title: Changes in regional ventilation after autologous blood clot pulmonary embolism.
abstract: BACKGROUND
  Previous studies have suggested that pulmonary embolism (PE) and pulmonary artery occlusion result in a shift in alveolar ventilation away from unperfused regions. This study aimed to directly assess changes in regional specific ventilation (sV(A)) due to autologous blood clot PE using positron emission tomography.
  
  
  METHODS
  Pulmonary embolism was created in six anesthetized, paralyzed, and mechanically ventilated sheep by injecting cylindrical clots of autologous blood (7 mm in diameter and height). Clots were progressively infused into a central vein until a stable mean pulmonary artery pressure between 30 and 40 mmHg was achieved. A multislice positron emission tomography camera was used to image 15 contiguous, 6.5-mm-thick transverse cross-sections of the chest beginning just above the diaphragm. sV(A) from perfused regions (sV(A),(p)) was assessed as the ventilatory turnover rate of the tracer NN after central venous injection of NN-labeled saline.
  
  
  RESULTS
  Pulmonary embolism obstructed flow to 64% of imaged areas. Before PE, (sV(A),(p))was equivalent in areas that would remain perfused and those that would become embolized after PE (0.021 +/- 0.007 0.021 +/- 0.006 s(-1); P = nonsignificant). After PE, sV(A),(p) of areas remaining perfused increased to 0.033 +/- 0.011 s (-1) (P < 0.005). This effect on regional sV(A),(p) could have been caused by active redistribution of sV(A),(p) or by a reduction in tracer concentration of perfused areas due to the dead space common to perfused and embolized regions. Model simulations indicated that the common dead-space effect could only explain a small part of the sV(A),(p) increase.
  
  
  CONCLUSIONS
  An increase in sV(A),(p) of perfused regions occurs following PE with 7-mm autologous blood clots. This increase is most likely caused by a shift in ventilation away from embolized areas mediated by hypocapnic pneumoconstriction.
authors.affiliation: Department of Anesthesia and Critical Care, Massachusetts General Hospital and Harvard Medical School, Boston 02114, USA. mvidalmelo@partners.org
authors.forename: Marcos F
authors.initials: MF
authors.lastname: Vidal Melo
authors.forename: R Scott
authors.initials: RS
authors.lastname: Harris
authors.forename: Dominick
authors.initials: D
authors.lastname: Layfield
authors.forename: Guido
authors.initials: G
authors.lastname: Musch
authors.forename: Jose G
authors.initials: JG
authors.lastname: Venegas
mesh_terms: D000465:Algorithms; D000818:Animals; D001777:Blood Coagulation / Q000502:physiology; D001784:Blood Gas Analysis; D001804:Blood Transfusion, Autologous; D006439:Hemodynamics / Q000502:physiology; D007091:Image Processing, Computer-Assisted; D008168:Lung / Q000000981:diagnostic imaging / Q000503:physiopathology*; D011652:Pulmonary Circulation / Q000502:physiology; D011655:Pulmonary Embolism / Q000000981:diagnostic imaging / Q000503:physiopathology*; D012129:Respiratory Function Tests; D015656:Respiratory Mechanics / Q000502:physiology*; D012756:Sheep; D013990:Tidal Volume / Q000502:physiology; D014055:Tomography, Emission-Computed