Why does Hgb concentration change in a CBC during a bleeding event?

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DrMetal

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Riddle me this: (good question posed by a medical student)

In an acutely bleeding patient, we often note a dropping Hgb in a series of CBCs (12 g/dL --> 10 --> 8, etc).

But this measured value from the CBC is a concentration of Hgb (g/dL), not a total amount.

It makes sense that the total amount of Hgb (or the total amount of blood volume) would drop in a bleeding patient, but why would the concentration change so abruptly? Shouldn't the concentration remain fairly constant? [If you had 10 L of sugar water of a certain concentration, 2 molar, then you drained out 5 L, the new concentration should be the same, 2 molar. total amount of sugar is decreased, but concentration, assuming uniformly dissolved, is the same.]

Or, is it the case that the Hgb we're getting from a CBC is not a true concentration, but some number more reflective of the total Hgb in the body?

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It probably has something to do with fluid shifts between the different fluid compartments in the acute stage, then in the more subacute stage you’ll probably have difficulty creating hemoglobin and new red blood cells as you also lose iron with acute blood loss.
 
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It probably has something to do with fluid shifts between the different fluid compartments in the acute stage, then in the more subacute stage you’ll probably have difficulty creating hemoglobin and new red blood cells as you also lose iron with acute blood loss.
Makes some sense. An acute fluid shift (say to keep BP elevated) would explain the drop in concentration.

The quantitative amount of Hgb though, I think, would be affected in the chronic or very subacute phase, only. (Your ability to make Hgb is not immediately impacted by say trauma, a GSW, but certainly is impacted by chronic anemia)
 
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A very rapid bleed (like arterial-enteric fistula, bad variceal bleed, surgical bleed etc) the hb won't change very quickly and isn't part of the resuscitation decision tree. Once a bleed is slower or believed to be controlled hb trending can be done to see how active it still is.

Like if a cirrhotic comes in and is having massive quantity of melena getting fluids and is hypotensive tachy to 130s you better bet that I don't give a **** if his hct on the ABG is normal he is getting 4-6 units of blood minimum while resuscitation is ongoing.
 
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It doesn’t change acutely.. the drop you see at about 24 hours is due to interstitial fluid reabsorption, or more commonly crystalloid resuscitation.
 
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Agree with above, and add that this is also due to ADH effect. After a bleed, circulating volume is decreased. This will trigger the pituitary to release ADH independent of the current Na concentration. It also will increase salt hunger. Both will work towards replacing the lost blood volume with plasma.
 
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At first, hemoglobin will not change. It takes a few hours for it to fall as the body tries to restore effective intravascular volume:
1. The quickest shift is interstitial fluid to intravascular. Transcapillary pressure = hydrostatic pressure - oncotic pressure, so because hydrostatic pressure is decreased in setting of significant bleeding, some interstitial fluid (water plus electrolytes) will diffuse into the intravascular space.
2. The next quickest is fluid shifting from the intracellular space to the extracellular space. I'm not 100% sure on the mechanism, but I believe some diffusion is involved.
3. The slowest is the renin-angiotensin-aldosterone system. Aldosterone leads to increased sodium reabsorption in the collecting duct, which results in increased water retention (and therefore increased extracellular volume) by osmosis. ADH secretion is increased as well, but ADH does not do much for volume. It is more for ensuring there is enough free water so that the solute concentration is appropriate. (i.e. aldosterone secretion without ADH would lead to hypernatremia)
 
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