Abstract 4144135: The Pulmonary Resistance-Compliance Relationship: Real or Mathematical Artefact?

Background: It has previously been suggested that pulmonary vascular resistance (PVR), the steady component of VA, and arterial compliance (PAC) are physiologically and inexorably linked through an inverse hyperbolic relationship and that their product, the pulmonary vascular time constant (τ), is roughly equal across a range of disease states. A critical and often overlooked concern, however, emerges from the way PAC has come to be estimated in many realms of clinical reearch as the ratio of stroke volume (SV) to pulse pressure (PA PP, PAC clinical ). We sought to explore the foundation of the reported link between PVR and PAC because they both share the value of SV in their determination.In other words, plotting a parameter that is dependent on SV (i.e., PVR) versus another that is dependent on 1/SV (i.e., PAC clinical ) is inherently prone to yield a hyperbolic relationship. Methods: We performed both joint density analysis (JDA) as well as a simple set of simulations using hemodynamic data from a cohort of patients with PH from left-sided disease. PAC clinical was calvulated as SV/PA PP. PVR was calculated as: (PA M – PCWP)/CO , expressed in Wood Units. Log values were plotted to determine PVR-PAC clinical relationships. Results: JDA of predicted PVR against PAC clinical demonstrated a Spearman’s R of -0.88 (CI -0.92 to -0.82). With bootstrapping, this increased to -0.92 (CI -0.93 to -0.91) demonstrating very high mathematical correlation and precision (Figure 1a). Hemodynamic model simulation demonstrated a consistent inverse dependence characterized by a first-order hyperbolic decay function ( PAC = τ avg /PVR ; r 2 0.86; p<0.001; Figures 1b-d). Compared with data from points associated with lower PCWP, the log 10 -transformed relationship was shift downward in a nearly parallel manner (Figures 1e-g). Conclusions: By performing JDA, as well as creating a random, albeit physiologically constrained hemodynamic simulation, we were able to recreate, with high-fidelity, the inverse hyperbolic relationship between PVR and PAC clinical reported in prior studies and the effect of PCWP on this relationship. Re-exploration of the PVR-PAC relationship, using more accurate methods of PAC determination, is now required to understand whether this relationship is truly physiological, or simply, mathematical artefact.