This subproject is one of many research subprojects utilizing theresources provided by a Center grant funded by NIH/NCRR. The subproject andinvestigator (PI) may have received primary funding from another NIH source,and thus could be represented in other CRISP entries. The institution listed isfor the Center, which is not necessarily the institution for the investigator.1. Resting minute ventilation (Ve) is increased in normocapnic patients with COPD.2. The ratio of CO2 production (VCO2) to resting Ve, is decreased in COPD3. Whilst the relationship VCO2/arterial PCO2 in COPD is similar to normals, the relationship Ve/arterial PCO2 is decreased. 4. VCO2 is similar in normocapnic and hypercapnic COPD, but Ve/VCO2 is decreased in hypercapnic vs normocapnic COPD. 5. In contrast to normal subjects, both normocapnic and hypercapnic COPD patients respond to an added respiratory resistive load with a decrease in Ve and increase in end-tidal PCO2.
SPECIFIC AIMS1. In patients with normocapnic COPD, and in healthy normal subjects, measure resting Ve, VCO2, end-tidal CO2 and anatomic deadspace (Vdan) and alveolar deadspace (Vdalv) and examine the relationship amongst these parameters and in relationship to arterial PCO2 (PaCO2).2. In patients with hypercapnic COPD, measure resting Ve, VCO2, end-tidal CO2, PaCO2, Vdan and Vdalv and examine the relationship amongst these parameters, and compare the results to normocapnic COPD patients.3. In normocapnic and hypercapnic COPD patients, and in healthy normal subjects, examine the effects of an added resistive load on Ve, VCO2, and end-tidal CO2 to approximate the effects of acute exacerbations of COPD on these parameters.Ventilatory failure is associated with an increased arterial PCO2 (PaCO2). Arterial PaCO2 is determined by the balance between CO2 production and excretion from the body (VCO2). CO2 production is known to be increased in obesity (1), during exercise (2), fever, and with high carbohydrate diets (3, 4). The critical importance of CO2 has been recognized for a very long time: Were it not for the peculiar properties of carbon dioxide - a very weak acid and a gas - our bodies would be unable to survive in their present state' (5). A great deal is known about the production of CO2 (VCO2) by the human body as a natural physiologic process: CO2 is produced in muscle as a product of metabolism, diffuses rapidly into blood where it is transported to the lungs and excreted. The production of CO2 is dependent on three factors: metabolism, blood carriage mechanisms (acid/base, buffering mechanisms), and pulmonary excretion.Dietary factors which alter CO2 production are due to the differences between carbohydrates and fat: in glycolysis, 1 mol of CO2 is produced in regenerating 6 mol of ATP, whereas in non-esterified fatty acid metabolism 1 mol of CO2 is produced for 8 mol of ATP. Thus CO2 production is dependent on the balance between fat and glycogen oxidation, and can be influenced by dietary changes (3, 4).CO2 is carried in the blood as dissolved CO2 and [HCO3-] and is affected by the acid -base state. The excretion of CO2 by the lungs is considered primarily a function of ventilation, and complete equilibration is assumed between the PCO2 of capillary blood and the alveoli (2). However, under stress, such as during exercise, a disequilibrium occurs, related to the breathing cycle and blood flow. In healthy normal subjects there is a direct, curvilinear relationship between alveolar ventilation (VA) and arterial PCO2.
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