Issue StoriesPitfalls, Perils, and Pearls of Pulse Oximetryby Patricia Carroll, RRT, RN, BC, CEN, MS Clinicians who take pulse oximetry readings at face value do so at their own risk.
In the past decade since pulse oximetry has become as common at the bedside as thermometers and blood pressure cuffs, SpO2 measurements have been called the fifth vital sign. As a result, many clinicians take pulse oximetry readings at face value, which could be more dangerous than not monitoring SpO2 at all. Potential Pitfalls in Pulse Oximetry At baseline, only 35% of nurses, 39% of physicians, and 76% of respiratory therapists knew that the statement pulse oximetry is a method for continuous noninvasive measurement of arterial oxygenation and ventilation was false. Forty percent of nurses, 35% of physicians, and 79% of respiratory therapists were aware that body position and ambient light can affect readings. And 39% of nurses, 46% of physicians, and 48% of respiratory therapists believed that spot checks of pulse oximetry readings are as helpful in assessing a patients oxygenation status as the evaluation of continuous monitoring over time, a statement not supported by the literature. Areas in which baseline knowledge was high included knowing that significant hypoxemia is likely to occur during patient transport (96% correct), vasoconstriction and low pulse pressure can limit the ability to detect hypoxemia with pulse oximetry (95% correct), and patients are at increased risk for desaturation during invasive procedures (97% correct). Several months after the educational program, the overall mean percentage of correct responses increased from 66% to 82% for all disciplines combined. While the clinicians knowledge improved, it would be interesting for this study to be replicated to see if increasing clinicians knowledge enhanced patient outcomes.
Pulse Oximetry Perils for Patients and Clinicians DeWitt describes a case from several years ago. A man had an anterior approach for a C-5 discectomy, developed swelling, and required reintubation in the PACU (post-anesthesia care unit). Anesthesia orders said the patient should remain intubated for 48 hours. However, the next morning, the medical doctor ordered immediate extubation, and the patient had stridor. The medical records over the next 10 hours read like a textbook case of impending hypercarbic respiratory failure, DeWitt says. The patient became confused and combative, and with every combative episode, the nurses gave lorazepam or midazolam. The patient ultimately arrested, and while the code was short and successful, the first arterial blood gas had a PaCO2 of 117 mmHg and a PaO2 of 45 mmHg. The patient suffered diffuse anoxic encephalopathy and was unable to return to work. The nurses defense rested on their frequent charting of pulse oximeter values of 92% to 93%. Clearly, the nurses lack of understanding of the role pulse oximetry should play as one part of an entire patient assessment, and their reliance on pulse oximetry alone as the key factor in assessing the patients pulmonary status in this case were below an acceptable standard of care. However, the actions of these nurses are consistent with the findings in the project reported in the American Journal of Critical Care1 in which only 38% of clinicians knew that pulse oximetry did not provide any information about a patients ventilatory status. Still, DeWitt would rather see a pulse oximeter used than abandoned. In another case, he explains, a 42-year-old woman was breathless after a hernia repair. Her PaO2 on room air was 46 mmHg, and her PaCO2 was 29 mmHg. She was not transferred to intensive care, and no one even placed a pulse oximeter on her finger to monitor her hypoxemia. She ultimately expired as a result of anoxic encephalopathy, and the defendant pulmonologist testified he didnt believe a pulse oximeter was necessary.
Pulse Oximetry Pearls From the Bedside Assess the site where the probe will be placed to make sure it is warm and has proximal pulses and brisk capillary refill. These quick assessments indicate perfusion to the probe site, which is critical for accuracy. Avoid sites distal to an automatic blood pressure cuffwhen it inflates, blood flow to the sensor will be cut off, causing the pulse oximeter to alarm. This can decrease nurses vigilance if they automatically attribute an alarm to an inflated cuff. Check the patients temperature (and understand the relationship between the oxygen-hemoglobin bond and body temperature). If the patient is hypothermic, the bond will be tighter, meaning less efficient oxygen delivery at the tissue level. In these patients, you will want to maintain the SpO2 at a higher level than in patients who are febrile. When body temperature rises, the bond is loosened, meaning better oxygen delivery at the tissue level. These patients can usually tolerate a lower SpO2. Rotate probe sites as your facility protocol or manufacturer recommends. When placing the probe on the patient, be sure the photodetector and the light emitting diode are properly aligned. Sarah Perry, RN, CCRN, MA, of Memorial Medical Center in Las Cruces, NM, echoes DeWitts concerns and confirms the results of the AJCC study.1 She says, The common misconception is that if the SpO2 is good, then the patient is doing all right. Lots of nurses (and a few doctors) Ive spoken with dont give much thought to the fact that O2 saturation doesnt tell us a thing about the patients CO2. Sometimes this results in a patient who is in big trouble while everyone focuses on the fact that the O2 saturation is just fine. She also offers these tips: If your patient is on a cardiac monitor, compare the heart rate from the ECG with the pulse rate reported by the pulse oximeter. If the numbers are not consistent, you probably do not have adequate perfusion to the probe site. If the patients fingers and toes are cold and vasoconstricted, move the sensor to the earlobe for a more accurate reading. Remember not to turn the patient to the side on which the sensor is placed. It not only is uncomfortable but also can result in inaccurate readings. You May Not Know
Methemoglobinemia may be caused by a genetic deficiency in the enzyme cytochrome b5 reductase, and presents as cyanosis in an infant with no signs of hypoxia. It can also occur after exposure to chemicals such as nitrites and benzene and therapeutic agents such as nitric oxide, Lidocaine, and sodium nitroprusside (Nipride). Sulfhemoglobinemia has been associated with long-term use of metoclopramide2 and exposure to dimethyl sulfoxide (DMSO). The widespread availability of pulse oximetry has been a major advance in monitoring patients with potential or actual oxygenation impairment. However, a SpO2 value cannot be taken at face value; it must be evaluated in the context of a complete patient assessment. Respiratory therapists can take the lead in replicating the AJCC1 study in their facilities, to identify knowledge needs across all clinical disciplines and provide education to enhance clinicians understanding of this important tool. Patricia Carroll, RRT, RN,BC, CEN, MS, is the owner of Educational Medical Consultants in Meriden, Conn, and is the Health Care Coordinator for Shelter NOW, a homeless shelter in Meriden, Conn. Reference |
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