Non-invasive blood gas interpretation
Lawrence Martin, M.D.

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4. Venous blood to check for CO or methemoglobin

Summary: If you suspect CO or methemoglobin toxicity, a venous blood sample will suffice to make the diagnosis, as venous and arterial values are the same.


All blood gas labs have a machine to measure pH, PaCO2 and PaO2, and to calculate (or allow for calculation of) the bicarbonate value. This is the "blood gas machine." In addition, many but not all labs also have anothermachine, called a co-oximeter (see Figure).

Blood gas machine & Co-oximeter

The co-oximeter is a machine separate from a blood gas analyzer and complimentary to it (see Figure). Every time a blood gas is done and it is important to know the SaO2 and/or the level of carbon monoxide (CO), a portion of the blood sample should be entered into the co-oximeter.

The co-oximeter can measure, on a small portion of the arterial blood sample, hemoglobin content (in grams/dl) and values related to hemoglobin binding: SaO2, %COHb, and %methemoglobin. From this information the arterial oxygen content (CaO2) can be calculated.

Carbon monoxide is a major cause of morbidity and mortality; in the U.S., each year there are 600 accidental deaths and 3000 suicides. CO is colorless and odorless, and poisoining can occur whenever there is incomplete combustion in a closed space. CO toxicity can mimic the flu, cause headaches and affect behavior in ways that may be difficult to diagnose.

CO affects tissue oxygen delivery in two ways: 1) it reduces arterial oxygen saturation by preventing oxygen binding to hemoglobin; and 2) it increases affinity for those oxygen molecules that do bind to hemoglobin, i.e., it causes a left shift of the oxygen dissociation curve.

Carbon monoxide is about 230 times more avid for hemoglobin than is oxygen. For every percent increase in COHb, there is a percent decreased in SaO2; the two together can never add up to more than 100%.

A partial pressure of CO only 1/230 that of oxygen will compete equally for hemoglobin binding sites. If PaO2 is 100 mm Hg and PaCO is only 0.43 mm Hg the blood will contain 50% oxyhemoglobin and 50% COHb. Obviously, it only takes tiny amounts of CO to induce poisoning.

There are several common misconceptions about diagnosing CO toxicity:

  • that the poisoned patient has "cherry red" skin color -- NOT TRUE; this sign is only evident at autopsy and only in some patients;
  • that arterial blood must be drawn to make the diagnosis -- NOT TRUE; a venous sample can be analyzed for CO in a co-oximeter; the value will be the same as in arterial blood;
  • that the PaO2 will be reduced -- NOT TRUE; CO toxicity does not affect PaO2, only the SaO2 (assuming the SaO2 is directly measured).

The result of these misconceptions can be a fatal error.

Even when the diagnosis is suspected, the physician may obtain an arterial sample, but only send it for "blood gas analysis," i.e. not for measurement in the co-oximeter. In this case the oxygen saturation will be calculated based on the measured PO2, which will be normal (unless the patient has concomitant lung disease). Since neither SaO2 nor CO is measured (both required the co-oximeter), the diagnosis WILL BE MISSED.

In fact, a much simpler test - sending a venous blood sample through the co-oximeter to directly measure CO -- would make the diagnosis (or rule it out).

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Methemoglobinemia (metHb) is much less common than CO toxicity, but the same principles apply: metHb will not affect PaO2, only the SaO2, but the SaO2 must be measured in the co-oximeter on an arterial blood sample. In lieu of this, one can directly measure methemoglobin on a venous sample, and the value will be just as accurate as on an arterial sample.

Patients susceptible to develop methemoglobinemia are those taking medications which can convert Fe+2 to FE+3 (which defines methemoglobin); the list of possible medications is large, but principally involves the nitrates and nitrates (e.g., coronary vasodilators).

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