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Influence of expiratory loading and hyperinflation on cardiac output during exercise

¹Department of Internal Medicine; Mayo Clinic and Foundation, Rochester, Minnesota 55905; and ²Physiological Imaging, Department of Radiology, University of Iowa Hospital, Iowa City, Iowa 52242

Submitted 22 July 2003 ; accepted in final form 30 December 2003

Patients with 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-cmH₂O 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 at 40 and 70% of peak work. At rest and during exercise, EL resulted in an increase in Pes and Pg (7-18 cmH₂O; P < 0.05) and a decrease in CO (from 5.3 ± 1.8 to 4.5 ± 1.4, 12.2 ± 2.2 to 11.2 ± 2.2, and 16.3 ± 3.3 to 15.2 ± 3.2 l/min for rest, 40% peak work, and 70% peak work, respectively; P < 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 = -0.58 and -0.60; P < 0.01), whereas the rise in CO with subsequent hyperinflation was related to a more negative Pes (R = 0.72; P < 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

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