DNURS 827 CV Microcirculation, Lymphatics, & Local Control of Blood Flow

Question 1

1. What is capillary filtration?

Answer 1

a. Net movement of water from capillary to interstitial space

Question 2

2. What is capillary reabsorption?

Answer 2

a. Net movement of water from interstitial space to capillary

Question 3

3. What are the Starling Forces with regard to capillary filtration/reabsorption?

Answer 3

a. Fluid filtered out from capillary pressure
b. Fluid reabsorbed from plasma osmotic pressure
c. Fluid in = fluid out

At the arteriolar end of the capillary, fluid is filtered through the semipermeable endothelium into the interstitial space. The driving pressure gradient here is the difference between the hydrostatic pressure of the interstitial fluid (Pi) and the much higher capillary hydrostatic pressure (Pc); this gradient favours the movement of fluid out of the capillaries and into the interstitium.

This (Pc- Pi) gradient is opposed by the oncotic pressure gradient (oncotic pressure being the carefully scrutinised subject of another chapter). The capillary oncotic pressure (Πc) is higher than the interstitial oncotic pressure (Πi) owing to the abundance of protein in the capillary blood. This gradient favours the movement of fluid out of the interstitium, and into the capillary.

At the arteriolar end of the capillary, the hydrostatic pressure gradient is a more powerful force than the oncotic pressure gradient. Oncotic pressure is defeated, and fluid is ultrafiltered into the interstitial space. In the postcapillary venules, the hydrostatic pressure is very low, and the oncotic forces become dominant, attracting some (but not all) of the ultrafiltered fluid back into the intravascular compartment. The remaining fluid relies on lymphatic drainage to mediate its return into the circulation.

Question 4

4. What is osmosis?

Answer 4

The movement of water across a semi-permeable membrane

Water moves from the region of high concentration to one that has a lower concentration of water

Question 5

5. If Net Driving Forces are positive, does it favor capillary filtration or reabsorption?

Answer 5

a. Capillary filtration
b. Negative net driving force= capillary reabsorption

Question 6

6. Are hydrostatic pressures within the capillary equal at the arteriolar end and the venous end?

Answer 6

a. No
b. Arterial capillary pressure = 30mmHg
c. Venous capillary pressure = 10mmHg

Question 7

7. Under normal circumstances, what Net Driving Force favors fluid movement INTO the capillary?

Answer 7

a. Interstitial fluid colloid osmotic pressure?
b. Reabsorption=negative net driving force?

Question 8

8. What would the Net Driving Forces be in a patient with congestive heart failure? Would they favor filtration or reabsorption?

Answer 8

a. Back-up of blood increases capillary hydrostatic pressure=capillary filtration

Question 9

9. What is the function of the lymphatic system?

Answer 9

Another route that pumps fluid, proteins, and large matter away from tissue space to capillaries

• An accessory route through which fluid can flow from the interstitial spaces into the blood

• The lymphatics can carry proteins and large particulate matter away from tissue spaces

• The return of proteins to the blood from the interstitial spaces is an essential function.

• Scavenger system that removes excess fluid, excess protein molecules, debris and other matter from tissue space

• When fluid enters the terminal lymphatic capillaries, the lymph vessel walls automatically contract for a few seconds and pump fluid into the blood circulation. This overall process creates the slight negative pressure that has been measured for fluid in the interstitial spaces.

Question 10

10. How is plasma filtrate returned to the circulation by the lymphatic system?

Answer 10

a. Tissue pressure, intermittent skeletal muscle activity, lymphatic vessel contraction, one-way valves

• Larger lymphatics have smooth muscle cells.
• Spontaneous and stretch-activated vasomotion serves to “pump” lymph. Vasomotion is the spontaneous rhythmic contraction and relaxation of lymphatic vessels
• Increased pressure stretched the vessel and induces myogenic contraction
• Sympathetic nerves can modulate vasomotion.
• One-way valves direct lymph away from tissues and eventually back into circulation via the thoracic duct and subclavian veins.
• 2-4L/day returned to the systemic circulation
• Filtration= reabsorption + lymph flow
• Tissue pressure
• Intermittent skeletal muscle activity
• Lymphatic vessel contraction
• System of one-way valves

Question 11

11. What is the thoracic duct? Where is it found and what does it connect to?

Answer 11

a. The largest lymphatic vessel
b. Found between left Internal Jugular and left subclavian vein
c. It collects most of body’s lymph
d. It connects/empties into the Left IJ, Left subclavian vein, or the angle between them.

Question 12

12. What things may cause edema?

Answer 12

a. Increased capillary hydrostatic pressure
b. Increased capillary permeability
c. Decreased plasma oncotic pressure
d. Lymphatic obstruction

Question 13

1. Name 3 endogenously found vaso-constricting substances.

Answer 13

a. Catecholamines (epi, norepi, dopamine), Endothelin, angiotensin II, vasopressin, serotonin

Question 14

2. Name 3 endogenously found vaso-dilating substances.

Answer 14

a. Histamine, adenosine, nitric oxide, carbon dioxide, hydrogen ions, prostaglandins, acetylcholine, bradykinin

Question 15

3. What is the Metabolic Mechanism? What substance is responsible for this mechanism?

Answer 15

a. An event that results in inadequate O2 supply for metabolic needs, causing formation of vasodilator substance to increase blood flow; adenosine, potassium ions, CO2, H+, lactic acid, inorganic phosphates

Question 16

4. What is the Myogenic Mechanism?

Answer 16

a. Sudden stretch of blood vessel causes smooth muscles to reactively contract to restore vessel diameter and resistance

Question 17

5. What is Reactive Hyperemia? Give a common clinical example of Reactive Hyperemia.

Answer 17

a. The rush of blood flow by 4-7x normal when the blood flow of a blocked tissue becomes unblocked. Increased blood flow lasts as long as period of occlusion.

b. the transient increase in organ blood flow that occurs following a brief period of ischemia (e.g., arterial occlusion)

c. Reactive hyperemia occurs following the removal of a tourniquet, unclamping an artery during surgery, or restoring flow to a coronary artery after recanalization (reopening a closed artery using an angioplasty balloon or clot dissolving drug)

Question 18

6. What is Autoregulation? What mechanism of blood flow regulation is thought to be involved?

Answer 18

a. Intrinsic ability of an organ to maintain a constant blood flow despite changes in perfusion pressure

b. This is done using both metabolic and myogenic mechanisms

Question 19

7. Name 3 endothelial factors that help regulate blood flow?

Answer 19

a. Nitric oxide (endothelium-derived relaxing factor), prostacyclin (vasodilator), endothelin (vasoconstrictor), endothelial-derived hyperpolarizing factor

Question 20

8. What is nitric oxide? How might it be helpful during one-lung ventilation?

Answer 20

a. Most important endothelial-derived relaxing factor; lipophilic gas made from L-arginine; decreases free calcium  increases cGMP; half-life= 6 seconds

b. Helpful because it causes pulmonary vasodilation preferentially in the ventilated lung which improves oxygenation and V/Q. Also recruits blood away from poorly ventilated areas of the lung. So in one lung, it would help to maintain oxygenation while the other lung is not being ventilated.

Question 21

9. Is Endothelin a vaso-dilator or -constrictor?

Answer 21

a. vasoconstrictor

Question 22

10. Why are blood vessels prone to vaso-constriction, vaso-spasm and thrombosis when the endothelium is damaged?

Answer 22

Where there is damage to the endothelial cells, there is a decrease in nitric oxide & prostacyclin and increased endothelin vasoconstriction, vasospasm, thrombosis

Increased endothelin release is believed to contribute to vasoconstriction when hypertension damages endothelium. When damage to the endothelium occurs, damage to the endothelial cells lead to a decreased nitric oxide and prostaglandin production, and increased endothelin production which leads to vasoconstriction, vasospasm and thrombosis.