Anemia-Induced Tissue Hypoxia

• Anemia-induced tissue hypoxia:
  • Oxygen consumption (VO2) is typically constant, until oxygen delivery drops below a critical point
    • Resting VO2 ~250 ml/min
  • Oxygen delivery (DO2) = cardiac output x arterial oxygen content (CaO2)
    • CaO2 = 1.34 x Hgb x SaO2 + 0.0031 x PaO2
      • Normal CaO2 ~20 ml/dL
    • Normal DO2 = 5 L/min x 20 ml/dL = 1000 ml/min
  • Normal oxygen extraction is about 25-30%, which results in the normal SvO2 of 70-75%
    • When DO2 drops, the body’s initial compensatory mechanism is to increase oxygen extraction, as occurred in this case
      • In our patient, her CaO2 was 4 ml/dL, resulting in an approximate DO2 of 200 ml/min (assuming normal cardiac output)
    • Thus, even with 100% extraction, her VO2 needs would not be met
    • If this increased extraction is insufficient to meet VO2 needs, cardiac output rises
    • If these two compensatory mechanisms fail, then VO2 drops
      • In acute setting, VO2 needs can be reduced by intubating and paralyzing a patient
• Role of hyperbaric oxygen:
  • At room air, the amount of oxygen dissolved in blood is minimal: 0.0031 x 100 = 0.3 ml/dL
  • Increasing FiO2 to 100% increases PaO2, and can increase amount of dissolved oxygen to 1.5 ml/dL
  • Hyperbaric oxygen can further increase amount of dissolved oxygen to 6 ml/dL
    • Assuming a cardiac output of 5 L/min, with no hemoglobin, DO2 in this setting would be 300 ml/min, which is sufficient to meet resting VO2 needs (see attached case report)
  • While interesting intellectually, from a practical standpoint, the closest hyperbaric chamber to us is an outpatient center in Los Altos which clearly cannot support critically ill patients such as this one

(Christopher Woo MD, 2/15/11)