End-Tidal Carbon Dioxide as a Prognostic Feature in Pulmonary Arterial Hypertension.

RATIONALE: Pulmonary arterial hypertension (PAH) is characterized in part by increased dead space ventilation, which can be estimated noninvasively at the bedside by measurement of end-tidal CO2 (ETco2). OBJECTIVES: Prior work has demonstrated that ETco2 is lower in patients with PAH than in control patients, but whether ETco2 has prognostic value is unknown. We hypothesized that lower measurements of ETco2 in patients with PAH correlate with worse long-term outcomes. METHODS: Patients with PAH seen in our referral clinic were prospectively recruited for ETco2 measurement between September 2009 and February 2010. Vital status as of July 2015 was documented using medical records and the Social Security Death Index. RESULTS: Eighty-two patients were followed for a median of 60 months. Twenty-six patients died, and two were lost to follow-up. Patients who died were more likely to be older (58.5 ± 14.9 vs. 47.6 ± 12.2 yr; P < 0.05) and to have shorter 6-minute walk distance (296 ± 127 vs. 401 ± 92 m; P < 0.05). Mean ETco2 in survivors was 30.5 ± 4.8 mm Hg, whereas mean ETco2 in patients who died was 27.1 ± 4.2 mm Hg (P = 0.004). After stratification by median baseline ETco2 of 29 mm Hg, survival in each group was analyzed. Patients with lower ETco2 had shorter survival (P = 0.006). Cox regression analysis with ETco2 as a continuous variable revealed the hazard ratio to be 0.88 (95% confidence interval, 0.80-0.97; P = 0.006). In 52 patients with more than one measurement a median of 17 months apart, ETco2 was unchanged. CONCLUSIONS: Our single-center data suggest that lower ETco2 is associated with shorter survival and that ETco2 is stable over time in patients with PAH.

End tidal CO(2) tension: pulmonary arterial hypertension vs pulmonary venous hypertension and response to treatment.

BACKGROUND: CO(2) excretion is impaired in pulmonary arterial hypertension (PAH) due to underlying vascular obstruction and increased dead space. Our aim was to determine whether resting end tidal CO(2) (Etco(2)) could differentiate patients with PAH from those with pulmonary venous hypertension (PVH) or patients without pulmonary hypertension (PH) and whether successful treatment of PAH resulted in higher Etco(2) values. METHODS: We performed Etco(2) measurements for five breaths at rest and after a 6-min walk test (6MWT) in patients seen at our pulmonary vascular center. Mean Etco(2) values were correlated with 6-min walk distance and right-sided heart catheterization data. RESULTS: We enrolled 84 patients with PAH, 17 with PVH without left ventricular systolic dysfunction, and seven with no PH and no severe alterations in pulmonary function testing. Etco(2) was significantly lower in patients with PAH than in those with no PH and PVH (P < .0001 PAH vs both groups). Etco(2) correlated with the pulmonary artery diastolic pressure-to-pulmonary artery occlusion pressure gradient (r = -0.50, P = .0002) and pulmonary vascular resistance (r = -0.44, P = .002). Etco(2) after 6MWT correlated with walk distance (r = 0.34, P = .003). In patients with prostaglandin therapy escalation, Etco(2) increased in those who had clinical improvement, whereas in patients who did not improve clinically, Etco(2) failed to rise (P = .04). CONCLUSIONS: Etco(2) is a promising tool to differentiate patients with PAH from those with PVH or no PH, correlates with diagnostic and prognostic hemodynamic indicators, and may increase with successful treatment of PAH.