obstructive lung disease are exposed to expiratory loads (ELs) and dynamic hyperinflation as a consequence of expiratory flow limitation. To understand how these alterations in lung mechanics might affect cardiac function, we examined the influence of a 10-cmH 2O EL, alone and in combination with voluntary hyperinflation (ELH), on pulmonary pressures [esophageal (Pes) and gastric (Pg)] and cardiac output (CO) in seven healthy subjects. CO was determined by using an acetylene method at rest and

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... t 40 and 70% of peak work. At rest and during exercise, EL resulted in an increase in Pes and Pg (7-18 cmH 2O; P Ͻ 0.05) and a decrease in CO (from 5.3 Ϯ 1.8 to 4.5 Ϯ 1.4, 12.2 Ϯ 2.2 to 11.2 Ϯ 2.2, and 16.3 Ϯ 3.3 to 15.2 Ϯ 3.2 l/min for rest, 40% peak work, and 70% peak work, respectively; P Ͻ 0.05), which remained depressed after an additional 2 min of EL. With ELH, CO increased at rest and both exercise loads (relative to EL only) but remained below control values. The changes in CO were due to a reduction in stroke volume with a tendency for stroke volume to fall further with prolonged EL. There was a negative correlation between CO and the increase in expiratory Pes and Pg with EL (R ϭ Ϫ0.58 and Ϫ0.60; P Ͻ 0.01), whereas the rise in CO with subsequent hyperinflation was related to a more negative Pes (R ϭ 0.72; P Ͻ 0.01). In conclusion, EL leads to a reduction in CO, which appears to be primarily related to increases in expiratory abdominal and intrathoracic pressure, whereas ELH resulted in an improved CO, suggesting that lung inflation has little impact on cardiac function. intrathoracic pressure; abdominal pressure; venous return; afterload