title: Pleural effusion decreases left ventricular pre-load and causes haemodynamic compromise: an experimental porcine study.
abstract: BACKGROUND
  Although pleural effusion is a common complication in critically ill patients, detailed knowledge is missing about the haemodynamic impact and the underlining mechanisms. The aim of this study was to evaluate the haemodynamic effect of incremental pleural effusion by means of invasive haemodynamic parameters and transthoracic echocardiography.
  
  
  METHODS
  This experimental interventional study was conducted using 22 female piglets (17.5-21.5 kg) randomized for right-side (n = 9) and left-side (n = 9) pleural effusion, or sham operation (n = 4). Pleural effusion was induced by infusing incremental volumes of saline into the pleural cavity. Invasive haemodynamic measurements and echocardiographical images were obtained at baseline, a volume of 45 ml/kg, a volume of 75 ml/kg and 45 min after drainage.
  
  
  RESULTS
  No difference (all P > 0.147) was found between right- and left-side pleural effusion, and the groups were thus pooled. At 45 ml/kg cardiac output, mean arterial pressure, stroke volume and mixed venous saturation decreased (all P < 0.003); central venous pressure and pulmonary arterial pressure increased (both P > 0.003) at this point. The changes accelerated at 75 ml/kg. At 45 ml/kg left ventricular pre-load in terms of end-diastolic area decreased significantly (P < 0.001). The effect on haemodynamics and cardiac dimensions changed dramatically at 75 ml/kg. Cardiac output, mean arterial pressure, central venous pressure and left ventricular end-diastolic area returned to normal during a recovery period of 45 min (all P > 0.061).
  
  
  CONCLUSIONS
  Incremental volumes of unilateral pleural effusion induced a significant haemodynamic impact fully reversible after drainage. Pleural effusion causes a significant decrease of left ventricular pre-load in a diverse picture of haemodynamic compromise.
authors.affiliation: Department of Anaesthesiology and Intensive Care, Aarhus University Hospital, Aarhus, Denmark.
authors.forename: K B
authors.initials: KB
authors.lastname: Wemmelund
authors.forename: R H
authors.initials: RH
authors.lastname: Lie
authors.forename: P
authors.initials: P
authors.lastname: Juhl-Olsen
authors.forename: C A
authors.initials: CA
authors.lastname: Frederiksen
authors.forename: J F
authors.initials: JF
authors.lastname: Hermansen
authors.forename: E
authors.initials: E
authors.lastname: Sloth
mesh_terms: D000818:Animals; D002302:Cardiac Output; D002305:Cardiac Tamponade / Q000000981:diagnostic imaging / Q000503:physiopathology; D004452:Echocardiography; D006352:Heart Ventricles / Q000000981:diagnostic imaging / Q000503:physiopathology*; D006439:Hemodynamics; D010996:Pleural Effusion / Q000150:complications / Q000503:physiopathology*; D011655:Pulmonary Embolism / Q000000981:diagnostic imaging / Q000503:physiopathology; D011897:Random Allocation; D016037:Single-Blind Method; D013318:Stroke Volume; D034421:Sus scrofa; D013552:Swine; D018487:Ventricular Dysfunction, Left / Q000000981:diagnostic imaging / Q000209:etiology* / Q000503:physiopathology