Eva Strömvall Larsson1, Bengt O Eriksson. 1. Department of Paediatric Cardiology, The Queen Sivia Children's Hospital, Göteburg University, sweden. eva.stromvall-larsson@vgregion.se
Abstract
OBJECTIVE: To assess the haemodynamic regulation at rest and during exercise in Fontan patients at a long-term follow-up. DESIGN: Cardiac output was measured with the dye-dilution technique. We examined 15 out of the surviving 20 patients operated upon in Göteborg between 1980 and 1991. Their mean age was 26.4 years. Four patients had to be excluded due to technical reasons. RESULTS: Median maximal oxygen uptake was 1.47 l/min, corresponding to 21.9 ml/kg/min. Cardiac output was lower than expected at all exercise levels, presumably due to a reduced pulmonary blood flow. The median maximal cardiac output value was 8.0 l/min. Stroke volume index was 33 ml/m (2). The subjects compensated for the reduced cardiac output with an increased arteriovenous oxygen difference. They had a normal increase in arterial blood pressure. This was achieved by an increase in total peripheral resistance. CONCLUSION: The low maximal exercise capacity was due to a reduced cardiac output and a reduced pulmonary blood flow. This was compensated for by an increased arteriovenous oxygen difference
OBJECTIVE: To assess the haemodynamic regulation at rest and during exercise in Fontan patients at a long-term follow-up. DESIGN: Cardiac output was measured with the dye-dilution technique. We examined 15 out of the surviving 20 patients operated upon in Göteborg between 1980 and 1991. Their mean age was 26.4 years. Four patients had to be excluded due to technical reasons. RESULTS: Median maximal oxygen uptake was 1.47 l/min, corresponding to 21.9 ml/kg/min. Cardiac output was lower than expected at all exercise levels, presumably due to a reduced pulmonary blood flow. The median maximal cardiac output value was 8.0 l/min. Stroke volume index was 33 ml/m (2). The subjects compensated for the reduced cardiac output with an increased arteriovenousoxygen difference. They had a normal increase in arterial blood pressure. This was achieved by an increase in total peripheral resistance. CONCLUSION: The low maximal exercise capacity was due to a reduced cardiac output and a reduced pulmonary blood flow. This was compensated for by an increased arteriovenousoxygen difference
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