OBJECTIVE: Acute right ventricular failure (RVF) is a life-threatening condition. This study investigated whether the combination of central venous pressure (CVP) and left ventricular functional preload parameters, such as stroke volume variation (SVV) and pulse pressure variation (PPV), can be used for the detection of acute RVF and for guidance of volume therapy. DESIGN AND SETTING: Experimental study in a university laboratory. PARTICIPANTS: Fifteen anesthetized and ventilated pigs. MEASUREMENTS AND MAIN RESULTS: For the induction of RVF, mean pulmonary artery pressure (MPAP) was increased by 50% with a continuous infusion of a thromboxane-A(2) analog (U46619). Then, blood removal (300 mL) and retransfusion (blood 200 mL + colloid solution 200 mL) were performed. An analysis of volume responders and nonresponders was implemented. Increasing MPAP (25.1 to 37.4 mmHg) led to decreases in mean arterial pressure (72.2 to 60.1 mmHg) and cardiac output (2.8 to 2.3 L/min, p < 0.05). CVP (11.3 to 12.6 mmHg), PPV (13% to 17%), and SVV (11 to 14%) increased significantly (p < 0.05). During volume removal, MPAP (37.4 to 34.1 mmHg), mean arterial pressure (60.1 to 53.2 mmHg), and cardiac output (2.3 to 2.1 L/min) decreased (p < 0.05), whereas PPV and SVV remained unchanged. During volume loading, CVP increased in volume responders and nonresponders; however, PPV decreased in responders only. CONCLUSIONS: Increases of CVP and SVV or PPV are suspicious for RVF. However, SVV and PPV fail to predict volume responsiveness in RVF. Changes in SVV and PPV during a volume-loading maneuver can be used to assess volume responsiveness.
OBJECTIVE: Acute right ventricular failure (RVF) is a life-threatening condition. This study investigated whether the combination of central venous pressure (CVP) and left ventricular functional preload parameters, such as stroke volume variation (SVV) and pulse pressure variation (PPV), can be used for the detection of acute RVF and for guidance of volume therapy. DESIGN AND SETTING: Experimental study in a university laboratory. PARTICIPANTS: Fifteen anesthetized and ventilated pigs. MEASUREMENTS AND MAIN RESULTS: For the induction of RVF, mean pulmonary artery pressure (MPAP) was increased by 50% with a continuous infusion of a thromboxane-A(2) analog (U46619). Then, blood removal (300 mL) and retransfusion (blood 200 mL + colloid solution 200 mL) were performed. An analysis of volume responders and nonresponders was implemented. Increasing MPAP (25.1 to 37.4 mmHg) led to decreases in mean arterial pressure (72.2 to 60.1 mmHg) and cardiac output (2.8 to 2.3 L/min, p < 0.05). CVP (11.3 to 12.6 mmHg), PPV (13% to 17%), and SVV (11 to 14%) increased significantly (p < 0.05). During volume removal, MPAP (37.4 to 34.1 mmHg), mean arterial pressure (60.1 to 53.2 mmHg), and cardiac output (2.3 to 2.1 L/min) decreased (p < 0.05), whereas PPV and SVV remained unchanged. During volume loading, CVP increased in volume responders and nonresponders; however, PPV decreased in responders only. CONCLUSIONS: Increases of CVP and SVV or PPV are suspicious for RVF. However, SVV and PPV fail to predict volume responsiveness in RVF. Changes in SVV and PPV during a volume-loading maneuver can be used to assess volume responsiveness.
Authors: Juan Carlos Lopez-Delgado; Francisco Esteve; Casimiro Javierre; Xose Perez; Herminia Torrado; Maria L Carrio; David Rodríguez-Castro; Elisabet Farrero; Josep Lluís Ventura Journal: Interact Cardiovasc Thorac Surg Date: 2012-12-12
Authors: Maria Helena Calixto Fernandes; Thomas Schricker; Sheldon Magder; Roupen Hatzakorzian Journal: Crit Care Date: 2018-01-25 Impact factor: 9.097
Authors: Wanhong Yin; Yi Li; Shouping Wang; Xueying Zeng; Yao Qin; Xiaoting Wang; Yangong Chao; Lina Zhang; Yan Kang; Chinese Critical Ultrasound Study Group Ccusg Journal: Biomed Res Int Date: 2018-06-11 Impact factor: 3.411