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Journal Article
Research Support, Non-U.S. Gov't
Cardiac output and pulmonary gas exchange at maximal exercise after atrial redirection for complete transposition.
European Heart Journal 1998 December
AIMS: To assess the determinants of exercise capacity and exercise oxygenation after atrial redirection for complete transposition.
METHODS AND RESULTS: At graded bicycle ergometry, including respiratory and arterial blood gas analyses, intra-arterial blood pressure recording, and cardiac output determination (dye-dilution technique), we tested 17 post-Mustard/Senning patients, 8.9-22.0 years old (mean 14.5, SD 4.0). Reference data were obtained by similar methods. At maximal exercise, oxygen uptake (29.6 ml x kg(-1) x min(-1)) and heart rate (167 beats x min(-1)) were low (P<0.001). Right-to-left shunts were detected in five patients. Arterial oxygen partial pressure and saturation fell in all subjects (P<0.0001). In 15/16 (94%) the alveolar-arterial oxygen partial pressure difference was > +2 SD. In 13/15 (87%) stroke volumes fell during exercise. Cardiac output per oxygen uptake was low (P<0.0001), which implies a high arteriovenous oxygen difference and a low mixed venous oxygen content at peak exercise.
CONCLUSION: The low exercise capacity was caused by a combination of low maximally attained heart rate and falling stroke volumes. The impaired arterial oxygenation may be caused by a combination of pulmonary ventilation/perfusion mismatch, a low mixed venous content and atrial shunting in some patients.
METHODS AND RESULTS: At graded bicycle ergometry, including respiratory and arterial blood gas analyses, intra-arterial blood pressure recording, and cardiac output determination (dye-dilution technique), we tested 17 post-Mustard/Senning patients, 8.9-22.0 years old (mean 14.5, SD 4.0). Reference data were obtained by similar methods. At maximal exercise, oxygen uptake (29.6 ml x kg(-1) x min(-1)) and heart rate (167 beats x min(-1)) were low (P<0.001). Right-to-left shunts were detected in five patients. Arterial oxygen partial pressure and saturation fell in all subjects (P<0.0001). In 15/16 (94%) the alveolar-arterial oxygen partial pressure difference was > +2 SD. In 13/15 (87%) stroke volumes fell during exercise. Cardiac output per oxygen uptake was low (P<0.0001), which implies a high arteriovenous oxygen difference and a low mixed venous oxygen content at peak exercise.
CONCLUSION: The low exercise capacity was caused by a combination of low maximally attained heart rate and falling stroke volumes. The impaired arterial oxygenation may be caused by a combination of pulmonary ventilation/perfusion mismatch, a low mixed venous content and atrial shunting in some patients.
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