title: Impaired ventilatory efficiency in chronic heart failure: possible role of pulmonary vasoconstriction.
abstract: BACKGROUND
  Patients with chronic heart failure show impairment of ventilatory efficiency, defined as the relation between ventilation and carbon dioxide output. It is caused by ventilation of excess physiologic dead space. We hypothesized a role of active vasoconstriction in the increase of physiologic dead space, presumed to lead to alveolar hypoperfusion.
  
  
  RESULTS
  In 57 patients with chronic heart failure (New York Heart Association classification II through IV, ejection fraction 25.6%+/-10.4%) and 7 control subjects, gas exchange at rest and on exercise was compared with hemodynamic measurements and, in a subgroup of 15 patients, with endothelin-1, epinephrine, and norepinephrine levels in the pulmonary and systemic circulation. Ventilatory efficiency at rest (VE/VCO2 ratio) correlated with ventilatory efficiency on exercise (VE vs VCO2 slope). Impairment of ventilatory efficiency correlated strongly negative with exercise tolerance (maximal oxygen uptake: r = -0.67) and cardiac output (r = -0.66) and positive with pulmonary hypertension (mean pulmonary artery pressure: r = 0.69, pulmonary vascular resistance: r = 0.60). None of the vasoconstrictors correlated with reduction of ventilatory efficiency in the subgroup studied.
  
  
  CONCLUSIONS
  Impairment of ventilatory efficiency in chronic heart failure is correlated with resting pulmonary artery pressures and associated with the impairment of exercise capacity. An imbalance of pulmonary vascular tone probably leads to both pulmonary hypertension and alveolar hypoperfusion.
authors.affiliation: Department of Internal Medicine and Working Group for Biometrics, Charité, Humboldt University Berlin, Germany.
authors.forename: I
authors.initials: I
authors.lastname: Reindl
authors.forename: K D
authors.initials: KD
authors.lastname: Wernecke
authors.forename: C
authors.initials: C
authors.lastname: Opitz
authors.forename: R
authors.initials: R
authors.lastname: Wensel
authors.forename: D
authors.initials: D
authors.lastname: König
authors.forename: T
authors.initials: T
authors.lastname: Dengler
authors.forename: I
authors.initials: I
authors.lastname: Schimke
authors.forename: F X
authors.initials: FX
authors.lastname: Kleber
mesh_terms: D000328:Adult; D002303:Cardiac Output, Low / Q000097:blood / Q000503:physiopathology*; D016022:Case-Control Studies; D019332:Endothelin-1 / Q000097:blood; D004837:Epinephrine / Q000097:blood; D005080:Exercise Test; D005260:Female; D006439:Hemodynamics; D006801:Humans; D008168:Lung / Q000098:blood supply*; D008297:Male; D008875:Middle Aged; D011659:Pulmonary Gas Exchange; D014661:Vasoconstriction; D014692:Ventilation-Perfusion Ratio
chemical_list: D019332:Endothelin-1; D004837:Epinephrine