title: Effects of increased intra-abdominal pressure on central circulation.
abstract: BACKGROUND
  In an experimental model we investigated the effects of a gradual increase in intra-abdominal pressure (IAP) on the central circulation.
  
  
  METHODS
  Seven pigs were anaesthetized, mechanically ventilated and instrumented. IAP was gradually increased by 5 mm Hg up to 30 mm Hg by abdominal banding in normovolaemic animals, and then they were made hypovolaemic after blood withdrawal. Right atrial pressure (RAP) and left ventricular end-diastolic pressure (LVEDP) at each step and aortic, femoral and inferior vena cava blood flows were measured. Left ventricular end-diastolic area (LVEDA) was determined using epicardial echocardiography.
  
  
  RESULTS
  Cardiac output maintained at mild IAP was reduced to 76 (24)% of the initial value at 30 mm Hg IAP [mean (sd)] in normovolaemic animals, and 72 (22)% (P<0.001) in hypovolaemic animals. In normovolaemic animals the LVEDA and LVEDP were significantly increased at an IAP of 10 and 15 mm Hg by 26 (24)% and 38 (23)%, respectively. At these IAP values, the difference between the RAP and IAP was positive. When this gradient became negative, that is beyond 15 mm Hg in normovolaemia and for all IAP values in hypovolaemic animals, the LVEDA declined, reaching 78 (16)% and 62 (22)% (P<0.05) of the initial values in normovolaemic and hypovolaemic groups at the highest IAP value.
  
  
  CONCLUSIONS
  These results showed that a gradual increase in IAP led to a redistribution of abdominal blood volume towards the thoracic compartment, at IAP lower than 15 mm Hg in normovolaemia, and at its expense at higher values of IAP. In hypovolaemia there was no thoracic compartment gain. Whereas the absolute or transmural RAPs were not informative of the direction of this blood shift, an RAP greater than IAP was associated with an intrathoracic compartment gain.
authors.affiliation: Department of Anaesthesiology and Intensive Care, Hôpital de la Croix-Rousse, Lyon, France.
authors.forename: E
authors.initials: E
authors.lastname: Vivier
authors.forename: O
authors.initials: O
authors.lastname: Metton
authors.forename: V
authors.initials: V
authors.lastname: Piriou
authors.forename: F
authors.initials: F
authors.lastname: Lhuillier
authors.forename: J M
authors.initials: JM
authors.lastname: Cottet-Emard
authors.forename: P
authors.initials: P
authors.lastname: Branche
authors.forename: S
authors.initials: S
authors.lastname: Duperret
authors.forename: J P
authors.initials: JP
authors.lastname: Viale
mesh_terms: D000005:Abdomen / Q000503:physiopathology*; D000818:Animals; D001794:Blood Pressure; D002245:Carbon Dioxide / Q000097:blood; D002302:Cardiac Output; D004837:Epinephrine / Q000097:blood; D005263:Femoral Artery / Q000503:physiopathology; D006439:Hemodynamics; D006973:Hypertension / Q000097:blood / Q000000981:diagnostic imaging / Q000503:physiopathology*; D020896:Hypovolemia / Q000097:blood / Q000000981:diagnostic imaging / Q000503:physiopathology; D009638:Norepinephrine / Q000097:blood; D010313:Partial Pressure; D013552:Swine; D014463:Ultrasonography; D014655:Vascular Resistance; D014682:Vena Cava, Inferior / Q000503:physiopathology; D016277:Ventricular Function, Left
chemical_list: D002245:Carbon Dioxide; D009638:Norepinephrine; D004837:Epinephrine