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1 Laboratory of Physiology, Free University of Brussels, B-1070 Brussels; 2 Department of Intensive Care, Erasme Hospital, B-1070 Brussels; 3 Department of Cardiac Surgery, Brugmann Hospital, B-1020 Brussels; and 4 Department of Anesthesiology, Bordet Institute, B-1000, Brussels, Belgium
Assessement of right ventricular (RV) contractility from end-systolic 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 (Pmax) 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 = 0.98 ± 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 < 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
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