Oxygen saturation in arterial blood (SaO₂) 

Binding sites for oxygen are the heme groups, the Fe++-porphyrin portions of the hemoglobin molecule. There are four heme sites, and hence four oxygen binding sites, per hemoglobin molecule. Heme sites occupied by oxygen molecules are said to be "saturated" with oxygen. The percentage of all the available heme binding sites saturated with oxygen is the hemoglobin oxygen saturation (in arterial blood, the SaO2). Note that SaO2 alone doesn't reveal how much oxygen is in the blood; for that we also need to know the hemoglobin content.

Oxygen saturation is an essential element in the management and understanding of patient care. Oxygen is tightly regulated within the body because hypoxemia can lead to many acute adverse effects on individual organ systems. These include the brain, heart, and kidneys. Oxygen saturation measures how much hemoglobin is currently bound to oxygen compared to how much hemoglobin remains unbound. At the molecular level, hemoglobin consists of four globular protein subunits. Each subunit is associated with a heme group. Each molecule of hemoglobin subsequently has four heme-binding sites readily available to bind oxygen. Therefore, during the transport of oxygen in the blood, hemoglobin is capable of carrying up to four oxygen molecules. Due to the critical nature of tissue oxygen consumption in the body, it is essential to be able to monitor current oxygen saturation. A pulse oximeter can measure oxygen saturation. It is a noninvasive device placed over a person's finger. It measures light wavelengths to determine the ratio of the current levels of oxygenated hemoglobin to deoxygenated hemoglobin. The use of pulse oximetry has become a standard of care in medicine. It is often regarded as a fifth vital sign. As such, medical practitioners must understand the functions and limitations of pulse oximetry. They should also have a basic knowledge of oxygen saturation. 

Anatomy and Physiology

One definition of oxygen consumption within the body is the product of arterial-venous oxygen saturation differences and blood flow. The body consumes oxygen partially through aerobic metabolism. In this process, oxygen is used to convert glucose to pyruvate, liberating two molecules of adenosine triphosphate (ATP). An important aspect of this process is the oxygen-hemoglobin dissociation curve. In the blood, hemoglobin binds free oxygen rapidly to form oxyhemoglobin leaving only a small percentage of free oxygen dissolved in the plasma. The oxygen-hemoglobin dissociation curve is a plot of the percent saturation of hemoglobin as a function of the partial pressure of oxygen (PO2). At a PO2 of 100 mmHg, hemoglobin will be 100% saturated with oxygen, meaning all four heme groups are bound. Each gram of hemoglobin is capable of carrying 1.34 mL of oxygen. The solubility coefficient of oxygen in plasma is 0.003. This coefficient represents the volume of oxygen in mL that will dissolve in 100 mL of plasma for each 1 mmHg increment in the PO2. A formula then calculates the oxygen content so that Oxygen Content = (0.003 × PO2) + (1.34 × Hemoglobin × Oxygen Saturation). This formula demonstrates that dissolved oxygen is a sufficiently small fraction of total oxygen in the blood; therefore, the oxygen content of blood can be considered equal to the oxyhemoglobin levels.[1]

As PO2 decreases, the percentage of saturated hemoglobin also decreases. The oxygen-hemoglobin dissociation curve has a sigmoidal shape due to the binding nature of hemoglobin. With each oxygen molecule bound, hemoglobin undergoes a conformational change to allow subsequent oxygens to bind. Each oxygen that binds to hemoglobin increases its affinity to bind more oxygen, meaning the affinity for the fourth oxygen molecule is the highest. 

In the lungs, alveolar gas has a PO2 of 100 mmHg. However, due to the high affinity for the fourth oxygen molecule, oxygen saturation will remain high even at a PO2 of 60 mmHg. As the PO2 decreases, hemoglobin saturation will eventually fall rapidly; at a PO2 of 40 mmHg, hemoglobin is 75% saturated. Meanwhile, at a PO2 of 25 mmHg, hemoglobin is 50% saturated. This level is referred to as P50, where 50% of heme groups of each hemoglobin have a molecule of oxygen bound. The nature of oxygen saturation becomes increasingly important in light of the effects of right and left shifts. A variety of factors can cause these shifts.

A right shift of the oxygen saturation curve indicates a decreased oxygen affinity of hemoglobin, which will allow more oxygen to be available to tissues.[2] The mnemonic, "CADET, face Right!" can help to remember factors that can lead to a right shift. Here, "CADET" stands for PCO2, acid, 2,3-diphosphoglycerate, exercise, and temperature. The hemoglobin dissociation curve shifts right with an increase in each of these factors.

A left shift of the oxygen saturation curve indicates an increase in the oxygen affinity of hemoglobin, which reduces oxygen availability to the tissues. Factors that cause a left shift in the oxygen-hemoglobin dissociation curve include decreases in temperature, PCO2, acidity, and 2,3-bisphosphoglyceric acid, formerly named 2,3-diphosphoglycerate.

Clinical Significance

The human eye's ability to detect hypoxemia is poor. The presence of central cyanosis, blue coloration of the tongue and mucous membranes, is the most reliable predictor; it occurs at an oxyhemoglobin saturation of about 75%.[3] Pulse oximetry provides a convenient, noninvasive method to measure blood oxygen saturation continuously. It can also help to eliminate medical errors. Pulse oximetry has a sensitivity of 92% and a specificity of 90% when detecting hypoxia at a threshold of 92% oxygen saturation.[9]

There is no set standard of oxygen saturation where hypoxemia occurs. The generally accepted standard is that a normal resting oxygen saturation of less than 95% is considered abnormal.[10] Therefore, it remains vital to observe patients for the clinical markers of hypoxemia. The brain is the most sensitive organ, and visual, cognitive, and electroencephalographic changes develop when the oxyhemoglobin saturation is less than 80% to 85%. It is unclear whether there are long-term deficits from hypoxemia. Patients with nocturnal hypoxemia do not seem to develop life-threatening complications despite abnormally low oxygen saturation.[3]

https://www.ncbi.nlm.nih.gov/books/NBK525974/

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1114160/

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