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Patient Care

The Balance Between Assessment and Monitoring

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As medical technology continues to advance and assessment tools become smaller, cheaper and more practical for use in the field, we are faced with the challenge of determining where these tools fit within our overall patient assessment.

In trying to emphasize the importance of a proper physical exam, it is often said that paramedics must “treat the patient and not the monitor.” This conventional wisdom is beginning to change, with one example being STEMI bypass programs that involve altering patient care based largely on what is seen on the cardiac monitor.

Furthermore, the 2010 American Heart Association guidelines recommend against routine supplemental oxygen for acute coronary syndrome because of the risks that are now recognized and likely result in part from free radical formation. Specifically, supplemental oxygen is not recommended for patients who are not short of breath, have an oxygen saturation of at least 94%, and are not showing signs of heart failure or shock.1

This increasing emphasis on these previously downplayed assessment findings requires a shift in our thinking where we will need to, at times, trust our monitor.

In a discussion with colleagues around this shift in thinking, it was suggested the monitor is a good tool, but you never want to be the paramedic who withholds oxygen from a patient who is cyanotic based on a high oxygen saturation level.

Having heard so many times about treating the patient and not the monitor, everyone seemed to agree. It certainly sounded like a nice idea, but it is one that must be carefully assessed. We must first exclude from the discussion any potential issues with the quality of the reading being obtained. For this, it is important that we examine the plethysmograph or pleth waveform from the oxygen saturation probe.

The most important component of this waveform for our purposes is the amplitude, which would be low if there is poor signal strength. Assuming there is a good waveform and the monitor is functioning properly, what would cause a patient to present with central cyanosis but also a high oxygen saturation? This question is more difficult to answer, but taking the time to work through the possibilities is an interesting exercise.

We should begin by briefly reviewing the normal physiology and essential components of respiration and oxygenation.

This begins with having adequate levels of oxygen in ambient air. Normally air consists of mainly nitrogen with approximately 21% oxygen. The movement of the diaphragm is responsible for decreasing pressure in the chest so that air travels down the pressure gradient and enters the lungs.

Upon reaching the alveoli where gas exchange takes place, it is essential there is sufficient surface area of thin respiratory membranes for gas exchange to take place. Fick’s Law reminds us of the importance of these membranes being thin and not obstructed by fluid. The pulmonary capillaries must be adequately perfused with hemoglobin-rich blood that can enter the lungs and become saturated with oxygen. Finally, there must be sufficient circulation of blood to deliver oxygen to tissues. Deficiencies in any of these components can leave a patient without adequate oxygenation.

If you were to ask what would cause a patient to present with central cyanosis as well as an erroneously high oxygen saturation, the first answer that you will likely receive is carbon monoxide poisoning. If we consider for a moment what causes cyanosis, we can quickly see how this will not be true. Cyanosis is due to deoxyhemoglobin, but in carbon monoxide poisoning, the hemoglobin is bound, just not to oxygen. This lack of deoxyhemoglobin and the presence of carboxyhemoglobin, means patients with carbon monoxide poisoning do not normally present with cyanosis.2

Another answer to this question is that patients with anemia may appear cyanotic but have a high oxygen saturation. To assess this possibility, we must recall that cyanosis is due to the deoxygenated hemoglobin. Patients with anemia have low levels of hemoglobin, so they actually may never become cyanotic because they cannot have a high enough concentration of deoxygenated hemoglobin in their blood to display the blue color.3 Even when their overall oxygen levels are decreasing, their oxygen saturation levels may remain high since the small amount of hemoglobin they have will be saturated. This is a worthwhile consideration when interpreting oxygen saturation readings, but it does not meet the type of patient we are trying to find.

At the other end of the spectrum, a patient with polycythemia could have cyanosis with only mild hypoxia.4 Because these patients have so much hemoglobin available, it may not all be saturated under normal conditions. Since the pulse oximeter is measuring the saturation of hemoglobin, the readings will be lower despite an otherwise normal arterial oxygen content. While this patient would have a low oxygen saturation along with cyanosis, it would not normally be due to hypoxemia. This is another interesting consideration when interpreting oxygen saturation, but it is not what we are trying to find.

If none of these will cause a patient with cyanosis to present with a falsely high oxygen saturation, maybe something with the reading, rather than the patient’s condition, could cause this. Nail polish, dirty fingers, poor perfusion and motion artifact are all possibilities we might consider. These should all be identifiable in the oxygen saturation waveform (the pleth waveform),5 which should make the astute clinician skeptical of a potentially unreliable reading. Specifically, poor perfusion or signal strength will be indicated by a low amplitude waveform while motion artifact will appear as a jagged waveform with a wandering baseline.

Another possibility worth considering, which also involves poor perfusion, is Raynaud’s phenomenon. A full description of this condition is beyond the scope of this discussion, but it involves episodic excessive vasoconstriction in the fingers and toes in response to stress or cold. This is normally symmetrical and can lead to cyanosis in the affected area.6 Given the poor peripheral perfusion, the oxygen saturation waveform is also likely to be poor. Even if perfusion was sufficient for a reliable reading, the oxygen saturation would be expected to be low, corresponding appropriately to the peripheral cyanosis. Since that would involve cyanosis presenting with a low oxygen saturation, that is not what we are looking for.

Let us consider for a moment that there was the uncommon patient with unilateral Raynaud’s. If you placed the oxygen saturation probe on the unaffected side, you may obtain a high oxygen saturation reading on the monitor along with peripheral cyanosis in the patient’s other hand. This is close but not quite the patient we are seeking, since the initial question was about a patient with central cyanosis and a high oxygen saturation. The spirit of the question also related to inappropriately withholding supplemental oxygen from someone who needed it, so we will need to continue our search.

After working through all of these possibilities, we are forced to shift our search toward more obscure conditions. This leads us to methemoglobinemia, which is an uncommon condition that most of us are not familiar with. Hemoglobin normally contains iron in the reduced, or ferrous, form (Fe2+). In this form, hemoglobin can combine with oxygen to transport it to the tissues. If the hemoglobin loses an electron and the iron becomes oxidized to the ferric form (Fe3+), it is no longer capable of oxygen transport. This form of hemoglobin is called methemoglobin.7

Under normal conditions, some hemoglobin is continually being converted to methemoglobin, but this is kept to around 1% by specialized enzyme systems. Cytochrome b5 reductase is the most important of these.8 The precise mechanisms are beyond the scope of this article, but these enzyme systems are able to reduce the iron (Fe3+) back to the functional form (Fe2+). When these systems are not functioning, or their capacity is exceeded, methemoglobin can rise above safe levels. When these levels reach 15% to 20%, the patient is likely to present with cyanosis or a brown coloration.8

It is important to be clear on the precise effects of these rising levels of methemoglobin. Recall that hemoglobin is a tetramer that has four iron molecules. Some of these will be directly affected by the conversion to the ferric (Fe3+) state, while others in the same hemoglobin molecule will remain in the ferrous (Fe2+ or functional) form. The non-functional parts of the hemoglobin will not be able to carry oxygen, but this is only part of the problem in methemoglobinemia. In addition to the direct impairment of hemoglobin due to the inability of the ferric form to transport oxygen, the otherwise functional ferrous heme groups’ ability to unload oxygen also becomes impaired.9 High levels therefore cause a left shift of the oxyhemoglobin dissociation curve because of this impaired unloading of oxygen at the tissues.

Though rare, this could be caused by a variety of agents such as lignocaine, nitroglycerin, metoclopramide or nitrites.10 In adults, it is most commonly caused by exposure to volatile nitrites due to inhalant abuse.10 In infants, it can be caused by topical benzocaine (sold under the trade name Orajel in the United States).11–13 Infections are another cause in this age group.14,15 Infants are particularly vulnerable to methemoglobinemia since they have relatively low cytochrome b5 reductase levels.16

Patients with methemoglobinemia will typically present with tachypnea, tachycardia and cyanosis.10 With traditional pulse oximetry, there is often an unreliable low reading in patients with mild methemoglobinemia and an unreliable high reading in patients with high-level methemoglobinemia.7, 17 There is no prehospital treatment for this condition available to most prehospital providers so treatment is generally supportive. Upon arrival at hospital, the patient may receive charcoal if the substance was ingested. Methylene blue may also be administered depending on the level of methemoglobin.10 Some specialist prehospital hazardous-materials teams may also be able to initiate this treatment.

The preceding discussion has two primary implications. The first implication, specific to the use of oxygen saturation monitoring, is that it is very unlikely you will ever come across a patient who presents with cyanosis and a high oxygen saturation with a good waveform on a functioning monitor. New technology has also now led to more sensitive probes that can detect methemoglobin.18 This technology is available on both monitors currently in the marketplace.

The second and more important implication is the importance of considering the underlying pathophysiology as it relates to the assessments we perform. Understanding the pathophysiology is the only way to truly understand the clinical findings. Even when technology helps us to assess patients, we must understand what these devices actually assess or measure.

Though it will be uncommon to see a case of methemoglobinemia, this structured examination of the possibilities helps prompt a review of the important physiology as it relates to oxygen saturation monitoring.

Through this discussion, we have reviewed a number of important considerations for using oxygen saturation as a part of overall patient assessment. It is only a single assessment, but when used with the underlying physiology and limitations in mind, it can offer crucial guidance for patient care.

Acknowledgement
We are grateful to Dr. Clayton Kazan, Cathryn MacKinnon and Dr. Steven Parrillo for their assistance with this article. We also appreciate the thorough review from an anonymous reviewer, which further helped to strengthen the article.

References
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12. Chung NY, Batra R, Itzkevitch M, et al. Severe methemoglobinemia linked to gel-type topical benzocaine use: a case report. J Emerg Med, 2010; 38(5):601–6.
13. Skold A, Cosco DL, Klein R. Methemoglobinemia: pathogenesis, diagnosis, and management. South Med J, 2011; 104(11):757–61.
14. Luk G, Riggs D, Luque M. Severe methemoglobinemia in a 3-week-old infant with a urinary tract infection. Crit Care Med, 1991; 19(10):1325–7.
15. Yano SS, Danish EH, Hsia YE. Transient methemoglobinemia with acidosis in infants. J Pediatr, 1982; 100(3):415–8.
16. Curry SC. “Hematologic consequences of poisoning.” In Shannon MW, Borron SW, Burns M. Haddad and Winchester’s Clinical Management of Poisoning and Drug Overdose, 4th ed. Philadelphia: Saunders; 2007.
17. Eisenkraft JB. Pulse oximeter desaturation due to methemoglobinemia. Anesthesiology, 1988; 68:279–282
18. Feiner JR, Bickler PE. Improved accuracy of methemoglobin detection by pulse CO-oximetry during hypoxia. Anesth Analg, 2010; 111(5):1160–1167.

Christopher R. Foerster, PCP, is a primary care paramedic with Lambton EMS in Ontario, Canada and a paramedic tutor for the University of Queensland. He can be reached at foerster@alumni.utoronto.ca.

Anthony G. Mendoza, BA, EMT-P, is an EMT/paramedic educator at UCLA’s Center for Prehospital Care. He works the field in Los Angeles and Ventura counties. He may be contacted at anthonymendoza@ucla.edu.
 

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