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Pao2, Sao2, Cao2 and Spo2


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#1 LifeguardsForLife

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Posted 27 December 2009 - 08:24 PM

In simplest terms the Pa02 is the amount of oxygent that is not bound to HB, but is in the plasma.

The Sao2 is the percent of oxygen bound to the heme portion of hemoglobin.

Neither the amount of hemoglobin, nor the binding characteristics of hemoglobin, should affect the amount of dissolved oxygen, and hence should not affect the PaO2). Stated another way, the number of dissolved oxygen molecules is independent of the amount of hemoglobin or what is bound to it. To repeat one more time (because it is so important), PaO2 is not a function of hemoglobin content or of its characteristics, but only of the alveolar PO2 and the lung architecture (alveolar-capillary interface). This explains why, for example, patients with severe anemia or carbon monoxide poisoning or methemoglobinemia can (and often do) have a normal PaO2.


Thus hemoglobin is like an efficient sponge that soaks up oxygen so more can enter the blood. Hemoglobin continues to soak up oxygen molecules until it becomes saturated with the maximum amount it can hold - an amount that is largely determined by the PaO2


Why wouldn't Pao2 and Sa02 vary inversly? It seems to me that if a low Sao2 existed(due to a deficiency of Hb, or inability of oxygen to bind to the Hb), one would find a higer Pa02, as no oxygen molecules are being removed from the plasma?

Would Co2 poisoning result in a low sa02, and a higher Pa02 as the heme bonding sites are occupied, thus preventing oxygen from bonding with hemeglobin?

Several sources seem to use Sp02 and Sa02 interchangebly. Spo2 and Sa02, while similiar, should represent 2 entirely differnet values, correct? If a patient has an Sp02/Sa02 level within an acceptable range, would that indicate that the Pa02 is also satisfactory?

Does the Ca02, simply combine the data gathered by the sa02 and the Pao2, in to a quantifiable amount?

If Cao2 is calculated with the following amount, would it stand to reason that a patient could be found to have an adequate Sa02 or Pao2 and still "not be oxygneating properly"?

CaO2 = Hb (gm/dl) x 1.34 ml O2/gm Hb x SaO2 + PaO2 x (.003 ml O2/mm Hg/dl).


Thank you in advance, and I hope my questions were phrased in a way that made sense to those of you reading(I can't seem to disable the bold font, so that is why this is typed boldly)



Edited by LifeguardsForLife, 27 December 2009 - 08:27 PM.

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#2 VentMedic

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Posted 27 December 2009 - 09:07 PM

Let's do a little more background work since each of your questions can get rather indepth.

The oxygen saturation measured by a pulse oximeter (SpO2) is not the same as the SaO2 measured by a laboratory cooximeter. The pulse oximeter measures the "functional" saturation of hemoglobin. Functional saturation represents the amount of oxygenated hemoglobin in a percentage form of the total reduced and oxygenated hemoglobin. The laboratory cooximeters use multiple wavelengths that distinguish other types of hemoglobin (methemoglobin and carboxyhemoglobin) and thus measure true fractional saturation, or amount of oxygenated hemoglobin in a percentage form of the total reduced + oxygenated hemoglobin + methemoglobin, + carboxyhemoglobin. This is why the SpO2 measurement can exceed the SaO2 reading in certain conditions.

Oxygen delivery is a product of cardiac output and oxygen content. The equation for arterial oxygen content is CaO2= (1.37 X Hb X SaO2) + (0.003 X PaO2). From this equation, it is noted that normoxemia does not necessarily guarantee adequate oxygen content. However, since the PaO2 contributes only 0.003 volume percent to the blood oxygen content, the most important factors in determining oxygen content become the hemoglobin concentration and the percent saturation. In order to interpret the results of pulse oximetry, keep in mind the shape of the oxygen hemoglobin dissociation curve, which is not linear and explains why the SpO2 is not a replacement for the SaO2 and the PaO2. Due to the shape of the curve, large decreases in PaO2 may be accompanied by only small changes in the SaO2 in areas other than the steep part of the curve, where a predictable correlation exists between SaO2 and PaO2. A patientís oxygen content may therefore drop steeply before it is detected by pulse oximetry. Shifts in the oxyhemoglobin saturation curve also influence the relationship between PaO2 and SpO2. The information provided by the pulse oximeter is not a replacement for the PaO2, but is complementary to the PaO2. However, the pulse oximeter becomes an ideal continuous monitor of tissue oxygen delivery in the face of normal hemoglobin concentration, and normal types of hemoglobin (vs. methemoglobin and carboxyhemoglobin).

http://www.lakesidep...ary/ABG/PO2.htm

Excellent for oxygen hemoglobin dissociation curve
http://www.ccmtutori...xygen/index.htm

As much as I hate to do this, I am going to reference a thread from the other forum since it also addresses some of the same questions.

http://www.emtlife.c...&highlight=PaO2

Now of course before one gets deeply into the physiology one should have an understanding of their oxygen equipment and the differences between oxygenation and ventilation. You may already have mastered that but many have not which is why I'm back tracking a little.
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#3 chbare

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Posted 27 December 2009 - 09:34 PM

In simplest terms the Pa02 is the amount of oxygent that is not bound to HB, but is in the plasma.

PaO2 is the pressure of dissolved oxygen in plasma. However, you are correct that PaO2 is not attached to hemoglobin; however, this dissolved oxygen can attach to hemoglobin as the hemoglobin looses oxygen. Of course, other concepts also come into play at the cellular level because CO2, biochemical, and PH changes effect the oxyhemoglobin affinity relationship.


The Sao2 is the percent of oxygen bound to the heme portion of hemoglobin.

It's the percent of hemoglobin that is oxidized or presumably oxidized by oxygen.



Why wouldn't Pao2 and Sa02 vary inversly? It seems to me that if a low Sao2 existed(due to a deficiency of Hb, or inability of oxygen to bind to the Hb), one would find a higer Pa02, as no oxygen molecules are being removed from the plasma?

There is a direct relationship in a person with a "normal" curve. Read up on the oxyhemoglobin dissociation curve. Vent posted some good links.



Would Co2 poisoning result in a low sa02, and a higher Pa02 as the heme bonding sites are occupied, thus preventing oxygen from bonding with hemeglobin?

I'm not quite sure what you mean by CO2 poisoning. Typically, elevated CO2 levels are the result of inadequate ventilation or increased CO2 production.


Several sources seem to use Sp02 and Sa02 interchangebly. Spo2 and Sa02, while similiar, should represent 2 entirely differnet values, correct? If a patient has an Sp02/Sa02 level within an acceptable range, would that indicate that the Pa02 is also satisfactory?


Pulse oximetry is an indirect method that relates to SaO2; however, they are not the same concept and can vary significantly depending on the patients condition.


Does the Ca02, simply combine the data gathered by the sa02 and the Pao2, in to a quantifiable amount?

Somewhat (The value is ml of oxygen per 100 ml of blood AKA vol%.); however, look at the left side of the equation. The concentration of well saturated hemoglobin makes up the vast majority of the CaO2. In fact, an FiO2 of 1 at MSL (760 mm/Hg) will do very little to add to the CaO2. This is part of the reasoning for hyperbaric oxygen therapy where we can significantly increase the partial pressure of oxygen.

If Cao2 is calculated with the following amount, would it stand to reason that a patient could be found to have an adequate Sa02 or Pao2 and still "not be oxygneating properly"?

Yes; however, many concepts go into this concept of cellular oxygenation. You could have a "normal" CaO2, yet have cell hypoxia because of conditions that alter oxygen offloading or utilisation.

CaO2 = Hb (gm/dl) x 1.34 ml O2/gm Hb x SaO2 + PaO2 x (.003 ml O2/mm Hg/dl).


Thank you in advance, and I hope my questions were phrased in a way that made sense to those of you reading(I can't seem to disable the bold font, so that is why this is typed boldly)




Take care,
chbare.

Edit for color problems.

Edited by chbare, 27 December 2009 - 09:39 PM.

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#4 LifeguardsForLife

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Posted 27 December 2009 - 10:05 PM

thank you vent and chbare for the information.

Chbare-I apologize, that should of read carbon monoxide poisoning not carbon dioxide. If the affinity between carbon monoxide and hemoglobin is roughly 200 times that of oxygen and hemoglobin, i figured that, carbon monoxide poisoning would result in a higher Pao2 and lower Sao2. Which seemed to conradict the refrenced passage.

I will go and review the oxyhemoglobin dissociation curve.

  • Carbon Monoxide. Hemoglobin binds with carbon monoxide 240 times more readily than with oxygen, and therefore the presence of carbon monoxide can interfere with the hemoglobin's acquisition of oxygen. In addition to lowering the potential for hemoglobin to bind to oxygen, carbon monoxide also has the effect of shifting the curve to the left. With an increased level of carbon monoxide, a person can suffer from severe hypoxemia while maintaining a normal PO2.

I think the above statements answers the question i was attempting to ask.

Edited by LifeguardsForLife, 27 December 2009 - 10:05 PM.

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#5 melclin

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Posted 29 December 2009 - 10:26 AM

This has already been said, but in the midst some complexity, so just to be clear, PaO2 is the partial pressure, not the amount, of oxygen (although they do obviously share a relationship). Do you understand the various gas laws and the concept of partial pressures and equilibrium reactions in chemistry in general? That's something you'd wanna cover before hand, other wise half this stuff won't make any sense.

I don't know where you stand educationally; I don't mean this to sound condescending.
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