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Updated: Feb 8, 2026

Invasive Hemodynamic Assessment for the Right Ventricular System and Hypoxia-Induced Pulmonary Arterial Hypertension in Mice
Published on: October 24, 2019
[Pathophysiology of right ventricular hemodynamics]
D Chemla1, E Berthelot2, P Assayag3
1Service de physiologie-hôpitaux universitaires Paris Sud-hôpital de Bicêtre, 94275, Le Kremlin Bicêtre, France; Faculté de médecine Paris-Sud, 94275, Le Kremlin-Bicêtre, France; Inserm UMR_S999, LabEx LERMIT, centre chirurgical Marie-Lannelongue, 92350 Le Plessis Robinson, France.
Abstract:
The right ventricle (RV) plays a key role in the maintenance of an adequate cardiac output whatever the demand, and thus contributes to the optimization of the ventilation/perfusion ratio. The RV has a thin wall and it buffers the physiological increases in systemic venous return without causing a deleterious rise in right atrial pressure (RAP). The RV is coupled to the pulmonary circulation which is a low pressure, low resistance, high compliance system. In the healthy subject at rest, the contribution of the RV to right heart systolic function is surpassed by the contribution of both left ventricular contraction and the respiratory pump. RV systolic function plays a contributory role during exercise and in patients with pulmonary hypertension. The RV compensates better for volume overload than for pressure overload and is more capable of sustaining chronic increases in load than acute ones. An impaired RV-pulmonary artery coupling leads to a major mismatch between RV function and arterial load ("afterload mismatch") and is associated progressively with a low cardiac output and a high RAP. Right ventricular dysfunction is involved in the pathophysiology of both cardiovascular and pulmonary diseases, and may partly explain the deleterious haemodynamic consequences of mechanical ventilation.
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