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Can Quantitative Capnometry Differentiate Between Cardiac and Obstructive Causes of Respiratory Distress?

Lawrence H. Brown; John E. Gough; Rosa H. Seim
Author and Funding Information

Affiliations: From the Department of Emergency Medicine, Pitt County Memorial Hospital, Greenville, NC.,  From the Department of Emergency Medicine, East Carolina University School of Medicine, and the Department of Emergency Medicine, Pitt County Memorial Hospital, Greenville, NC.,  From the East Carolina University School of Medicine, and the Department of Emergency Medicine, Pitt County Memorial Hospital, Greenville, NC.

Affiliations: From the Department of Emergency Medicine, Pitt County Memorial Hospital, Greenville, NC.,  From the Department of Emergency Medicine, East Carolina University School of Medicine, and the Department of Emergency Medicine, Pitt County Memorial Hospital, Greenville, NC.,  From the East Carolina University School of Medicine, and the Department of Emergency Medicine, Pitt County Memorial Hospital, Greenville, NC.

Affiliations: From the Department of Emergency Medicine, Pitt County Memorial Hospital, Greenville, NC.,  From the Department of Emergency Medicine, East Carolina University School of Medicine, and the Department of Emergency Medicine, Pitt County Memorial Hospital, Greenville, NC.,  From the East Carolina University School of Medicine, and the Department of Emergency Medicine, Pitt County Memorial Hospital, Greenville, NC.


1998 by the American College of Chest Physicians


Chest. 1998;113(2):323-326. doi:10.1378/chest.113.2.323
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Published online

Abstract

Study objective: To determine whether quantitative measurement of end-tidal carbon dioxide (ETCO2) can differentiate between cardiac and obstructive causes of respiratory distress.

Design: Prospective observational study.

Setting: Emergency department (ED) of a tertiary care hospital.

Patients: Adult patients who presented to the ED with moderate-to-severe dyspnea. Patients were excluded if they were unable to cooperate with the performance of peak expiratory flow rate (PEFR) or ETCO2 tests, were younger than 18 years of age, or had received prehospital intervention for their respiratory distress.

Interventions: Physicians obtained an ETCO2 level and PEFR prior to ED pharmacologic intervention. A hand-held capnometer with digital read-out was used to obtain the ETCO2 level. The patient's age, sex, initial vital signs, breath sounds and medication history, the presence or absence of diaphoresis and/or orthopnea, the duration of symptoms, the chest radiograph interpretation, and final diagnosis were also recorded.

Measurements and results: Forty-two patients were eligible for inclusion in the analysis. The mean ETCO2 level was 31.1±9.4 mm Hg; the mean PEFR was 161.3±53.1 L/min. The ETCO2 levels for pulmonary edema/congestive heart failure (CHF) patients differed significantly from those of asthma/COPD patients (27.1±7.8 mm Hg vs 33.4±9.6 mm Hg; p=0.0375). However, no single ETCO2 level was found to be a reliable predictor of diagnosis.

Conclusion: ETCO2 levels for pulmonary edema/CHF patients differ significantly from those of asthma/COPD patients. However, no single ETCO2 level reliably differentiates between the two disease processes.


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