title: Resting alveolar gas tensions as a mortality prognosticator in chronic heart failure.
abstract: BACKGROUND
  Increased end-tidal oxygen (ET-O(2)) and decreased end-tidal carbon dioxide (ET-CO(2)) gas tensions are noninvasively measurable correlates of ventilatory inefficiency, leading to increased ventilatory requirements relative to gas exchange among patients with chronic heart failure (CHF). We investigated the prognostic value of ET-O(2) and ET-CO(2) as predictors of CHF mortality.
  
  
  METHODS
  We measured resting ET-O(2) and ET-CO(2) electrochemically in 134 patients with symptomatic CHF in the supine position. We used Kaplan-Meier analysis, Cox proportional hazard models, and receiver operating characteristic curves to test our hypothesis.
  
  
  RESULTS
  At a median follow-up of 16.5 months, 32 patients had died. ET-O(2) levels were increased (P = .001) and ET-CO(2) levels decreased (P = .002) with increased New York Heart Association class (I-IV). Survivors showed lower ET-O(2) (121 vs 118 mm Hg; P = .021) and higher ET-CO(2) (33.2 vs 32.1 mm Hg; P = .032) levels than nonsurvivors. Patients with ET-O(2) values ≥121 mm Hg and/or ET-CO(2) values <31 mm Hg had an increased risk of death with hazard ratios of 2.93 (95% confidence interval [CI], 1.43-6.01) and 2.47 (95% CI, 1.23-4.97), respectively. Kaplan-Meier estimates for follow-up mortality with ET-O(2) ≥121 mm Hg and/or ET-CO(2) <31 mm Hg were 83.8% (vs 60.1%; P = .0014) and 80.3% (vs 60.2%; P = .0061), respectively. Areas under the receiver operating characteristic curves for prediction of death with ET-O(2) and ET-CO(2) were both significant and similar to that of echocardiographic left ventricular function.
  
  
  CONCLUSIONS
  In CHF, high levels of ET-O(2) and low levels of ET-CO(2) are associated with increased mortality. We suggest that the measurements may be useful prognostic markers for risk stratification.
authors.affiliation: Department of Internal Medicine B-Cardiology, Intensive Care, Pulmonary Medicine and Infectious Diseases, University of Greifswald, Germany. christoph.schaeper@gmail.com
authors.forename: C
authors.initials: C
authors.lastname: Schäper
authors.forename: S
authors.initials: S
authors.lastname: Gläser
authors.forename: B
authors.initials: B
authors.lastname: Wolff
authors.forename: B
authors.initials: B
authors.lastname: Koch
authors.forename: G
authors.initials: G
authors.lastname: Vietzke
authors.forename: S B
authors.initials: SB
authors.lastname: Felix
authors.forename: F X
authors.initials: FX
authors.lastname: Kleber
authors.forename: C F
authors.initials: CF
authors.lastname: Opitz
authors.forename: R
authors.initials: R
authors.lastname: Ewert
mesh_terms: D000368:Aged; D002245:Carbon Dioxide / Q000032:analysis; D002908:Chronic Disease; D004452:Echocardiography; D005260:Female; D005541:Forced Expiratory Volume; D006333:Heart Failure / Q000209:etiology / Q000401:mortality / Q000503:physiopathology*; D006801:Humans; D008297:Male; D008875:Middle Aged; D017202:Myocardial Ischemia / Q000000981:diagnostic imaging / Q000503:physiopathology; D010100:Oxygen / Q000032:analysis; D011379:Prognosis; D016016:Proportional Hazards Models; D011650:Pulmonary Alveoli / Q000503:physiopathology*; D016683:Supine Position; D013990:Tidal Volume / Q000502:physiology; D018487:Ventricular Dysfunction, Left / Q000503:physiopathology
chemical_list: D002245:Carbon Dioxide; D010100:Oxygen