Abeer Rizvi1, Patricia Macedo2, Lydia Babawale2, Hannah C Tighe2, J Michael B Hughes3, James E Jackson4, Claire L Shovlin5. 1. 1 School of Medicine, Imperial College London. 2. 2 Respiratory Medicine, Imperial College Healthcare NHS Trust. 3. 3 Respiratory Sciences, National Heart and Lung Institute, Imperial College London. 4. 4 Imaging, Imperial College Healthcare NHS Trust; and. 5. 5 Cardiovascular Sciences, National Heart and Lung Institute, Imperial College London, London, United Kingdom.
Abstract
RATIONALE: PaO2 and SaO2 are commonly measured in respiratory practice, but arterial oxygen content (CaO2) refers to the volume of oxygen delivered to the tissues per unit blood volume. CaO2 is calculated from SaO2 and the hemoglobin concentration in blood, recognizing that each gram of hemoglobin can transport approximately 1.34 ml of oxygen when fully saturated. OBJECTIVES: To prospectively evaluate serial changes in CaO2 in humans, incorporating and excluding dynamic changes to oxygenation and hemoglobin parameters that may occur during life. METHODS: A cohort of 497 consecutive patients at risk of both hypoxemia and anemia were recruited. The patients had radiologically proven pulmonary arteriovenous malformations (PAVMs), which result in hypoxemia due to right-to-left shunting, and concurrent hereditary hemorrhagic telangiectasia, which placed them at risk of iron deficiency anemia due to recurrent hemorrhagic iron losses. Presentation SaO2 (breathing room air, by pulse oximetry), hemoglobin, red cell and iron indices were measured, and CaO2 calculated as SaO2 × hemoglobin × 1.34 ml/g. Serial measurements were evaluated in 100 cases spanning up to 32.1 (median, 10.5) years. RESULTS: Presentation CaO2 ranged from 7.6 to 27.5 (median, 17.6) ml/dl. CaO2 did not change appreciably across the SaO2 quartiles. In contrast, hemoglobin ranged from 5.9 to 21.8 g/dl (median, 14.1 g/dl), with a linear increase in CaO2 across hemoglobin quartiles. After PAVM embolization and an immediate increase in SaO2, hemoglobin fell and CaO2 was unchanged 1.6-12 (median, 4) months later. When hemoglobin fell because of iron deficiency, there was no change in SaO2. Similarly, when hemoglobin rose after iron treatment, there was no change in SaO2, and the expected CaO2 increment was observed. These relationships were not evident during pregnancy when hemoglobin fell, and PAVMs usually deteriorated: in pregnancy SaO2 commonly increased, and serial CaO2 values (incorporating hemodilution/anemia) more accurately reflected deteriorating PAVM status. An apparent fall in CaO2 with age in females was attributable to the development of iron deficiency. There was an unexplained increase in CaO2 with age in follow-up of males after embolization. CONCLUSIONS: Hemoglobin/CaO2 should be further incorporated into oxygenation considerations. More attention should be given to modest changes in hemoglobin that substantially modify CaO2.
RATIONALE: PaO2 and SaO2 are commonly measured in respiratory practice, but arterial oxygen content (CaO2) refers to the volume of oxygen delivered to the tissues per unit blood volume. CaO2 is calculated from SaO2 and the hemoglobin concentration in blood, recognizing that each gram of hemoglobin can transport approximately 1.34 ml of oxygen when fully saturated. OBJECTIVES: To prospectively evaluate serial changes in CaO2 in humans, incorporating and excluding dynamic changes to oxygenation and hemoglobin parameters that may occur during life. METHODS: A cohort of 497 consecutive patients at risk of both hypoxemia and anemia were recruited. The patients had radiologically proven pulmonary arteriovenous malformations (PAVMs), which result in hypoxemia due to right-to-left shunting, and concurrent hereditary hemorrhagic telangiectasia, which placed them at risk of iron deficiency anemia due to recurrent hemorrhagiciron losses. Presentation SaO2 (breathing room air, by pulse oximetry), hemoglobin, red cell and iron indices were measured, and CaO2 calculated as SaO2 × hemoglobin × 1.34 ml/g. Serial measurements were evaluated in 100 cases spanning up to 32.1 (median, 10.5) years. RESULTS: Presentation CaO2 ranged from 7.6 to 27.5 (median, 17.6) ml/dl. CaO2 did not change appreciably across the SaO2 quartiles. In contrast, hemoglobin ranged from 5.9 to 21.8 g/dl (median, 14.1 g/dl), with a linear increase in CaO2 across hemoglobin quartiles. After PAVM embolization and an immediate increase in SaO2, hemoglobin fell and CaO2 was unchanged 1.6-12 (median, 4) months later. When hemoglobin fell because of iron deficiency, there was no change in SaO2. Similarly, when hemoglobin rose after iron treatment, there was no change in SaO2, and the expected CaO2 increment was observed. These relationships were not evident during pregnancy when hemoglobin fell, and PAVMs usually deteriorated: in pregnancy SaO2 commonly increased, and serial CaO2 values (incorporating hemodilution/anemia) more accurately reflected deteriorating PAVM status. An apparent fall in CaO2 with age in females was attributable to the development of iron deficiency. There was an unexplained increase in CaO2 with age in follow-up of males after embolization. CONCLUSIONS: Hemoglobin/CaO2 should be further incorporated into oxygenation considerations. More attention should be given to modest changes in hemoglobin that substantially modify CaO2.
Authors: Claire L Shovlin; Ilenia Simeoni; Kate Downes; Zoe C Frazer; Karyn Megy; Maria E Bernabeu-Herrero; Abigail Shurr; Jennifer Brimley; Dilipkumar Patel; Loren Kell; Jonathan Stephens; Isobel G Turbin; Micheala A Aldred; Christopher J Penkett; Willem H Ouwehand; Luca Jovine; Ernest Turro Journal: Blood Date: 2020-10-22 Impact factor: 22.113