Work-up for hypoxia (or relative hypoxia) is a bit sophisticated. But big picture, there are few key issues to think about. And I am going to think out loud. So take this with grain of salt. Seek a formal evaluation. And hopefully eveyone reading sees this more as physiology class than "what could be wrong with me?"
Breathe in, oxgen goes into your lungs, into your alveoli, the air sacs that are filled with gas (mixture of O2 and CO2 among other gases). Lungs are sponges that absorb the oxygen. Venous blood is passing from right heart -> to the lungs -> through the pulmonary capillaries to pick up the oxygen -> returns to the left heart oxygenated -> and then gets pumped out to the systemic arterial circulation. Deliver your oxygen, return to venous system, back to right heart, back to lungs, repeat.
Sat probes detect oxygen concentration in your arterial circulation, bound to your hemoglobin. If your O2 saturation is low, numerous possiblities. Where is the defect? Is it mild, moderate, severe? And is it transient or persistent?
I am going to presume for this discussion that you don't have a major cardiac or pulmonary dysfunction. Same for most people following,
What you describe sounds mild and more persistent. One plausible explanation for you is your asthma. People with asthma can have airway inflammation/narrowing/obstruction all the way down to their distal, small airways. This can cause some people to have air trapping, +/- some excess mucus. What that means is you don't fully exhale all of your gas, which can impair O2 reabsorption in those distal alveoli. Can lead to slightly lower O2 concentration.
Another very common explanation is some sort of shunt. Shunt is where venous, deoxygenated blood somehow gets mixed into the arterial circulation, thus lowing the arterial oxygen concentration. A patent foramen ovale (failure to close a communication between right and left atria at birth) can cause small shunt. This occurs and is normal in 15-25% of people (depending on the literature). Next, Arterial-Venous malformations. A tangle of venous-arterial capillary beds where for some reason the veins and artery blends and venous blood mixes with arterial blood in that malformation. This puts a small amount of venous blood into the arterial circulation. They can occur various places. People can have random AVM's in the lungs (I actually have a few small ones, and my baseline O2 saturation lives at 94-95%). Cirrhosis and liver disease causes shunts. Many people often have mild shunts and may not know.
Whatever the cause, sleeping can make baseline hypoxia, transiently worse. When you sleep, you lay on your lungs, can get some very mild atelectasis (airways and alveoli can collapse), and then periodic shallow breathing while asleep can lead to some hypoventilation. Which will take someone with mild hypoxia, and make it a little bit worse. This often ties in with sleep apnea.
Obstructive sleep apnea is transient, when sleeping, It is a structural problem. When people fall asleep who have it, their airway occludes, most often from crowding or collapse of soft tissue in the posterior pharynx. Inhalation brings O2 in, then the airway occludes, which inhibits passive exhalation, which then leads to lack of another respiratory effort, which then leads to O2 levels to drift down until your brain tells you don't die, and you startle, wake up and start to breathe again. There are also episodes of low or shallow respirations that can occur in sleep apnea. This hypoventialtion also contributes to low O2 levels.
These are the very common and not overly concerning causes of hypoxia. Again, separate from a more concerning cardiopulmonary diagnosis. There also weird genetic issues and hemoglobinopathies. I am not going to cover those.
I would say make sure you are evaluated. Consider Pulmonary Function Testing (or repeat if you have had in past), and Arterial Blood Gas to get an accurate measurement of your arterial concentration, calculate an A-a gradient, and then determine role for further studies. To include a screen for sleep apnea, and potential formal sleep study.
Breathe in, oxgen goes into your lungs, into your alveoli, the air sacs that are filled with gas (mixture of O2 and CO2 among other gases). Lungs are sponges that absorb the oxygen. Venous blood is passing from right heart -> to the lungs -> through the pulmonary capillaries to pick up the oxygen -> returns to the left heart oxygenated -> and then gets pumped out to the systemic arterial circulation. Deliver your oxygen, return to venous system, back to right heart, back to lungs, repeat.
Sat probes detect oxygen concentration in your arterial circulation, bound to your hemoglobin. If your O2 saturation is low, numerous possiblities. Where is the defect? Is it mild, moderate, severe? And is it transient or persistent?
I am going to presume for this discussion that you don't have a major cardiac or pulmonary dysfunction. Same for most people following,
What you describe sounds mild and more persistent. One plausible explanation for you is your asthma. People with asthma can have airway inflammation/narrowing/obstruction all the way down to their distal, small airways. This can cause some people to have air trapping, +/- some excess mucus. What that means is you don't fully exhale all of your gas, which can impair O2 reabsorption in those distal alveoli. Can lead to slightly lower O2 concentration.
Another very common explanation is some sort of shunt. Shunt is where venous, deoxygenated blood somehow gets mixed into the arterial circulation, thus lowing the arterial oxygen concentration. A patent foramen ovale (failure to close a communication between right and left atria at birth) can cause small shunt. This occurs and is normal in 15-25% of people (depending on the literature). Next, Arterial-Venous malformations. A tangle of venous-arterial capillary beds where for some reason the veins and artery blends and venous blood mixes with arterial blood in that malformation. This puts a small amount of venous blood into the arterial circulation. They can occur various places. People can have random AVM's in the lungs (I actually have a few small ones, and my baseline O2 saturation lives at 94-95%). Cirrhosis and liver disease causes shunts. Many people often have mild shunts and may not know.
Whatever the cause, sleeping can make baseline hypoxia, transiently worse. When you sleep, you lay on your lungs, can get some very mild atelectasis (airways and alveoli can collapse), and then periodic shallow breathing while asleep can lead to some hypoventilation. Which will take someone with mild hypoxia, and make it a little bit worse. This often ties in with sleep apnea.
Obstructive sleep apnea is transient, when sleeping, It is a structural problem. When people fall asleep who have it, their airway occludes, most often from crowding or collapse of soft tissue in the posterior pharynx. Inhalation brings O2 in, then the airway occludes, which inhibits passive exhalation, which then leads to lack of another respiratory effort, which then leads to O2 levels to drift down until your brain tells you don't die, and you startle, wake up and start to breathe again. There are also episodes of low or shallow respirations that can occur in sleep apnea. This hypoventialtion also contributes to low O2 levels.
These are the very common and not overly concerning causes of hypoxia. Again, separate from a more concerning cardiopulmonary diagnosis. There also weird genetic issues and hemoglobinopathies. I am not going to cover those.
I would say make sure you are evaluated. Consider Pulmonary Function Testing (or repeat if you have had in past), and Arterial Blood Gas to get an accurate measurement of your arterial concentration, calculate an A-a gradient, and then determine role for further studies. To include a screen for sleep apnea, and potential formal sleep study.