I would like to discuss on Perfusion and Diffusion limited
Ok, let see, how could we make things easier. Let us put few things for us to remember (this is just for the sake of understanding) before we go into deeper part of it
1. Each gas fights to reach its partial pressure equilibrium between the alveolar and capillaries, regardless by diffusing into or diffusion out from the capillaries
2. Each gas has its own partial pressure, but in certain condition it will not exert its partial pressure value for example when it binds to protein; in this case Heamoglobin
3. It means, partial pressure value can only be measured when the gas is free in the plasma
Too much? This is just a fraction of it lol, still miles to go =)
Let us take it one step at a time
Why does O2 and CO2 is perfusion limited but not diffusion limited? This might be the question that has been lingering in your mind in Respiratory physiology isn’t it?
Let us discuss on O2.
1. This is the partial pressure for O2, both in capillary and alveolar
a) Alveolar – ~105mmHg
b) Capillary – ~40mmHg
So, just do some a simple mathematic here, 105mmHg – 40mmHg = 65mmHg. This dictates that there is 65mmHg difference between partial pressure of O2 in the alveolar space and capillary. This simply shows to us how great the gradient it is, this is why the diffusing capacity of O2 through the respiratory membrane is very high, means a lot of O2 can enter into the blood. But it is need to be remembered that eventhough O2 has a high diffusing capacity, it has a slower diffusing rate compared to CO2 (I know its started to become confusing here, never mind, let us proceed)
2. What can you tell from the number 40mmHg of capillary O2 partial pressure? It shows to us that there is still remaining O2 in the venous return. So, simply to say, pulmonary artery that enters the lung is already preloaded with O2.
3. Now we have two things in hand, one is partial pressure of O2 between the alveolar and capillary is very high (65mmHg), and two – O2 is already preloaded in the pulmonary artery.
4. From the beginning we already agreed the fact that all gases are trying to reach their partial pressures equilibrium between alveolar and capillary, same goes to O2. O2 needs at least 65mmHg to reach its equilibrium between alveolar and capillary which ~105mmHg.
5. Because the O2 is already preloaded in the pulmonary artery and the pressure gradient between the alveolar space and capillary is so high, extensive amount of O2 can enter the blood in a short period of time, in fact – O2 can reach its equilibrium even before the capillary exits the alveoli.
6. So, O2 doesn’t have problem with its diffusing capacity, thus showing to us that the only thing that may effect the amount of O2 enters the blood is the BLOOD ITSELF.
7. Normal amount of O2 entering the blood per tidal volume is ~500ml. How does this value can increase or decrease. Simple, if the cardiac output decreases, lesser amount of O2 can enter the blood and vice versa.
What about CO2? Why it is Perfusion limited?
1. Here are the partial pressure values of CO2 in both alveolar and capillary
a) Alveolar – ~40mmHg
b)Capillary – ~46mmHg
Again, let us do some kids maths 46mmHg – 40mmHg = 6mmHg. Ermm, now we have started to wonder, this value is too low for CO2 to diffuse into the blood isn’t it? Ok, scroll up, see what I’ve written above, ok2 I know you were too anticipated to scroll up, let me quote it back for you ” eventhough O2 has a high diffusing capacity, it has a slower diffusing rate compared to CO2“. It means that, CO2 can pass through the respiratory membrane with lower pressure gradient but in a higher rate. Thus, CO2 can reach its equilibrium just before capillary exits the alveolar.
2. You got your bell ringing there! So, CO2 is perfusion limited since it doesn’t have problem with its diffusing capacity, cause it manages to reach its equilibrium within the transit time of blood through the alveolar capillary.
3. How could the amount of CO2 can be changed? Change the amount of blood perfuses to the lungs isn’t it? =) As simple as that
We have been wondering, what with the CO? What makes it becomes Diffusion limited?
1. It must be clear that in normal condition, we don’t inhale CO for fun lol (Ok its not funny). So, we purposely introduce CO to the lung in the safest amount ~1mmHg for us to understand the nature of CO toxicity.
2. It is agreed that CO has a higher affinity towards heamoglobin compared to O2, in fact 200 folds of difference between CO affinity to O2 affinity towards heamoglobin.
3. This shows to us that CO can easily occupy the heamoglobin without giving a chance for O2 to bind to heamoglobin.
4. Like what I’ve said, we don’t inhale CO for fun, so, the partial pressure of CO in capillary is always ~0mmHg. We introduce 1mmHg of CO in the alveolar and we have 0mmHg of CO in the capillary, means that we only have 1mmHg pressure gradient between the alveolar and the capillary.
5. It means that very little amount of CO can enter the blood. Lets say, 2 molecules of CO enters the blood, and these 2 molecules immediately bind to heamoglobin without having a chance to diffuse into the plasma, let me remind of a fact that I’ve stated above “Each gas has its own partial pressure, but in certain condition it will not exert its partial pressure value for example when it binds to protein; in this case Heamoglobin“. It takes too long for the CO to reach its equilibrium before capillary exits the alveoli.
6. Because of this, CO is diffusion limited – regardless how much blood you perfuse the lungs, CO won’t be able to reach it’s equilibrium cause of two major things
a) Diffusing capacity is too low in respect to its low pressure gradient between alveolar and capillary
b) High affinity towards heamoglobin makes its impossible for CO to diffuse into the blood plasma
Does it help? I hope so… Let us have some discussion on more interesting topics in the future. Goodluck pals =)
P/s – Try to figure out in which condition do O2 and CO2 will shift from Perfusion limited to Diffusion limited. I will try to discuss on it in future post