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Original Research: PULMONARY VASCULAR DISEASE |

End Tidal CO2 TensionEnd Tidal CO2 in Pulmonary Hypertension: Pulmonary Arterial Hypertension vs Pulmonary Venous Hypertension and Response to Treatment

Anna R. Hemnes, MD; Meredith E. Pugh, MD; Alexander L. Newman, BA; Ivan M. Robbins, MD; James Tolle, MD; Eric D. Austin, MD, MSCI; John H. Newman, MD
Author and Funding Information

From the Division of Allergy, Pulmonary and Critical Care Medicine (Drs Hemnes, Pugh, Robbins, Tolle, and J. H. Newman and Mr A. L. Newman) and Division of Allergy, Immunology and Pulmonary Medicine (Dr Austin), Department of Pediatrics, Vanderbilt University Medical Center, Nashville, TN.

Correspondence to: Anna R. Hemnes, MD, Division of Allergy, Pulmonary and Critical Care Medicine, Vanderbilt University Medical Center, T1218 Medical Center N, 1161 21st Ave S, Nashville, TN 37232; e-mail: anna.r.hemnes@vanderbilt.edu


Funding/Support: The authors have reported to CHEST that no funding was received for this study.

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (http://www.chestpubs.org/site/misc/reprints.xhtml).


© 2011 American College of Chest Physicians


Chest. 2011;140(5):1267-1273. doi:10.1378/chest.11-0155
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Background:  CO2 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 CO2 (Etco2) 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 Etco2 values.

Methods:  We performed Etco2 measurements for five breaths at rest and after a 6-min walk test (6MWT) in patients seen at our pulmonary vascular center. Mean Etco2 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. Etco2 was significantly lower in patients with PAH than in those with no PH and PVH (P < .0001 PAH vs both groups). Etco2 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). Etco2 after 6MWT correlated with walk distance (r = 0.34, P = .003). In patients with prostaglandin therapy escalation, Etco2 increased in those who had clinical improvement, whereas in patients who did not improve clinically, Etco2 failed to rise (P = .04).

Conclusions:  Etco2 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.

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