Co Oximetry
Co Oximetry
Elizabeth Mack
Pediatr. Rev. 2007;28;73-74
DOI: 10.1542/pir.28-2-73
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focus on diagnosis
Co-oximetry
Elizabeth Mack, MD* Each of the dyshemoglobins has a
unique absorption spectrum, and the
Introduction concentration can be derived from
A co-oximeter is a blood gas analyzer the Beer-Lambert law by measuring
that, in addition to the status of gas absorption at four specific wave-
tensions provided by traditional lengths. Normal values are reported
Author Disclosure blood gas measurements, measures as a percentage of normal hemoglo-
Dr Mack did not disclose any concentrations of oxygenated hemo- bins and include oxyHb, 45% to 70%;
financial relationships relevant to globin (oxyHb), deoxygenated he- deoxyHb, 0% to 5% (arterial) or 15%
moglobin (deoxyHb or reduced to 40% (venous); MetHb, 0% to
this article.
Hb), carboxyhemoglobin (COHb), 1.5%; and COHb 0% to 2.5% (non-
and methemoglobin (MetHb) as a smoker) or 1.5% to 10% (smoker).
percentage of the total hemoglobin The total hemoglobin level is age-
concentration in the blood sample. dependent in children. An oxygen
Use of co-oximetry is indicated when saturation gap is defined as a differ-
a history is consistent with toxin ex- ence of more than 5% between the
posure, hypoxia fails to improve with saturation that is calculated from a
the administration of oxygen, there is standard arterial blood gas analyzer
a discrepancy between the PaO2 on a and the saturation that is measured
blood gas determination and the ox- by co-oximetry. The presence of an
ygen saturation on pulse oximetry oxygen saturation gap is consistent
(SpO2), or the clinician suspects with the presence of dyshemoglo-
other dyshemoglobinemias such as bins.
methemoglobinemia or carboxyhe- Accurate collection techniques
moglobinemia. are necessary for appropriate inter-
Pulse oximetry measures the oxy- pretation of co-oximetry. Co-
gen saturation (SaO2) of hemoglobin oximeter gases require a minimum of
in arterial blood or the average 0.3 mL of blood (venous or arterial).
amount of oxygen bound to each The blood must be collected in an
hemoglobin molecule. Blood gas an- air-free, heparinized syringe, be
alyzers calculate oxygen saturation mixed well, have the air bubbles re-
from the measured parameters PO2 moved, and be placed on ice.
and pH on the basis of standard
oxygen-dissociation curves. Unfor- Methemoglobinemia
tunately, pulse oximetry, a noninva- Methemoglobinemia is diagnosed
sive procedure, does not distinguish definitively by co-oximetry. Congen-
among the different types of hemo- ital defects in erythrocyte enzyme
globins. For example, in the case of systems may result in inherited met-
methemoglobinemia, pulse oximetry hemoglobinemia. More common
may read 88%, but desaturation can causes include drug effects (classi-
be demonstrated with co-oximetry, cally, local anesthetics such as lido-
recording 70% oxyHb and 30% caine or benzocaine), gastroenteritis
MetHb. resulting in nitrite production, expo-
sure to nitric oxide, or ingestion of
*Dr Mack wrote this article when she was a third- nitrite-containing well water. These
year resident at Palmetto Richland Hospital in compounds oxidize normal ferrous
Columbia, SC. She is now a pediatric critical care
fellow at Cincinnati Children’s Hospital, Cincinnati, (Fe⫹⫹) hemoglobin to the ferric
Ohio. (Fe⫹⫹⫹) form (ie, MetHb).
MetHb has no oxygen-carrying ca- the baseline COHb concentration ance, polycythemia, and cardiomeg-
pacity and is unable to unload oxy- found in healthy people. In patients aly. Chronic exposure often occurs in
gen into the tissues. afflicted with hemolytic anemias, smokers, who may have concentra-
Healthy persons should have 0% COHb can reach concentrations of tions of COHb up to 8% or even 10%
to 1.5% MetHb. Mild cyanosis oc- 8%. Values also may be elevated in immediately after a cigarette.
curs at levels below 10%, and symp- severe sepsis. Treatment of acute poisoning in-
toms of fatigue, dizziness, and nau- CO binds Hb with an affinity cludes oxygen administration (hy-
sea usually develop at concentrations 200 times that of oxygen and causes perbaric oxygen may be considered
above 20%. Concentrations higher a leftward shift in the oxygen- in specific cases) and the usual sup-
than 45% may result in tissue isch- hemoglobin dissociation curve, re- port of airway, breathing, and circu-
emia, leading to arrhythmias, sei- sulting in decreased oxygen delivery lation. Administering higher FIO2
zures, acidosis, and coma. Concen- and tissue hypoxia. CO also binds decreases the half-life of the COHb.
trations higher than 70% may be fetal Hb with greater affinity, making Room air results in a half-life of
fatal. Patients who have methemo- infants more vulnerable to its effects. 320 minutes, 100% oxygen causes a
globinemia may have the classic CO often is called the “great mim- half-life of 80 minutes, and adminis-
“chocolate-colored blood.” icker” because it produces flulike or tration of hyperbaric oxygen reduces
Treatment is indicated for pa- gastroenteritis-type symptoms; diag- the half-life to 25 minutes.
tients who have more than 30% nosis requires a high degree of suspi-
MetHb and includes removal of the cion. The cherry-red color of the skin
offending agent and administration described in textbooks rarely is seen. Sulfhemoglobinemia
of methylene blue, a cofactor of Pulse oximetry is not adequate to Sulfhemoglobinemia is a rare condi-
NADP-MetHb reductase. Methyl- diagnose CO poisoning because tion that may result from exposure to
ene blue increases the capacity of this COHb and oxyHb both absorb at sulfonamides, acetanilide, phenazo-
enzyme to reduce ferric iron concen- 660 nm with the same absorption pyridine, nitrates, trinitrotoluene,
trations and usually is administered coefficient, thus falsely elevating the and phenacetin. Sulfhemoglobin is
intravenously in doses of 1 to 2 mg/ SpO2 value. In addition, when a pa- unique because its presence is not
kg. Clinicians can expect MetHb tient who already has received sup- detected by co-oximetry. Unlike the
concentrations to fall in 1 to 2 hours. plemental oxygen presents to an other dyshemoglobins, sulfhemoglo-
If this decrease does not occur, the emergency department, his or her bin shifts the oxygen dissociation
dose may need to be repeated. How- COHb concentration by co- curve to the right, resulting in oxy-
ever, caution is advised at total doses oximetry may have normalized. gen being more readily available to
greater than 15 mg/kg because this Common symptoms of acute CO tissues. Sulfhemoglobinemia should
amount of methylene blue paradoxi- intoxication include headache, dizzi- be suspected when a patient who has
cally can cause methemoglobinemia. ness, weakness, nausea, confusion, cyanosis has a normal PaO2 and ele-
In refractory cases, exchange transfu- shortness of breath, and vision vated methemoglobin concentration
sion is recommended. changes. Severe poisoning may result by co-oximetry but does not respond
in dysrhythmias, hypotension, rhab- to methylene blue therapy. Treat-
Carbon Monoxide (CO) domyolysis, myocardial ischemia, ment involves administering oxygen
Poisoning cardiac or respiratory arrest, noncar- and discontinuing the offending
CO is a colorless, odorless, nonirri- diogenic pulmonary edema, seizures, agent.
tating gas produced by incomplete and coma. Late clinical effects (not
combustion of organic matter. CO seen for 2 to 40 d) involve delayed
poisoning is the most common cause neurologic sequelae, which may in-
of death by poisoning in the United clude any conceivable psychiatric or Suggested Reading
States. Sources of CO poisoning in- neurologic symptom. Kao LW, Nanagas KA. Toxicity associated
with carbon monoxide. Clin Lab Med.
clude house fires, car exhaust, indoor Effects of chronic exposure to CO
2006;26:99 –125
heaters, and stoves. Endogenous include headache, nausea, cerebellar Konig MW, Dolinski SY. Pulmonary and
production occurs during the degra- dysfunction, mood disorders, low critical care pearls. Chest. 2003;123:
dation of heme and contributes to birthweight, reduced exercise toler- 613– 616