PubMed · 4565795
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D H Simmons, P S Kasnitz. 1972. Continuous positive-pressure ventilation.. https://doi.org/10.7326/0003-4819-77-2-327
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BACKGROUND: The management of neonates with complex congenital anomalies depends on careful interpretation of arterial blood gas values. Improved interpretation of these oxygen parameters may allow clinicians to avoid unexpected cardiovascular events. This study examined whether systemic oxygen delivery (DO2) can be maximized by the use of indices derived from oxygen saturation measurements in neonates with hypoplastic left heart syndrome. METHODS AND RESULTS: For the single-ventricle heart with both circulations in parallel, we used a previously developed computer simulation to obtain DO2 as a function of systemic arterial (SaO2) and venous (SvO2) oxygen saturation, arteriovenous oxygen difference (Sa-vO2), or pulmonary-to-systemic flow ratio (Qp/Qs). We also examined the oxygen excess factor, SaO2/Sa-vO2 (Omega). We found that (1) slight increases in SaO2 may be associated with large decreases in DO2. (2) Low values for SvO2 indicate low values for DO2. (3) Curves for Sa-vO2 and Qp/Qs are redundant in the data provided. (Qp/Qs, however, provides these data in more physiologically relevant terms.) (4) High values for Qp/Qs (>4) are associated with low DO2. (5) Estimating Qp/Qs from oxygen saturation measurements may result in errors when pulmonary venous oxygen saturation is not available. (6) Maximizing DO2 is extremely difficult using SaO2, SvO2, and Qp/Qs. (7) A linear relationship exists between Omega and DO2, and this linear relationship is not altered by changes in cardiac output. CONCLUSIONS: Patients with low SvO2 values require attention. Ideally, after reducing Qp/Qs to <1.5, Omega might be a better index to guide further therapy and maximize DO2. Interventions that increased Omega would be considered beneficial, whereas interventions that decreased Omega would be considered detrimental.
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Hereditary hemorrhagic teleangiectasia, or M. Osler (Osler-Weber-Rendu disease), is an autosomal dominant, systemic fibrovascular dysplasia. This may lead to increased liver blood flow from arteriovenous fistulas. A 45-year-old woman with a known M. Osler was admitted for liver transplantation. On admission, exertional dyspnea was the predominant symptom. Radiological investigations revealed multiple intrahepatic arteriovenous fistulas and consecutive high-output heart failure. Laboratory findings revealed remarkably elevated bilirubin and alkaline phosphatase. To alleviate the high-output cardiac failure, the hepatic artery was ligated. Fourteen months later, the patient presented again with increased levels of bilirubin and recurrent bleeding episodes from esophageal varices grade IV. The patient underwent liver transplantation and post-transplant recovery was excellent. A hyperdynamic circulatory state due to a hepatic M. Osler has been treated in several cases by ligation or embolization of the hepatic artery. This procedure, however, is recommended only for patients with normal liver function and carries a considerably risk of bile duct necrosis.