University of Aberdeen, Aberdeen, United Kingdom.
Heart Lung Circ. 2013 Jul;22(7):507-11. doi: 10.1016/j.hlc.2013.03.072. Epub 2013 Apr 12.
The functions of the left and right ventricles are intimately linked. The right ventricle (RV) has transverse muscle fibres in its free wall and also shares oblique fibres in the interventricular septum with the left ventricle (LV). The latter constitute a link between left and right ventricular contractile function such that LV contraction augments RV contraction - a phenomenon called systolic ventricular interaction. When RV afterload is increased (by raised pulmonary artery pressure) overall contractile performance becomes increasingly dependent on this systolic ventricular interaction because the oblique septal fibres are more mechanically efficient than the free wall transverse fibres in conditions of high RV afterload. When LV end diastolic pressure is increased by heart failure due to LV systolic dysfunction, pulmonary artery pressure becomes raised, imposing an increased afterload on the RV. In such patients global LV performance is reduced, consequently systolic ventricular interaction is reduced resulting in a reduction in RV contractile performance even if the RV is not directly involved in the disease process causing LV systolic dysfunction. Furthermore, as the left ventricle becomes progressively more spherical the septal fibres become less oblique, dramatically reducing their mechanical advantage and further impairing RV contractile function. This ultimately leads to clinical right ventricular failure. This in turn typically results in tricuspid regurgitation and a vicious cycle of right ventricular enlargement with further reduction in the oblique nature of the septal fibres. In addition to the systolic interaction of the LV on the RV, when the RV is enlarged and stretches the pericardium, pericardial and right ventricular diastolic pressures may become markedly increased and this can result in constraint to filling of the LV by the pericardium (pericardial constraint) and by the RV via the interventricular septum (diastolic ventricular interaction).
左右心室的功能密切相关。右心室(RV)的游离壁有横向的肌肉纤维,室间隔也与左心室(LV)共享斜向纤维。后者构成了左右心室收缩功能之间的联系,使得左心室收缩增强右心室收缩——这种现象称为收缩性室间相互作用。当 RV 后负荷增加(肺动脉压升高)时,整体收缩性能越来越依赖于这种收缩性室间相互作用,因为在 RV 后负荷较高的情况下,斜向室间隔纤维比游离壁横向纤维在机械效率上更有优势。当由于 LV 收缩功能障碍导致心力衰竭时 LV 舒张末期压力增加,肺动脉压升高,对 RV 施加更大的后负荷。在这些患者中,整体 LV 性能降低,因此收缩性室间相互作用降低,导致 RV 收缩性能降低,即使 RV 本身并未直接参与导致 LV 收缩功能障碍的疾病过程。此外,随着左心室逐渐变得更加球形,室间隔纤维变得不那么倾斜,其机械优势显著降低,进一步损害 RV 收缩功能。这最终导致临床右心室衰竭。反过来,这通常会导致三尖瓣反流以及 RV 扩大的恶性循环,进一步降低室间隔纤维的斜向特性。除了 LV 对 RV 的收缩性相互作用外,当 RV 增大并拉伸心包时,心包和 RV 舒张压力可能会显著增加,这可能导致心包(心包约束)和 RV 通过室间隔(舒张性室间相互作用)对 LV 充盈的限制。