Pulmonary vascular resistance and compliance relationship in pulmonary hypertension

• Published in: The European respiratory journal Vol. 46; no. 4; pp. 1178 - 1189
• Main Authors: Chemla, Denis, Lau, Edmund M.T., Papelier, Yves, Attal, Pierre, Hervé, Philippe
• Format: Journal Article
• Language: English
• Published: England 01.10.2015
• Subjects: Blood Pressure; Elasticity; Heart Ventricles - physiopathology; Humans; Hypertension, Pulmonary - physiopathology; Lung - physiopathology; Prognosis; Pulmonary Artery - pathology; Pulmonary Artery - physiopathology; Pulmonary Circulation; Pulmonary Medicine - methods; Pulmonary Wedge Pressure; Reference Values; Reproducibility of Results; Stroke Volume; Systole; Vascular Resistance; Ventricular Dysfunction, Right - physiopathology
• ISSN: 0903-1936; 1399-3003; 1399-3003
• DOI: 10.1183/13993003.00741-2015

Right ventricular adaptation to the increased pulmonary arterial load is a key determinant of outcomes in pulmonary hypertension (PH). Pulmonary vascular resistance (PVR) and total arterial compliance (C) quantify resistive and elastic properties of pulmonary arteries that modulate the steady and pulsatile components of pulmonary arterial load, respectively. PVR is commonly calculated as transpulmonary pressure gradient over pulmonary flow and total arterial compliance as stroke volume over pulmonary arterial pulse pressure (SV/PApp). Assuming that there is an inverse, hyperbolic relationship between PVR and C, recent studies have popularised the concept that their product (RC-time of the pulmonary circulation, in seconds) is “constant” in health and diseases. However, emerging evidence suggests that this concept should be challenged, with shortened RC-times documented in post-capillary PH and normotensive subjects. Furthermore, reported RC-times in the literature have consistently demonstrated significant scatter around the mean. In precapillary PH, the true PVR can be overestimated if one uses the standard PVR equation because the zero-flow pressure may be significantly higher than pulmonary arterial wedge pressure. Furthermore, SV/PApp may also overestimate true C. Further studies are needed to clarify some of the inconsistencies of pulmonary RC-time, as this has major implications for our understanding of the arterial load in diseases of the pulmonary circulation.