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

Abstract

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.

Exercise-induced Arteriovenous Intrapulmonary Shunting in Dogs

“…No dog was found to have an intracardiac shunt during postmortem examination, which, combined with the isolated lung data demonstrating 25-to 50-m microspheres in the pulmonary venous outflow, indicates that the conduits allowing microspheres to bypass the pulmonary microcirculation in the intact animal were I-P arteriovenous pathways, and not of cardiac origin. Consistent with previous human exercise studies (1)(2)(3), these data confirm that large-diameter (Ͼ 25 m) I-P arteriovenous pathways are recruited with exercise.…”

Intense hypoxic cycle exercise does not alter lung density in competitive male cyclists

“…This uncoupling of EVLW and disrupted gas exchange (further supported by McKenzie et al 1999) points to an alternate mechanism of exercise-induced arterial hypoxaemia. Several candidate mechanisms exist, including reduced pulmonary diffusing capacity, inadequate hyperventilation, ventilation/perfusion mismatch, reduced red cell transit time in the pulmonary capillaries, a temperature and pH induced rightward shift in the oxyhaemoglobin dissociation curve (reviewed in Dempsey and Wagner 1999) or intrapulmonary shunt (Stickland et al 2006). However, it is also possible that an undetected disruption of the alveolarcapillary membrane did occur in our subjects and contributed to the demonstrated impairment in gas exchange.…”

Note technique : validation des outils de monitorage du débit cardiaque

“…La précision et la résolution n'en ont pas besoin. Le principe de Fick énoncé dès 1870 [3], est toujours considéré comme la meilleure mesure du DC au laboratoire de physiologie [4]. En pratique clinique, en dehors de situations très particulières de chirurgie cardiaque permettant l'utilisation de la circulation extracorporelle ou de bague Doppler interne [5,6], un étalon du DC manque le plus souvent.…”