Hi folks, Gavin Greenfield here. I'm going to have a quick chat about dead space. Dead space is a term that refers to any gas in the respiratory system that does not participate in gas exchange.
The easiest concept to understand would be anatomic dead space. So this is gas in the conducting system. So anything from the mouth, nose, and you'll see the note over here, mouth, nose to the terminal bronchial. So you take a breath in and anything from here all the way down the trachea, all the way down the main stem bronchi, and these will continue dividing into smaller and smaller conducting airways and they'll eventually end in terminal bronchioles, which will terminate in alveoli.
So from here all the way down to these... terminal bronchioles, there is no capillary beside any of those areas and there's no gas exchange there. They're simply conducting airways.
So that is anatomic dead space. Once that air is conducted to the alveoli, this is where gas exchange takes place. So here's a schematic of a single alveoli with a capillary going beside it. So of course, O2 will diffuse from the alveoli into the capillary.
CO2 will diffuse from the capillary into the alveoli. So that's anatomic deadspace. Alveolar deadspace is represented by this alveolus right here.
And so what we have with alveolar deadspace is an increased VQ ratio because Q typically because Q falls. And so here we're showing Q or perfusion schematically much less than the Q or perfusion that's happening here. So you can imagine a much decreased ability for gas exchange.
There just won't be the capacity, there won't be as many hemoglobin molecules flowing through here for O2 to diffuse. Now whatever O2 does diffuse will fully saturate that hemoglobin molecule, but the total amount of oxygenated hemoglobin returning to the left side of the heart will be... decrease because there will be decreased blood flow to the left side of the heart.
What is coming back will be fully oxygenated, but there just won't be that much blood coming back because this is the state that's happening. And of course, you can also imagine a decreased CO2 delivery to this alveoli that can diffuse into here and be breathed out. So, you know, on an extreme state, if we go from here, so remember our normal venous PV CO2 is is somewhere around on the venous side 45 for a PV CO2.
So in normal physiology it comes here it diffuses in and once it equilibrates there will be no further diffusion and it will breathe out and with full exhalation the end tidal which which since the sensor is sitting up here by the mouth will will read the CO2 concentration of that alveolar gas. And of course in healthy physiology it'll be pretty close to that venous and pretty close to that arterial value. The brackets will be pretty narrow. So we might get an end tidal of you know 40 or something like that in this case.
However if this same venous CO2 of 45 comes into this situation there is not nearly the ability for that 45 to diffuse into the alveoli because very little is getting to the alveoli because we have this situation as far as the blood flow goes. And so then this will not, the volume of CO2 in this alveoli will not get up in the range of 40. It will be closer to what it was when you breathed in. And remember the CO2 concentration in the atmosphere is very, very low.
We essentially, from a math perspective, treat it as zero. So therefore any gas breathed out from this alveoli when it flows by this end title is going to be much much lower and read much lower. So that is a situation where we will have wide brackets where we'll have an end title that is markedly lower than the venous and the arterial value and it's because of because of this situation. A little further explanation on this concept of O2 and CO2 diffusion.
Recall that in this situation from an O2 perspective, I said whatever blood flow is flowing by here, oxygen will saturate that hemoglobin. It's just that there's very little blood flow flowing by. So normally there's kind of an equilibrium. O2 flows in, CO2 flows out.
In this situation that happens, but you can imagine very little O2, there's very little capacity for the blood to take up O2 because there's very little blood there. So much less O2 is going to flow into the capillary here. This is a relatively fixed space and if the O2 remains, think of it as there's not much room for CO2. So whatever CO2 does get in or whatever blood flow flows through here, CO2 will diffuse.
But there's just going to be very little ultimate CO2 diffusion because very little O2 is left. So unlike here where lots of O2 is going in, leaving lots of space for CO2 to diffuse out, there's very little flow going this way and there will be thus very little capacity to accept flow this way. So CO2 will not fully diffuse out of here and we'll get a rise in our blood values of CO2.
And again, the end tidal CO2 will fall because this will be mostly representative of atmospheric CO2, which we have discussed, and it is very low. So back to our dead space. So dead space is any space in the respiratory system that does not participate in gas exchange. Typically, we think of the anatomic dead space.
That's the mouth and nose to the terminal bronchioles. In a healthy person, there's very little alveolar dead space. So the physiologic dead space, which is the sum of those two things, the anatomic dead space and the alveolar dead space, typically is somewhere around the anatomic dead space.
However, when we have a person that is unhealthy and has a significantly increased VQ ratio, significant increased alveolar dead space, then we'll have a higher physiologic dead space because it is the sum of 1 plus 2. And in disease states, 2 will take on... a higher significance. So what causes increased alveolar dead space?
I've got a note here, certainly this is not exhaustive, but we've talked about PE. PE on a regional level, wherever that clot is, will give rise to this situation. We still have alveoli that are full of gas, but because the clot is sitting somewhere over here, we don't have any perfusion there.
So we'll have an increased alveolar dead space from PE. Shock in general, if we have somebody in... most causes of shock, certainly obstructive and hypovolemic as well as cardiogenic, will schematically result in decreased output from the right ventricle. And overall, there'll be less perfusion through the lung. And so schematically, it will look like this.
So shock will cause increased alveolar dead space and will cause a drop in your end tidal CO2. Positive pressure ventilation can do it. So you can imagine in our normal physiology here, if we really significantly increased the intrathoracic pressure from positive pressure ventilation, we can distend this alveoli and when you distend the alveoli, it's going to push on the surrounding capillary.
And again, we will increase the VQ ratio in that situation. And we'll get to something schematically that may look like this. So those are all things that can result in a fall of your end tidal CO2 relative to your PV and PaCO2.
So we talked about physiologic dead space, which again is the sum of the anatomic dead space and the alveolar dead space. The thing we haven't talked about is mechanical dead space. So when we start to add ventilator... tubing here, a circuit, and our end tidal CO2 detector for that matter, our HME filter. Those are all areas of mechanical dead space.
And we will touch on that in your upcoming vent course. So I think that's all I have to say about dead space. Please fire any questions to my STARS email. Thanks everybody.