L17 Microcirculation and Lymphatics

Question 0

Capillary blood flow

Answer 0

Flow is via Rouleaux formation – RBCs are single file and slightly slanted
Precap sphincters can control whether or not capillaries will receive flow. If they shut off, BF directed somewhere else.
Vasomotion is irregular and movement is not uniform. Direction based on P gradients

Question 1

Structure of microcirculation

Answer 1

arterioles –> pre-capillary sphincters (can shut off flow through a capillary bed)–> metarterioles (like bridges that do not participate in O2 exchange) –> capillaries –> venules (no control in resistance)

Question 2

Transcapillary fliud exchange (TCF)

Answer 2

Capillary hydrostatic pressure pushes fluid out

Capillary oncotic pressure pulls fluid in based on [proteins] inside

Inerstitial oncotic and hydrostatic should both be 0 in normal conditions

Question 3

TCF in hemorrhage

Answer 3

In hemorrhage, Blood volume is reduced so fluid would be taken into the capillary from the interstitium

Question 4

TCF in nephrosis

Answer 4

Glomerular cap walls get more permeable, so more proteins are filtered into the urine. If more proteins are taken out of the blood, the oncotic pressure will decrease and hydrostatic P will win out, pushing fluid out.

Question 5

TCF in liver damage

Answer 5

Liver damage results in less albumin, the main factor in oncotic pressure. Therefore, the oncotic P is lower and fluid will be pushed out

Question 6

TCF in portal hypertension

Answer 6

Portal hypertension is caused by a backup of blood in the liver. This will …../?????????????

Question 7

TCF in burns

Answer 7

Burns increase the permeability of capillaries, mean that fluid leaks out. Edema will ensue

Question 8

TCF in CHF

Answer 8

CHF causes an increase in blood volume and hypertension. This is an increase in the hydrostatic P and fluid will be pushed out. Edema.

Question 9

Pre-Post capillary resistance

Answer 9

Pre capillary resistance comes from arterial side. Since this side is very low compliance, changes in resistance are not as easily transferred to the caps
Post cap resistance comes from the venous side. Since veins are so compliant, they are the PRIMARY DETERMINANT OF CAPILLARY PRESSURE. if the veins are high p, the caps are high p

Question 10

Endothelial-derived mediators (NO, endothelin, metabolites, prostacyclins, EDRF)

Answer 10

These factors are released when the resistance through a vessel increases. When the R goes up, the shear stress against the vessel wall goes up and this shearing against the endothelium releases the above factors to vasodilate. (Endothelin is a constrictor - this is released when shear stress is reduced)

Question 11

Lymphatic system

Answer 11

This is a system of one-way flow with valves (like the venous system) that is responsible for taking interstitial fluid back to the Subclavian veins. The endothelial cells are non-fenestrated so nothing can leak. There is no smooth muscle, so fluid moves along with skeletal muscle pumps.

Question 12

Edema

Answer 12

an accumulation of excess fluid in the interstitium that is not taken up by the lymphatics.
Causes:
Liver failure - lack of albumin in blood leads to less oncotic pressure
Burns - increases cap permeability and thus fluid leaks out
Renal disease - loss of protein in blood = less oncotic P
Obstruction of venous return
CHF - venous side of the system is backed up due to decreased CO, which means the post-cap resistance is higher, and the hydrostatic pressure of the capillaries in increased.