Abstract

Pulmonary artery capacitance (PaCAP) is the ability of the pulmonary artery to accept a volume of blood at a given pressure. Measured invasively with heart catheterization; PaCAP can be estimated non‐invasively through the measurement of end‐tidal CO2 (PETCO2) and stroke volume (SV), known as gas‐exchange capacitance (GXCAP). We have shown that GXCAP is decreased at rest as well as during peak exercise in patients with cystic fibrosis (CF), when compared to healthy subjects. To determine whether GXCAP is different in CF and controls at a workload that matches for SV. 9 CF patients (age=22±3yrs, BMI=23±1kg/m2, VO2=19±1mL/kg/min, FEV1=81±8%pred.) and 13 healthy subjects (age=28±3yrs, BMI=25±1kg/m2, VO2=23±2L/min, FEV1=93±3%pred.) were studied. Exercise testing was performed on a cycle ergometer. PETCO2 was assessed using a metabolic cart, SV was calculated from heart rate and cardiac output (Q) using the acetylene rebreathe technique and GXCAP was calculated as the product of PETCO2 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 GXCAP in healthy and CF was abolished (GXCAP=32±2 vs. 32±2mL/BEAT • min). PETCO2 was similar between CF and healthy subjects (PETCO2 36±1 and 35±1mmHg). When matched for SV, GXCAP was statistically similar in CF. In relatively healthy CF there is no evidence of pulmonary vasculature dysfunction. NIH RO1 HL108962‐02

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