How come some people with higher FEV1 than 20% are on O2 and I am not?*

My FEV1 is about 20% and I am not on O2. My sat was 95 last week at rest.
How come some people with higher FEV1 than 20% are on O2?

Folks, I thought I'd offer this attempt at a more complete reason 'WHY' and define/explain the WHAT of emphysema, a little better while I'm at it.
There is NO necessarily direct correlation between FEV-1 and the ability to 'oxygenate' (I define 'oxygenate', as ability to transfer oxygen from the air in the alveoli [air sacs] to the blood plasma). Further, 'ventilation' (defined as the movement of a volume of gas [air] into and out of the lungs) has insignificant influence upon oxygenation until it approaches extremes of inadequacy. In other words, you can be "breathing" very POORLY, but if there is adequate oxygen in the air you breathe in relation to your ability to transfer it through the membrane that separates your alveoli from the blood flowing by it, then you can have perfectly adequate oxygenation, despite poor ventilation.

This would be evident by presence of an elevated carbon dioxide level, but a relatively normal oxygen level, if a blood gas were to be measured.
Emphysema is a disease characterized by the destruction and loss of lung tissue. In particular, what we call 'terminal conducting airways' and 'alveoli' are directly affected. To best picture what happens, imagine a bunch of grapes on the vine. The vine, represents the bronchial tubes ("conducting airways"). Now imagine that instead of being many 'individual' grapes acting 'independently', each grape shares a 'common wall' with those adjacent to it, so that what you have in the end is a bunch of individual, yet inter-connected grapes. This is pretty much how your alveoli relate to each other, forming each lung unit then lung segments and so on up to the lung as a whole.
In emphysema there is destruction and breakdown in two ways. First and foremost, the individual, yet inter-connected alveoli lose more and more of the 'common walls' that separate them. The end result is like those many grapes 'coalescing' (blending, merging) into one big grape. Second, further damage causes loss and destruction of the conducting airways. (A third way there is destruction in emphysema is through loss of blood vessels and circulation, but at this point, I am trying to describe the just the tissue destruction.)
When you take into account the effect of both kinds of damage occurring, it is not hard to understand why it is so hard to effectively 'ventilate', and how the 'air-trapping' that you are told about happens. Again, to picture the trapping part, imagine that you only have the one 'skinny, little stem' (bronchial tube) through which air must pass in and out to 'ventilate' that one 'big grape' (alveolus). You only have enough opportunity to breathe in your 'normal' breath, in pretty much your 'normal' amount of time. The amount of "fresh" air you are able to take in to 'mix' with the huge amount of air contained in that one big alveolus is very small, therefore, unable to make a big difference in the quality of the air already in the big alveolus.
To picture this further, think of a balloon. When you first begin to blow it up, a little bit of air goes a long way to make it bigger from one breath to the next. Now, as you make that balloon bigger and bigger, it only grows a small amount with each breath - - - even though ALL of the breaths you have blown into it are the same size. Normal lungs - - alveoli - - would equate with the balloon, when you first blow it up (except for the point that alveoli do not 'collapse' between breaths, but always have 'some' air left in them). Lungs with emphysema equate with the big, inflated balloon.

The last point is that depending upon how widespread the destruction and over-distention is throughout your lungs, will determine the degree of disturbance in your 'ventilation'. But also figuring into the equation is the effect of all those over-distended lung units pressing on the blood vessels moving blood through your lungs and the loss of blood vessels to the structural changes that occur when the many individual alveoli become one big one. And finally, the circulation can be disturbed further by the presence of a low oxygen level in your blood, which acts as a stimulant for the lung's blood vessels to constrict (narrow). The more disturbed the circulation is going through your lungs, the worse your ability to exchange carbon dioxide and oxygen. On top of the disturbance in exchanging gases, is the effect upon your heart, in that it has to pump HARDER, against more resistance, to fewer blood vessels in the face of constriction. This ultimately causes the heart to fail against the increasingly difficult workload.
There are different ways in which emphysema develops and is present in different people. For some, the damage is evenly spread throughout the lungs. For others it occurs inconsistently throughout the lungs, as with the formation of 'blebs' (bubble-like structures), and in yet others, large areas such as segments or lobes can be destroyed. The type of damage and destruction you have determines how and to where air most easily moves when you breathe and influences the points made in the next paragraph.
Some have said that the diffusion study determines whether you need oxygen or not. That is true only if you can move enough air into and out of the lungs to provide for an accurate diffusion measurement in the time allotted for making the measurement. In emphysema the problem is precisely that you CANNOT move enough air into and out of the lungs and time required to move air in and out is greatly increased. On top of that, WHERE the air goes once it is in your lungs is of consequence. You must be able to disburse ('spread') the fresh air you breathe in EVENLY throughout your lungs for diffusion measurements to be meaningful. In emphysema, we know that air is disbursed Unevenly throughout the lungs.
This means that we cannot easily measure diffusion, and that we have to look at the other 'major' measurements of the PFT to be able to determine what meaning to give diffusion test results.
To sum it up, you can have very poor air movement as indicated by very low FEV-1, and even very low measured diffusion, and still have adequate ability to oxygenate. By the same token, you can have a relatively higher FEV-1 and under many circumstances, adequate diffusion measurements and still have very poor oxygenation. As you can see, there are many different factors which 'add up' to the end total effect. They differ to varying degrees in each individual according to their particular emphysema changes and the presence and influence those factors that contribute to having low oxygen in their blood.

Regards,
Mark Mangus, RPFT, RRT, RCP
Respiratory Care Practitioner in Pulmonary Rehabilitation

Hope this helps someone,

Love to all,
Holly