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Evolution of Blood Gas Analysis - Focusing on the Source of I m paired O 2 Supply to the Tissue Ellis Jacobs, Ph.D, DABCC, FACB Associate Professor of Pathology, NYU School of Medicine Director of Pathology, Coler-Goldwater Hospital and Nursing


  1. Evolution of Blood Gas Analysis - Focusing on the Source of I m paired O 2 Supply to the Tissue Ellis Jacobs, Ph.D, DABCC, FACB Associate Professor of Pathology, NYU School of Medicine Director of Pathology, Coler-Goldwater Hospital and Nursing 14/ 11/ 2013 Facility

  2. Agenda Part 1  Why measure blood gases  Overview of acid-base disturbances  Use of the Acid- Base Chart Part 2 (Today)  Full value of the p O 2 assessment via  Oxygen uptake, Oxygen transport, Oxygen release  Why a measured saturation is the best  Assessment of tissue perfusion - Lactate

  3. 3 The traditional picture Oxygen  Traditionally, p O 2 (a) has uptake been the sole parameter used for evaluation of patient ? Oxygen oxygen status transport ? Oxygen release ? Tissue oxygenation

  4. 4 The traditional picture Oxygen  Traditionally, p O 2 (a) has uptake been the sole parameter used for evaluation of patient Oxygen oxygen status transport  For a complete evaluation of the oxygen status, it is necessary to consider lactate Oxygen and all parameters involved release in oxygen uptake, transport, and release Tissue oxygenation

  5. 5 Example of a flowchart [ Adapted from different textbooks and Siggaard-Andersen, O et al. Oxygen status of arterial and mixed venous blood. Crit Care Med. 1995 Jul; 23(7): 1284-93.

  6. 6 Phase one: Oxygen uptake

  7. 7 p O 2 (a) – the key parameter  p O 2 (a) is the key parameter for evaluation of oxygen uptake in the lung  When the p O 2 (a) is low, the supply of oxygen to cells might be compromised

  8. 8 Conditions affecting p O 2 (a)  The amount of oxygen F O 2 ( I ) available  The degree of intra- and extrapulmonary shunting F Shunt  Hypercapnia, high blood p CO 2  The ambient pressure p ( am p)

  9. 9 F O 2 (I) – fraction of inspired oxygen  Oxygen diffuses from the alveoli into the blood O 2  The higher the oxygen O 2 O 2 content of the air, the O 2 higher p O 2 (a)  Breathing room air equals an F O 2 (I ) of 21 %  A patient breathing supplemental oxygen may have a p O2(a) as high as 400 mmHg (and the oxygen saturation is normal)

  10. Evaluation of PO 2 in Adult, Neonatal, and Geriatric Patients Breathing Room Air Arterial PO 2 (mmHg) Condition above 80 Normal for adult (< 60 y) above 70 Adequate for age > 70 y above 60 Adequate for age > 80 y 50 to 75 Normal neonatal at 5 min 60 to 90 Normal neonatal at 1-5 days 40 to 60/ 70/ 80 Moderate to mild hypoxemia below 40 Severe hypoxemia

  11. Evaluating Arterial Oxygenation in Patients Breathing O 2 -Enriched Air Lowest FI-O 2 (% ) Acceptable PO 2 (mmHg) 30 150 40 200 50 250 80 400 100 500 Patients with a lower PO 2 may be assumed to be hypoxic on room air.

  12. Estimated FI-O 2 of Air When Breathing 100% Oxygen from Nasal Cannula Rough estimate: For each L/min of oxygen flow, add 4% to the estimated FI-O 2 of air in the room, usually 21%. Example: What is the estimated FIO 2 of the air being inhaled by a person receiving 2 L/min oxygen from a nasal cannula?

  13. Goals of Oxygen Therapy  Treat hypoxemia  Decrease work of breathing  Hyperventilation typical response to hypoxemia.  Decrease myocardial work  Increased cardiac output is a mechanism to compensate for hypoxemia.

  14. 14 F Shunt FShunt is the fraction of venous blood not oxygenated when passing the pulmonary capillaries Examples of different types of shunt I ntrapulmonary respiratory I ntrapulmonary circulatory Cardiac shunt: shunt: shunt: • By some called true shunt • Also called ventilation- • I ncomplete oxygenation in • Heart defects allowing perfusion disturbance lung venous blood from left chamber of heart to enter • I ncomplete oxygenation in • I nsufficient blood perfusion right chamber lung of the lungs • Lung diseases with inflammation or edema that causes the membranes to thicken

  15. 15 F Shunt – measured vs calculated  Shunt is calculated with values from simultaneously drawn arterial and mixed venous samples  The mixed venous sample must be drawn from the pulmonary artery, as indicated in the illustration  A simpler and faster way to estimate F Shunt is from a single arterial sample  Assuming that the arterio-venous difference is normal, i.e. extraction of 5.1 mL O 2 per dL blood

  16. 16 Hypercapnia, high p CO 2  Strong hypercapnia significantly decreases alveolar p O 2 , a condition known as hypoventilatory hypoxemia  The hypoxemia develops because the alveolar gas equation dictates a fall in p O 2 (a); p O 2 (A) = p O 2 (air) – p CO 2 (A)/ RQ  At any given barometric pressure, any increase in alveolar p CO 2 (caused by hypoventilation) leads to a fall in alveolar p O 2 and therefore also in arterial p O 2

  17. 17 Oxygen uptake – a recap  The amount of oxygen F O 2 ( I ) available  The degree of intra- and extrapulmonary shunting F Shunt  Hypercapnia, high blood p CO 2  The ambient pressure p ( am p)

  18. 18 Phase two: Oxygen transport

  19. 19 c tO 2 – the key parameter  Oxygen content , c tO 2 is the key parameter for evaluating the capacity for oxygen transport  When c tO 2 is low, the oxygen delivery to the tissue cells may be compromised

  20. 20 Does c tO 2 / p O 2 correlate?  A multicenter study on 10079 blood samples [ 1]  c tO 2 / p O 2 correlation unpredictable  c tO 2 is almost independent of p O 2 , so full information is needed  E.g. p O 2 of 60 mmHg (8 kPa ) corresponds to a c tO 2 of 4.8 – 24.2 mL/ dL [ 1] Gøthgen IH et al. Variations in the hemoglobin-oxygen dissociation curve in 10079 arterial blood samples. Scand J Clin Lab Invest 1990; 50, Suppl. 203: 87-90

  21. 21 Oxygen content  The blood’s oxygen content, c tO 2 , is the sum of  Oxygen bound to hemoglobin and  Physically dissolved oxygen  98% of oxygen is carried by hemoglobin  The remaining 2% is dissolved in a gas form  c tO 2 normal range 18.8-22.3 mL/dL c tO 2 = s O 2 × c tHb × (1 – F COHb – F MetHb) + α O 2 × p O 2 α is the solubility coefficient of oxygen in blood

  22. 22 Conditions affecting c tO 2  The concentration of hemoglobin c tHb  The fraction of oxygenated hemoglobin F O 2 Hb  The arterial oxygen saturation s O 2  The presence of dyshemoglobins F COHb and F MetHb

  23. 23 Improving c tO 2  The oxygen content can be improved by the variable factors in the equation c tO 2 = s O 2 × c tHb × (1 – F COHb – F MetHb) + α O 2 × p O 2 blood increasing Dyshemoglobins: transfusion F IO 2 can be removed

  24. 24 Types of hemoglobin tHb Total hemoglobin HHb Reduced hemoglobin HbO 2 O 2 Hb Oxyhemoglobin O 2 COHb Carboxyhemoglobin MetHb Methemoglobin MetHb O 2 O 2  tHb is defined as the sum of COHb HHb+ O 2 Hb+ COHb+ MetHb O 2 HbO 2  COHb and MetHb are called dyshemoglobins because they are incapable of oxygen transport

  25. 25 Hemoglobin O 2  Hemoglobin consists of 4 identical subunits Fe 2+  Each subunit contains an iron atom, Fe 2+ Fe 2+  Each iron can bind to one O 2 O 2 oxygen molecule, O 2 Fe 2+  Oxygen binding is cooperative Fe 2+  Typical reference range is O 2 12-17 g/ dL

  26. 26 Carboxyhemoglobin  Causes of raised COHb: CO  Increased endogeneous production of CO  Breathing air polluted with CO (carbon-monooixde CO CO poisoining)  CO’s affinity to Hb is 210 times higher than that of O 2  The blood turns cherry-red, CO but is not always evident  COHb is normally less than 1-2 % but in heavy smokers up to 10 %

  27. 27 Endogeneous increase in COHb  Hemolytic condition leads to heme catabolism and thus increased production of CO [ 1]  Hemolysis induced increase in COHb can be up to 4 % but 8.3 % is also reported [ 2]  Slight increase in COHb is also a feature of a inflammatory disease, and is thus also seen in critically ill patients [ 3] [ 1] Higgins C. Causes and clinical significance of increased carboxyheomoglobin. www.acutecaretesting.org . Oct 2005. [ 2] Necheles T, Rai U, Valaes T. The role of hemolysis in neonatal hyperbilirubinemia as reflected in carboxyhemoglobin values. Acta Paediatr Scand. 1976; 65: 361-67 [ 3] Morimatsu H, Takahashi T, Maeshima K et al. Increased heme catabolism in critically ill patients: Correlation among exhaled carbon monoxide, arterial carboxyhemoglobin and serum bilirubin IX { alpha} concentrations. Am J Physiol Lung Cell Mol Physiol. (EPub) 2005 Aug 12th doi: / 0.1152/ ajplung.00031.2005

  28. 28 COHb intoxication  COHb intoxication may be deliberate or accidential  In the US is accounts for 40,000 ED visits and between 5 and 6,000 death a year (2004) [ 1]  Sources of CO – common [ 2]  Fire, motor-vehicle exhaust and faulty domestic heating systems  Less commonly, gas ovens, paraffin (kerosene) heaters and even charcoal briquettes [ 1] Kao L. Nanagas K. Carbon monoxide poisoning. Emerg Clin N Amer 2004; 22: 985-1018 [ 2] Higgins C. Causes and clinical significance of increased carboxyheomoglobin. www.acutecaretesting.org . Oct 2005.

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