Oxyhaemoglobin | ABG Interpretation - MedSchool
Sign up to start your free trial of MedSchool Premium!Get Started
 
ABG Interpretation
 
 
ABG Interpretation
 
 
Bookmark
Oxyhaemoglobin refers to the percentage of haemoglobin that is bound to oxygen.
 

Oxyhaemoglobin

 
 
Bookmark

Overview

  • Oxyhaemoglobin refers to the percentage of haemoglobin that is bound to oxygen.
      • Normal Range

      • >90%

Reduced Oxyhaemoglobin

  • The level of haemoglobin saturated by oxygen may be reduced in the context of reduced oxygen, right shift of the oxygen saturation curve, displacement of oxygen by carbon dioxide, or in the setting of haemoglobinopathies.
    • Causes of Reduced Oxyhaemoglobin

    • Reduced Environmental Oxygen

    • High altitude
    • Hypoventilation

    • CNS - drugs, trauma, encephalopathy, motor neurone disease, Guillain-Barré
    • Muscular / neuromuscular - myaesthenia, paralytics, myopathy, fatigue, malnutrition
    • Airway obstruction - foreign body, asthma, COPD, bronchiectasis
    • Decreased compliance - interstitial lung disease
    • Chest wall abnormalities
    • Ventilation / Perfusion Mismatch

    • Physiological shunt - atelectasis, pulmonary oedema, pneumonia, ARDS
    • Anatomical shunt - cardiac shunt e.g. tetralogy of Fallot
    • Dead space - asthma, COPD, pulmonary embolus, heart failure
    • Other

    • Right shift of the oxygen dissociation curve - acidaemia, hyperthermia, high 2,3-DPG
    • Carbon monoxide poisoning
    • Haemoglobinopathy - methaemoglobinaemia, foetal haemoglobin

Oxygen Dissociation Curve

    • Oxygen Dissociation Curve
    • The oxyhaemoglobin dissociation curve describes the relationship between PaO₂ and HbO₂:
    • At high PaO₂ (e.g. at the alveolar-capillary membrane) oxygen readily binds to haemoglobin.
    • At low PaO₂ (e.g. at systemic capillaries) oxygen is readily released from haemoglobin.
  • As the curve shifts to the left, oxygen will more readily bind to haemoglobin. As the curve shifts to the right, oxygen will more readily be released from haemoglobin.
    • Causes of Left Shift

    • Alkalaemia (Bohr effect)
    • Hypothermia
    • Decreased 2,3-DPG
    • Causes of Right Shift

    • Acidaemia (Bohr effect)
    • Hyperthermia
    • Increased 2,3-DPG
Last updated on February 7th, 2020
 
----------------------------------------------------------------------------------------------------------------------------------------------------------------------------
 
 

Read More...

 Andersen L, Mackenhauer J, Roberts J, Berg K, Cocchi M, Donnino M. Etiology and Therapeutic Approach to Elevated Lactate Levels. Mayo Clin Proc. 2013;88:1127-1140.
Beasley R, McNaughton A, Robinson G. New look at the oxyhaemoglobin dissociation curve. The Lancet. 2006;367:1124-1126.
 Bellomo R. Bench-to-bedside review: lactate and the kidney. Critical Care 2002;6(4):1. Berend K, de Vries A, Gans R. Physiological Approach to Assessment of Acid-Base Disturbances. N Engl J Med. 2014;371:1434-1445. Brenner BE. Alveolar-arterial oxygen gradients. Ann Emerg Med. 1980;9:648-648. Brindley PG, Butler MS, Cembrowski G, Brindley DN. Falsely elevated point-of-care lactate measurement after ingestion of ethylene glycol. Canadian Medical Association Journal 2007;176(8):1097-9. Donnino MW, Carney E, Cocchi MN, Barbash I, et al. Thiamine deficiency in critically ill patients with sepsis. Journal of critical care 2010;25(4):576-81. Gore DC, Jahoor F, Hibbert JM, DeMaria EJ. Lactic acidosis during sepsis is related to increased pyruvate production, not deficits in tissue oxygen availability. Annals of surgery 1996;224(1):97. Kraut JA, Madias NE. Lactic acidosis. N Engl J Med. 2014; 371: 2309-2319. Levraut J, Ciebiera JP, Chave S, Rabary O, et al. Mild hyperlactatemia in stable septic patients is due to impaired lactate clearance rather than overproduction. Am J RespirCrit Care Med. 1998; 157(4 Pt 1):1021-6. Levy B, Gibot S, Franck P, Cravoisy A, et al. Relation between muscle Na+ K+ ATPase activity and raised lactate concentrations in septic shock: a prospective study. The Lancet 2005;365(9462):871-5. Marino PL. Marino's the ICU Book. Fourthition. ed. Philadelphia: Wolters Kluwer Health/Lippincott Williams & Wilkins; 2014. McCarter FD, Nierman SR, James JH, Wang L, et al. Role of skeletal muscle Na+–K+ ATPase activity in increased lactate production in sub–acute sepsis. Life sciences 2002;70(16):1875-88. Moreau R, Hadengue A, Soupison T, Kirstetter P, et al. Septic shock in patients with cirrhosis: hemodynamic and metabolic characteristics and intensive care unit outcome. Critical care medicine 1992;20(6):746. Perriello G, Jorde R, Nurjhan N, Stumvoll M, et al. Estimation of glucose-alanine-lactate-glutamine cycles in postabsorptive humans: role of skeletal muscle. American Journal of Physiology-Endocrinology and Metabolism 1995;269(3):E443-50. Phypers B, Pierce JT. Lactate physiology in health and disease. Continuing education in Anaesthesia, critical care & pain. 2006 Jun 1;6(3):128-32. Stacpoole PW. Lactic acidosis. Endocrinol Metab Clin North Am 1993 Jun; 22(2) 221-45.
Tunney P, Chinnan NK. Serum Lactate in Intensive Care: Practical Points and Pitfalls. inflammation. 2016;6:7.
 Vary TC. Sepsis-induced alterations in pyruvate dehydrogenase complex activity in rat skeletal muscle: effects on plasma lactate. Shock 1996;6(2):89-94. Venkatesh B, Morgan T, Garrett P. Measuring the lactate gap. The Lancet 2001;358(9295):1806.
Feedback