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The physiology of cyanotic congenital heart disease Tadahito KATO 1 , Atsushi KAWAGUCHI 2 1Department of Intensive Care Medicine, Pediatric Critical Care Medicine, Tokyo Women's Medical University 2Department of Pediatrics, St. Marianna University School of Medicine pp.363-374
Published Date 2022/4/1
DOI https://doi.org/10.11477/mf.3102200972
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Cyanotic congenital heart disease (CCHD) is a highly diverse anatomical and hemodynamic entity. Basic physiology can be applied to improve the understanding of the complex hemodynamics. It is not easy to determine the optimal level of SaO2 in patients with CCHD, but it is important to assess whether the oxygen supply is adequate to meet the oxygen demand of the tissues in each condition. Oxygen delivery (DO2) is mainly regulated by arterial oxygen saturation (SaO2), hemoglobin concentration (Hb), and cardiac output (CO). In patients with decreased SaO2, the Hb, and CO can act as compensatory mechanisms to preserve DO2. In single ventricle physiology with parallel circulation, SaO2 is determined by the pulmonary venous oxygen saturation (SpvO2), systemic venous oxygen saturation (SsvO2), and pulmonary to systemic blood flow ratio (Qp/Qs). While an increase of Qp/Qs leads to an increase in SaO2, it may also cause a decrease in DO2 due to decreased systemic blood flow. SsvO2 is an important indicator of DO2. A decrease in SsvO2 is critical, especially for these patients since it directly affects SaO2, thereby further decreasing DO2. Therefore, to maximize DO2, it is necessary to balance Qp/Qs and prevent anemia and low cardiac output.


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電子版ISSN 2186-7852 印刷版ISSN 1883-4833 メディカル・サイエンス・インターナショナル

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