Introduction – Hypoxemia and Hypercapnia

by Thad Wilson, PhD

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    00:01 Hello! In this lecture, we’re going to cover hypoxemias and hypercapneas.

    00:06 And our learning goals will be pretty diffused, but we’ll cover them one by one.

    00:10 And that is the arterial venous and then alveolar to arterial O2 gradient.

    00:16 We’ll then describe hypoxia, which is different than hypoxemias, and their potential difference and underlying mechanisms.

    00:24 We’ll predict the mechanisms of hypoxemias and we’ll be able to go through some clinical scenarios and some actual test data that will able to highlight these particular principles.

    00:37 And then finally, we’re going to go through the relationship between alveolar ventilation and hypercapneas.

    00:43 So there’s a lot of hypo- and hypers- today, but if it has to do with –oxia, that’s oxygen and –capneas with CO2.

    00:52 Let’s go through now what normally, when you breathe in air, what the different O2s and CO2s are.

    01:01 So when you breath in dry air at sea level, your PO2 will be about 160 millimeters of mercury.

    01:09 And you might ask, “How in the world do I know that?” You take barometric pressure times the percent of fraction of O2 in the air.

    01:18 So it’s about 20.93 or we oftentimes round it to 21%.

    01:24 CO2 is very low in atmospheric air.

    01:30 Now once you humidify air, there’s a decrease in the PO2.

    01:34 And this doesn’t mean that the amount of O2 has changed in the air, it's still 21%.

    01:41 But we have to account for the amount of water of vapor and humidify the air.

    01:46 Because by the time you get air from the mouth all the way down to the alveoli, there is about 99.5% saturation of that air.

    01:56 And we have to account for that and that accounts for about 47 millimeters of mercury and that difference of 47 millimeters of mercury lowers the PO2 to about 150.

    02:10 Once you’re in the air sacs themselves, PO2 is lower.

    02:15 In fact, about 100 millimeters of mercury versus the air sac, CO2 has risen to about 40 47 millimeters of mercury.

    02:24 And at first, when you think through this process, you will always will think, “Oh, wow! It went from a 150 and 0 down to a 140. What causes that change?” Now remember in the air sacs, this is where gas exchange is occurring.

    02:38 So you’re removing the O2 and you’re adding CO2 and that accounts for that difference.

    02:43 In the blood on the arterial side of the circulation, you have a PaO2 of about 95 and CO2 of about of about 40.

    02:53 On the mixed venous side, it’ s about 40 O2 and about 46 millimeters of mercury of CO2.

    03:00 You’ll notice that we used the word mixed venous so this is in the pulmonary artery and the reason why this is mixed is all the venous circulation from the body are combined together.

    03:13 So when you have your blood returning to the heart from the inferior and superior vena cavas, they will be mixed together in the right side of the heart, right atrium, right ventricle, and by the time they get into the pulmonary artery, this is all mixed together and so this is a general venous blood across the whole body.

    03:33 Okay.

    03:34 Now with those in place, let’s talk through our two gradients.

    03:38 So these gradients will be arterial to venous, small A minus small V, or alveolar to arterial, which is capital A minus small A O2 gradients.

    03:51 Okay.

    03:51 Let’s start off with systemic venous blood.

    03:55 This comes in at about a PO2 of 40 millimeters of mercury.

    04:00 You’ll notice in the pulmonary capillaries, there’s a dramatic rise in the amount of PO2.

    04:06 And that is because there’s gas exchange occurring between the pulmonary capillaries and the alveoli.

    04:14 In the systemic arterial blood, it’s a little bit lower than what occurred at the end of the pulmonary capillary and that is because there’s some blood that deoxygenated is mixed with the oxygenated blood.

    04:29 Where does this blood come from? It usually comes from a thebesian veins that drain the heart and the bronchial circulation.

    04:36 So these two circulations will dump a little bit of deoxygenated blood into the oxygenated blood and that accounts for a small decrease and we call that a shunt any time there is some deoxygenated blood mixed with the oxygenated blood.

    04:56 Then finally, in the systemic capillaries, you remove that O2.

    05:00 And therefore, you can see the dramatic decrease as you reach down to a number of about 40.

    05:06 So what are these two gradients? That first gradient is A to a.

    05:12 So that’s the difference between what is in the pulmonary capillary minus the arterial blood.

    05:18 So there’s always a small gradient that occurs because that has to do with physiological shunt.

    05:24 But it should be a number less than 15.

    05:27 If it gets greater than 15, we’re starting to reach an amount of an A to a gradient that is pathological.

    05:37 The A to V gradient is very much dependent on metabolism.

    05:41 And why do we know that? Is because you’re going to fully oxygenate your blood at the level of the lung, but how much you pull out in the systemic capillaries will be very dependent upon how high a person’s metabolism is.

    About the Lecture

    The lecture Introduction – Hypoxemia and Hypercapnia by Thad Wilson, PhD is from the course Respiratory Physiology.

    Included Quiz Questions

    1. Humidified tracheal air.
    2. Alveolar air.
    3. Arterial blood..
    4. Mixed venous blood.
    1. 40
    2. 0
    3. 10
    4. 20
    5. 30
    1. The partial pressure of oxygen decreases in the humidified air in trachea.
    2. The partial pressure of oxygen increases in the humidified tracheal air.
    3. The partial pressure of carbon dioxide decreases in the air sacs.
    4. The partial pressure of oxygen is the greatest in the air sacs as compared to trachea.
    5. The partial pressure of carbon dioxide is greatest in the trachea.

    Author of lecture Introduction – Hypoxemia and Hypercapnia

     Thad Wilson, PhD

    Thad Wilson, PhD

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