after left ventricular support because of two factors. First, pulmonary vascular resistance begins to rise due to secondary effects of pulmonary vascular endothelial injury due to prolonged cardiopulmonary bypass and multiple intraoperative blood and platelet transfusions Second, the venous return to the LV diminishes because the RV cannot maintain output against the rising pulmonary vascular resistance. Consequently, the LV collapses (Fig. 14
) and displaces the septum toward the left side further compromising RV function. Right ventricular failure supervenes after delayed pulmonary hypertension occurs as the lungs become vulnerable to edema formation that occurs despite with normal cardiac output.
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Fig. 14. Echocardiographic view of the failing left ventricle before (left panel) and after LV decompression, as described by Robert Korsmo. Note: In the left panel, the thin stretched akinetic septum, pushed or bowed into right ventricular chamber by distended left ventricle and in the right panel, note thickened septum, after LV decompression, with distended RV mass now bowing the septum into the left side.
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Contributory factors to RV failure include underlying septum dysfunction with absence of twisting action, and raised pulmonary vascular resistance. A right ventricular assist device (RVAD) is sometimes needed following the onset of RV failure to mechanically insure adequate pulmonary blood flow, retain oxygenation, and simultaneously decompress the dilated right ventricle. Increased pulmonary vascular resistance is initially lowered with milrinone and nitric oxide [36,37], and adequate LVAD function to reduce left-sided pressure. Right-sided failure improves following resolution of pulmonary hypertension and then the RVAD can be removed. Satisfactory right-sided free wall function allows efficient RV performance with normal pulmonary vascular resistance, despite persistent septal damage.
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8. Cardiac transplantation
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Cardiac transplantation is uniformly associated with right ventricular dysfunction as evidenced by a high right atrial pressure [38]. RV failure is attributed to ongoing pulmonary hypertension in the recipient because of chronic heart failure [24], which, unmasks the septal injury caused in the donor during cardiac transplant procurement and implantation. This iatrogenic septal injury prevents the RV from twisting to eject blood into the high vascular resistance lungs. The problem is the cardiac septum, not the pulmonary vasculature.
This damage may be overcome by utilizing methods to avoid reperfusion damage during heart implantation with methods similar to those employed routinely during non-transplant procedures [39]. Proper protection of the septum will avoid septal and hence RV dysfunction and thereby permit cardiac transplantation in patients with high pulmonary vascular resistance who are now excluded from consideration. Such protection of the septum with resultant normal septal performance may decrease the need for postoperative nitric oxide and prolonged use of inotropic agents to treat the after effects of septal injury that may be preventable.
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9. Congenital heart disease
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Septal structure/function interaction is a key to understanding why the septal contribution to biventricular events is important in congenital heart disease. For example, right-sided ventricular dilation from either pressure or volume overload will stretch the free wall, increase RV chamber size, and bow the septum to the left side to create septal hypokinesia or akinesia and limit its functional contribution to left- and right-sided outputs. Perhaps the most obvious, but often unrecognized example was reported by Dexter [27], when he described the ‘reverse Bernheim [26] effect’ after closing large atrial septal defects causing RV volume overload; left-sided performance improved as the bowed septum became a functional midline structure.
As with ASD, adverse septal and biventricular change may also occur with pulmonary hypertension and right ventricular volume overloading [23]. RV failure may also evolve postoperatively following repair of Tetralogy of Fallot, because of RV dilation, when chronic pulmonary insufficiency follows treatment of RV outflow tract obstruction. Of equal importance, correction of this late problem by pulmonary valve implantation may not remedy chronic right heat failure, prevent sudden death from arrhythmias (due to fiber stretch [33]) or correct left-sided functional impairment [40]. The underlying mechanism is ongoing dilation of the RV free wall and septum that persists despite pulmonary valve implantation. Under these circumstances the solution of this structure/function problem includes, restoration of the RV anatomic configuration by excluding the aneurysm, and imbricating the free wall and septum [32].
The occurrence of septal dysfunction that results from the congenital heart disease process becomes accentuated if the methods of myocardial protection during surgical correction do not prevent septal stunning. For example, patients with preoperative pulmonary hypertension and normal septal function may develop sudden acute right ventricular failure following successful correction of the underlying lesion causing high pulmonary vascular resistance. Septal damage that is induced intraoperatively causes hypokinesia, and this injury becomes evident during postoperative episodes of acute pulmonary vasospasm. This intraoperative damage offsets the protective capacity of a large thickened right ventricle that preoperatively, efficiently ejected against raised pulmonary vascular resistance. Loss of septal twisting capacity places the hemodynamic burden upon the RV free wall, whose function is predominantly a compression force due to the working transverse muscle from basal loop; this constrictive action, may be insufficient to generate output against high pulmonary vascular resistance without septal twisting.
Septal stunning from inadequate protection may be a short-lived event. For example, a dual reason exists in children undergoing correction of anomalous left coronary artery. Preoperatively, there is ischemia and akinesia of left ventricular anterior wall and underlying anterior septum. Additionally, there is bowing of the septum from ongoing left ventricular dysfunction with associated pulmonary hypertension. Superimposed intraoperative septal damage will cause dysfunction of the inferior portion of the septum. Cardiac decompression with ECMO (Extracorporeal membrane Oxygenation) allows such stunning to abate to allow subsequent left and right ventricular recovery.
The univentricular heart provides a clear example of the vital septal role in biventricular function. Ventricular twisting to produce sequential motion is related to the oblique muscle of the septum and free wall. Deficiency of the septal structure implies absence of the myocardial fold that is responsible for the oblique fiber orientation that generates the natural twisting action of the septum and free wall during embryonic development [41]. The predictable consequence of this malady is a circular chamber that retains the more transverse fiber orientation and is functionally inefficient. This deficient design cannot be expected to be cured by surgical interventions that fail to restore natural fiber orientation.
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10. Resynchronization
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The conduction delay existing in wide QRS or left bundle branch block causes a delayed septal thickening, and is associated with impaired LV function, as the earlier contracting LV free wall bows the septum to the right side, and simultaneously causes tethering of the posterior medial papillary muscle to produce pre-systolic mitral insufficiency. While septal muscle is viable and thick walled, its lack of function resembles the scarred septum existing in patients with ischemic heart disease. However, the response to biventricular septal pacing may differ between ischemic non-viable and non-functional viable muscle.
Biventricular pacing corrects the architectural disadvantage, only if the septum is viable and conduction reasons are responsible for septal dyssynergy. We have shown recently that early electrical stimulation of the posterior LV wall with a biventricular unit causes simultaneous contraction of all myocardial segments. The septum becomes a midline structure by earlier shortening, and mitral insufficiency is reduced due to the return of the papillary muscle to its correct position. However, the natural longitudinal shortening of the septum does not occur, and there is marginal improvement of body oxygen uptake [42,43]. Prior sonomicrometer studies of sequential contraction during biventricular pacing show that the paced region shorten, but does not resume the normal sequential pattern for twisting [44,45]. We suspect that biventricular pacing returns the septum into midline location to create a rigid central curtain with movement of the papillary muscles to a normal position, but does not restore the natural septal twisting motion.
The role of the septum that is functionally akinetic during the electrical state of either wide QRS or LBBB differs from the ischemic process. This contrast exists because motion can be achieved in patients with an electrical reason for septal dysfunction by early stimulation with a biventricular pacing device. Conversely, this movement cannot be achieved in dead tissue.
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11. Cardiac surgery
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Postoperative right ventricular dysfunction is a difficult problem for clinical management and may develop, even in patients that enter the operating room with normal septal function. The dilemma that exists is that septal hypokinesia or akinesia is considered a usual occurrence postoperatively because of its frequency after many forms of cardioplegic myocardial protection [16,46,47]. The role of the septum in this process is critical, yet there is usually some confusion about its impact. The RV free wall is the only observable index of right ventricular performance that is followed by the surgeon because the septum is not visible. Monitoring septal function by echocardiography before bypass is discontinued will readily demonstrate hypokinesia and help predict the presence and degree of RV dysfunction.
Despite normal free wall contraction, central venous pressure increases when bypass is discontinued, suggesting underlying right ventricular dysfunction. This process can only occur if the septal contribution to cardiac output is the major determinant of RV output. The observed subsequent dilation of the free wall reflects a late secondary event that follows volume overloading of the right heart.
The importance of the septal role is evident in off bypass procedures, where septal and right ventricular dysfunctions are rare. More importantly, septal dysfunction is likely a reflection of stunning from inadequate myocardial protection, since some methods of integrated protection avoid septal injury [48] and result in normal septal function on postoperative studies. The magnitude of this issue does not become apparent when there is normal pulmonary artery pressure, since the normally contracting transverse muscle of the free wall can constrict the right ventricular wall and deliver RV output into the low resistance pulmonary vascular bed.
However, even this bellows action of the free wall may not be necessary, since the conduit function of the RV is exemplified in the Fontan procedure, where the RV is excluded. However, this conduit action works only with low pulmonary vascular resistance. Conversely, the twisting action is vital when there is pulmonary hypertension, an event that can occur preoperatively in valve disease or chronic congestive heart failure or postoperatively as a result of pulmonary vascular or parenchymal injury.
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12. Treatment options relating to structure/function
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It follows, from these anatomic principals, that the rational treatment protocol for RV dysfunction should consist of (1) avoidance of septal dysfunction by adequate myocardial protection; (2) lowering of pulmonary artery resistance by use of pulmonary vasodilators (milrinone, isoproterenol, nitric oxide) to compensate for the inability of the twisting aspect of RV performance to overcome the high after load; (3) optimize filling pressures to avoid over distention of the RV, since stretching the chamber bows the septum to further compromise LV function; and (4) inotropic support to try to reverse stunning with either catecholamines or calcium sensitizing agents (like levosimendan). Catecholamine drugs that increase pulmonary vascular constriction should be used with caution, since the vasoconstrictive effects may counteract the inotropic effects. These pharmacologic interventions are first line therapy and precede mechanical support by intrapulmonary balloon pump or RVAD [49].
It becomes clear the usual recommendation of volume loading to improve cardiac output and using the right ventricle as a conduit is no longer tenable; instead a balanced approach of optimizing preload and minimizing right ventricular after load and inotropic support with agents that do not constrict pulmonary vasculature would be preferable.
Damage to the septum is not altered by the foregoing maneuvers, yet there is an observable improvement in cardiac function. This can be readily predicted from the anatomic principles of septal dynamics and RV performance. The theme of these interventions is to maximize the benefits of the transversely contracting basal loop, and simultaneously place the non-functioning septum into a midline position, so that its stretch cannot further impair biventricular function. In the RV, there is reduction of size to diminish the adverse effects of tethering of tricuspid apparatus that causes regurgitation. In the LV, reduction of septal bowing restores the normal cavity dimensions with improved left-sided filling.
In this context, it is clear that right ventricular dysfunction is not benign and may be associated with high mortality. On occasion these patients manifest hemodynamic instability during the time when they are taken off cardiopulmonary bypass in spite of normal contractility of the RV free wall. It will become apparent that understanding the mechanisms of these phenomena will have profound bearing on the rational therapy of these conditions. Clearly, protecting the septum is of paramount importance in operative planning. Fuller understanding how to protect the septum and ways to manage its dysfunction will have great impact upon successful surgical outcome.
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13. Summary and conclusions
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The understanding of myocardial structure and normal function provides a context to explain and unify a variety of clinical observations that can be evaluated and corrected rationally. The concept of the septum as ‘the biventricular motor’ is useful to explain both the function of the right ventricle and its derangement as well as the interdependence of both ventricles. This concept emphasizes the importance of the septum, because of not only the amount of myocardial mass it represents but also its critical importance in right ventricular function in the setting of elevation of pulmonary vascular resistance. In the case of the left ventricle which has a free wall made up of oblique and therefore twisting fibers, the manifestation of septal dysfunction is less clinically apparent since the free wall is able to compensate better than the right ventricular free wall with muscle, predominantly composed, of transverse fibers. The aphorism ‘left heart failure begets right heart failure’ is linked to the septal ‘biventricular motor’ motion hypothesis, and explains why absence of septal motion is caused by distortion of its structure from stretching.
Given the importance of the septum to biventricular function, it is no longer acceptable to take for granted the septal dysfunction postcardiac surgery if this can in any way be avoided. Understanding the central role of the septum in RV function provides the theoretical basis for treatment of entities such as right ventricular infarction and postcardiac surgery RV dysfunction. Knowledge of the anatomy and physiology of the septum also allows the rational design of operations to treat various cardiac conditions such as RV dysplasia, RV failure from pulmonary insufficiency, transplantation RV dysfunction, right-sided congenital defects that affect LV function, development of techniques of myocardial protection, planning physiologic treatment of RV dysfunction by use of a structure/function relationship, and improving left ventricular restoration.
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Appendix A
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Supplementary data
Supplementary data associated with this article can be found, in the online version, at doi:10.1016/j.ejcts.2006.02.048.
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Top
Abstract
1. Introduction
