Hemodynamic effects of experimental acute right ventricular overload

• Published in: Arquivos brasileiros de cardiologia 2011-04, Vol.96 (4), p.284-292
• Main Authors: Brito Filho, Flávio, Campos, Kleber Nogueira de, Oliveira, Humberto Alves de, Fernandes, Josué, Silva, César Augusto Melo e, Gaio, Eduardo, Parra, Edwin Roger, Carvalho, Paulo Henrique Cândido de, Fernandes, Paulo Manoel Pêgo
• Format: Article
• Language: English
• Subjects: Acute Disease; Animals; Blood Pressure - physiology; Disease Models, Animal; Heart Rate - physiology; Hemodynamics - physiology; Male; Pulmonary Artery - physiopathology; Pulmonary Embolism - physiopathology; Swine; Time Factors; Ventricular Dysfunction, Right - physiopathology
• ISSN: 1678-4170
• DOI: 10.1590/S0066-782X2011005000029

Acute right ventricular overload is associated with high morbidity and mortality clinical situations such as: extensive lung resection, pulmonary thromboembolism, lung transplantation and high altitude pulmonary edema. Some points of its pathophysiology remain unclear. To assess the hemodynamic effects of experimental acute right ventricular overload in pigs. Right ventricular overload was induced through the occlusion of the pulmonary arteries using ligationss. Twenty pigs were used in the study, divided into 04 groups: one control group not subject to pulmonary vascular occlusion, and three right ventricular overload groups subject to occlusion of the following pulmonary arteries: SVD1 (left pulmonary artery); SVD2 (left pulmonary artery and right lower lobe) and SVD3 (left pulmonary artery, right lower lobe and mediastinal lobe), obstructing the pulmonary vasculature in 42, 76 and 82.0% respectively. Hemodynamic variables were measured every 15 minutes during one hour of study. The statistical analysis employed mixed linear models with variance and covariance structures. Group comparisons revealed significant increases in heart rate (p = 0.004), mean pulmonary artery pressure (p = 0.001) and pulmonary capillary wedge pressure (p < 0.0001). There was no significant difference in cardiac index (p = 0.94). Despite the severe right ventricular overload promoted by 82.0% obstruction of the pulmonary vasculature and the significant increase in pulmonary arterial pressure, there was no severe cardiovascular dysfunction and/or circulatory shock during the study period.