Fetal Circulation Question

[Sammy1024]

2. Some children persist in forming fetal hemoglobin for months or even years after birth. Such children would likely:

A. be able to withstand environments having low oxygen content.
B. be able to shunt blood from the right to the left side of the heart.
C. be unable to survive in the absence of an artificial oxygen supply.
D. be unable to bear children.

So in the passage it gave some facts like fetal blood is 67% saturated while humans have 98/99% saturation.

I was wondering why the answer would be A instead of C. I eliminated B and D because they're those "random" or "completely irrelevant" answers. So then I was thinking that a baby would need the 98/99% saturation once born and if it keeps producing fetal hemoglobin, then only 67% of it will be saturated which isn't enough?

I'm under the assumption that the answer is saying that since fetal hemoglobin can bind Oxygen better, then if you're in a poor O environment, it can bind whatever is necessary to reach the 98/99% saturation?

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[DrknoSDN]

I'm under the assumption that the answer is saying that since fetal hemoglobin can bind Oxygen better, then if you're in a poor O environment, it can bind whatever is necessary to reach the 98/99% saturation?

Yes. Option A is describing that scenario where fetal hemoglobin is able to pull oxygen from the air better than adult hemoglobin.
In normal atmospheric conditions fetal hemoglobin saturation would be the same or higher than adult hemoglobin because oxygen more readily binds fetal hemoglobin.

The only difference would be in delivery to the tissues. Fetal hemoglobin does not release oxygen at the tissues as readily so some tissues might become slightly hypoxic on exertion but not to a degree that would be fatal. The 67% number is because the fetus is having to extract oxygen from the mothers blood supply instead of directly from the air.
If you look at the saturation curves there really is not a large difference, just enough for oxygen to transfer from mother to fetus.

 

[Sammy1024]

Oh thank you! I need to remember to look at the big picture. For some reason I thought the 67% meant it only is 67% saturated ever. So dumb of me. Thanks so much! :]]

 

[Mantis Toboggin]

Yes. Option A is describing that scenario where fetal hemoglobin is able to pull oxygen from the air better than adult hemoglobin.
In normal atmospheric conditions fetal hemoglobin saturation would be the same or higher than adult hemoglobin because oxygen more readily binds fetal hemoglobin.

The only difference would be in delivery to the tissues. Fetal hemoglobin does not release oxygen at the tissues as readily so some tissues might become slightly hypoxic on exertion but not to a degree that would be fatal. The 67% number is because the fetus is having to extract oxygen from the mothers blood supply instead of directly from the air.
If you look at the saturation curves there really is not a large difference, just enough for oxygen to transfer from mother to fetus.

I'm sorry to bump this but why exactly does this imply slight hypoxia for the fetus? I get that at the tissue level, due to the left shift, o2 won't be delivered as readily, but don't these children have a higher po2 to begin with? Wouldn't this cause metabolic alkalosis if anything?

Deox Fetal hb will bind to atmospheric o2 more readily in the lungs.

 

[DrknoSDN]

I'm sorry to bump this but why exactly does this imply slight hypoxia for the fetus? I get that at the tissue level, due to the left shift, o2 won't be delivered as readily, but don't these children have a higher po2 to begin with? Wouldn't this cause metabolic alkalosis if anything?

Deox Fetal hb will bind to atmospheric o2 more readily in the lungs.

For clarification I was referring to a child with only fetal hemloglobin, under exertion, breathing atmospheric pressure air.

I am not certain but I believe hypoxia on exertion could be possible because at atmospheric pO2 (of around 160 mmHg), Hb saturation is near 100% for both types of hemoglobin (adult and fetal).
If you look at the graph they level out around 100 mmHg pO2, and after that the main factor would be tissue delivery of oxygen as both would bind standard atmospheric oxygen normally. (The fetal hemoglobin would bind better in low oxygen environments like the question said)

Having a stronger oxygen affinity could cause fetal hemoglobin to release less oxygen than the adult hemoglobin. Also adult hemoglobin is made of sub-units that form a binding pocket for 2,3-BPG while fetal hemoglobin does not allow significant binding to aid oxygen delivery. The idea that a child with only fetal hemoglobin could experience tissue hypoxia on exertion came from the oxygen delivery graphs. The images shows a significantly lower partial pressure required to get to 50% Hb saturation. (26.8 to 19 mmHg).

Also this image shows the tissue pressure region around 19 mmHg with 50% saturation for fetal vs 25% adult bound oxygen. This link (and other research) suggests an 18 mmHg pO2 as a minimum value during cardiovascular endurance exercise but it probably varies.
At that very low cellular pO2 adult hemoglobin would deliver around 25% more oxygen to the tissues that need it.

 

[Mantis Toboggin]

For clarification I was referring to a child with only fetal hemloglobin, under exertion, breathing atmospheric pressure air.

I am not certain but I believe hypoxia on exertion could be possible because at atmospheric pO2 (of around 160 mmHg), Hb saturation is near 100% for both types of hemoglobin (adult and fetal).
If you look at the graph they level out around 100 mmHg pO2, and after that the main factor would be tissue delivery of oxygen as both would bind standard atmospheric oxygen normally. (The fetal hemoglobin would bind better in low oxygen environments like the question said)

Having a stronger oxygen affinity could cause fetal hemoglobin to release less oxygen than the adult hemoglobin. Also adult hemoglobin is made of sub-units that form a binding pocket for 2,3-BPG while fetal hemoglobin does not allow significant binding to aid oxygen delivery. The idea that a child with only fetal hemoglobin could experience tissue hypoxia on exertion came from the oxygen delivery graphs. The images shows a significantly lower partial pressure required to get to 50% Hb saturation. (26.8 to 19 mmHg).

Also this image shows the tissue pressure region around 19 mmHg with 50% saturation for fetal vs 25% adult bound oxygen. This link (and other research) suggests an 18 mmHg pO2 as a minimum value during cardiovascular endurance exercise but it probably varies.
At that very low cellular pO2 adult hemoglobin would deliver around 25% more oxygen to the tissues that need it.

Do you mind explaining the significance of the p50 mark in general?

I'm still trying to understand the big picture here.

With high po2 levels, the child would have to breath in less to gain basal metabolic pco2 levels back to normal.

The opposing force here is the higher affinity for po2 in fetal HB, which means that normally pco2 levels would be higher than if the HB was that of a healthy child.

So for high pco2 (co2/h+ cannot as readily compete for o2 for HB binding), the body normally breathes more, but the fetal HB helps to do this with higher o2 affinity.

Would it be correct to say that while the pco2 and po2 levels would be metabolically the same, the actual delivery of o2 to the baby's tissue would be lower, therefore hypoxia would occur? So neither alkalosis nor acidosis.

I'm just terribly confused at what the net effect is going to be on overall po2 and pco2 levels, if we are assuming normal resting state.

 

[DrknoSDN]

In general this is all very unlikely to be on the MCAT. Even the OP question is probably a stretch for realistic questioning.

I'm just terribly confused at what the net effect is going to be on overall po2 and pco2 levels, if we are assuming normal resting state.

I don't think you should worry about this hypothetical.

If you are interested the condition is called "Hereditary persistence of fetal hemoglobin" (HPFH), and in the medical field is usually considered asymptomatic.

Some endurance exercise studies have been done for venous blood po2 and pco2 in rested and exercised individuals.
Additionally the normal distribution of fetal hemoglobin in adults with HPFH is usually far less than 100%. So the sample size of people with very high levels of HbF that can test for muscle/tissue hypoxia would be small. This abstract talks about 2 brothers who have the condition but do not show symptoms of increased muscle hypoxia as judged by lactate turnover. But again this is 25% HbF and not homozygous 100% HbF.
From what I found the child/adult with fetal hemoglobin should be asymptomatic unless another condition is present like anemia/thalassemia etc.


Far too much information for MCAT. Don't worry about the questions that require searching pubmed.