Related Experiment Video
Updated: May 13, 2026

Closed Chest Biventricular Pressure-Volume Loop Recordings with Admittance Catheters in a Porcine Model
Published on: May 18, 2021
Fixed Volume-Intercept Approach for Serial Contractility Assessment with Closed-Chest Pressure-Volume Loops in a
Oskar Kjærgaard Hørsdal1, Kristoffer Berg-Hansen2, Nigopan Gopalasingam3
1Department of Cardiology, Aarhus University Hospital; Department of Clinical Medicine, Aarhus University; osho@clin.au.dk.
Abstract:
The end-systolic pressure-volume relationship (ESPVR) is widely regarded as the gold standard, load-independent descriptor of left-ventricular (LV) contractility. Practically, ESPVR is often approximated as a straight line defined by its slope - end-systolic elastance (Ees), a direct index of contractile state - and its volume-axis intercept (V₀), the theoretical LV volume at zero pressure. In vivo, ESPVR is classically derived from serial inferior vena cava (IVC) occlusions performed with simultaneous LV pressure-volume (PV) catheter monitoring. However, in disease states such as cardiogenic shock, the requisite preload depletion may provoke reflex tachyarrhythmias and transient or sustained hemodynamic instability, limiting feasibility and interpretability. Thus, methods for in vivo assessment of inotropy during hemodynamically fragile states are warranted. This protocol aims to describe a practical experimental model in which V₀ is determined once under stable baseline conditions and then held fixed for subsequent, single-beat Ees estimation from LV PV loops. This approach, detailed step-by-step for use in acute large-animal studies, allows continuous serial assessment of contractility without repeated IVC occlusions. In a porcine cardiogenic shock model, it reliably tracked load-independent changes in myocardial performance while avoiding arrhythmias and hemodynamic instability otherwise provoked by preload reduction. The method is therefore well suited for acute, closed-chest experiments in which the ventricular geometry remains unchanged, and contractility primarily modulates the ESPVR slope rather than its intercept. Nonetheless, the fixed-V₀ assumption represents a methodological simplification that introduces deliberate systematic error and should only be applied when repeated preload manipulation is impractical or unsafe. When structural remodeling, profound LV dilation, or marked thoracic pressure changes occur, V₀ must be re-estimated. Overall, this protocol provides a feasible and physiologically sound approach for serial contractility assessment in unstable large-animal models, balancing methodological rigor with experimental safety and practicality.
