Bedside End Tidal Carbon Dioxide in Evaluation for Pulmonary Embolism.
Bedside End Tidal Carbon Dioxide in Evaluation for Pulmonary Embolism.
- 2018
Available online from MWHC library: 1997 - present, Available in print through MWHC library:2005-2007
Copyright This article is protected by copyright. All rights reserved. Pulmonary embolism (PE) is associated with approximately 100,000 deaths per year in the United States and the incidence of deep vein thrombosis/pulmonary embolism in the US is estimated at more than 350,000 cases annually (1). The diagnosis of pulmonary embolism poses a diagnostic challenge in the Emergency Department (ED), despite, validated decision rules, lab tests, and radiographic imaging (2, 3). While a simple lab test would be ideal for diagnosis, the well-known D-dimer test is, at its best, only about 54% specific (4). The gold standard pulmonary artery Computed Tomography Angiography (CTA) has numerous downsides including a requirement of clinical stability for transport to radiology, administration of potentially nephrotoxic contrast agents, and radiation exposure to patients, some of whom may be pregnant. Hemodynamically significant PE increases pulmonary dead space and therefore increases the alveolar dead space fraction, however calculating this involves invasive testing with ABG and a slightly cumbersome calculation (5, 6). Studies suggest that it is possible to use ETCO2 alone to screen for PE with the resultant increase in dead space causing the amount of exhaled ETCO2 to be lower in patients with clinically significant PE as opposed to invasive ABG testing (7, 8). However, these studies have typically included patients admitted to the hospital, which represent a fraction of those seen in the ED, and likely have a higher prevalence of PE. No study has prospectively evaluated real-time ETCO2 in ED patients suspected of having PE. We sought to determine if ETCO2 can rule out hemodynamically significant PE, hypothesizing that no patients with hemodynamically significant PE would have an ETCO2 greater than 35 mm Hg. Our secondary hypothesis was that the mean ETCO2 would be significantly lower in patients with PE versus those without PE. Full IRB approval was obtained through MedStar Washington Hospital Center's IRB prior to initiation of this study. This article is protected by copyright. All rights reserved.
English
1069-6563
10.1111/acem.13546 [doi]
IN PROCESS -- NOT YET INDEXED
MedStar Health Research Institute
MedStar Washington Hospital Center
Emergency Medicine
Journal Article
Available online from MWHC library: 1997 - present, Available in print through MWHC library:2005-2007
Copyright This article is protected by copyright. All rights reserved. Pulmonary embolism (PE) is associated with approximately 100,000 deaths per year in the United States and the incidence of deep vein thrombosis/pulmonary embolism in the US is estimated at more than 350,000 cases annually (1). The diagnosis of pulmonary embolism poses a diagnostic challenge in the Emergency Department (ED), despite, validated decision rules, lab tests, and radiographic imaging (2, 3). While a simple lab test would be ideal for diagnosis, the well-known D-dimer test is, at its best, only about 54% specific (4). The gold standard pulmonary artery Computed Tomography Angiography (CTA) has numerous downsides including a requirement of clinical stability for transport to radiology, administration of potentially nephrotoxic contrast agents, and radiation exposure to patients, some of whom may be pregnant. Hemodynamically significant PE increases pulmonary dead space and therefore increases the alveolar dead space fraction, however calculating this involves invasive testing with ABG and a slightly cumbersome calculation (5, 6). Studies suggest that it is possible to use ETCO2 alone to screen for PE with the resultant increase in dead space causing the amount of exhaled ETCO2 to be lower in patients with clinically significant PE as opposed to invasive ABG testing (7, 8). However, these studies have typically included patients admitted to the hospital, which represent a fraction of those seen in the ED, and likely have a higher prevalence of PE. No study has prospectively evaluated real-time ETCO2 in ED patients suspected of having PE. We sought to determine if ETCO2 can rule out hemodynamically significant PE, hypothesizing that no patients with hemodynamically significant PE would have an ETCO2 greater than 35 mm Hg. Our secondary hypothesis was that the mean ETCO2 would be significantly lower in patients with PE versus those without PE. Full IRB approval was obtained through MedStar Washington Hospital Center's IRB prior to initiation of this study. This article is protected by copyright. All rights reserved.
English
1069-6563
10.1111/acem.13546 [doi]
IN PROCESS -- NOT YET INDEXED
MedStar Health Research Institute
MedStar Washington Hospital Center
Emergency Medicine
Journal Article