Blood Flow 2 Flashcards
Cardiovascular system as a circuit (we are going to ignore capacitance for now)
Watch lecture at ~21 mins
Factors determining heart rate vs. peripheral resistance vs. stroke volume
- Heart rate is determined strictly at the level of the heart
- Peripheral resistance is determined strictly at the level of the vascular system
- Stroke volume is impacted by both the heart (e.g. contractility, degree of sympathetic tone) and the vascular system (venous return determines preload (Frank Starling)
Changes in pressure in arteries
- Most of the blood in the body is in the veins
- Because there’s a limit on how quickly the blood can go from arterial to venous, the pressure in the arteries will go up
- When arterial pressure increases, that means that more blood is being displaced from veins
What would happen if you were to stop the heart while it is pumping normally with high pressure and arteries and none in veins
- The blood that had been pressurizing on the arterial side is no longer going to fed any blood from the venous side by the heart
- Arterial pressure will go down substantially
- Venous pressure goes up, but not as substantially because that blood from the arteries is draining into the veins and it’s not being replaced by fresh blood from the heart
- E.g. the pressure in the arteries will drop from 100 to 7 mmHg and rise in the veins from 0 to 7
- The pressure in the exact system will be exactly the same in the arteries and veins
- If the heart starts working again, pressure in the arteries goes up, pressure in the veins drops, there’s peripheral resistance that prevents blood from shooting back to the veins, giving a pressure gradient
Equation for pressure gradient
(HR x SV) x TPR
How is TPR determined?
- Strictly in the periphery
- It is independent of cardiac output (??)
- However, cardiac output and pressure will be directly impacted by changes in other systems
How would an increase in cardiac output affect pressure and TPR
Pressure would go up but TPR would not be affected directly
How would increased arterial pressure affect TPR and stroke volume?
- Won’t affect TPR
- Decreased stroke volume (more work in the ventricle goes into generating pressure, less work is available to eject the volume)
Cardiac Function Curve
- For a given amount of contractility (sympathetic tone) and a given heart rate, the higher the right atrial pressure, the higher the cardiac output
- Right atrial pressure is typically around 0 mmHg
- The higher the right atrial pressure, the greater the venous return to the heart, and the greater the preload will be in the left ventricle
- The greater the preload, the greater the stroke volume
Vascular Function Curve
- Independent variable is on the Y axis (venous return) and the dependent variable is on the X axis (right atrial pressure)
- If the cardiac output (venous return) is 0, the pressure on the venous side and arterial side are equal to each other because there’s no flow through the system. Right atrial pressure rests at 7 mmHg.
- The greater the cardiac output, the lower the right atrial pressure
Venous return is the same thing as ___
Cardiac output
What three factors impact a vascular function curve
-Total peripheral resistance
Mean circulatory filling pressure:
- Blood volume
- Capacitance of veins
Pressure change in arteries vs. veins
Greater in arteries than in veins because they’re smaller in volume and the walls are stiffer
How can you modify the vascular function curve?
- Increase blood volume (= higher filling pressure) (doesn’t typically change)
- Tensing up the smooth muscles in the walls of the veins (decreased capacitance & increased pressure) (can be altered by NS)
What is arterial and venous pressure when cardiac output is 0?
- Venous and arterial rest are at the same pressure and it’s around 7 mmHg
- This is mean circulatory filling pressure
What can affect mean circulatory filling pressure?
- Blood volume
- Capacitance of veins
If you change cardiac output from 0 to 1, and eventually 5, what would happen to arterial, venous, and atrial pressure?
- Arterial pressure will go up
- Venous pressure will go down
- By the time you get to 5 l/m, right atrial pressure is ~0 mmHg
- This is because blood it being sucked out of the veins, and crammed into arteries and there’s a resistance in the return of that blood back to the veins.
- Volume is displaced from veins to arteries and the blood is trapped in the arteries because theres a resistance (??)
- The higher the pressure gets, the more the blood will squirt through the resistance
What happens when there’s negative pressure in the veins
- The walls floppy and walls suctioned in, which restricts flow back to the heart
- As venous pressure gets more negative, the harder you try to suck blood out of the veins, the more restricted movement of blood out will be (collapses in on itself just outside the right atrium)
How does decreased capacitance (in veins) affect (left ventricular) filling pressure?
- It increases it
- Decreased capacitance, so increased muscle tension, squeezes blood in and increases venous pressure
- This causes more blood to be pumped back to the heart
How would having 0 TPR (total peripheral resistance) change the vascular function curve?
- There’s a shift in the slope
- Right atrial pressure is not going down to 0 because blood is returning right to the veins and there’s no significant gradient
Explain what would happen in the vascular system if you decreased TPR to 0
- Blood would be sucked from the venous side and crammed into the arterial side in a futile attempt to make the pressure go up, but it immediately flows back to the veins
- You could have a cardiac output of 10 l/m but the pressure on the arterial side won’t go up that much and venous won’t go down much
What would happen if you increased TPR to infinity?
- RAP starts at 7 when the cardiac output is 0
- As soon as the cardiac output starts, blood is crammed into the arteries, but nothing is returning to the veins, so arterial is going to skyrocket quickly and venous pressure will go down really quickly
What is the intersection point between the cardiac and vascular curves?
- It signifies where the system is operating at any point in time
- Textbook value for intersection:
RAP: 0 mmHg
Cardiac output: 5 l/m
What would happen if all you did was increase heart rate and contractility but not change the vascular system?
- Venous pressure would go into the negative values, veins would collapse, and you can’t get any venous return –> preload too low –> low stroke volume
- So we have to also affect the vascular system
What would happen if all you did was change the vascular system but not cardiac?
-You could increase mean circulatory filling pressure by:
- Increasing blood volume (not available)
- Decrease capacitance of veins (+)
- You can decrease TPR to get the slope to shift to the right
- New intersection point is not bad, but still, far from where we want to be
How would the changes brought on by the sympathetic NS during blood loss affect the cardiovascular curve?
- The cardiac curve would shift upwards (purple line) because of increased HR and contractility
- RAP would go even lower if all you’re doing is pumping the heart faster and stronger
What changes in the cardiovascular system occur during exercise?
- Increased sympathetic, decreased parasympathetic
- Local override in muscle decreases peripheral resistance, so TPR drops a lot
- Increased sympathetic tone causes increased heart rate and contractility
- Decreased capacitance –> dramatic boost in filling pressure
- Shift in the slope because of decreased peripheral resistance
Flow chart showing the baroreceptor reflex and the response to orthostatic hypotension (standing up quickly –> blood pressure drops)
Flow chart showing the baroreceptor reflex - the response to increased blood pressure
Summary diagram showing the forces that impact cardiac output
Flow chart showing effects of hemorrhage (blood loss)
Another diagram for effects of hemorrhage
- Arrow shows the time at which hemorrhage occurs
Compensation effects of hemorrhage
Change in pressure triggers the delayed compensatory responses:
- Increased stroke volume (still lower than before)
- Increased heart rate (higher than before)
- Increased CO (still lower than before)
- Increased TPR
- Increased arterial pressure (still lower than before)
Fluid compartment shift due to blood loss
- Fluid compartment shift from interstitial fluid into blood vessels
- So you can kind of change blood volume
Mechanism:
- Blood loss causes decreased capillary hydrostatic pressure
- Fluid absorption from interstitial compartments
- Increased plasma volume
- Restoration of arterial pressure towards normal
Helps but does not make up for everything
Flow chart of arterial pressure and blood volume (the kidney’s role in maintaining blood volume will be covered in renal lectures)
Graph showing the Frank-Staling effect for a failing heart
- With a failing heart, there’s a danger of going down the wrong end of length-tension
- With normal EDVs (50-200/300 ml), the overlap of actin and myosin is ideal (length of sarcomere is 1.9-2.2 micrometers)
- Stretching a little bit engages the stretch-sensitive calcium channels and the stretch-sensitivity of troponin to give you more cross-bridges
- If a heart fails, for a normal preload, you’re getting much less stroke volume, so contractility decreases.
- If you lose 30% of the ventricular muscle, 70% is contracting, the 30% that isn’t contracting is not only not contributing, to increasing pressure in that ventricle, but it could also be bulging out and allowing pressure to dissipate into the elasticity of the wall of the ventricle.
Flow chart of exercise cardiovascular changes
- Set point for BP goes up
- Local changes in muscles
- Upstream artery effect
- Other changes- look at diagram
