Why does mannitol produce Pulmonary Edema

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Aconitase

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I don't understand why mannitol would cause pulmonary edema. It seems counterintuitive to me.

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It's because the increase in hydrostatic pressure overcomes the increase in osmotic pressure in the lung. This is most apparent in a case of CHF, where cardiac output is diminished. Everywhere else, water is leaving the interstitium to enter the vasculature; in the lungs this increased blood volume pushes water out into the lungs and causes edema.
 
It's because the increase in hydrostatic pressure overcomes the increase in osmotic pressure in the lung. This is most apparent in a case of CHF, where cardiac output is diminished. Everywhere else, water is leaving the interstitium to enter the vasculature; in the lungs this increased blood volume pushes water out into the lungs and causes edema.

In physiological conditions, is the hydrostatic pressure in the pulmonary vasculaure higher than the rest of the body by default?
 
I don't understand why mannitol would cause pulmonary edema. It seems counterintuitive to me.

I think it's because mannitol is confined to the extracellular volume and raises the osmolarity of the extracellular fluid exclusively -> draws water out of the intracellular volume -> higher overall extracellular volume -> volume overload and edema.
 
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In CHF, the increased hydrostatic pressure proximal to the left atrium causes transudation in the lungs. Although mannitol can act as a diuretic, it initially increases plasma volume due to its effects on elevating plasma oncotic pressure. Increased plasma volume --> increased left atrial preload in the face of decompensation that already occurred even at a lower preload --> increased LAP (PCWP) with further decompensation --> exacerbation of pulmonary venular transudation.
 
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In CHF, the increased hydrostatic pressure proximal to the left atrium causes transudation in the lungs. Although mannitol can act as a diuretic, it initially increases plasma volume due to its effects on elevating plasma oncotic pressure. Increased plasma volume --> increased left atrial preload in the face of decompensation that already occurred even at a lower preload --> increased LAP (PCWP) with further decompensation --> exacerbation of pulmonary venular transudation.

I just read in UW that in high doses it elevates the hydrostatic pressure by pulling water out of the cells :)
 
My understanding is Mannitol is an osmotic diuretic-> increases plasma osmolarity->water and potassium come out of the interstitium& cells to compensate for this increase in osmolarity (wonder why potassium comes out)-> decrease in ICF+ increase in ECF(->if major increase in ECF-> increase in hydrostatic pressure-> pulm.edema).
Pls correct if its wrong :)
 
My understanding is Mannitol is an osmotic diuretic-> increases plasma osmolarity->water and potassium come out of the interstitium& cells to compensate for this increase in osmolarity (wonder why potassium comes out)-> decrease in ICF+ increase in ECF(->if major increase in ECF-> increase in hydrostatic pressure-> pulm.edema).
Pls correct if its wrong :)

Hyperosmolarity always shifts potassium into the ECF. If plasma is hyperosmolar, then ICF is going to move into the ECF, which results in an increased intracellular potassium concentration. To get back to equilibrium potassium will move into the ECF.

how would it increase oncotic pressure if the proteins are getting diluted?

Start at equilibrium (i.e. normal body before you throw mannitol in it)

1. Equilibrium
2. Add mannitol
3. Mannitol = osmotic --> transient shift of water from ICF to ECF
4. Increase in ECF volume in pulmonary circuit = increased hydrostatic pressure --> pulmonary edema
 
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