Right Heart Failure in Patients With Mechanical Circulatory Support

Introduction

For end-stage heart failure (HF), heart transplantation or implantation of a left ventricular assist device (LVAD) is lifesaving and provides a significant improvement in quality of life. Despite the therapeutic success of LVADs, concomitant right ventricular failure (RVF) and the lack of appropriate long-term, right ventricular (RV) support devices has limited the full potential that mechanical circulatory support (MCS) can offer to patients with biventricular failure.

Despite the relatively low rate of temporary RV assist device (RVAD) support in the United States, a significant number of patients who have been successfully discharged after receiving an LVAD remain symptomatic from RVF and undergo recurrent readmissions for the management of HF. In addition, delayed RVF is being increasingly recognized in a subset of patients on chronic LVAD support. In this chapter, we will discuss the pathophysiology of RVF, which can be potentially exacerbated after LVAD implantation, and the nonsurgical and surgical management strategies to address this extremely important issue.

Physiology and anatomy of the right ventricle

The RV is a complex three-dimensional structure that appears triangular in sagittal section, unlike the cone-shaped left ventricle (LV) chamber ( Fig. 14.1 ). Both the RV and LV are linked with a common meshwork of fibers that encircle the ventricles ( Fig. 14.2 ). The muscle mass of the RV is approximately one-sixth that of the LV and, under normal conditions, it functions in a low-pressured working environment.

Another uniqueness of RV structure is its high level of “reinforcement” with interweaving strands of muscle (trabeculae carneae) and a coarse endocardial inner surface. The pattern of RV trabeculae carneae in the ventricle is an efficient means of gaining power without excessively thickening the wall of the chamber (normally 3–5 mm in thickness). In patients with increased RV pressure, the trabeculae are more likely to be coarser, which may result in substantial alterations of RV volume, mass, and ejection fraction.

In addition, the shared interventricular septum (IVS) plays an important role in RV output. It has been suggested that a substantial portion of RV systolic pressure and stroke volume results from LV contraction, much of which is contributed through the IVS. As the IVS contracts, it adds to the contraction effort of the RV free wall and may in fact contribute as much as 40% to the output of the RV. In addition, the contracting free wall of the RV pushes against the IVS as its supporting structure. This ventricular interdependence of RV output on the IVS and on LV contractility has been demonstrated in animal models. As discussed later in the chapter, this has particular importance once an LVAD is implanted because it can significantly alter the loading conditions of both the RV and LV and their respective geometric relationship to each other.

Under normal baseline conditions, the unique anatomy, myocardial ultrastructure, and coronary blood flow physiology of the RV reflect the characteristics of a high-volume/low-pressure pump. Because of low pulmonary vascular resistance (PVR), the RV pumps the same stroke volume as the LV does, but with ~ 25% of the stroke work. Contraction of the extremely compliant, thin-walled RV (by virtue of the Laplace relationship) is a process starting at the inlet, then free wall, and subsequently ending at the infundibulum. Of note, unlike the LV, in which coronary perfusion is predominately during diastole, the low-pressured RV is perfused throughout the cardiac cycle. Hence, significant elevations in the RV end-diastolic pressure, without a concomitant increase in mean arterial pressure, may be accompanied by ischemia in a relatively hypertrophied RV. In chronic HF, the RV pressure-volume loop shifts from a normal trapezoidal shape, reflecting its high efficiency/low impedance, to a rectangular shape, which becomes indistinguishable from a normal LV pressure-volume loop, suggesting an ongoing RV adaptation to increased volume overload ( Fig. 14.3 ).

Right ventricular failure in patients with chronic heart failure after lvad