Is there a place for intra-aortic balloon counterpulsation support in acute right ventricular failure by pressure-overload?

Abstract

BackgroundMost therapeutic strategies for acute right ventricular failure (RVF) by pressure-overload are directed to improve cardiac output and coronary perfusion pressure by vasopressive agents. The eventual role of intra-aortic balloon counterpulsation (IABP) support remains questionable. This study investigates the contribution of IABP for acute RVF by pressure-overload, in comparison with phenylephrine (PE) and norepinephrine (NOR). MethodsAcute RVF is induced by fixed pulmonary artery constriction in 6 pigs, pursuing a 50% reduction of cardiac output. Assessment of the treatment interventions included biventricular PV-loop analysis, and continuous measurement of aortic and right coronary artery flow. ResultsRestoration of baseline cardiac output was only observed by administration of NOR (Baseline=3.82±1.52ml/min — RVF=2.03±0.59ml/min — IABP=2.45±0.62ml/min — PE=2.98±0.63ml/min — NOR=3.95±0.73ml/min, p<0.001). NOR had most effect on biventricular contractility (PRSW-slope-RV: IABP +24% — PE +59% — NOR +208%, p<0.001 and PRSW-slope-LV: IABP +36% — PE +53% — NOR +196%, p<0.001), heart rate acceleration (IABP +7% — PE +12% — NOR +51%, p<0.001), and RCA flow (IABP +31% — PE +58% — NOR +180%, p<0.001), concomitant to a higher increase of LV-to-RV pressure ratio (IABP: +7% versus −3%, PE: +36% versus +8%, NOR: +101% versus 42%). The hemodynamic contribution of IABP was limited, unless a modest improvement of LV compliance during PE and NOR infusion. ConclusionIn a model of acute pressure-overload RV failure, IABP appears to offer limited hemodynamic benefit. The administration of norepinephrine is most effective to correct systemic output and myocardial perfusion through adding an inotropic and chronotropic effect to systemic vasopression.