title: Hemodynamic effects of experimental acute right ventricular overload.
abstract: BACKGROUND
  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.
  
  
  OBJECTIVE
  To assess the hemodynamic effects of experimental acute right ventricular overload in pigs.
  
  
  METHODS
  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.
  
  
  RESULTS
  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).
  
  
  CONCLUSIONS
  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.
authors.affiliation: Unidade de Cirurgia Torácica, Hospital de Base do Distrito Federal, Brazil. flavio@cirurgiatoracicadf.com.br
authors.forename: Flávio
authors.initials: F
authors.lastname: Brito Filho
authors.forename: Kleber Nogueira de
authors.initials: KN
authors.lastname: Campos
authors.forename: Humberto Alves de
authors.initials: HA
authors.lastname: Oliveira
authors.forename: Josué
authors.initials: J
authors.lastname: Fernandes
authors.forename: César Augusto Melo e
authors.initials: CA
authors.lastname: Silva
authors.forename: Eduardo
authors.initials: E
authors.lastname: Gaio
authors.forename: Edwin Roger
authors.initials: ER
authors.lastname: Parra
authors.forename: Paulo Henrique Cândido de
authors.initials: PH
authors.lastname: Carvalho
authors.forename: Paulo Manoel Pêgo
authors.initials: PM
authors.lastname: Fernandes
mesh_terms: D000208:Acute Disease; D000818:Animals; D001794:Blood Pressure / Q000502:physiology; D004195:Disease Models, Animal; D006339:Heart Rate / Q000502:physiology; D006439:Hemodynamics / Q000502:physiology*; D008297:Male; D011651:Pulmonary Artery / Q000503:physiopathology*; D011655:Pulmonary Embolism / Q000503:physiopathology; D013552:Swine; D013997:Time Factors; D018497:Ventricular Dysfunction, Right / Q000503:physiopathology*