Intern report PEARLS 2/11: oxygen dissociation curve, methemoglobinemia, and hemolytic anemias!

Going to start with an approach to hemolytic anemias, even though this came up later in the case!

Approach to hemolytic anemias

  • A great review by our very own Goop, Pat Cornett, and LT:
  • One approach is to think intravascular vs extravascular:
    • Intravascular: MAHAs (DIC, TTP, HUS, shear stress from mechanical valves), AIHA, toxin-mediated lysis, complement mediated (eg PNH)
    • Extravascular: liver, spleen
  • Another approach is intrinsic vs extrinsic:
    • Intrinsic: think anatomically!
      • membrane defects (eg hereditary spherocytosis) à smear with spherocytes
      • enzyme deficiencies (eg G6PD, pyruvate kinase, and a slew more!) à smear with bite cells, Heinz bodies
      • hemoglobinopathies (eg sickle cell disease) à smear with sickled cells, target cells
    • Extrinsic: usually acquired!
      • MAHAs à smear with schistocytes
      • AIHA à smear with spherocytes; +direct coombs test
      • Infections (eg malaria, babesia)
      • Liver disease
      • Hypersplenism
    • Lab workup:
      • For all, expect: indirect hyperbili, elevated retics, high LDH, low haptoglobin
      • To differentiate further: get a smear, coags, and other tests depending on clinical suspicion (eg coombs, hgb electrophoresis, infectious w/u, G6PD level, etc)


And, a review of the oxyhemoglobin dissociation curve, co-oximetry, and methemoglobinemia (mostly copied from previous AM report PEARLs, found here!)


Oxyhemoglobin dissociation curve:

*First, remember that hypoxia and hypoxemia are different! Hypoxia = low O2 sat; hypoxemia = low PaO2

 O2 dissoc

Note the curve is sigmoidal, so changes in PaO2 have very little effect on O2 sat when PaO2 is >60 (i.e. PaO2 increase from 60-100 translates to O2 sat going from 90 to 98%), however, for PaO2s from 20-60, there is a more dramatic drop in O2 sat. For O2sats <70%, accuracy is questionable!


  • Methemoglobinemia: PaO2 is too high for a given pulse ox reading.
  • Carbon monoxide poisoning: falsely high % sat on pulse ox (because pulse ox can’t differentiate carboxyHgb from oxyHgb)


Quick word on co-oximetry: order this separate from your standard ABG/VBG! Measures 4 different hemoglobin derivatives (using different wavelengths): oxyhemoglobin, deoxyhemoglobin, carboxyhemoglobin, and methemoglobin


Patient-related factors for inaccurate pulse ox readings (didn’t discuss this today, but helpful!)

  • Abnormal hemoglobin
  • Vasoconstriction (hypoperfusion, hypothermia) – move the pulse ox to the earlobe!
  • Anemia with Hgb<5
  • High A1c (overestimates O2sat)
  • Venous congestion (low O2sat because of venous pulsation)
  • Nail polish


  • Cause: congenital vs acquired (in adults, often the latter)
    • For the acquired causes, can be from medication overdose/poisoning, OR normal doses in patients with certain enzyme deficiencies (like G6PD). Major categories of drugs to think of: dapsone, topical anesthetics (e.g. benzocaine), inhaled nitric oxide, aniline and its derivatives (e.g. Aniline dyes)
  • Symptoms: can be asymptomatic at low levels. When there are symptoms, they include headache, fatigue, dyspnea, and lethargy. At high levels >40%, can have respiratory depression, AMS, shock, seizures and death (admit to ICU!)
  • Pulse ox and PaO2: suspect methemoglobin and order co-oximetry when the pulse ox shows an O2sat <90 but PaO2 on ABG is >70!
    • O2 sat on pulse ox decreases by about half the methemoglobin percentage up to a methemoglobin level of 20%. At higher levels, the O2 sat by pulse ox plateaus at about 85%
  • Treatment:
    • 1) remove the offending agent (for acquired methemoglobinemia)
    • 2) consider methylene blue when level is >30% (***BUT should not be used in patients with known G6PD deficiency since reduction of methemoglobin by methylene blue depends on NADPH generated by G6PD!). Response is rapid!
    • 3) If very severe: give adjunctive blood transfusion, exchange transfusion, and/or hyperbaric oxygen



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