Department of Cardiology, Erasme University Hospital, ULB, Brussels, Belgium.
Department of Cardiovascular and Respiratory Science, Sapienza University of Rome, Rome, Italy.
Cardiovasc Res. 2017 Oct 1;113(12):1474-1485. doi: 10.1093/cvr/cvx160.
The right and the left ventricle are interdependent as both structures are nested within the pericardium, have the septum in common and are encircled with common myocardial fibres. Therefore, right ventricular volume or pressure overloading affects left ventricular function, and this in turn may affect the right ventricle. In normal subjects at rest, right ventricular function has negligible interaction with left ventricular function. However, the right ventricle contributes significantly to the normal cardiac output response to exercise. In patients with right ventricular volume overload without pulmonary hypertension, left ventricular diastolic compliance is decreased and ejection fraction depressed but without intrinsic alteration in contractility. In patients with right ventricular pressure overload, left ventricular compliance is decreased with initial preservation of left ventricular ejection fraction, but with eventual left ventricular atrophic remodelling and altered systolic function. Breathing affects ventricular interdependence, in healthy subjects during exercise and in patients with lung diseases and altered respiratory system mechanics. Inspiration increases right ventricular volumes and decreases left ventricular volumes. Expiration decreases both right and left ventricular volumes. The presence of an intact pericardium enhances ventricular diastolic interdependence but has negligible effect on ventricular systolic interdependence. On the other hand, systolic interdependence is enhanced by a stiff right ventricular free wall, and decreased by a stiff septum. Recent imaging studies have shown that both diastolic and systolic ventricular interactions are negatively affected by right ventricular regional inhomogeneity and prolongation of contraction, which occur along with an increase in pulmonary artery pressure. The clinical relevance of these observations is being explored.
左右心室相互依存，因为两者都嵌套在心包膜内，有共同的室间隔，并被共同的心肌纤维环绕。因此，右心室容积或压力超负荷会影响左心室功能，而这反过来又可能影响右心室。在正常休息的受试者中，右心室功能与左心室功能几乎没有相互作用。然而，右心室对运动时正常的心输出量反应有重要贡献。在没有肺动脉高压的右心室容量超负荷患者中，左心室舒张顺应性降低，射血分数降低，但收缩性没有内在改变。在右心室压力超负荷患者中，左心室顺应性降低，左心室射血分数最初保持不变，但最终会出现左心室萎缩性重塑和收缩功能改变。呼吸会影响心室相互依存，在健康受试者运动时、肺部疾病和呼吸系统力学改变的患者中都会出现这种情况。吸气会增加右心室容积，减少左心室容积。呼气会减少右心室和左心室的容积。完整的心包膜会增强心室舒张的相互依存性，但对心室收缩的相互依存性几乎没有影响。另一方面，右心室游离壁僵硬会增强收缩的相互依存性，而室间隔僵硬则会降低收缩的相互依存性。最近的影像学研究表明，舒张和收缩心室相互作用都会受到右心室区域性不均匀性和收缩延长的负面影响，这些变化与肺动脉压升高同时发生。正在探索这些观察结果的临床意义。
