The answer to this isn't the traditional explanation. The traditional theory is wrong.
A normal SpO 2 is 95 to 100%. A value below 95% is reduced but considered adequate if it is above 88%. In fact, for oxygen to be paid by an insurance company, the SpO 2 needs to be 88% or below. The oxygen saturation is normally measured by a pulse oximeter placed on a finger, but a Wrist Bracelet can also be used. Raising the admission threshold to 92% entails 1 additional hospitalization for every 14 patients discharged. Conclusions: among outpatients with pneumonia, oxygen saturations 92% would be safer and clinically better justified.
The traditional theory argues that oxygen administration to CO2 retainers causes loss of hypoxic drive, resulting in hypoventilation and type 2 respiratory failure.
This is not the case in patients with COPD. Patients suffering from COPD exacerbation, regardless of whether they have CO2 retention, generally have a supra-normal respiratory drive (unless there is impending hypercapnic coma)
The real answer to the question involves two mechanisms:
- Increased V/Q mismatch.
- The Haldane effect.
V/Q mismatch:
A V/Q mismatch occurs when part of the lung receives oxygen without blood flow or it receives blood flow without oxygen.
In COPD, patients optimize their gas exchange by hypoxic vasoconstriction leading to altered alveolar ventilation-perfusion (Va/Q) ratios.
Excessive oxygen administration overcomes this, leading to increased blood flow to poorly ventilated alveoli, and thus increased Va/Q mismatch and increased physiological dead space.
This increase in Va/Q mismatch occurs in both CO2 retainers and non-retainers, the difference is presumably one of degree.
The Haldane effect
Deoxygenated hemoglobin (Hb) binds CO2 with greater affinity than oxygenated hemoglobin (HbO2). Therefore, oxygen induces a rightward shift of the CO2 dissociation curve, which is known as the Haldane effect.
Deoxygenated blood can carry increasing amounts of carbon dioxide, whereas oxygenated blood has a reduced carbon dioxide capacity.
The Haldane Effect results from the fact that deoxygenated hemoglobin has a higher affinity (about 3.5 x) for CO2 than does oxyhemoglobin. Deoxygenated hemoglobin has a higher affinity for CO2 because it is a better proton acceptor than oxygenated hemoglobin.
Therefore, when hemoglobin is deoxygenated there is a right shift of the carbonic acid-bicarbonate buffer equation to produce hydrogen ions which in turn increases the amount of CO2 which can be carried by the blood back to the lungs to be exhaled. Then, with oxygenation at the lungs CO2 dissociates more readily from hemoglobin.
In patients with severe COPD who cannot increase minute ventilation, the Haldane effect accounts for about 25% of the total PaCO2 increase due to O2 administration.
Oxygen saturation is the fraction of oxygen-saturated hemoglobin relative to total hemoglobin (unsaturated + saturated) in the blood. The human body requires and regulates a very precise and specific balance of oxygen in the blood. Normal arterial blood oxygen saturation levels in humans are 95–100 percent. If the level is below 90 percent, it is considered low and called hypoxemia.[1] Arterial blood oxygen levels below 80 percent may compromise organ function, such as the brain and heart, and should be promptly addressed. Continued low oxygen levels may lead to respiratory or cardiac arrest. Oxygen therapy may be used to assist in raising blood oxygen levels. Oxygenation occurs when oxygen molecules (O
2) enter the tissues of the body. For example, blood is oxygenated in the lungs, where oxygen molecules travel from the air and into the blood. Oxygenation is commonly used to refer to medical oxygen saturation.
Definition[edit]
In medicine, oxygen saturation, commonly referred to as 'sats', measures the percentage of hemoglobin binding sites in the bloodstream occupied by oxygen.[2] At low partial pressures of oxygen, most hemoglobin is deoxygenated. At around 90% (the value varies according to the clinical context) oxygen saturation increases according to an oxygen-hemoglobin dissociation curve and approaches 100% at partial oxygen pressures of >11 kPa. A pulse oximeter relies on the light absorption characteristics of saturated hemoglobin to give an indication of oxygen saturation.
Physiology[edit]
The body maintains a stable level of oxygen saturation for the most part by chemical processes of aerobic metabolism associated with breathing. Using the respiratory system, red blood cells, specifically the hemoglobin, gather oxygen in the lungs and distribute it to the rest of the body. The needs of the body's blood oxygen may fluctuate such as during exercise when more oxygen is required [3] or when living at higher altitudes. A blood cell is said to be 'saturated' when carrying a normal amount of oxygen.[4] Both too high and too low levels can have adverse effects on the body.[5]
Measurement[edit]
An SaO2 (arterial oxygen saturation, as determined by an arterial blood gas test[6]) value below 90% indicates hypoxemia (which can also be caused by anemia). Hypoxemia due to low SaO2 is indicated by cyanosis. Oxygen saturation can be measured in different tissues:[6]
- Venous oxygen saturation (SvO2) is the percentage of oxygenated hemoglobin returning to the right side of the heart. It can be measured to see if oxygen delivery meets the tissues' demands. SvO2 typically varies between 60% and 80%.[7] A lower value indicates that the body is in lack of oxygen, and ischemic diseases occur. This measurement is often used under treatment with a heart lung machine (extracorporeal circulation), and can give the perfusionist an idea of how much flow the patient needs to stay healthy.
- Tissue oxygen saturation (StO2) can be measured by near infrared spectroscopy. Although the measurements are still widely discussed, they give an idea of tissue oxygenation in various conditions.
- Peripheral oxygen saturation (SpO2) is an estimation of the oxygen saturation level usually measured with a pulse oximeter device. It can be calculated with pulse oximetry according to the formula[6] where HbO2 is oxygenated hemoglobin (oxyhemoglobin) and Hb is deoxygenated hemoglobin.
Spo2 92
Pulse oximetry[edit]
Spo2 92% Life Threatening
Pulse oximetry is a method used to estimate the percentage of oxygen bound to hemoglobin in the blood.[8] This approximation to SaO2 is designated SpO2 (peripheral oxygen saturation). The pulse oximeter consists of a small device that clips to the body (typically a finger, an earlobe or an infant's foot) and transfers its readings to a reading meter by wire or wirelessly. The device uses light-emitting diodes of different colours in conjunction with a light-sensitive sensor to measure the absorption of red and infrared light in the extremity. The difference in absorption between oxygenated and deoxygenated hemoglobin makes the calculation possible.[6]
Medical significance[edit]
Healthy individuals at sea level usually exhibit oxygen saturation values between 96% and 99%, and should be above 94%. At 1,600 meters' altitude (about one mile high) oxygen saturation should be above 92%.[9]
Spo2 92 With 6 Minute Walk
An SaO2 (arterial oxygen saturation) value below 90% causes hypoxia (which can also be caused by anemia). Hypoxia due to low SaO2 is indicated by cyanosis, but oxygen saturation does not directly reflect tissue oxygenation. The affinity of hemoglobin to oxygen may impair or enhance oxygen release at the tissue level. Oxygen is more readily released to the tissues (i.e., hemoglobin has a lower affinity for oxygen) when pH is decreased, body temperature is increased, arterial partial pressure of carbon dioxide (PaCO2) is increased, and 2,3-DPG levels (a byproduct of glucose metabolism also found in stored blood products) are increased. When the hemoglobin has greater affinity for oxygen, less is available to the tissues. Conditions such as increased pH, decreased temperature, decreased PaCO2, and decreased 2,3-DPG will increase oxygen binding to the hemoglobin and limit its release to the tissue.[10]
See also[edit]
References[edit]
Spo2 92 Meaning
- ^'Hypoxemia (low blood oxygen)'. Mayo Clinic. mayoclinic.com. Retrieved 6 June 2013.
- ^Kenneth D. McClatchey (2002). Clinical Laboratory Medicine. Philadelphia: Lippincott Williams & Wilkins. p. 370. ISBN9780683307511.
- ^'Understanding Blood Oxygen Levels at Rest'. fitday.com. fitday.com. Retrieved 6 June 2013.
- ^Ellison, Bronwyn. 'NORMAL RANGE OF BLOOD OXYGEN LEVEL'. Livestrong.com. Livestrong.com. Retrieved 6 June 2013.
- ^'Hypoxia and Hypoxemia: Symptoms, Treatment, Causes'. WebMD. Retrieved 2019-03-11.
- ^ abcd'Understanding Pulse Oximetry: SpO2 Concepts'. Philips Medical Systems. Retrieved 19 August 2016.
- ^https://www.lhsc.on.ca/critical-care-trauma-centre/central-venous/mixed-venous-oxygen-saturation
- ^Peláez EA, Villegas ER (2007). 'LED power reduction trade-offs for ambulatory pulse oximetry'. Conf Proc IEEE Eng Med Biol Soc. 2007: 2296–9. doi:10.1109/IEMBS.2007.4352784. ISBN978-1-4244-0787-3. PMID18002450. S2CID34626885.
- ^'Normal oxygen level'. National Jewish Health. MedHelp. February 23, 2009. Retrieved 2014-01-28.
- ^Schutz (2001). 'Oxygen Saturation Monitoring by Pulse Oximetry'(PDF). American Association of Critical Care Nurses. Archived from the original(PDF) on January 31, 2012. Retrieved September 10, 2011.
External links[edit]
Spo2 92 Normal