Happy hypoxia in COVID-19: New study may have found possible causes behind this biology-defying complication
In happy hypoxia, a person’s oxygen levels are so low that they should be fainting or experiencing organ damage, but instead, they are seemingly well, until eventually, they collapse
The first case of COVID-19 was reported in December 2019. Since then it seems like scientists are discovering something new about the disease every other day.
Happy hypoxia is one such condition that has been seen in a lot of patients with COVID-19 .
In happy hypoxia, a person’s oxygen levels are so low that they should be fainting or experiencing organ damage, but instead, they are seemingly well, until eventually, they collapse. The idea is so baffling that experts around the world are calling it a biology-defying phenomenon since theoretically, it should be impossible.
Now, a group of scientists at the Loyola University Health System have come up with an explanation for the condition.
The blood oxygen saturation level (SaO2, amount of hemoglobin carrying oxygen) of a normal person is around 95 percent or more. However, in conditions that affect the lungs like pneumonia, the blood saturation levels drop below 94 percent. This condition is called hypoxemia.
Blood oxygen levels below 90 percent are considered to be too low and oxygen therapy is needed for such patients. A person with low oxygen levels would have symptoms like shortness of breath and chest pain. However, in happy hypoxia, the person shows no such symptoms.
In an article published in the peer-reviewed journal Science, Reuben Strayer, an emergency physician at Maimonides Medical Center in New York City said, “There is a major mismatch between how the patient looks like and what the monitors show.”
A pulse oximeter is used to detect blood oxygen levels in a COVID-19 patient. Also, in conditions like pneumonia, the reduction in blood oxygen saturation levels are accompanied by fluid collection and raised carbon dioxide levels in the lungs. The latter is what makes them unable to breathe properly instead of the low blood oxygen levels.
Hypoxemia, if left unchecked, leads to a condition called hypoxia (low tissue levels of oxygen), which can cause organ damage.
The study mentions the following possible causes of happy hypoxia:
1. Difficulty in breathing is a symptom, not a sign: Dyspnea (difficulty in breathing) is a symptom, only experienced by the patient, and not a sign that can be observed by others around the patient. A healthcare practitioner or a caregiver cannot catch it until the patient shows signs like rapid breathing, fast heartbeats or any other signs associated with the condition.
2. Carbon dioxide (and not oxygen) tells the brain about hypoxia: Our brain senses carbon dioxide levels not oxygen levels in our blood. Minute changes in ventilation only occur after PaO2 starts to drop below 60 mmHg. PaO2 is the measure of the pressure of oxygen in the blood in arteries. It tells you how well the oxygen is passing through the lungs and into the blood. Normal PaO2 levels are between 75-100 mmHg.
In a previous study, it was found that even a decrease of end-tidal PaO2 (partial pressure of oxygen during exhalation) below 60 mmHg only increased dyspnea in half of the subjects even though all subjects should have experienced it.
On the other hand, even a small increase in the pressure of carbon dioxide in arterial blood (PaCO2) would show large changes in ventilation. Even a reduction of blood carbon dioxide saturation level by 10mm Hg can cause respiratory issues that a person cannot tolerate for even a minute. But, severe hypoxia only leads to an increase in ventilation when the PaCO2 goes above 39 mmHg.
3. ACE2 receptors are present on brain cells that respond to hypoxia: Hypoxemia induces breathing difficulty through special chemical receptors called carotid bodies present in the brain. ACE2 receptors, the cell surface receptors that the COVID-19 causing virus uses to enter healthy cells, are present on carotid bodies too. So, it is a possibility that these receptors may play a role in dyspnea, however, more studies are needed to understand this.
4. Pulse oximeters are not as effective in critically-ill patients: Pulse oximeters are not as efficient in noting low oxygen saturation levels.
The readings from a pulse oximeter have about 4 percent difference from true arterial oxygen saturation, SaO2. Oximetry is much less reliable at SaO2 levels below 80 percent.
5. Fever may affect the way our body responds to hypoxia: Fever, a symptom of COVID-19 , may have something to do with happy hypoxia. The carotid bodies in the brain only respond to PaO2 and not SaO2. However, the two could vary at different temperatures.
More findings from the study
In the latest study, the researchers at Loyola University took a poll from about 58 hospitals and healthcare practitioners to see if they have seen any patients with happy hypoxia. They found that 16 patients had PaO2 less than 60 mmHg but were not experiencing any discomfort. Seven of these patients had their PaCO2 levels above 39 mmHg (in the range between 41-49), which is the sign of silent hypoxia. However, the rest had PaCO2 levels below 39 mmHg. Since this level can blunt the effects of hypoxia on the brain, these patients were not considered to have happy hypoxia.
A lot of COVID-19 patients are either diabetic or old — two conditions that reduce the response of the respiratory system to hypoxia. It has been indicated that diabetics and people older than 65 years have a 50 percent reduced response to hypoxia. So the study suggested that such patients with COVID-19 may be more prone to silent hypoxia.
Furthermore, most people have around 300-600 percent difference in their respiratory drive (the response of their respiratory muscles to the respiratory centres in their brain). So, while one patient may quickly develop shortness of breath with higher blood carbon dioxide levels, another one may not.
For more information, read our article on Oxygen therapy
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