Vol. 14 •Issue 7 • Page 36
Blood Gas Analysis
Putting CO-oximetry in Your Toolbox
Dysfunctional Hemoglobin May Be a Factor in More Cases Than You Think
Even though CO-oximetry is now integrated into many arterial blood gas analyzers, respiratory therapists working outside of trauma and critical care tend not to perform it routinely or be familiar with it.
In a survey conducted at the 2004 American Association for Respiratory Care International Respiratory Congress, 87 percent of the 430 RTs responding said there was a gap in understanding the benefits of integrated CO-oximetry in blood gas analysis.
Although it may not be needed as frequently as standard blood gas panels, CO-oximetry offers a more accurate assessment of a patient’s oxygenation status.
Understanding the differences and knowing when to order a CO-oximetry panel outside of critical care can make your respiratory protocols more effective and provide lifesaving answers quickly in some unexpected circumstances.
WHERE TO FIND IT
CO-oximetry uses a multi-wavelength spectrophotometer to measure the percentages of normal and abnormal or dysfunctional forms of hemoglobin (Hb) simultaneously in arterial blood. This indicates how much of the total Hb is functional and capable of carrying oxygen at a given time.
CO-oximetry is performed primarily in the emergency room, trauma unit and critical care units to detect and measure compromised forms of Hb such as carboxyhemoglobin (COHb) and methemoglobin (metHb) that prevent Hb from carrying a full load of oxygen.
Typical clinical applications of CO-oximetry include identification of carbon monoxide poisoning in suspected suicide attempts, detection of internal bleeding in cases where the patient appears unharmed externally but is unconscious and nonrespondent, or other clinical situations that alter Hb’s ability to carry oxygen.
Many of today’s blood gas analyzers include a CO-oximetry analyzer in some form, either side-by-side or fully integrated into the same sample and reagent pathway as the blood gas panel. Sample preparation requirements are the same as for blood gas — the blood needs to be anticoagulated, kept cold, and tested within a few minutes after the blood draw so that leukocytes don’t start breaking down the Hb or consuming the dissolved oxygen.
Fully integrated analyzers are becoming more common in point-of-care settings, as well as in critical care units and STAT labs. True integration has numerous advantages for the therapist and the patient, not least of which is the ability to perform both complete panels in just 60 seconds or so on a single arterial sample. Calibration and quality assurance/quality control procedures can be run once for the machine as a whole.
For analyzers without full integration, CO-oximetry requires a separate sample, as well as separate calibration and quality control procedures, but it still provides the rapid turnaround and response needed to deal with hypoxia cases that don’t respond to supplemental oxygen therapy.
The most important advantage of CO-oximetry is that it provides a definitive diagnosis of compromised or dysfunctional Hb states that are likely to be missed by relying on the more common pulse oximetry or arterial blood gas panel alone. (See Table)
COHb and metHb are the two most common dysfunctional forms of Hb. Carbon monoxide attaches strongly to the heme iron and blocks it from accepting new oxygen molecules. Sulfhemoglobin acts in a similar fashion. In metHb, the heme iron hasn’t been returned to its ferrous (Fe2+) state after releasing oxygen to the tissues, and it can’t attach another oxygen molecule.
Any one dysfunctional Hb subunit also prevents the other Hb subunits in the molecule from releasing or picking up new oxygen efficiently. Until it regenerates or is removed from the blood, it will lower the patient’s actual functional oxygen transport. Given that CO has a much higher affinity for hemoglobin than oxygen does, even relatively small percentages of COHb can cause large drops in functional oxygen transport that can’t be overcome easily even with 100-percent oxygen supplementation.
Contrary to popular assumption, pulse oximetry and blood gas aren’t good substitutes for CO-oximetry when there’s a chance that Hb may have been damaged or compromised. Blood gas derives its O2 saturation value from the partial pressure of O2 dissolved in plasma, rather than measuring oxygenated Hb directly. Pulse oximetry measures arterial O2 saturation (SpO2) by taking the ratio of oxyhemoglobin and deoxygenated Hb optical absorbances through a fingertip. Under normal circumstances, these measures correlate well with actual O2 saturation and therefore functional Hb.
But when dysfunctional Hb is present, blood gas SpO2 may appear near normal because plasma O2 concentration hasn’t changed. Pulse oximetry fails to distinguish between normal oxygenated Hb and some of the dysfunctional Hbs, notably COHb, and can show desaturation that stabilizes at about 85 percent regardless of the patient’s status.1 Blood gas and pulse oximetry results in this case may conflict with each other. Until CO-oximetry is performed, the blood gas or pulse oximetry result may be mistakenly deemed contaminated or inconclusive.
CO-OXIMETRY OUTSIDE THE CRITICAL CARE UNIT
Most commonly, CO poisoning and methemoglobinemia are first picked up in the emergency room or trauma unit during triage, often as the cause of admittance to the hospital. However, a number of infrequent but significant cases exist in which CO-oximetry has an important role outside these settings. Most obviously, it should be used to follow the effec-tiveness of respiratory and ventilation therapy in cases that were flagged COHb or metHb in triage, and to determine when the dysfunctional Hb levels are low enough to discontinue or cut back therapy.
Methemoglobinemia also can arise in the hospital after the patient has been admitted or during surgery or common respiratory procedures. It can greatly increase the risk of neurological and circulatory complications if not recognized and treated promptly.
Signs of compromised Hb often include cyanosis, lethargy, a tell-tale chocolate brown color of the blood that doesn’t redden on exposure to air, and patient nonresponsiveness to standard oxygen supplementation. As mentioned earlier, blood gas and pulse oximetry results that don’t match the patient’s condition or agree with each other are another sign of trouble.
In recent years, numerous case studies and several comprehensive reviews of induced Hb compromise have been reported during routine respiratory procedures such as bronchoscopy and intubation for ventilation.2-4 The patients had been stable prior to the procedures, and the cause of their sudden hypoxia wasn’t detected right away. Blood gas and pulse oximetry gave confusing results, and in each case considerable time passed — in one case more than a day — before the attending physician or RT realized CO-oximetry might hold the answers they were seeking. CO-oximetry detected elevated metHb levels in less than a minute, and appropriate therapy (O2 supplementation with or without intravenous methylene blue, depending on the level of metHb and the condition of the patient) was initiated.
Each of the case studies traced the syndrome back to the topical anesthetic spray used to prepare the patient for intubation. Lidocaine, benzocaine, and a large number of other anesthetic and analgesic drugs are known to compromise Hb oxygenation in a small but significant percentage of patients. Topical sprays are hard to dose consistently, and in these cases, the spray appeared to have been applied somewhat enthusiastically. After identifying the common cause, the hospitals revised their protocols and training to reduce the chance of overdose by sticking to the minimum recommended spray times and having the patient spit out any residue rather than swallow it.5
The fact that these are such common procedures in patients with multiple vulnerabilities may be a sign that induced methemoglobinemia is underdiagnosed and undertreated.
Several populations other than critical care patients are at increased general risk of methemoglobinemia or dyshemoglobinemia and may show some degree of reduced oxygen transport. They may not develop severe or acute hypoxia, but their underlying conditions can affect response to respiratory therapy and may make standard blood gas and pulse oximetry tests misleading.
• The elderly are particularly vulnerable to methemoglobinemia because Hb turnover efficiency decreases with aging liver and kidney function.
• Neonates, especially premature infants, have incompletely developed respiratory function. Their functional Hb is also still largely fetal Hb, which is gradually replaced by the adult form throughout childhood. Fetal Hb has a slightly different O2 saturation curve from the adult form, so both pulse and CO-oximetry may need adjustments to compensate.6
• Both adult and pediatric patients with sickle cell anemia often show functional oxygen transport a few percent lower than indicated by pulse oximetry and blood gas.7,8 Those being treated with hydroxyurea to reduce acute chest syndrome and painful crises also should be producing some fraction of fetal Hb, perhaps as much as 10 percent to 20 percent of their functional Hb.9,10
• Smokers tend to have an elevated COHb fraction.
• A small fraction of the general population has genetically dysfunctional cytochrome b5 reductase or abnormal Hbs other than sickle cell Hb.
How do you get CO-oximetry on the units when you need it? The first step is to locate the right machines. You may already have them as part of your freestanding blood gas unit(s) or point-of-care cartridge analyzers and just haven’t been using the CO-oximetry feature. If your blood gas analyzer doesn’t include CO-oximetry, you may need to order CO-oximetry results from your STAT lab or arrange to switch to an integrated blood gas/CO-oximetry unit.
The second step is to get the extra training you need to run CO-oximetry yourself or prepare the sample correctly for the lab. The hospital point-of-care coordinator should be able to guide you. For integrated blood gas/CO-oximetry analyzers, the differences are generally minimal and sometimes boil down to “select the CO-oximetry option, too.”
The third factor is communication. Any blood gas or CO-oximetry panels you run from a freestanding unit need to be recorded not only in the patient chart but reported to the central laboratory and/or hospital information system (LIS and/or HIS), both for patient tracking and for Clinical Laboratory Improvement Amendment ’88 and Joint Commission on Accreditation of Healthcare Organizations compliance. Most blood gas/CO-oximetry analyzers include some kind of software interface for automated communication to the LIS or HIS, but sometimes they require customization. The hospital’s point-of-care coordinator should be able to help you connect with the LIS or HIS either directly or by manual input for reporting.
Finally, seek professional resources. Clinical guidelines and white papers are available on all aspects of blood gas and CO-oximetry from the Clinical and Laboratory Standards Institute (formerly the National Committee for Clinical Laboratory Standards; www.nccls.org or www.clsi.org), American Association for Respiratory Care (www.aarc.org) or Society of Critical Care Medicine (www.sccm.org).
Dysfunctional Hb isn’t an incredibly common source of hypoxia outside of trauma or critical care, but it may be a factor in more of your cases than you think. Blood gas and pulse oximetry, while essential routine tools, can’t substitute for CO-oximetry in these cases. Recognizing situations when your patients may be vulnerable and considering CO-oximetry early in cases of acute suspected hypoxia or cyanosis can prevent life-threatening complications, simplify recovery, and reduce the workload on your staff.
1. Haymond S, Cariappa R, Eby CS, Scott MG. Laboratory assessment of oxygenation in methemoglobinemia. Clin Chem. 2005;51(2):434-44.
2. Rodriguez LF, Smolik LM, Zbehlik AJ. Benzocaine-induced methemoglobinemia: report of a severe reaction and review of the literature. Ann Pharmacother. 1994;28(5):643-9.
3. Ash-Bernal R, Wise R, Wright SM. Acquired methemoglobinemia: a retrospective series of 138 cases at two teaching hospitals. Medicine (Baltimore). 2004;83(5):265-73.
4. Wurdeman RL, Mohiuddin SM, Holmberg MJ, Shalaby A. Benzocaine-induced methemoglobinemia during an outpatient procedure. Pharmacotherapy. 2000;20(6):735-8.
5. Pasternack AS. A puzzling case of methemoglobinemia in the intensive care unit. Hospital Physician. Feb 2004;30-32,38.
6. Whyte RK, Jangaard KA, Dooley KC. From oxygen content to pulse oximetry: completing the picture in the newborn. Acta Anaesthesiol Scand Suppl. 1995;107:95-100.
7. Blaisdell CJ, Goodman S, Clark K, Casella JF, Loughlin GM. Pulse oximetry is a poor predictor of hypoxemia in stable children with sickle cell disease. Arch Pediatr Adolesc Med. 2000;154(9):900-3.
8. Needleman JP, Setty BN, Varlotta L, Dampier C, Allen JL. Measurement of hemoglobin saturation by oxygen in children and adolescents with sickle cell disease. Pediatr Pulmonol. 1999;28(6):423-8.
9. Fitzhugh CD, Wigfall DR, Ware RE. Enalapril and hydroxyurea therapy for children with sickle nephropathy. Pediatr Blood Cancer. 2005 Feb 9;in process (Epub ahead of print).
10. Teixeira SM, Cortellazzi LC, Grotto HZ. Effect of hydroxyurea on G gamma chain fetal hemoglobin synthesis by sickle-cell disease patients. Braz J Med Biol Res. 2003;36(10):1289-92.
Marc Schlessinger, BS, RRT-NPS, RPFT, is director of cardiorespiratory services and physical medicine for Frankford Hospital, Philadelphia.
Table: Analytes CO-oximetry Measures
• hematocrit (Hct)
• hemoglobin or total hemoglobin (Hb or tHb)
• oxygen saturation (SaO2) — the percentage of oxygen attached to Hb compared to the maximal Hb binding capacity
• oxyhemoglobin (O2Hb) — percentage of normal Hb currently bound to O2
• deoxygenated hemoglobin (HHb) — percentage of normal Hb not currently bound to O2 but capable of binding to it
• carboxyhemoglobin (COHb) — anything above 1 percent of tHb is considered a sign of CO poisoning
• methemoglobin (metHb) — anything above 3 percent of tHb indicates toxicity from drugs or other chemical sources