Kasak, Alexander

Pulmonary artery capacitance (Pa CAP ) is the ability of the pulmonary artery to accept a volume of blood at a given pressure. Measured invasively with heart catheterization; Pa CAP can be estimated non‐invasively through the measurement of end‐tidal CO 2 (P ETCO2 ) and stroke volume (SV), known as gas‐exchange capacitance (GX CAP ). We have shown that GX CAP is decreased at rest as well as during peak exercise in patients with cystic fibrosis (CF), when compared to healthy subjects. To determine whether GX CAP is different in CF and controls at a workload that matches for SV. 9 CF patients (age=22±3yrs, BMI=23±1kg/m 2 , VO 2 =19±1mL/kg/min, FEV 1 =81±8%pred.) and 13 healthy subjects (age=28±3yrs, BMI=25±1kg/m 2 , VO 2 =23±2L/min, FEV 1 =93±3%pred.) were studied. Exercise testing was performed on a cycle ergometer. P ETCO2 was assessed using a metabolic cart, SV was calculated from heart rate and cardiac output (Q) using the acetylene rebreathe technique and GX CAP was calculated as the product of P ETCO2 and SV. When matched for workload which sought to match SV, there was a significant difference in CF and healthy subjects in workload (Watts=72±6 vs. 90±4W), but no difference in percent of max watts (%MaxW=63±4 vs. 66±5W), Q (11±1 vs. 13±1L/min), or SV (89±4 vs. 90±4ml/beat). When matched, the previous difference in GX CAP in healthy and CF was abolished (GX CAP =32±2 vs. 32±2mL/BEAT • min). P ETCO2 was similar between CF and healthy subjects (P ETCO2 36±1 and 35±1mmHg). When matched for SV, GX CAP was statistically similar in CF. In relatively healthy CF there is no evidence of pulmonary vasculature dysfunction. NIH RO1 HL108962‐02