Pulse Oximetry Myths in Critical Care

Pulse Oximetry Myths in Critical Care: Separating Fact from Fiction

Dr Neeraj Manikath , claude.ai

Abstract

Pulse oximetry has become ubiquitous in modern critical care, often described as the "fifth vital sign." However, numerous misconceptions persist regarding its accuracy and limitations, particularly in anemia, carbon monoxide poisoning, and shock states. This review critically examines common myths surrounding pulse oximetry, explores the underlying physiological and technical principles, and provides evidence-based guidance for interpretation in challenging clinical scenarios. Understanding these limitations is essential for postgraduate trainees in critical care to avoid diagnostic errors and optimize patient management.

Keywords: Pulse oximetry, SpO₂, anemia, carbon monoxide poisoning, shock, oxygen saturation, critical care

---

Introduction

Since its introduction into clinical practice in the 1980s, pulse oximetry has revolutionized patient monitoring and become an indispensable tool in critical care medicine. The ability to non-invasively and continuously monitor arterial oxygen saturation (SpO₂) has improved patient safety and guided therapeutic interventions across diverse clinical settings.^1,2

However, the widespread availability and ease of use of pulse oximetry have paradoxically led to overconfidence in its reliability and misunderstanding of its fundamental limitations. Critical care practitioners frequently encounter clinical scenarios where pulse oximetry accuracy is compromised, yet common myths persist that can lead to misinterpretation and potentially harmful clinical decisions.^3,4

This review addresses three prevalent myths in critical care practice: the effects of anemia on pulse oximetry accuracy, the response to carbon monoxide poisoning, and performance in shock states. We provide evidence-based clarification of these misconceptions and practical guidance for optimal utilization in complex clinical situations.

---

Principles of Pulse Oximetry: A Brief Primer

Basic Physics and Technology

Pulse oximeters utilize spectrophotometry, exploiting the different light absorption characteristics of oxygenated and deoxygenated hemoglobin. Conventional pulse oximeters emit light at two wavelengths: red light (approximately 660 nm) and infrared light (approximately 940 nm).⁵

Deoxygenated hemoglobin (HHb) absorbs more red light, while oxygenated hemoglobin (HbO₂) absorbs more infrared light. The device calculates the ratio of pulsatile absorption at these wavelengths to determine the "functional" oxygen saturation:⁶

SpO₂ = HbO₂ / (HbO₂ + HHb) × 100

This calculation is critically important because it only accounts for hemoglobin capable of carrying oxygen, excluding dyshemoglobins such as methemoglobin (MetHb) and carboxyhemoglobin (COHb).

🔑 Pearl: Conventional pulse oximeters measure "functional saturation," not "fractional saturation." This distinction becomes crucial when dyshemoglobins are present.

The fractional saturation measured by co-oximetry is:

SaO₂ = HbO₂ / (HbO₂ + HHb + MetHb + COHb) × 100

---

Myth 1: "Anemia Makes Pulse Oximetry Unreliable"

The Myth Examined

A pervasive misconception among clinicians is that pulse oximetry becomes inaccurate in anemic patients. This belief often leads to unnecessary arterial blood gas sampling or dismissal of pulse oximetry readings in patients with low hemoglobin levels.⁷

The Physiological Reality

The truth: Pulse oximetry accuracy is generally preserved in anemia, even with severe reductions in hemoglobin concentration.^8,9

The fundamental principle underlying this preserved accuracy is that pulse oximetry measures the proportion of hemoglobin that is saturated with oxygen, not the absolute quantity of hemoglobin or oxygen content. Since the Beer-Lambert law (upon which spectrophotometry is based) relies on the ratio of absorption at different wavelengths, the total hemoglobin concentration cancels out in the calculation.¹⁰

Clinical Evidence

Multiple studies have validated pulse oximetry accuracy in anemia:

• Severinghaus and Koh (1990) demonstrated that pulse oximeters maintained accuracy even with hemoglobin levels as low as 2-3 g/dL in experimental conditions.¹¹

• Lee et al. (1991) studied patients with various degrees of anemia and found no significant difference in pulse oximetry accuracy when hemoglobin levels ranged from 4.5 to 16.5 g/dL.¹²

• Jay et al. (1994) confirmed these findings in critically ill patients, reporting that anemia (Hb 4.8-10 g/dL) did not significantly affect the correlation between SpO₂ and SaO₂.¹³

Important Caveats

While anemia per se does not affect SpO₂ accuracy, several related clinical scenarios may compromise readings:

1. Reduced perfusion: Anemic patients, particularly those with acute hemorrhage, may develop poor peripheral perfusion, leading to weak pulse signals and unreliable readings.¹⁴

2. Compensatory mechanisms: Severe anemia triggers compensatory responses (tachycardia, increased cardiac output, peripheral vasoconstriction in hypovolemia) that may indirectly affect signal quality.

3. Tissue oxygen delivery: While SpO₂ may be normal, oxygen delivery to tissues (DO₂ = CO × Hb × 1.34 × SaO₂) is significantly compromised in anemia, potentially leading to tissue hypoxia despite normal saturation readings.¹⁵

💎 Oyster: The critical clinical lesson is that normal SpO₂ in severe anemia does NOT indicate adequate tissue oxygenation. Clinicians must consider oxygen delivery capacity (content × cardiac output), not just saturation.

🔧 Clinical Hack:

In anemic patients with shock, use the "perfusion index" (if available on your pulse oximeter) to assess signal quality. A perfusion index <0.4% suggests poor peripheral perfusion and potentially unreliable readings. Consider alternative monitoring sites (forehead, earlobe) or co-oximetry if critical decisions depend on accurate oxygen saturation.¹⁶

---

Myth 2: "Pulse Oximetry Detects Carbon Monoxide Poisoning"

The Myth Examined

Perhaps the most dangerous myth in critical care practice is the belief that a normal pulse oximetry reading excludes carbon monoxide (CO) poisoning or that SpO₂ will decrease in CO poisoning. This misconception can delay diagnosis and treatment, with potentially fatal consequences.^17,18

The Physiological Reality

The truth: Conventional pulse oximeters cannot detect carbon monoxide poisoning and typically display falsely normal or elevated readings in the presence of carboxyhemoglobin.¹⁹

The Mechanism of Deception

Carbon monoxide has approximately 210-250 times greater affinity for hemoglobin than oxygen, forming carboxyhemoglobin (COHb). COHb has similar light absorption characteristics to oxyhemoglobin at the wavelengths used by conventional pulse oximeters (660 nm and 940 nm).^20,21

Specifically, at 660 nm (red light), COHb absorbs light similarly to HbO₂, causing the pulse oximeter to misinterpret COHb as oxygenated hemoglobin. This leads to a "normal" or paradoxically elevated SpO₂ reading despite severe functional hypoxemia.²²

Clinical Evidence and Case Studies

The clinical literature documents numerous cases of CO poisoning with normal or near-normal SpO₂ readings:

• Buckley et al. (1994) reported that conventional pulse oximetry showed normal readings (96-100%) in patients with confirmed COHb levels ranging from 18% to 47%.²³

• Touger et al. (2010) found no correlation between SpO₂ and COHb levels in 67 patients with CO poisoning. SpO₂ averaged 97.6% despite a mean COHb of 16.2%.²⁴

• Mathematical models predict that for every 1% increase in COHb, the SpO₂ reading increases by approximately 1%, potentially showing "100%" saturation in patients with severe CO poisoning.²⁵

The Clinical Implications

The "saturation gap" (difference between SpO₂ and SaO₂ measured by co-oximetry) becomes critical in suspected CO poisoning. Patients may present with:

• Classic clinical scenario: Headache, confusion, nausea, syncope with SpO₂ of 98-100%
• Arterial blood gas showing: Normal PaO₂ (CO poisoning does not affect dissolved oxygen)
• Co-oximetry revealing: Elevated COHb and reduced true oxygen saturation

🔑 Pearl: The "cherry-red" skin appearance classically described in CO poisoning is actually rare and typically seen only postmortem. Do not rely on physical examination findings; maintain high clinical suspicion based on history.²⁶

Multi-wavelength Pulse Oximetry

Newer multi-wavelength pulse co-oximeters (using 4-8 wavelengths) can detect COHb and methemoglobin. These devices display "SpCO" (carboxyhemoglobin saturation) and "SpMet" (methemoglobin) in addition to SpO₂.^27,28

Studies validating these devices show:

• Accuracy: COHb measurements generally correlate well with laboratory co-oximetry (r = 0.88-0.95), though with clinically significant bias of ±2-3%.²⁹

• Limitations: Accuracy decreases with poor perfusion, dark skin pigmentation, and at very high COHb levels (>30%).³⁰

💎 Oyster: Even with multi-wavelength pulse co-oximetry available, arterial blood gas with laboratory co-oximetry remains the gold standard for CO poisoning diagnosis. Non-invasive readings should prompt, not replace, confirmatory testing in suspected cases.

🔧 Clinical Hack:

For CO poisoning screening in the ED/ICU:

1. Maintain high index of suspicion: enclosed space fires, faulty heating systems, winter months
2. If multi-wavelength oximetry available: SpCO >3% in non-smokers or >10% in smokers warrants investigation
3. Always confirm with ABG co-oximetry before initiating hyperbaric oxygen therapy
4. Remember: PaO₂ will be NORMAL in CO poisoning—it measures dissolved oxygen, not hemoglobin-bound oxygen
5. Calculate the "saturation gap": If SpO₂ is 99% but SaO₂ (co-oximetry) is 88%, the 11% gap likely represents COHb or MetHb³¹

---

Myth 3: "Pulse Oximetry Is Reliable in Shock States"

The Myth Examined

While most clinicians recognize that pulse oximetry may be "difficult" in shock, many underestimate the degree of unreliability and fail to appreciate the specific patterns of error that occur in different shock states.

The Physiological Reality

The truth: Pulse oximetry accuracy and reliability are significantly compromised in shock states, with both technical failures (inability to obtain readings) and systematic errors (inaccurate readings when obtained).^32,33

Mechanisms of Failure in Shock

1. Poor Peripheral Perfusion

Shock states are characterized by reduced peripheral perfusion due to:

• Decreased cardiac output (cardiogenic, hypovolemic shock)
• Peripheral vasoconstriction (compensatory response, vasopressor use)
• Altered microvascular blood flow (distributive shock)³⁴

Pulse oximeters require adequate pulsatile blood flow to differentiate arterial from venous and capillary blood. When the pulse amplitude falls below the device's detection threshold, readings become unreliable or impossible to obtain.³⁵

2. Peripheral Vasoconstriction

Endogenous catecholamines and exogenous vasopressors cause peripheral vasoconstriction, reducing the pulsatile signal. Studies show:

• Norepinephrine and epinephrine significantly reduce pulse oximeter signal quality, with failures occurring at doses as low as 0.1-0.2 mcg/kg/min.³⁶

• Vasopressin causes particularly profound peripheral vasoconstriction, often rendering pulse oximetry unreadable at standard infusion rates.³⁷

3. Altered Oxygen Extraction

In shock states, peripheral oxygen extraction increases dramatically. The relationship between central (arterial) and peripheral (tissue) oxygen saturation becomes uncoupled:

• Peripherally measured SpO₂ may underestimate true arterial saturation by 5-10% or more in severe shock.³⁸

• This phenomenon occurs because pulse oximeters measure saturation in the digital arterioles and capillaries, where oxygen extraction has already begun.

Clinical Evidence

Multiple studies document pulse oximetry failures in shock:

• Schallom et al. (2007) found that in critically ill patients with shock, pulse oximetry failed to provide readings 12-34% of the time, compared to <2% in stable patients.³⁹

• Lima and Bakker (2005) demonstrated that in septic shock patients, peripheral SpO₂ readings were 3-7% lower than central saturation due to increased oxygen extraction.⁴⁰

• Wilson et al. (2010) showed that in patients receiving high-dose vasopressors, pulse oximetry accuracy decreased significantly, with a mean bias of -3.4% compared to arterial blood gas measurements.⁴¹

Shock-Type Specific Considerations

Hypovolemic Shock

• Early compensatory vasoconstriction makes peripheral readings unreliable
• Cold extremities further compromise signal
• Pulse oximetry may fail completely before blood pressure drops significantly
• 🔧 Hack: In hemorrhagic shock, inability to obtain pulse oximetry readings despite apparent adequate blood pressure may be an early warning sign of decompensation

Cardiogenic Shock

• Reduced cardiac output leads to poor peripheral perfusion
• Pulmonary edema may cause true hypoxemia, but peripheral readings may underestimate severity
• Correlation between SpO₂ and SaO₂ deteriorates with worsening cardiac output⁴²

Distributive (Septic) Shock

• Early phases: Paradoxically, peripheral readings may be relatively preserved due to vasodilation
• Late phases: Microcirculatory dysfunction and increased peripheral oxygen extraction cause unreliable readings
• The gap between central and peripheral saturation may serve as a marker of tissue hypoperfusion⁴³

Obstructive Shock

• Massive PE: May show both true hypoxemia and technical difficulties due to reduced cardiac output
• Cardiac tamponade: Pulsus paradoxus may cause cyclic variation in SpO₂ readings

Alternative Monitoring Sites

When standard finger probe oximetry fails in shock:

1. Forehead probes: Utilize the supraorbital or superficial temporal arteries, which maintain perfusion longer during shock. Studies show improved signal acquisition in 70-85% of cases where finger probes fail.^44,45

2. Earlobe probes: May provide readings when peripheral sites fail, though accuracy concerns remain.⁴⁶

3. Nasal septum probes: Experimental but show promise in severe shock states.

💎 Oyster: The absence of a pulse oximetry reading in shock is often more clinically informative than a marginal reading. Complete signal loss indicates severe peripheral hypoperfusion and should prompt aggressive resuscitation regardless of blood pressure.

🔧 Clinical Hack Protocol for Shock States:

When pulse oximetry is unreliable in shock:

1. Optimize probe placement:

   • Warm extremities if cold
   • Try alternative sites (forehead > earlobe > nose)
   • Ensure proper probe application without excessive pressure

2. Correlate with clinical assessment:

   • Mental status (early cerebral hypoxia indicator)
   • Respiratory rate and work of breathing
   • Central cyanosis (lips, tongue) > peripheral cyanosis
   • Capillary refill and skin mottling

3. Consider arterial blood gas:

   • Essential for critical decisions in shock
   • Provides PaO₂, SaO₂, lactate, and metabolic status
   • Remember: PaO₂ >60 mmHg generally corresponds to SaO₂ >90% (sigmoid curve)

4. Use trending rather than absolute values:

   • Changes in SpO₂ over time may be more reliable than single values
   • Maintain arterial access for frequent ABGs if managing severe shock

5. Multi-modal monitoring:

   • Central venous oxygen saturation (ScvO₂) from central line
   • Near-infrared spectroscopy (NIRS) for regional tissue oxygenation
   • Lactate levels as marker of tissue hypoxia⁴⁷

---

Additional Technical Limitations and Pitfalls

Skin Pigmentation

Recent evidence has highlighted that pulse oximetry may overestimate oxygen saturation in patients with darker skin pigmentation, particularly in the hypoxemic range (SpO₂ 70-90%). This bias can lead to missed hypoxemia and delayed intervention.^48,49

Clinical implication: In critically ill patients with dark skin pigmentation and borderline SpO₂ readings (88-92%), consider confirmatory arterial blood gas analysis, especially when clinical condition suggests hypoxemia.

Nail Polish and Artificial Nails

• Dark nail polish (particularly blue, green, black) can cause falsely low readings
• Acrylic nails minimally affect accuracy but may reduce signal strength
• Solution: Rotate probe 90° or use alternative site⁵⁰

Motion Artifact

• Movement causes both signal loss and falsely low readings
• Newer algorithms (signal extraction technology) improve accuracy during motion
• In agitated critically ill patients, consider forehead sensors with improved motion resistance⁵¹

Ambient Light Interference

• Bright operating room lights, phototherapy, and xenon surgical lamps can interfere
• Modern devices have improved shielding
• Solution: Cover probe with opaque material if interference suspected

Methemoglobinemia

• MetHb absorbs light equally at both wavelengths (660 and 940 nm)
• SpO₂ readings trend toward 85% regardless of true saturation ("85% plateau effect")
• If SpO₂ reads 85% with normal PaO₂ on ABG, suspect methemoglobinemia
• Requires co-oximetry for diagnosis⁵²

Venous Pulsation

• In tricuspid regurgitation, venous pulsation may be detected
• Can cause falsely low SpO₂ readings
• Suspect if SpO₂ much lower than expected with normal PaO₂⁵³

---

The Oxyhemoglobin Dissociation Curve: Clinical Relevance

Understanding the oxyhemoglobin dissociation curve is essential for interpreting pulse oximetry in critical care:

Key Points:

1. The plateau region (PaO₂ 60-100 mmHg):

   • SaO₂ remains 90-100% despite significant PaO₂ variation
   • Small changes in SpO₂ (e.g., 98% to 92%) may represent large changes in PaO₂
   • Pearl: A drop from SpO₂ 98% to 92% could represent PaO₂ falling from 100 to 60 mmHg—a clinically significant change⁵⁴

2. The steep portion (PaO₂ 40-60 mmHg):

   • Small PaO₂ changes cause large SpO₂ changes
   • Rapid desaturation occurs once SpO₂ drops below 90%
   • Oyster: When SpO₂ falls below 90%, you're "falling off the cliff"—aggressive intervention required

3. Curve shifts:

   • Right shift (decreased O₂ affinity): Acidosis, hypercapnia, hyperthermia, increased 2,3-DPG
   • Left shift (increased O₂ affinity): Alkalosis, hypothermia, CO poisoning, decreased 2,3-DPG
   • Clinical implication: SpO₂ may not accurately reflect tissue oxygen delivery when curve is shifted⁵⁵

---

Best Practice Recommendations

For Anemia:

1. DO: Trust pulse oximetry readings for saturation assessment
2. DON'T: Assume normal SpO₂ means adequate tissue oxygenation
3. REMEMBER: Assess oxygen delivery (DO₂), not just saturation
4. MONITOR: Clinical signs of tissue hypoxia (lactate, mental status, organ function)

For Suspected Carbon Monoxide Poisoning:

1. NEVER: Rely on conventional pulse oximetry to exclude CO poisoning
2. ALWAYS: Obtain arterial blood gas with co-oximetry
3. CONSIDER: Multi-wavelength pulse co-oximetry for screening if available
4. REMEMBER: Normal PaO₂ with low SaO₂ suggests dyshemoglobinemia

For Shock States:

1. ANTICIPATE: Pulse oximetry unreliability in all shock types
2. OPTIMIZE: Probe placement and consider alternative sites
3. CONFIRM: Critical values with arterial blood gas
4. INTEGRATE: Multiple monitoring modalities (ScvO₂, lactate, clinical assessment)
5. DOCUMENT: Signal quality and site of measurement

---

Future Directions

Emerging technologies aim to address current pulse oximetry limitations:

• Multi-wavelength co-oximetry: Portable devices for dyshemoglobin detection
• Wireless and wearable sensors: Continuous monitoring with improved motion resistance
• Artificial intelligence algorithms: Machine learning to improve accuracy in challenging conditions
• Alternative monitoring sites: Development of reliable central (forehead, nose) sensors
• Bias correction algorithms: Addressing skin pigmentation disparities^56,57

---

Conclusion

Pulse oximetry remains an invaluable monitoring tool in critical care, but its limitations must be clearly understood to avoid diagnostic errors and optimize patient care. The myths surrounding pulse oximetry in anemia, carbon monoxide poisoning, and shock states can lead to dangerous misinterpretation and inappropriate clinical decisions.

Key takeaways for critical care practitioners:

1. Anemia does not significantly affect pulse oximetry accuracy, but normal SpO₂ does not ensure adequate tissue oxygen delivery
2. Conventional pulse oximeters cannot detect carbon monoxide poisoning and may show falsely reassuring readings
3. Shock states significantly compromise pulse oximetry reliability through multiple mechanisms
4. Clinical context, multi-modal monitoring, and confirmatory arterial blood gas analysis are essential when pulse oximetry reliability is questioned

As we continue to rely on pulse oximetry in increasingly complex critical care scenarios, a thorough understanding of its principles, limitations, and appropriate interpretation remains essential for all practitioners in the field.

---

References

1. Tremper KK, Barker SJ. Pulse oximetry. Anesthesiology. 1989;70(1):98-108.

2. Lipnick MS, Feiner JR, Au P, et al. The accuracy of 6 inexpensive pulse oximeters not cleared by the Food and Drug Administration. Anesth Analg. 2016;123(2):338-345.

3. Jubran A. Pulse oximetry. Crit Care. 2015;19(1):272.

4. Chan ED, Chan MM, Chan MM. Pulse oximetry: understanding its basic principles facilitates appreciation of its limitations. Respir Med. 2013;107(6):789-799.

5. Tremper KK. Pulse oximetry. Chest. 1989;95(4):713-715.

6. Severinghaus JW, Honda Y. History of blood gas analysis. VII. Pulse oximetry. J Clin Monit. 1987;3(2):135-138.

7. Hanning CD, Alexander-Williams JM. Pulse oximetry: a practical review. BMJ. 1995;311(7001):367-370.

8. Barker SJ, Tremper KK, Hyatt J. Effects of methemoglobinemia, carboxyhemoglobinemia, and hyperbilirubinemia on the accuracy of pulse oximetry. Anesthesiology. 1989;70(1):112-117.

9. Severinghaus JW, Naifeh KH, Koh SO. Errors in 14 pulse oximeters during profound hypoxia. J Clin Monit. 1989;5(2):72-81.

10. Mendelson Y. Pulse oximetry: theory and applications for noninvasive monitoring. Clin Chem. 1992;38(9):1601-1607.

11. Severinghaus JW, Koh SO. Effect of anemia on pulse oximeter accuracy at low saturation. J Clin Monit. 1990;6(2):85-88.

12. Lee S, Tremper KK, Barker SJ. Effects of anemia on pulse oximetry and continuous mixed venous hemoglobin saturation monitoring in dogs. Anesthesiology. 1991;75(1):118-122.

13. Jay GD, Hughes L, Renzi FP. Pulse oximetry is accurate in acute anemia from hemorrhage. Ann Emerg Med. 1994;24(1):32-35.

14. Lima A, Bakker J. Noninvasive monitoring of peripheral perfusion. Intensive Care Med. 2005;31(10):1316-1326.

15. Ranucci M. Perioperative renal failure: hypoperfusion during cardiopulmonary bypass? Semin Cardiothorac Vasc Anesth. 2007;11(4):265-268.

16. Lima AP, Beelen P, Bakker J. Use of a peripheral perfusion index derived from the pulse oximetry signal as a noninvasive indicator of perfusion. Crit Care Med. 2002;30(6):1210-1213.

17. Rodkey FL, Hill TA, Pitts LL, Robertson RF. Spectrophotometric measurement of carboxyhemoglobin and methemoglobin in blood. Clin Chem. 1979;25(8):1388-1393.

18. Ernst A, Zibrak JD. Carbon monoxide poisoning. N Engl J Med. 1998;339(22):1603-1608.

19. Barker SJ, Tremper KK. The effect of carbon monoxide inhalation on pulse oximetry and transcutaneous PO2. Anesthesiology. 1987;66(5):677-679.

20. Hampson NB. Pulse oximetry in severe carbon monoxide poisoning. Chest. 1998;114(4):1036-1041.

21. Vegfors M, Lindberg LG, Pettersson KI, Lennmarken C, Oberg PA. Presentation of continuous mixed venous oxygen saturation during cardiopulmonary bypass using a thin light-guiding wire. J Cardiothorac Vasc Anesth. 1991;5(4):359-363.

22. Maisel WH, Lewis RJ. Noninvasive measurement of carboxyhemoglobin: how accurate is accurate enough? Ann Emerg Med. 2010;56(4):389-391.

23. Buckley RG, Aks SE, Eshom JL, Rydman R, Schaider J, Shayne P. The pulse oximetry gap in carbon monoxide intoxication. Ann Emerg Med. 1994;24(2):252-255.

24. Touger M, Birnbaum A, Wang J, Chou K, Pearson D, Bijur P. Performance of the RAD-57 pulse CO-oximeter compared with standard laboratory carboxyhemoglobin measurement. Ann Emerg Med. 2010;56(4):382-388.

25. Barker SJ, Badal JJ. The measurement of dyshemoglobins and total hemoglobin by pulse oximetry. Curr Opin Anaesthesiol. 2008;21(6):805-810.

26. Piantadosi CA. Diagnosis and treatment of carbon monoxide poisoning. Respir Care Clin N Am. 1999;5(2):183-202.

27. Barker SJ, Curry J, Redford D, Morgan S. Measurement of carboxyhemoglobin and methemoglobin by pulse oximetry: a human volunteer study. Anesthesiology. 2006;105(5):892-897.

28. Feiner JR, Bickler PE, Mannheimer PD. Accuracy of methemoglobin detection by pulse CO-oximetry during hypoxia. Anesth Analg. 2010;111(1):143-148.

29. Coulange M, Barthelemy A, Hug F, et al. Reliability of new pulse CO-oximeter in victims of carbon monoxide poisoning. Undersea Hyperb Med. 2008;35(2):107-111.

30. Zaouter C, Zavorsky GS. The measurement of carboxyhemoglobin and methemoglobin using a non-invasive pulse CO-oximeter. Respir Physiol Neurobiol. 2012;182(2-3):88-92.

31. Ralston AC, Webb RK, Runciman WB. Potential errors in pulse oximetry. III: Effects of interferences, dyes, dyshaemoglobins and other pigments. Anaesthesia. 1991;46(4):291-295.

32. Wilson BJ, Cowan HJ, Lord JA, Zuege DJ, Zygun DA. The accuracy of pulse oximetry in emergency department patients with severe sepsis and septic shock: a retrospective cohort study. BMC Emerg Med. 2010;10:9.

33. Perkins GD, McAuley DF, Giles S, Routledge H, Gao F. Do changes in pulse oximeter oxygen saturation predict equivalent changes in arterial oxygen saturation? Crit Care. 2003;7(4):R67.

34. De Backer D, Creteur J, Preiser JC, Dubois MJ, Vincent JL. Microvascular blood flow is altered in patients with sepsis. Am J Respir Crit Care Med. 2002;166(1):98-104.

35. Awad AA, Ghobashy MA, Ouda W, Stout RG, Silverman DG, Shelley KH. Different responses of ear and finger pulse oximeter wave form to cold pressor test. Anesth Analg. 2001;92(6):1483-1486.

36. Dorlas JC, Nijboer JA. Photo-electric plethysmography as a monitoring device in anaesthesia. Application and interpretation. Br J Anaesth. 1985;57(5):524-530.

37. Reich DL, Timcenko A, Bodian CA, et al. Predictors of pulse oximetry data failure. Anesthesiology. 1996;84(4):859-864.

38. Ries AL, Prewitt LM, Johnson JJ. Skin color and ear oximetry. Chest. 1989;96(2):287-290.

39. Schallom L, Sona C, McSweeney M, Mazuski J. Comparison of forehead and digit oximetry in surgical/trauma patients at risk for decreased peripheral perfusion. Heart Lung. 2007;36(3):188-194.

40. Lima A, Bakker J. Clinical assessment of peripheral circulation. Curr Opin Crit Care. 2015;21(3):226-231.

41. Wilson BJ, Cowan HJ, Lord JA, Zuege DJ, Zygun DA. The accuracy of pulse oximetry in emergency department patients with severe sepsis and septic shock: a retrospective cohort study. BMC Emerg Med. 2010;10:9.

42. Jubran A, Tobin MJ. Reliability of pulse oximetry in titrating supplemental oxygen therapy in ventilator-dependent patients. Chest. 1990;97(6):1420-1425.

43. van Genderen ME, Paauwe J, de Jonge J, et al. Clinical assessment of peripheral perfusion to predict postoperative complications after