Prior to the late 1950s, it was assumed that the single most important factor in sustaining life was maintaining a normal blood pressure. In critically ill patients, all efforts were centered on keeping the systolic blood pressure at 100 mm Hg or more.1 With the availability of arterial blood-gas (ABG) measurement in the 1960s, it was realized that other factors were equally (if not more) important. Clinicians discovered that there were certain levels of oxygen and carbon dioxide that the body could not tolerate. As blood-gas data became more readily available, it became obvious that just having the data was not enough. Accurate interpretation and clinical correlation were equally important if the proper course for care was to be followed.
Most clinicians would probably agree that having high-quality data is a prerequisite for delivering high-quality patient care. Westgard2 has questioned how we can distinguish reliable from unreliable data. He suggests that, unfortunately, data take on a certain level of credibility by the mere fact that they are printed. While today’s blood-gas analyzers have come a long way in terms of speed, accuracy, and sophistication, they are not foolproof. It is still up to the clinician to perform the most important tasks in the process. Those would include an independent review of the data and correlation of the data with the patient’s condition.
Measurements and Calculations
The newest analyzers can perform calibrations and process data in 2 minutes or less, and they can do this with a fraction of the amount of blood needed by older machines. Several types of analyzers can even be carried in one hand to the bedside to provide point-of-care testing.
Regardless of the type of analyzer used, pH, Pco2, and Po2 are measured values. Other reported values, such as oxygen saturation, bicarbonate (HCO3), and base excess, are calculated using the measured values and other factors. Other, less commonly reported values also are calculated. These could include total carbon dioxide, oxygen content, or a serum HCO3 level corrected for a Pco2 of 40.
If measured values for oxygen saturation and other hemoglobin values such as carboxyhemoglobin and methemoglobin are desired, they are made with the use of a CO-oximeter.
While measured values are generally considered more reliable than calculated values, there are times when either may be inaccurate. The conflicts observed between oxygen saturation measured by pulse oximetry (Spo2) and the oxygen-saturation value calculated from an ABG are a case in point. Disparities between these parameters can be a source of confusion to those who care for the patient. The numbers on the oximeter’s display are influenced by the quality of the blood flow and the integrity of the sensor. Other factors3 that contribute to inaccurate readings include severe anemia; the presence of fetal hemoglobin, methemoglobin, or carboxyhemoglobin; dyes, such as methylene blue; probe placement on a dependent limb with poor venous return; and vasopressors used in the management of shock.4
Similarly, the calculated oxygen saturation reported by the analyzer could be inaccurate. ABG analysis assumes that the patient has a normal hemoglobin affinity for oxygen. It also assumes a normal level of the dysfunctional hemoglobins.5 These assumptions may not always be accurate. Metabolism also may account for a disparity. Immature leukocytes consume significant amounts of oxygen. Fox et al6 have described a leukemia patient whose white blood cell count was 27,600 per cubic millimeter (27.6 x 109/L). He demonstrated a decline in Pao2 from 130 mm Hg to 58 mm Hg in 2 minutes. This type of patient may demonstrate a falsely low Po2 and oxygen saturation, while the oxygen saturation displayed on the monitor reflects normal oxygen levels.
Preanalytical and Analytical Errors
|Figure 1. Bad ABG data.|
Analysis of blood specimens begins with a sample of blood being aspirated by or introduced into a machine (or into a cartridge that is then inserted into the machine). Errors can occur during this analytical phase, but they are relatively uncommon if the analyzers are properly maintained. If cartridges are used, they may release their calibrating solutions prematurely. Cartridges also can be overfilled or underfilled. A failed calibration or electrode, a clot in the sample, or a problem with a membrane also could account for an error. If an error does occur during this analytical phase, it is very obvious. An error code or message appears somewhere in a display, alerting the analyst, and either no data or very limited data are reported (Figure 1).
The potential for error in the preanalytical phase was outlined by Mottram and Blonshine7 and includes six main problem areas:
- collection of demographic data (incorrect patient identification number, name, sex, or ordering physician);
- patient conditions (position, activity, ventilator settings, oxygen, and delivery device);
- failure to observe (recent suction, ventilator changes, or repositioning);
- sample sites (site location and manner of sampling, such as line versus puncture);
- sample error (venous sampling, air bubbles, flush solution, or heparin); and
- delayed analysis.
After a blood specimen has been obtained, it is handled by the staff and transported to the analyzer. The time that passes until the blood is actually introduced into the analyzer, the methods used to collect and prepare the blood for analysis, and the way in which the sample is transported could all contribute to erroneous results.8,9 If the sample is transported to the laboratory via pneumatic tube system, for example, values can be adversely affected to a greater degree. McKane et al10 showed that using a pneumatic tube system to get the samples to the laboratory in a more expeditious manner exaggerated the values of Po2 and Pco2. Errors made during the preanalytical phase are suggested as some of the most common causes of inaccurate data.7
The ABG sample must be collected anaerobically in a syringe made from either glass or high-density propylene. If the sample is obtained from an arterial line, consider the length of the line and withdraw enough blood to eliminate the possibility of dilution by the flush solution. Values are far less likely to be influenced by heparin dilution if the sample is obtained by arterial puncture and collected in a commercially available plastic syringe. The syringe’s inner barrel is already coated with a dry form of heparin (or the needle hub may have a heparin crystal already placed inside). Unless a very small sample (less than 2 mL) is obtained, values are unlikely to be altered using this method.9 Of the values reported, however, Pco2 is the measurement most likely to be affected by heparin dilution and will fall significantly if the blood sample is not large enough. Po2 will rise, but to a lesser degree. The pH remains unchanged due to the buffering potential of oxyhemoglobin and plasma proteins.11
Any air bubbles in the sample must be expelled immediately. Exposure to air will alter Pco2, Po2, and pH. The partial pressure of ambient air is approximately 150 mm Hg. Exposure to air and the process of diffusion will cause a decrease in Po2 if the value is greater than 150 mm Hg. If the Po2 is less than 150 mm Hg, the Po2 will decrease.9
Samples should be analyzed within 10 to 15 minutes from the time they are drawn. If the analysis will be delayed, the sample should be placed on ice to slow the metabolic process (which has been shown to alter results). Diffusion of oxygen through plastic syringes may be a consideration where calculation of a shunt fraction is requested and the fraction of inspired oxygen (FIo2) is 100%. Smeenk et al12 recommend that the sample be drawn using a glass syringe and then be kept on ice.
|Figure 2. PO2 too high.|
As Westgard2 has noted, it should be clear that not all data that are printed are possible. Consider the example shown in Figure 2. An arterial oxygen level of 354 mm Hg is within the realm of possibility in human blood, but the reported FIo2 is 35%. Could the addition of 35% oxygen have accounted for this level of hyperoxia? An air bubble could not have caused this, since the arterial oxygen tension of room air is only 150 mm Hg. It is likely that a mistake was made in the reporting of the FIo2. An analyzer error is another possible explanation for this questionable result, but a simple mathematical test could have uncovered this mistake.
This test, used to estimate the patient’s Pao2, is to consider the ratio of Pao2 to FIo2.13 If the FIo2 is approximately 20% and the Pao2 is 100, the Pao2/FIo2 ratio is 5. In the preceding case, multiplying the FIo2 by a factor of 5 would have shown that the highest Pao2 possible would have been 185 mm Hg. The rule of five also may be used to determine the relative severity of the patient’s degree of hypoxemia. If the FIo2 for a given patient is 80% and his Pao2 is 80, the ratio is 1. If the FIo2 is later decreased to 60% and the Pao2 is 50, the ratio is only 0.8. Relatively speaking, the patient has become more hypoxemic.
The relationship between pH, Pco2, and HCO3 has been shown to be very predictable. Malley14 has described how acute changes in Pco2 and pH are closely related and, in fact, predictable (if metabolic status remains normal). Using accepted normal values for pH (7.4) and Pco2 (40 mm Hg), he suggests that if Paco2 decreases by 1 mm Hg, pH should increase by 0.01. Being able to perform this quick mental check of ABG data can be helpful. Malley gives the example of a patient whose ABG results were reported as a pH of 7.6, a Paco2 of 30 mm Hg, a base excess of 1 mEq/L, and an HCO3 of 23 mEq/L. Application of the formula shows that the value for pH is actually too high, given the values for the other parameters. The pH should have been 7.5, but there was a transcription error that caused it to be misreported.
Detecting Venous Samples
Inadvertent venous sampling occurs when a vein overlies, or is in proximity to, an intended arterial-puncture site. This could easily occur if arterial puncture is attempted in the patient’s groin because the femoral vein is posterior to the femoral artery. Patients also could have anatomical anomalies where veins are adjacent to the more commonly used sites like the radial or brachial artery. In either case, a small amount of venous blood will contaminate the arterial sample. It has been estimated that if 10% of a sample comes from a venous source, the Pao2 can drop by as much as 25%.15
Venous sampling should be suspected if the analysis shows slight hypercarbia and hypoxemia. Unfortunately, these conditions are common in critically ill patients. Data from another source should be used for comparison. If the patient’s Spo2 was 90% when the sample was drawn, but the oxygen saturation is reported as 75%, there is a good chance that the sample is not arterial.
Another method used to rule out venous sampling is to rely on the intuitive powers of the person evaluating the data. Suppose the Po2 of the sample is in the 30s or 40s. If this were taken from an artery, it would indicate severe hypoxemia. Next, look at the pH, base excess, and HCO3 levels. If these values are only slightly different from normal arterial values, then the sample must be venous. A severely hypoxic patient could not have a nearly normal acid-base balance.
The postanalytical phase of blood-gas analysis requires the clinician to make an observation of the patient and determine whether the data confirm suspicions about the patient’s status. If there is any question, that sample should be reanalyzed. A repeat puncture of another site also should be considered. The best data are the data that are most reliable. They come not only from well-maintained analyzers, but also from well-trained analysts.
Mark Grzeskowiak, RRT, is clinical supervisor, adult critical care, Long Beach Memorial Medical Center, Long Beach, Calif. For more information, contact [email protected].
- Eckenhoff JE. Foreword to the first edition. In: Shapiro BA, Harrison RA, Cane RD, Kozlowski-Templin R, eds. Clinical Application of Blood Gases. 4th ed. Chicago: Year Book Medical Publishers Inc; 1989:vii.
- Westgard JO. Good Data Wanted—Bad Data Should Not Apply (The STARD Initiative). Available at: [removed]www.westgard.com/essay49htm[/removed]. Accessed November 11, 2006.
- Shapiro BA, Harrison RA, Cane RD, Kozlowski-Templin R, eds. Clinical Application of Blood Gases. 4th ed. Chicago: Year Book Medical Publishers Inc; 1989:233-4.
- Malley WJ. In: Pederson D, ed. Clinical Blood Gases: Application and Noninvasive Alternatives. Philadelphia: WB Saunders; 1990:290.
- P02 and calculated values for saturated oxygen (s02). Article 714180-00A. In: ISTAT System Manual. Revised April 16, 2001. East Windsor, NJ: ISTAT Corp.
- Fox MJ, Brody JS, Weintraub LR. Leukocyte larceny: a case of spurious hypoxemia. Am J Med. 1979;67:742-6.
- Mottram CD, Blonshine SB. Blood gas QC for the future. AARC Times. November 2005:30-5.
- AARC Clinical Practice Guideline: Sampling for Arterial Blood Gas Analysis. Respir Care. 1992;37:913-17.
- Shapiro BA, Harrison RA, Cane RD, Kozlowski-Templin R, eds. Clinical Application of Blood Gases. 4th ed. Chicago: Year Book Medical Publishers Inc; 1989:262-3.
- McKane MH, Southorn PA, Santrach PJ, Burritt MF, Plevak DJ. Sending blood gas specimens through pressurized transport tube systems exaggerates the error in oxygen tension measurements created by the presence of air bubbles. Anesth Analg. 1995; 81:179-82.
- 11. Drake MD, Peters J, Teague R. The effect of heparin dilution on arterial blood gas analysis. West J Med. 1984;140:792-3.
- 12. Smeenk FW, Janssen JD, Arends BJ, et al. Effects of four different methods of sampling arterial blood and storage time on gas tensions and shunt calculations in the 100% oxygen test. Eur Respir J. 1997;10:910-3.
- 13. Shapiro BA, Harrison RA, Cane RD, Kozlowski-Templin R, eds. Clinical Application of Blood Gases. 4th ed. Chicago: Year Book Medical Publishers Inc; 1989:83.
- 14. Malley WJ. In: Pederson D, ed. Clinical Blood Gases: Application and Noninvasive Alternatives. Philadelphia: WB Saunders; 1990:151.
- 15. Malley WJ. In: Pederson D, ed. Clinical Blood Gases: Application and Noninvasive Alternatives. Philadelphia: WB Saunders; 1990:28.