Thread by @aryadoctoryet

#medtwitter #tweetorial on one of my favorite, elegant little mechanisms. This is something every #resident and #medstudenttwitter will see ALL the time! Bonus inclusion: a simple way to think about macro/micro-cytosis.

So, why is basically everyone in the hospital anemic?

1/

Principles:

- it is useful to remember that the venous blood “drawn” for a lab test is composed of many parts: plasma, RBCs and WBCs.

- Hemoglobin (Hgb) is a direct measure of the actual Hgb molecule within the RBCs

&

- hematocrit (Hct) is the % volume of RBCs

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So why can we “cheat” and just multiply the hemoglobin by 3 to get the hematocrit?

Well - in a healthy RBC, approximately 1/3 of its space is a hemoglobin molecule!

So, imagine each RBC as just a Hgb molecule wearing a coat! The Hgb is 1/3 of the space, the coat 2/3s!

3/

So,

Naked Hgb x 3 = a dressed in coat Hgb = a RBC!

This means if we know what our Hgb is, and we dress up all of our Hgb, we have RBCs and know how much space they’re taking! How much space the RBCs are taking is....the hematocrit!

This is why Hgb x 3 ~= Hct!

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Let’s get fancy. What if our coat was...much bigger? Or much smaller?

If the coat is bigger, then our Hgb x3 “estimate” is too low since it should be Hgb x4 or x5 because the coat is larger!

Lucky for us, our lab can literally see that the RBCs are taking more space.

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Which means, when we do our Hgb x 3 estimate, our number is going to be smaller than the Hct!

Because our “coat” is very big, the RBC is big....aka the MCV (mean “coat” volume 😉) is big....aka macrocytosis!

So, if our Hgb x3 is < Hct, we can suspect macrocytosis!

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Likewise, if our “coat” is very tight around the Hgb, then our RBC is tiny, and our Hgb x 3 calculation will be >> Hct.

Tiny coat, tiny RBCs, Hgb x 3 > Hct = suspect MICROcytosis!

7/

So, how does this help us understand why everyone is basically anemic in the hospital?

Well, just like with our Hgb coat size, if the other stuff in our sample changes, the space our RBCs take up relative to the sample also changes!

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In the hospital setting, or really, any type of stressful setting, we’ve got a lot of catecholamines floating around!

These catecholamines hit the sympathetic receptors, preferentially vasoconstricting ARTERIOLES.

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Remember the two forces for fluids in the body: hydrostatic and oncotic.

With our arteriole vasoCONSTRICTION, our oncotic (protein) pressure pulling fluid INTO vessels doesn’t change, the proteins are all hanging out still in the arterioles and venules.

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However, our hydrostatic pressure DOES change. How?

Well, the arteriole constricts, preventing as much blood from flowing to to the venule, which means, the venules “see” a LOWER hydrostatic pressure!

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They don’t like this! They wana be normal so they PULL MORE FLUID IN from the surrounding tissue & via the lymph system!

Vasoconstriction at the arteriole causes the venules to pull in more fluid.

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More fluid in the veins = more “stuff” besides our RBCs when we draw our blood! So we see an anemia! This is known as a “dilutional” anemia because it’s not that we HAVE less RBCs, it’s just that we are SEEING less because of the other “stuff!”

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In a hospital setting — stress, pain, anxiety, etc cause catechols to float around which cause vasoconstriction @ arterioles.

Vasoconstriction at the arteriole causes decreased DOWNSTREAM hydrostatic pressure & the body compensates @ the venule and pulls more fluid in!

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This causes us to “see” a dilutional anemia!

Now when your in significant pain patient has anemia, you can tell your staff it’s not because you think they’re bleeding! 🙌🏽

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To summarize:

- Hgb x 3 ~= RBC size ~= Hct

- Hgb x 3 >> Hct = small coat = suspect microcytosis

- Hgb x 3 << Hct = big coat = suspect macrocytosis

16/17

- stress/anxiety/pain in hospital settings cause arteriolar vasoconstriction leading to decreased downstream venule hydrostatic pressure and so the body compensates by pulling in fluid from the tissue & lymph system @ the venule causing venodilution and dilutional anemia!

FIN.