Lymph flow rate is usually low. It is influenced primarily by the rate of lymph formation. For example, if blood capillary pressure is increased by arterial vasodilation or venous constriction, the flow rate of lymph increases. Also, the flow rate is affected by compression of lymphatics by contraction of neighboring musculature and by negative intrathoracic pressure (breathing).
Interstitial pressure (so pressure in the ECF, which would increase if given IV saline) and lymph flow are positively related. A small increase in interstitial volume greatly increases its pressure, promoting lymph flow that acts to restore the interstitial volume to normal.
more on this topic: https://www.ncbi.nlm.nih.gov/books/NBK53448/
Vasoconstriction (narrowing of a tube) will cause the flow rate to increase through that tube, which decreases radial/outward pressure. The faster a fluid moves through a tube, the less โoutwardโ force it exerts. (This is known as the Venturi effect.)
I think the more correct explanation is that lymph mostly is hyrdostatically pressed out of the thinner walled small arterioles, capillaries, venules
If you vasoconstricted the pulmonary arteriole, youd get hydrostatic backup but not into the smaller arteries, capillaries, veinules but actually less flow (due to constriction) and less lymph formation.
20% albumin is HYPERtonic and causes drawing of fluid out of the interstitum and into the blood.
"Albumin (Human) 20% is indicated in the emergency treatment of hypovolemia with or without shock. Its effectiveness in reversing hypovolemia depends largely upon its ability to draw interstitial fluid into the circulation. It is most effective in patients who are well hydrated. When blood volume deficit is the result of hemorrhage, compatible red blood cells or whole blood should be administered as quickly as possible."
https://www.drugs.com/pro/albumin-human-20.html
Vasoconstriction decreases blood flow and thus decreases hydrostatic pressure. Seems counter intuitive but I had to look this up after I got it wrong, too.
Can someone help a brother out? My thinking was that increased fluid in the interstitial leads to increased lymph, so I thought they were looking for something to simulates high altitude pulmonary edema or arterial pulmonary HTN, which I am pretty sure both lead to pulmonary edema. Where did I go wrong?
submitted by โandro(269)
First Point : Lymph forms at the Capillary level of blood vessels ( as this is where fluid moves in and out of vessels along with metabolites and nutrients ) .
The function of lymph is to return excess proteins and interstitial fluid back to the bloodstream ( Recall Lymph eventually drains into the large veins)
Second Point : We may increase lymph either by increasing 1. the rate at which we form it . 2. Decreasing the rate of drainage ( i.e - obstructing lymph vessels )
To increase lymph formation we have to increase the rate at which fluid filters out of the capillaries . This can be done by altering Starlings forces in the capillary
Going through the options
Option A : Endothelin will cause vasoconstriction of Pulmonary artery .This is precapillary meaning we will have less blood/ fluid getting to the capillaries - decreased hydrostatic pressure and decreased lymph formation
Option B : Constriction of pulmonary artery again
Option C and D : lead to the physiologic response of hypoxic vasoconstriction
Option E : Increased oncotic pressure decreases the amount of fluid moving out of capillaries