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1 Department of Internal Medicine, Mayo Clinic and Foundation, Rochester, MN, USA
2 Physiological Imaging, Department of Radiology, University of Iowa Hospitals, Iowa City, IA, USA
* To whom correspondence should be addressed. E-mail: johnson.bruce{at}mayo.edu.
Patients with obstructive lung disease are exposed to expiratory loads 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 expiratory load (EL), alone, and in combination with voluntary hyperinflation (ELH), on pulmonary pressures (esophageal, Pe, and gastric, Pg) and cardiac output (CO) in 7 healthy subjects. CO was determined using an acetylene method at rest, 40 and 70% of peak work (Wpeak). At rest and during exercise EL resulted in an increase in Pe 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% Wpeak and 70% Wpeak, 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 (SV) with a tendency for SV to fall further with prolonged EL. There was a negative correlation between CO and the increase in expiratory Pe and Pg with EL (R=-0.58 and -0.60, p<0.01), while the rise in CO with subsequent hyperinflation was related to a more negative Pe (R=0.72, p<0.01). In conclusion, EL leads to a reduction in CO that appears primarily related to increases in expiratory abdominal and intrathoracic pressure, while voluntary hyperinflation during EL resulted in an improved CO suggesting lung inflation has little impact on cardiac function.
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