Right Versus Left Ventricular Failure

Abstract

1033V entricular failure manifests in many forms, its underlying physiology ranging from overt left ventricular (LV) systolic dysfunction to isolated right ventricular (RV) diastolic dysfunction, and the wide portfolio of resulting symptoms vary from chronic fluid retention to acute multiorgan dysfunction and death. In this review, we discuss the morphological, functional, and molecular similarities and differences in RV and LV responses to adverse loading and failure. We further discuss whether LV and RV function and failure can truly be discussed as separate entities and thereby examine interactions between the ventricles that on one hand contribute to ventricular dysfunction but on the other may be harnessed for therapeutic benefit. Embryological and Physiological Differences Between the RV and LVThe RV and LV have different embryological origins.1 The LV originates from the primary heart field; the RV, from the secondary heart field. Consequently, several genes specifically control RV formation, including, among others, Hand2 and Tbx20.2 During gestation, the RV functions as the systemic ventricle ( Figure 1A). During fetal life, in addition to supplying the modest amount of pulmonary blood flow, the RV pumps blood to the lower body and placenta and contributes more than half of the combined cardiac output.3 With the transition from fetal to postnatal physiology and with the reduction in pulmonary vascular resistance, the subpulmonary RV transforms its morphology and geometry, becoming a thin-walled chamber to adopt its postnatal physiological characteristics. 4 Because it faces a low impedance pulmonary circulation, the normal postnatal RV maintains a cardiac output equal to that of the LV at approximately a fifth of the energy cost. The trapezoidal RV pressure-volume loop reflects this difference, with few if any isovolumic periods. Consequently, RV output starts early during pressure generation and is later maintained by a "hangout period" when antegrade flow continues into the pulmonary artery despite the onset of RV relaxation.5 In contrast, the rectangular LV pressure-volume loops reflect the LV square-wave pump function with distinct and well-developed isovolumic contraction and relaxation periods.6 Likewise, RV myocytes display faster twitch velocities than LV myocytes. 7The physiological differences are reflected in morphological differences between the ventricles (Table 1). The low-pressure RV is triangular in the sagittal plane and crescent-shaped in cross section as a result of the concave RV free wall and convex interventricular septum wrapping around the high-pressured, thick-walled, bullet-shaped LV. Consequently, although the normal RV has a lower ratio of volume to surface area and a thinner wall than the LV, 8 the low cavity pressure determines a lower wall stress and lower oxygen demands.Anatomic differences are also apparent in myocardial architecture. LV subepicardial and subendocardial fibers are oblique and helical with fiber angles ranging from 30° to 80° with a mean of ≈60°, whereas ...

Transthoracic Echocardiography in the Evaluation of Pediatric Pulmonary Hypertension and Ventricular Dysfunction

“…16 Although not the focus of this review, evaluation of the left heart, including LV systolic function (LV ejection fraction [EF], fractional shortening), longitudinal systolic LV function (mitral annular plane systolic excursion), and inflow and outflow Doppler of all valves, should be an integral part of the echocardiographic assessment of PH, to assess detrimental RV-LV interactions. 17 After the initial diagnostic evaluation for PAH, TTEs are usually performed at 6-12-month intervals and when there is a clinical change. TTE assessment of RV function is commonly known to be technically difficult in both children and adults.…”

Echocardiographic assessment of right ventricular systolic function in conscious healthy dogs following a single dose of pimobendan versus atenolol

“…Consequently, some of the measured change seen with pimobendan may relate to alterations in pulmonary vascular resistance; however, the increased inotropic effect of pimobendan is well documented in the dog 19 and this, coupled with the effect measured by atenolol, argues that these indices can be used as a surrogate to track changes in RV systolic function. Studies show that RV function is partially determined by left ventricular function 38 ; as such, we cannot be certain how much of an effect pharmacologic alteration of left ventricular function had on these measures of RV function. An additional limitation of the current study is the lack of longitudinal follow-up for the dogs enrolled in this study.…”

Hypoxia-Induced Molecular and Cellular Changes in the Congenitally Diseased Heart: Mechanisms and Strategies of Intervention

“…The different morphology and metabolism between the left and the right ventricle can in part explain the different susceptibility [28]. Furthermore, the anatomy of most of the CHD exposes the right ventricle to higher stresses, making it more prone to fail than the left counterpart [24].…”