Sickle Cell Anemia Question

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Hey guys. So I am doing a Sickle Cell Anemia research paper/case study and I seem to be stuck on this one question. "Discuss how these lab results are consistent with patients who have SCA". The lab results are as follows:

white blood cell count (WBC) 18 x 109/L (higher than norms)

red blood cell count (RBC) 3x1012/L (lower than norms)

hemoglobin (Hgb) 75 g/L (lower than norms)

hematocrit (Hct) 0.218 (lower than norms)

reticulocyte count 0.23 (lower than norms)

ABG'S

pH 7.54 (alkalosis)

PaCO2 32 (lower than norms)

HCO3 22 (in range)

PaO2 87 (in range, but on the low end)

I understand why the RBC, Hgb, Hct, retic count, and WBC count are outside of norms considering the diagnosis, but I don't understand why the ABG's are affected. All thoughts are appreciated!

desperately waiting for clarification still

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Specializes in Adult Internal Medicine.

Sorry I was having dinner.

Want the simple explanation or the long one?

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the long one :)

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Specializes in Adult Internal Medicine.

The body wants to balance the PCO2/HCO3 ratio because when the ratio is small there is a reduction of hydrogen ion concentration (alkaline). Conversely when the ratio is large there is a increase of hydrogen ion concentration (acid).

The body buffers this via two mechanisms. First, hydrogen ions are released which binds to HCO3 to make carbonic acid reducing HCO3 to match the drop in PCO2. This causes a mild compensatory reduction in the HCO3 levels.

Eventually the kidneys start to compensate for the imbalance by increasing resorption of hydrogen ions and increasing excretion of HCO3 to maintain a balanced ratio. This results in a more pronounced compensatory reduction of HCO3.

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The bloods pH is not made acidic by Carbonic Acid, rather by free hydronium (H+) ions in the blood. In order to compensate for the acute respiratory alkalosis, the already formed carbonic acid should be dissociating to form more HCO3 and H+ ions, thereby decreasing the pH. But i agree with your third statement "Eventually the kidneys start to compensate for the imbalance by increasing resorption of hydrogen ions and increasing excretion of HCO3 to maintain a balanced ratio. This results in a more pronounced compensatory reduction of HCO3."

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Specializes in Adult Internal Medicine.
The bloods pH is not made acidic by Carbonic Acid rather by free hydronium (H+) ions in the blood. [/quote']

The carbonic acid is the buffer, recusing the concentration of HCO3 to match the drop in PCO2.

Free hydrogen ions don't cause the blood to be acidic, they are what makes the blood acidic. The PCO2/HCO3 imbalance causes the low concentration of hydrogen ions which makes the blood alkaline.

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The body wants to balance the PCO2/HCO3 ratio because when the ratio is small there is a reduction of hydrogen ion concentration (alkaline). Conversely when the ratio is large there is a increase of hydrogen ion concentration (acid).

The body buffers this via two mechanisms. First, hydrogen ions are released which binds to HCO3 to make carbonic acid reducing HCO3 to match the drop in PCO2. This causes a mild compensatory reduction in the HCO3 levels.

Eventually the kidneys start to compensate for the imbalance by increasing resorption of hydrogen ions and increasing excretion of HCO3 to maintain a balanced ratio. This results in a more pronounced compensatory reduction of HCO3.

I think this just made everything click after the 3rd time I read it. :'D

Thank you!

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The bloods pH is not made acidic by Carbonic Acid rather by free hydronium (H+) ions in the blood. In order to compensate for the acute respiratory alkalosis, the already formed carbonic acid should be dissociating to form more HCO3 and H+ ions, thereby decreasing the pH. But i agree with your third statement "Eventually the kidneys start to compensate for the imbalance by increasing resorption of hydrogen ions and increasing excretion of HCO3 to maintain a balanced ratio. This results in a more pronounced compensatory reduction of HCO3."[/quote']

What I'm perceiving is this...

In basic terms: More co2 more acidic. More HCO3 more basic.

This patient had a drop of CO2 due to respiratory patterns. Making them go into respiratory alk.

The body is trying to "use" the BASIC HCO3 by combining it with hydrogen ions to make Carbonic acid.

The carbonic acid IS the temporary fix.

This subtle drop in HCO3 is evidenced in the ABGs in your patient.

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correct, the carbonic acid is the temporary fix as it is using the basic HCO3 ions in the blood (so less freely roaming HCO3 so the bloods pH drops because of that, not because Carbonic Acid is actually acidic in itself)

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correct the carbonic acid is the temporary fix as it is using the basic HCO3 ions in the blood (so less freely roaming HCO3 so the bloods pH drops because of that, not because Carbonic Acid is actually acidic in itself)[/quote']

Yay! C:

That was some awesome nerdy student nurse action.

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This is the conclusion i am trying to make: Because the red blood cells take on a sickle shape and harden, they cannot easily pass through capillaries or other small vessels and can cause vascular occlusion, leading to acute or chronic tissue injury. The red blood cells cannot effectively carry out internal gas exchange which has lead to local hypoxia and hypocapnia. For the same reason, although her PaO2 is in range, it is still low. In an attempt to compensate, her respiratory rate has increased to 25 beats per minute.

Is this correct?

No, it isn't. She is not remotely hypoxic. Normal PaO2 on room air at sea level is 80-100, and 87 is close to midrange, not low. Hypoxia is not the first respiratory driver, anyway, elevated CO2 or acidosis is, and hers is not elevated and she is not acidotic.

Localized hypoxemia can make someone acidotic if there is lactic acidosis as a byproduct of anaerobic metabolism, but that would give you a very low bicarb. You see this in nasty things like mesenteric artery thrombosis, where a big honking piece of gut has no decent arterial flow and goes anaerobic resulting in metabolic acidosis. You would see a low, not high, pH in that case, and a low CO2 as the body attempts to compensate by getting rid of as much CO2 as it can. NOT what you see here.

She is alkalotic because she is hyperventilating and losing CO2, right. But even if her RBCs aren't capable of delivering normal tissue oxygenation (and you don't know that's true because you have no acidosis going on), you have no indication that her tissues are hypoxic. You have a respiratory alkalosis, which means her ABD represents a respiratory, not a metabolic derangement.

I gave you a really good hint earlier, a common finding in SCA :)

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Dear nurse, I see you're being a typical intolerant nurse. These SCD patients need your help, not your judgments, or your semi-racial bias. Yeah, some SCD patients are addicted, but people like you make their disease worse! In fact, attitudes like that can kill these patients, unless that's what you want huh, dead SCD patients. Stay away from racist nurses and doctors who badmouth these patients. Lead, not follow. If you hate SCD patients that much, take up another career. See, you are part of the problem, when you should stick up for the patient, even when they're a problem. They act the way they do because of attitudes like yours. All their lives, they've had to fight to get respect, and you and your nurse pals had better give it to them, got that. How dare you treat them like that. A nurse is supposed to soothe, love, listen and learn from their patients. How would you like it if a stranger passed judgment on you? You're not fit to be a nurse. It takes a massive amount of patience, and you just don't have it. Tell us something. Is the Hippocratic oath just a joke to you? "First do no harm" doesn't mean much anymore does it?

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