W P Santamore1, L A Gray. 1. Division of Thoracic and Cardiovascular Surgery, University of Louisville, Kentucky 40292, USA.
Abstract
BACKGROUND: In patients with postcardiotomy low cardiac output syndromes, right ventricular (RV) failure develops in approximately 25% of patients receiving left ventricular (LV) assist device support. Depressed RV function have been attributed to abnormalities of the RV myocardium, excessive load imposed on the RV during systole or diastole, or obstruction to RV inflow. However, recent studies also suggest that LV function may significantly affect RV function through ventricular interdependence. METHODS: We reviewed the data showing the importance of systolic ventricular interaction. We then related these observations to the RV response during LV assist device support, and present our ideas regarding the mechanisms responsible for this RV failure. RESULTS: Using an electrically isolated right heart preparation, Damiano observed double-peaked waveforms for RV pressure, and pulmonary artery blood flow occurred over a wide range (0 to 300 ms) of pacing intervals between the LV and RV. Numeric analysis indicated that RV systolic pressure and pulmonary artery blood flow were composed of both RV and LV components, with the LV component dominating (63.5% versus 36.5%). CONCLUSIONS: The experimental studies indicate a very consistent RV response during LV assist device support: a decrease in RV afterload, increased compliance, and decreased contractility. In normal hearts, the net effect is an increase or no change in cardiac output. With a preexisting pathologic condition, the RV responses is qualitatively the same, but anatomic ventricular interaction is accentuated, leading to a greater decrease in RV contractility. The net effect is a decrease in cardiac output, which may require inotropic or RV mechanical support.
BACKGROUND: In patients with postcardiotomy low cardiac output syndromes, right ventricular (RV) failure develops in approximately 25% of patients receiving left ventricular (LV) assist device support. Depressed RV function have been attributed to abnormalities of the RV myocardium, excessive load imposed on the RV during systole or diastole, or obstruction to RV inflow. However, recent studies also suggest that LV function may significantly affect RV function through ventricular interdependence. METHODS: We reviewed the data showing the importance of systolic ventricular interaction. We then related these observations to the RV response during LV assist device support, and present our ideas regarding the mechanisms responsible for this RV failure. RESULTS: Using an electrically isolated right heart preparation, Damiano observed double-peaked waveforms for RV pressure, and pulmonary artery blood flow occurred over a wide range (0 to 300 ms) of pacing intervals between the LV and RV. Numeric analysis indicated that RV systolic pressure and pulmonary artery blood flow were composed of both RV and LV components, with the LV component dominating (63.5% versus 36.5%). CONCLUSIONS: The experimental studies indicate a very consistent RV response during LV assist device support: a decrease in RV afterload, increased compliance, and decreased contractility. In normal hearts, the net effect is an increase or no change in cardiac output. With a preexisting pathologic condition, the RV responses is qualitatively the same, but anatomic ventricular interaction is accentuated, leading to a greater decrease in RV contractility. The net effect is a decrease in cardiac output, which may require inotropic or RV mechanical support.
Authors: Stavros G Drakos; Abdallah G Kfoury; Craig H Selzman; Divya Ratan Verma; John N Nanas; Dean Y Li; Josef Stehlik Journal: Curr Opin Cardiol Date: 2011-05 Impact factor: 2.161
Authors: Christopher T Dibble; Joao A C Lima; David A Bluemke; Julio A Chirinos; Harjit Chahal; Michael R Bristow; Richard A Kronmal; R Graham Barr; Victor A Ferrari; Kathleen J Propert; Steven M Kawut Journal: Chest Date: 2011-02-17 Impact factor: 9.410