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 +35  upvote downvote
submitted by โˆ—hayayah(1212)

LV stopped working, pressure backed up into pulm circuit. Pulm circuit roughly is made of 3 "parts" - the capillaries, interstitial space, and the alveoli.

In cardiogenic shock, the extra blood increases capillary hydrostatic pressure, driving fluid into the interstitial space. Compared to the alveoli, the interstitial space now has more fluid (thus more interstitial hydrostatic pressure and less oncotic pressure due to ratio of fluid to protein), and as a result of this unbalancing of forces, fluid moves into the alveoli --> pulmonary edema.

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  • cirrhosis = liver issues = liver not producing albumin.

= decreased plasma colloid osmotic pressure (pressure pulling fluid into the vessels)

= fluid moves out of the vasculature and into the interstitial space (third spacing)

 +32  upvote downvote
submitted by โˆ—hello(429)

Patient's symptoms began 30 min after mowing lawn (i.e. after doing physical activity). He has severe chest pain and is cool, clammy, diaphoretic. He has increased pulmonary artery pressure and increased left atrial pressure. Taken altogether, this is cardiogenic shock.

Cardiogenic shock is a heart pump problem -- the LV isn't working.

When the LV, isn't working, it causes a back up in the direction opposite to how blood normally flows. Therefore, blood will back up in the lungs.

This causes increased capillary hydrostatic pressure --> this drives more fluid into the interstitium --> this causes increased interstitial hydrostatic pressure --> there is now more fluid than normal in the interstitium --> this affects the protein ratio within the interstitum --> this causes decreased interstitial oncotic pressure.

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targetusmle  awesomely explained :) +
lilyo  This was amazingly explained Thank you @Hello! +
pseudopseudopth  For edema to occur shouldn't interstitial oncotic pressure be increased?(when proteins are there, they can pull the fluid) +1
pseudopseudopth  And when increased interstitial hydrostatic pressure is pressure, shouldn't it oppose the edema by pushing against it? +1
pseudopseudopth  *when interstitial hydrostatic pressure is increased +2
pmofmalasia  You don't necessarily need to have increased oncotic pressure, you're correct in that decreased oncotic pressure would act against causing edema but as long as the net change in forces still acts "for" edema it will still occur. For example in this scenario, if the capillary hydrostatic pressure is greater than the change in interstitial hydrostatic and oncotic pressures. Also, the change in interstital hydrostatic and oncotic pressures is a direct result of the edema in this scenario, so it's more like they're responsible for setting the new equilibrium - if they didn't counteract it, you'd never come to a point where the leakage of fluid stops. +
kcyanide101  Hey guys please help me affirm.... so based off your explanation, if it were hypovolemic chock.... capillary Hydrostatic pressure will drop, due to blood loss... interstitial hydrostatic Pressure will drop as fluid will move into the capillaries to balance things out and interstitial oncotic pressure will increase due to fluid loss from the interstitium.... IS THIS CORRECT? tnx +

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