title: Pulmonary endarterectomy improves dyspnea by the relief of dead space ventilation.
abstract: BACKGROUND
  In chronic thromboembolic pulmonary hypertension (CTEPH), dyspnea is considered to be related to increased dead space ventilation caused by vascular obstruction. Pulmonary endarterectomy releases the thromboembolic obstruction, thereby improving regional pulmonary blood flow. We hypothesized that pulmonary endarterectomy reduces dead space ventilation and that this reduction contributes to attenuation of dyspnea symptoms.
  
  
  METHODS
  In this follow-up study we assessed dead space ventilation, hemodynamic severity of disease, and symptomatic dyspnea in 54 consecutive CTEPH patients, before and 1 year after pulmonary endarterectomy. Dead space ventilation was calculated using the Bohr-Enghoff equation. Dyspnea was assessed by Borg scores and the New York Heart Association functional classification.
  
  
  RESULTS
  Preoperatively, dead space ventilation was increased (0.40 +/- 0.07) and correlated with severity of disease (mean pulmonary artery pressure: r = 0.49, p < 0.001; total pulmonary resistance: r = 0.53, p < 0.001), and resting (r = 0.35, p < 0.05) and post-exercise Borg dyspnea scores (r = 0.44, p < 0.01). Postoperatively, dead space ventilation (0.33 +/- 0.08, p < 0.001) and dyspnea symptoms decreased significantly. Changes in symptomatic dyspnea were independently associated with changes in pulmonary hemodynamics and absolute dead space.
  
  
  CONCLUSIONS
  Dead space ventilation in CTEPH is increased and correlates significantly with hemodynamic severity of disease and dyspnea symptoms. Pulmonary endarterectomy decreases dead space ventilation. The induced change in dead space upon surgical removal of chronic thromboembolism contributes to the postoperative recovery of symptomatic dyspnea.
authors.affiliation: Department of Respiratory Medicine, Academic Medical Centre, University of Amsterdam, Amsterdam, The Netherlands. m.n.vanderplas@amc.uva.nl
authors.forename: Mart N
authors.initials: MN
authors.lastname: van der Plas
authors.forename: Herre J
authors.initials: HJ
authors.lastname: Reesink
authors.forename: Carel M
authors.initials: CM
authors.lastname: Roos
authors.forename: Reindert P
authors.initials: RP
authors.lastname: van Steenwijk
authors.forename: Jaap J
authors.initials: JJ
authors.lastname: Kloek
authors.forename: Paul
authors.initials: P
authors.lastname: Bresser
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D002245:Carbon Dioxide / Q000097:blood; D002908:Chronic Disease; D004417:Dyspnea / Q000503:physiopathology / Q000601:surgery*; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D006976:Hypertension, Pulmonary / Q000503:physiopathology / Q000601:surgery; D008168:Lung / Q000098:blood supply; D008297:Male; D008875:Middle Aged; D010100:Oxygen / Q000097:blood; D011655:Pulmonary Embolism / Q000503:physiopathology / Q000601:surgery*; D011659:Pulmonary Gas Exchange / Q000502:physiology; D011669:Pulmonary Wedge Pressure / Q000502:physiology; D012126:Respiratory Dead Space / Q000502:physiology*; D014655:Vascular Resistance / Q000502:physiology; D055815:Young Adult
chemical_list: D002245:Carbon Dioxide; D010100:Oxygen