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In young, healthy people the alveolar–arterial P difference (A-aDO2) is small at rest, but frequently increases during exercise. Previously, investigators have focused on ventilation/perfusion mismatch and diffusion abnormalities to explain the impairment in gas exchange, as significant physiological intra-pulmonary shunt has not been found. The aim of this study was to use a non-gas exchange method to determine if anatomical intra-pulmonary (I-P) shunts develop during exercise, and, if so, whether there is a relationship between shunt and increased A-aDO2. Healthy male participants performed graded upright cycling to 90% while pulmonary arterial (PAP) and pulmonary artery wedge pressures were measured. Blood samples were obtained from the radial artery, cardiac output was calculated by the direct Fick method and I-P shunt was determined by administering agitated saline during continuous 2-D echocardiography. A-aDO2 progressively increased with exercise and was related to (r= 0.86) and PAP (r= 0.75). No evidence of I-P shunt was found at rest in the upright position; however, 7 of 8 subjects developed I-P shunts during exercise. In these subjects, point bi-serial correlations indicated that I-P shunts were related to the increased A-aDO2 (r= 0.68), (r= 0.76) and PAP (r= 0.73). During exercise, intra-pulmonary shunt always occurred when A-aDO2 exceeded 12 mmHg and was greater than 24 l min−1. These results indicate that anatomical I-P shunts develop during exercise and we suggest that shunt recruitment may contribute to the widened A-aDO2 during exercise.
During aerobic exercise, there is typically an impairment in pulmonary gas exchange as demonstrated by an increase in the alveolar–arterial pressure difference for oxygen (A-aDO2). Depending on the ventilatory response and magnitude of A-aDO2, exercise-induced arterial hypoxemia can develop (Dempsey & Wagner, 1999). Abnormalities in pulmonary gas exchange could result from ventilation/perfusion mismatch, diffusion impairment, right to left extra-pulmonary or intra-pulmonary (I-P) shunt. Current theories to explain the widened A-aDO2 during exercise include inadequate blood transit time in the lung (Dempsey et al. 1984), and a mismatch of secondary to pulmonary hypertension (Wagner et al. 1986).
Intra-pulmonary shunt has been previously dismissed as an explanation for the increased A-aDO2 during exercise because oxygen breathing (Dempsey et al. 1984; Torre-Bueno et al. 1985; Hammond et al. 1986; Wagner et al. 1986) and the multiple inert gas elimination technique (MIGET; Hopkins et al. 1994; Dempsey & Wagner, 1999; Rice et al. 1999) consistently failed to detect significant right to left mixed-venous shunt. However, precapillary gas exchange has been documented in both humans (Jameson, 1963, 1964; Sobol et al. 1963) and cats (Conhaim & Staub, 1980). Conhaim & Staub (1980) reasoned that because of precapillary gas exchange, 100% O2 breathing underestimates shunt. Similarly, MIGET may underestimate I-P shunt during exercise if precapillary gas exchange occurs. Large arteriovenous vessels have been demonstrated in normal post-mortem human lungs (Tobin & Zariquiey, 1950; Tobin, 1966), and we previously questioned whether these arterial–venous anastamoses could act as shunt vessels during exercise (Stickland et al. 2002). Whyte et al. (1992) have previously documented an increase in shunt during exercise using technetium-99m labelled albumin microspheres in normal control subjects, and Eldridge et al. (2004) demonstrated I-P shunts during exercise with agitated saline contrast echocardiography. Accordingly, the purpose of this investigation was to confirm that I-P shunts occur during exercise and if so, determine the relationship to A-aDO2 and haemodynamic responses. We hypothesized that the recruitment of anatomical I-P shunts contributes to the widened A-aDO2 during exercise.