Determinants of maximal right ventricular function: role of septal shift

Klima UP, Lee M-Y, Guerrero JL, LaRaia PJ, Levine RA, Vlahakes GJ. J Thorac Card-iovasc Surgery 2002;123:72-80

Reviewer: Andrew D. Maslow, MD
Rhode Island Hospital
Providence, RI

Right ventricular (RV) failure is associated with poor outcome. RV failure can be caused by infarct, pulmonary hypertension, trauma, cardiomyopathy, or congenital defects. The mechanism of hemodynamic compromised caused by RV failure is not completely understood, but likely involves the interaction between the left and right ventricles because changes in the pressure and volume of one chamber affects the pressure and volume of the other chamber.

Ventricular interdependence is affected by the pericardium, the interventricular septum, and the pulmonary vasculature. The intact pericardium imposes a mechanical restraint to outward expansion so an increase in volume in one ventricle impairs filling of the other ventricle. For example, left ventricular (LV) failure and dilation impairs RV diastolic and systolic function. Removing the pericardial constraint may improve RV filling, but the increase in RV preload may unmask underlying RV systolic dysfunction. An intact pericardium enhances interdependence at the ventricular septum. Normally, the greater LV pressures cause the septum to bulge toward the RV during both systole and diastole. In LV failure, septal wall motion is reduced and its position is shifted more towards the right impairing both RV filling and systolic function. With primary RV failure, septal wall motion is also reduced and its position shifted to the left impairing LV diastolic filling. Finally, LV dysfunction may be transmitted through the pulmonary vascular system and increase RV afterload causing RV dysfunction.

Maintenance or even increasing right coronary artery (RCA) perfusion pressure may be especially important to prevent or treat RV dysfunction regardless of etiology. The purpose of the experiment by Kilma, et al was to evaluate the effect of systemic blood pressure and interventricular septal function on RV performance independent of the pulmonary circulation and pericardial restraint. The experiment was performed using dogs employing an isovolemic RV preparation. A bypass circuit removed systemic venous return, oxygenated it, and returned it to the left heart. RV volume was controlled using an intracavitary balloon. The developed pressure of the right ventricle (RVDP) was used to assess RV function. RV failure was defined as when the RVDP decreased in response to an increase in RV preload. The experiment consisted of increasing the RV volume in increments while varying LV output. RV function was studied at different mean systemic pressures and after inactivation of the ventricular septum.

RV systolic function or RVDP was found to increase in response to increased systemic blood pressure independent of the LV output. At increased systemic pressure, RV failure occurred later and at higher RV volumes. RCA blood flow increased incrementally at increasing systemic pressures regardless of LV output. While a significant decrease in RCA flow was seen in the presence of RV failure, increasing systemic pressure increased RCA flow and improved RV function. Inactivation of the interventricular septum caused a rightward shift in septal position and a significant decrease in RV function.

The authors concluded that maintenance of systemic pressure was important to maximize RV function at rest or in the presence increased RV volume and strain. The corresponding increases in RCA flow likely improved the balance between oxygen demand and supply to improve RV function. Inactivation of the interventricular septum affected RV function significantly.

This study demonstrated the importance of maintaining systemic arterial pressure and RCA blood flow when there is a risk of RV dysfunction. Clinical scenarios may include pulmonary hypertension from any cause, heart transplantation, or left ventricular assist device implantation, where attention may be concentrated on LV function and less on biventricular function or the interaction between the two ventricles. The findings of this study highlighted also that interventricular septal contraction and position had an important contribution to RV function even in the presence of an open pericardium, which may reduce the affects of the ventricular septal position on ventricular interdependence. As stated in the article, "the end diastolic position of the septum influences septal [position, and] motion during systole." These data add further support for the importance of interventricular septal function on both diastolic and systolic ventricular function.

A separate study in the same journal demonstrated the impact of RV failure on LV function.1 In that study, RV dysfunction was induced by occluding 4-6 acute marginal arteries resulting in RV systolic failure, increased chamber pressure, and cavity enlargement. This ischemic model of RV failure caused secondary changes that led to LV systolic and diastolic dysfunction as well. RV decompression by a modified Glenn shunt (superior vena cava to main pulmonary artery bypass) decreased RV volume and an led to an improvement in biventricular function. An explanation for the findings was that RV dilation caused a leftward shift of the interventricular septum and impaired LV systolic and diastolic function. RV decompression restored the position of the interventricular septum and normalized ventricular interdependence to improve LV geometry and function.

These two studies confirm that the loading conditions of one ventricle will influence the function of the other ventricle. In the study by Kilma et al, maintenance of RCA perfusion pressure was also critical for maintaining RV performance. Both studies demonstrated that septal position or "septal preload" had an important impact on systolic as well as diastolic function. The study by Danton, et al showed that RV failure not only impaired LV diastolic filling, but also impaired LV systolic function by altering both LV preload and interventricular septal position. The clinical implications of these findings suggest that hemodynamic compromise is compounded in RV failure as a consequence of its negative impact on LV function. The subsequent reduction in systemic pressure generated by the LV leads to further impairment of RV function as a consequence of reduced coronary perfusion. The ability to assess interventricular septal position and function may help to optimize biventricular function caused by RV or LV dysfunction.

Reference
Danton MH, Byrne JG, Flores KQ, Hsin M, Martin JS, Laurence RG, Cohn LH, Aklog L. Modified Glenn connection for acutely ischemic right ventricular failure reverses secondary left ventricular dysfunction. J Thorac Cardiovasc Surgery 2001; 122:80-91.

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