Oxygen in the body + during ventilation responses

a) technically speaking PGas is the pressure exerted by the dissolved gas, but this is directly proportional to the concentration so it's used interchangeably

b) the solvation of oxygen in plasma is dictated primarily by the solubility of oxygen, so i don't imagine the change will be all that great even in hyperventilation. CO2 is a different story as it reacts with water to make carbonic acid.

2) ventilation (breathing) affects Hb saturation because it affects the PO2 in the lungs. more & faster breathing = higher PO2. it likely has minimal effect in the periphery.

Like bleargh said, ventilation would affect Hb saturation because it affects the levels of pO2 and pCO2 in the blood.

In acidosis, when breathing rate increases to expel CO2, the pO2 in the blood increases (since you're expelling CO2 primarily while inhaling O2). However, I don't think the increase is a significant one.

To understand what happens to Hb saturation during hyperventilation and hypoventilation, I think it helps to think of hyperventilation as a decrease in pC02 (an increase in pH) and of hypoventilation as an increase in pCO2 (a decrease in pH). Thinking like this, you just need to look at Hb saturation curves and how they're affected by changes in pH and pCO2. A decrease in pH shifts the curve to the right while and increase in pH shifts the curve to the left.

Hope this helps.

Transformers said:

I was curious about the levels of oxygen in the body

1.) When we refer to PO2, we are referring to the 2% of the oxygen in the body that is dissolved in the blood right? This is relatively constant correct?
a.) What about in metabolic acidosis when PCO2 is high and you need to compensate by hyperventilation? We know as a result PCO2 drops and pH rises....but does PO2 rise up OR does it stay relatively constant? What actually occurs here?

2.) Basically this leads me to ask about the O2 bound to hemoglobin. I understand the % saturation curves + the Bohr and Haldane effects. 98% of O2 is in the Hemoglobin (2% is dissolved) with nearly fully saturated in the lungs and about 70% in metabolically resting systemic tissues or 40% in metabolically active tissues...my question is how do ventilation responses affect the saturation of Hemoglobin or are they unrelated? That is if you hyperventilate, how does this affect %saturation of Hb (and thus ultimately levels of HB-O2) at the lungs and tissues?

My overall inquiry is to find out what happnes to your oxygen levels (in Hb and in the blood pO2) during periods of ventilation.

Thanks.

Click to expand...

I think it is wrong to say "the 2% of the oxygen dissolved in the blood". 2% of what? I think we are stating that 98% of the Hb is bound to O2, and the rest of the O2 is dissolved. 2% is the amount of Hb not bound.

I would assume that PO2 remains relatively stable. You are breathing in more O2 but you also are not allowing it to exchange as much as in deep breathing. The body is just trying to expel CO2 here. This knowledge is likely beyond the MCAT.

you keep stating that 98% of the O2 in the body is bound. I think it is supposed to be 98% of the Hb is bound, these are two different statements. I don't think 98% of O2 is on the Hb, this is backwards thinking.

Hyperventilation likely does NOT affect Hb saturation, at least directly. The reason I state this is because we are at a near saturation point for O2 already, why would increasing O2 slightly from hyperventilation cause you to bind more? The slope is flattening and conc increases have negligible effects. Hyperventilation to increase blood pH would directly affect Hb saturation and push the saturation curve to the left, increasing the affinity to bind to O2.

Like Kaushik just said, understand that pH and CO2 affect the sat curve (I think you already knew this).

I wouldn't think if there were 100 molecules of O2 in the body that 98 of them are attached to Hb. Instead we are saying if there were 100 Hb's in the body, 98 of them are attached to O2.