Cardiovascular - End bit Flashcards
One way valves: venous side : Hemodynamics of Veins
Veins have 2 major functions:
- Volume storage
- Bring blood back to heart – venous return, coupled with cardiac output
- Veins have series of one-way valves, which we don’t have on arterial side
- Venous return depends on venous pressure
La Place and Veins
- Law of LaPlace – applies to alveoli, arterial side, AND venous side
- For venous side, look at wall tension. Tension = Transmural pressure (pressure on the wall itself) * radius
- Transmural pressure on venous side is very low. So the amount of wall tension we need to keep things together is not high.
- The veins are far less likely to rupture than the arteries
Factors that influence venous pressure:
- Blood volume. (Increase volume –> increase pressure)
- Cardiac output. (Increase CO –> increase pressure)
- Veno-motion changes. (Increasing sympathetic veno constriction –> increase pressure.)
- Constrict the smooth muscle to squeeze down on vessels
•Skeletal muscle pump (see diagram above)
- When muscle contracts, can squeeze on one-way valve which increase pressure
•Respiratory Cycle
- During inhalation, increase in venous return.
- During exhalation, pressure increases a little and venous return decreases.
How Capillaries facilitate exchange
- Capillaries have thin wall of epithelial cells, make it easy for exchange
- Epithelial cells exchange gases and lipid soluble material through cell membrane
- However, larger molecules like glucose and amino acid have to move through pores
- Having pores between cells is extremely important. Most pores are 6-7 nm in diameter, allowing glucose and amino acids to go out, but keeping larger proteins (like plasma) in.
- Continuous capillaries = have pores between cells (skeletal muscle)
- Fenestrated = more holes. Between cells and also within them (intestine, kidney)
- Sinusoidal capillaries = have big holes, allow cells (like RBCs) to pass through, into circulation. (Bone marrow, liver)
- Some transcytosis also occurs (but in this class we just focus on pores)
Capillary Types
- Continuous capillaries = have pores between cells (skeletal muscle)
- Fenestrated = more holes. Between cells and also within them (intestine, kidney)
- Sinusoidal capillaries = have big holes, allow cells (like RBCs) to pass through, into circulation. (Bone marrow, liver)
Precapillary Sphincter
Precapillary sphincter = smooth muscle that controls blood flow into capillary
•Has a role in regulating how much blood flow gets into capillary bed – this is the last layer of regulation.
Capillary - Filtration and Reabsorption w/2 forces
In capillary: filtration and reabsorption
The two forces: hydrostatic pressure and oncotic pressure
- Oncotic pressure can also be called colloid osmotic pressure, due to plasma proteins
- Hydrostatic pressure denoted by Pc (Pressure capillary), Oncotic pressure denoted by π
- When blood comes in arterial side, Pc = 37 mmHg (force pushing water out), and π =25 mmHg (force to keep things in)
- Interstitial fluid pressure PIF outside capillary is +1 mmHg, which pushes fluid in. Oncotic pressure outside capillary is zero. So net force pushing things in is 26 mmHg (from plasma proteins and interstitial fluid)
- Net on arterial side is 11 mmHg pushing fluid out (glucose, ions, amino acids go with it) –> filtration
- As you go through the capillary, convert pressure to flow (PE to KE). On the venous end, pressure is much lower
- PC on venous end is 17 mmHg. π= same 25 mmHg. PIF and π the same. So net force is -9 mmHg
•Negative means will draw fluid in,–> reabsorption.
- At some point in the center of the capillary, filtration = absorption
- Center is dynamic, can move left or right
- We always filter a little more than we absorb. Risk of putting too much fluid in tissue. The fact that we have a little excess filtration means that the excess fluid has to be handled in some way –>lymph system takes it away.
- If the lymph doesn’t take care of that, over time the fluid will build up and you’ll get edema, fluid accumulation.
Capillary Hydrostatic pressure
Decrease in hydrostatic pressure across the capillary:
•When the hydrostatic aka capillary pressure is greater, get filtration
When drops below oncotic pressure, you get reabsorption
Net filtration
- Net filtration and net reabsorption along the vessel length
- The inward pressure (pP + PIF) remains constant throughout the length of the capillary whereas the outward pressure (PC + pIF) progressively declines throughout the capillary’s length
- first half of the vessel, where the declining outward pressure still exceeds the constant inward pressure, <ing> filtered out (depicted by the upward red arrows)</ing>
- last half of the vessel, progressively increasing quantities of fluid are reabsorbed (depicted by the downward blue arrows) as the declining outward pressure falls farther below the constant inward pressure.
Study this graph:
- Oncotic pressure stays constant, whereas capillary pressure changes.
- If you have an individual with compromised nutrition, who does not make enough plasma protein, the green line drops down. This will result in more filtration, less reabsorption.
So dynamic center can change either when oncotic pressure changes, or when capillary pressure changes:
- Ex: capillary pressure is higher when exercising, so the dynamic center shifts to the right
- Ex: If your blood pressure is low, then center would shift to the left
FIltration vs. reabsorption
we usually have more filtration than reabsorpiton, we have to take excess away in the lymph
- Lymph system has vessels very similar to veins. Overlapping endothelial cells are set up for one-way flow in, not out.
- So once you trap fluid in the lymph system, you can easily take it away
- If you block lymph capillaries, get edema
Precapillary sphincter is final gate keeper
Precapillary sphincters = the final gatekeeper for how much blood flow a capillary bed gets
- Involved in autoregulation of blood flow
- Smooth muscle, can constrict or relax
- If it relaxes, radius increases, and flow increases
- Precapillary sphincters in lungs can also work in reverse
- If there is a decrease in pO2, precapillary sphincters will constrict
Sphincter is sensitive to local metabolites:
- Increase in pCO2 causes relaxation (this is because increased metabolism means you need more nutrients)
- Decrease in pO2 causes relaxation
- Histamine or allergic responses causes relaxation (this leads to increased filtration, more fluid flowing out of nose)
- Increase in lactic acid (when exercising, anaerobic metabolism)
- Increase in potassium
Application for cardiorespiratory responses: high altitude scenario
pO2 is lower. We can compensate:
- Chemoreceptors increase cardiac output AND increase RMV respiratory minute volume (increase rate and increase depth)
- You blow off more CO2. so pCO2 in blood goes down. Now chemoreceptors are confused. This blocks a strong increase in RMV, temporarily. After a few days, you can really increase the RMV.
- Over time, increase # of RBCs. Hematocrit increases.
- This is stimulated by increase in EPO (erythropoietin from kidney, kidney is sensitive to decrease CO2)
- Increase in 2,3 DPG, over a couple of days
- Remember oxygen dissociation curve. If we b_low off too much CO2, the curve shifts left._ That makes it harder to unload. But if you increase 2, 3 DPG, will shift curve back to the right, normalizes.
- As you adapt to high altitude, you also increase diffusion capacity of the lungs over time (takes about a month):
- Increase # pulmonary capillaries, increase blood volume, increase alveolar surface area
2 types of altitude sickness
•Two kinds of altitude sickness:
Acute – due to cerebral edema, pulmonary edema
- Tissues are oxygen starved and blood vessels dilate
- Fluid build up is especially dangerous in the brain. If you have a headache at high altitude, get out.
Chronic symptoms
- Increase in hematocrit. If people make too many RBCs, increases viscosity of their blood.
- Increase in pulmonary arterial pressure.
- Increase in right ventricular hypatrophy – this can lead to heart failure, heart cannot generate enough pressure