[Calculated pulmonary vascular resistance, is definitively a worthless variable. Current methods for a better definition]

Abstract

The term pulmonary vascular resistance [PVR] describes, in part, the forces opposing the flow across the pulmonary vascular bed. The equation traditionally used is based on the assumption that the pulmonary capillaries, as well as some others vessels in series behave like a Poiseuille resistance. This assumption implies a laminar type of flow of a homogeneous Newtonian fluid, however blood is not a Newtonian fluid and flow is pulsatile in the pulmonary circulation. Neglecting these factors [which only slightly undermines the application of the equation] and others as well [like distension and recruitment of the vessels], will, however, not give us a true clinically practical solution for the calculation of PVR, because the concept of the equation is only true or partially true for part of the pulmonary circulation. In other parts of the lung, flow depends mainly on the behaviour of capillaries as a Starling resistor. If we considered always pulmonary venous pressure [measured clinically as left atrial pressure or pulmonary wedge pressure] as the effective downstream pressure for the calculation of PVR and we ignore or disregard the existence of a significant "critical closing pressure" [whatever the cause] in the lung it will lead to additional erroneous concept regarding PVR calculations and, in addition for the real hemodynamic conditions of the pulmonary vascular bed. Because, at least two different models of perfusion exist in the lung it is inadmissible from a theoretical point of view to calculate PVR, based on only in one of these models. According to the present knowledge of the pulmonary circulation hemodynamics, an improved definition for the PVR could be obtained: 1. by a multipoint pulmonary vascular pressure/flow plot at high flows and 2. with the use of the pulmonary artery occlusion pressure [PAOP] in addition to the determination of the pulmonary wedge pressure technique [PWP], in order to establish the estimated downstream pressure of the pulmonary circulation at zero flow. Therefore, pulmonary hemodynamic determinations of the PVR are better defined with the analysis of the pressure-flow relationships in addition to the information derived from the PAOP/PWP measurements. However, if none of the previous pressure-flow relationships [in order to obtain the slope = PVR at high flows] or the effective downstream pressure measurements [in order to estimate the critical closing pressure at zero flow] are applied for the analysis of the pulmonary circulation, a cautious interpretation of the measured variables [mean pulmonary artery pressure and cardiac output] is preferable to wrong conclusions made from a meaningless variable, the "calculated PVR".