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Effect of acute increases in pulmonary vascular pressures on exercise pulmonary gas exchange

¹Faculties of Physical Education and Recreation, ²Medicine and Dentistry, and ³Rehabilitation Medicine, University of Alberta, Edmonton, Alberta; and ⁴Department of Critical Care Medicine, Thunder Bay Regional Health Sciences Centre, Thunder Bay, Ontario, Canada

Submitted 23 November 2005 ; accepted in final form 23 February 2006

The purpose of this study was to determine the effect of acute increases in pulmonary vascular pressures, caused by the application of lower-body positive pressure (LBPP), on exercise alveolar-to-arterial PO₂ difference (A-aDO₂), anatomical intrapulmonary (IP) shunt recruitment, and ventilation. Eight healthy men performed graded upright cycling to 90% maximal oxygen uptake under normal conditions and with 52 Torr (1 psi) of LBPP. Pulmonary arterial (PAP) and pulmonary artery wedge pressures (PAWP) were measured with a Swan-Ganz catheter. Arterial blood samples were obtained from a radial artery catheter, cardiac output was calculated by the direct Fick method, and anatomical IP shunt was determined by administering agitated saline during continuous two-dimensional echocardiography. LBPP increased both PAP and PAWP while upright at rest, and at all points during exercise (mean increase in PAP and PAWP 3.7 and 4.0 mmHg, respectively, P < 0.05). There were no differences in exercise oxygen uptake or cardiac output between control and LBPP. Despite the increased PAP and PAWP with LBPP, A-aDO₂ was not affected. In the upright resting position, there was no evidence of shunt in the control condition, whereas LBPP caused shunt in one subject. At the lowest exercise workload (75 W), shunt occurred in three subjects during control and in four subjects with LBPP. LBPP did not affect IP shunt recruitment during subsequent higher workloads. Minute ventilation and arterial PCO₂ were not consistently affected by LBPP. Therefore, small acute increases in pulmonary vascular pressures do not widen exercise A-aDO₂ or consistently affect IP shunt recruitment or ventilation.

pulmonary circulation; ventilation; arteriovenous anastomoses; pulmonary shunt; pulmonary edema

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