Interface IV: Right Ventricular Function
The RV should not be understood as a smaller or weaker version of the LV. Although they work in series, the RV and LV are embryologically, anatomically, and functionally distinct chambers, each adapted to a different circulation. Whereas the left ventricle is designed to generate pressure against the high-impedance systemic circulation, the right ventricle is designed to generate flow into a pulmonary vascular bed that, under normal conditions, is low resistance, highly compliant, and weakly wave-conductive/reflective. This is why the healthy RV performs with remarkable energetic efficiency, but also why it becomes so vulnerable when its vascular load rises.
RV Anatomical and Physiological Particularities
Its anatomy reflects that specialization. The RV is thin-walled, compliant, and geometrically complex. It has a crescentic shape in cross-section, a triangular profile in longitudinal view, and three functional components: (1) the inlet, (2) the trabeculated apical myocardium, and (3) the infundibulum or outflow tract.
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Compared with the LV, it has far less muscle mass, generates much lower systolic pressures, and performs much less stroke work (the energy needed for one pump cycle), despite ejecting the same effective stroke volume. These are not signs of lesser importance, but of unique function. The RV is built to transport blood efficiently rather than to sustain large pressure loads.
Figure: Unique anatomic and functional features which distinguish the RV from the LV.
Its contraction is equally distinctive. The LV contracts with a concentric and rotational squeeze. The RV contraction occurs as a coordinated and sequential event, as shown below. The systolic contraction begins in the inlet and trabeculated regions and reaches the infundibulum slightly later, creating a peristaltic wave-like pattern of ejection. Functionally, RV contraction results from three principal mechanisms: longitudinal shortening that draws the tricuspid annulus toward the apex, inward movement of the free wall, and traction transmitted through septal and left ventricular attachments.
Of these, longitudinal shortening appears to be the dominant component in normal physiological states, while radial shortening contributes to a lesser degree. This explains why indices such as the Tricuspid Anular Plane Systolic Excursion (TAPSE) and the Tricuspid Annular Systolic Velocity (S’) are so informative when assessing RV function with echocardiography; they capture a fundamental feature of how the RV ejects.
Table 1: Physiological comparison between the right and left ventricles
Systolic Interaction and Ventricular Interdependence
Yet the RV should never be imagined as a chamber acting in isolation. A major portion of its systolic performance depends on septal mechanics and on its intimate structural and functional relationship with the left ventricle. The septum is therefore not simply a partition between chambers, but an important contributor to RV ejection. In this sense, the RV is a chamber of interaction. Its function depends not only on its intrinsic contractility, but also on the geometry and performance of the septum, the synchrony of biventricular contraction, the restraining effect of the pericardium, and the characteristics of the pulmonary vascular bed into which it ejects.
Because the two ventricles share myocardial fibers, a common septum, and the same pericardial space, the size, shape, and compliance of one ventricle influences the performance of the other; this is called systolic interaction. Specifically, systolic interaction refers to the contribution of left ventricular contraction and septal shortening to RV systolic ejection. Under normal circumstances the septum should bow slightly into the right ventricle as shown in the image on the left below. This can account for a significant proportion of the total RV stroke volume.
Although the view of the septum most often is seen on short axis imaging demonstrates bowing into the RV, normal fluctuations in RV and LV loading across the respirophasic cycle or following postural changes can cause the septum to transiently and subtly shift toward the left ventricle. This motion and the effect of the septum itself on RV and LV function is called ventricular interdependence. Generally, these small movements are normal and do not affect cardiac performance.
However, when the RV is exposed to abnormal loading, whether from volume excess or pressure overload, the interventricular septal shifts become accentuated. In these cases, the septum may "flatten" or bow leftward for part or all of the cardiac cycle, altering LV geometry and impairing LV diastolic filling. Importantly, the timing of septal displacement helps identify the dominant mechanism. Septal shift during systole reflects RV pressure overload, when RV systolic pressure rises abnormally relative to LV systolic pressure during ejection. By contrast, septal shift during diastole alone is more characteristic of RV volume overload and increased RV end diastolic filling pressures, when excess RV filling and chamber distention displace the septum before systolic contraction begins.
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In the above figure, a normal RV:LV interaction is displayed on the left graphic. In this setting, the contraction of the septum into the RV during systole augments the RV ejection fraction. In cases where RV volume or pressure are increased, the septum begins to bow into the LV, as shown in the right graphic. The influence of the septum on both RV and LV function and the interactions between the two is called ventricular interdependence.
The role of preload on RV function
Preload must also be handled with refinement. As in the left ventricle, the Frank-Starling mechanism applies within physiological limits and moderate increases in filling will augment RV output. This process is called heterometric adaptation. But the therapeutic window is narrow. Once the chamber becomes excessively distended, increased pericardial constraint causes septal flattening and stretches myofibrils beyond their optimal sarcomere length (actin–myosin overlap). In addition, septal flattening contributes to increased LV diastolic pressures and impaired LV filling. At this point, further filling occurs without a concomitant increase in cardiac output. In these situations, additional preload becomes part of the problem rather than part of the solution. RV dilation is therefore not merely an imaging observation; it is a mechanical and hemodynamic event that can convert a potentially compensatory response into a source of biventricular compromise.
This is why reducing RV distention can improve stroke volume without directly increasing inotropy (Ees). By restoring septal geometry and relieving pericardial constraint, unloading the RV may allow the chamber to recover some of the mechanical benefit derived from ventricular ventricular interdependence. In the failing right heart, improving contractility is not only a matter of stimulating myocardium. It is often requires a mulitfaceted approach of restoring geometry, optimizing coupling, and allowing the septum to function effectively again.