Single-beat estimation of right ventricular end-systolic pressure-volume relationship

Abstract

Brimioulle, Serge, Pierre Wauthy, Patricia Ewalenko, Benoît Rondelet, Franç oise Vermeulen, Franç ois Kerbaul, and Robert Naeije. Single-beat estimation of right ventricular end-systolic pressure-volume relationship. Am J Physiol Heart Circ Physiol 284: H1625-H1630, 2003. First published January 16, 2003 10.1152/ajpheart.01023.2002.-Assessement of right ventricular (RV) contractility from endsystolic pressure-volume relationships (ESPVR) is difficult due to problems in measuring RV instantaneous volume and to effects of changes in RV preload or afterload. We therefore investigated in anesthetized dogs whether RV ESPVR and contractility can be determined without measuring RV volume and without changing RV preload or afterload. The maximal RV pressure of isovolumic beats (P max) was predicted from isovolumic portions of RV pressure during ejecting beats and compared with Pmax measured during the first beat after pulmonary artery clamping. In RV pressure-volume loops obtained from RV pressure and integrated pulmonary arterial flow, end-systolic elastance (Ees) was assessed as the slope of Pmax-derived ESPVR, pulmonary artery effective elastance (Ea) as the slope of end-diastolic to end-systolic relation, and coupling efficiency as the Ees-to-Ea ratio (Ees/ Ea). Predicted Pmax correlated with observed Pmax (r ϭ 0.98 Ϯ 0.02). Dobutamine increased Ees from 1.07 to 2.00 mmHg/ml and Ees/Ea from 1.64 to 2.49, and propranolol decreased Ees/Ea from 1.64 to 0.91 (all P Ͻ 0.05). After adrenergic blockade, preload reduction did not affect Ees, whereas hypoxia and arterial constriction markedly increased Ea and somewhat increased Ees due to the Anrep effect. Low preload did not affect Ees/Ea and high afterload decreased Ees/Ea. In conclusion, in the right ventricle 1) Pmax can be calculated from normal beats, 2) Pmax can be used to determine ESPVR without change in load, and 3) Pmax-derived ESPVR can be used to assess ventricular contractility and ventricular-arterial coupling efficiency. contractility; preload; afterload; pulmonary hypertension; hypoxia LEFT VENTRICULAR CONTRACTILITY is commonly defined by the end-systolic pressure-volume relationship (ESPVR) (15,16,24). In the right ventricle (RV), the concept of ESPVR is also valid (8, 20) but it is difficult to apply in practice. The major problem is the difficulty in measuring instantaneous RV volume in vivo. In 1988, Kass (13) summarized the limitations of available methods and mentioned the potential of conductance volumetry. Although not completely validated for measurement of instantaneous volume, conductance has been used repeatedly to generate pressure-volume loops in animals and humans (34). The method remains difficult and time consuming and is therefore predominantly used as a research tool (31). A second problem may be the identification of end systole on triangle-shaped RV pressure-volume curves. Several investigators (9, 20) determined ESPVR from end-ejection pressures and volumes, but end ejection and end systole are known to occur at different times in the ...

Magnetic Resonance Imaging Analysis of Right Ventricular Pressure-Volume Loops

“…E max was determined by a single-beat estimation method of the RV end-systolic pressure-volume relationship. 15,21 In this approach, the maximal RV pressure of isovolumic beats (P max ) is computed by sine wave extrapolation of the pressure curve from the ejecting beat before maximal and after minimal dP/dt. 15 Maximal ventricular elastance (E max ) is determined from the slope of the tangent between the P max and V es points (Figures 2 and 3).…”

“…From these measurements, RV pressure-volume loops were constructed, and the slope of the end-systolic pressure volume relationship (E max ), a load-independent parameter of myocardial contractility, was determined by applying a single-beat estimation method. 15 The aims of the present study were to validate MRI-derived assessment of E max in a swine model and then to apply this technique in patients with chronic RV pressure overload from pulmonary hypertension (PHT) for assessment of E max , ventricular pump function and the efficiency of VA coupling.…”

Biomechanics of the Right Ventricle in Health and Disease (2013 Grover Conference Series)

“…The acute hypoxia-induced increase in PVR was associated with preserved RV-arterial coupling because of increased RV contractility. 15,19,[29][30][31] The adapted increase in RV contractility with preserved RV-arterial coupling was also reported in pulmonary hypertension following either microembolism or pulmonary arterial banding. 19 Endotoxic shock-induced increase in PVR was associated with early preservation of RV-arterial coupling but deterioration as soon as 1 hour after the initial insult because of an unsustained adaptive increase in contractility.…”

“…This is why single-beat methods have been developed, initially for the LV 14 and then for the RV. 15 The single-beat method relies on a maximum-pressure (P max ) calculation from a nonlinear extrapolation of the early and late portions of an RV pressure curve, an integration of pulmonary flow, and synchronization of the signals. The E max is estimated from the slope of a tangent from P max to the pressure-volume curve ( Figure 3).…”

State of the Art: Advanced Imaging of the Right Ventricle and Pulmonary Circulation in Humans (2013 Grover Conference Series)

“…Using this method, arterial elastance (Ea) as a measure of RV afterload can also be determined. [30][31][32] The ratio of Ees to Ea represents efficiency of the ventriculo-arterial coupling. In addition, CMR approaches have been developed to estimate Ees noninvasively.…”