how is driving force for blood flow maintained during ventricular diastole?
When arteries stretch due to ejection of blood during ventricular systole they will recoil to push blood along and maintain pressure
pulse pressure is
- gravity force
- pulse pressure = systolic pressure - diastolic pressure
40 = 120-80
Mean arterial pressure is
MAP = 80 + 1/3 (pulse pressure)
= 93mm Hg
- this is normal resting MAP and it is skewed towards diastolic because your heart spends more time in it
what does “MAP illustrates mass balance” mean
- what comes in must go out
MAP is proportional to
cardiac output x resistance
what is the minimum MAP required to perfuse the systemic organs
60 mm Hg
Describe how the cardiovascular and renal system work together to respond to an increase in blood volume
- Increase in blood volume leads to increase in blood pressure:
Compensation by cardiovascular system: fast response
- arterioler vasodilation or vasoconstriction (decrease or increase resistance)
ANS: vasodilate, decrease resistance
- increase or decrease CO and HR as needed
ANS: decrease CO and HR, so contractility and SV decrease
Compensation by kidneys: slow response
- retain fluid or offload fluid in form of urine
ANS: excretion of fluid will decrease blood volume which will decrease blood pressure
Factors to regulate blood flow locally
- myogenic response
- paracrine response
- sympathetic nervous system regulation
resistance is mostly determined by
- arteriolar radius (r^4)
- length of vessel and viscosity of blood remain constant
Factors to increase MAP
Factors to increase MAP
1. decrease in diameter of the veins
- so if we decrease the volume of the veins or increase the action of the skeletal muscle it will increase venous return which will increase the length of the sarcomere
- This is shown in the frank starling law of the heart, so if you stretch the sarcomere (by stuffing blood inside) the heart will contract more forcefully because the heart will pump all blood returned to the heart
- This increases EDV which increases sarcomere length which increases contractility which then increases stroke volume which increased in turn increases MAP
2. Increase systemic resistance therefore decreasing diameter of arteriole we will systemically vasoconstrict which will increase MAP
3. Blood volume
- if we increase fluid intake we have more volume of stuff in our cardiovascular system which increases the pressure in that system
- If we decrease fluid loss it would also increase the volume of that system and increase MAP that could be regulated at kidneys
4. Increase heart rate and stroke volume (CO = HR X SV)
Local factors: myogenic autoregulation
- in this case we have to much pressure, to much flow and we want to turn it down locally
- Increase in pressure (constriction of blood vessel) —> increase in flow —> results in stretch of arteriole
- This will cause stretch activated channels to open and they will let in cations (maybe Na+) which will result in depolarization
- Depolarization causes opening of voltage gated Ca2+ channels open
- Ca 2+ into smooth muscle causes more cross bridge cycling, more force production, higher arteriolar resistance
- Now when we have an arteriole that is contracting it will vasoconstrict which will decrease the flow to that area and reduce the pressure on that wall
- Problem fixed
Example: kidney blood flow (we don’t want blood flow all over your body to depend exclusively on blood pressure we want regulatory local mechanisms)
Local factors: Paracrines will be released in response to changes in tissue needs
- Active hyperemia: will match blood flow to metabolic demands
- your at the gym so you need greater blood flow to certain muscles
- Tissue metabolism increases because muscles are working harder and the overworking muscle cells will release metabolites ( O2, CO2, NO, H+ and ADP) which will act on arteriole smooth muscle
- Smooth muscle cells will relax and decrease cross bridge cycling
- All metabolites act as vasodilators therefore resistance decreases and blood flow will increase to where it’s needed - Reactive hyperemia: compensation following a period of reduced blood flow
- when there is a clot in the way or prevent muscles or tissues to receive adequate blood flow
- because blood flow is inadequate because of clotting, metabolites produced during normal tissue metabolism will build up in ECF and not be washed away like they usually do
- Metabolites still act as vasodilators which will cause smooth muscle to relax
- Vasodilation will increase diameter, decrease resistance and increase flow so metabolites and clot can be washed out and arterioles can regain their normal tone
Norepinephrine on arteriole resistance
- neurotransmitter released from postganglionic sympathetic neurons (when we have NE we also have epinephrine)
- When we have elevated levels of norepinephrine it will bind to a1-adrenergic receptors on most smooth muscle cells
- a1-adrenergic receptors are coupled to Gq proteins (activates PLC)
- Which results in an increase of IP3 which increases calcium release from SR
- Then smooth muscle will contract which will increase resistance and arterioles will vasoconstrict and we will decrease flow
- Blood will be diverted away from these regions (GI tract)
- Anywhere there is a1-receptors and sympathetic input you will vasoconstrict and blood will be diverted away
Epinephrine on arteriole resistance
- epinephrine is released from adrenal medulla
- Norepinephrine and epinephrine (but epinephrine is better) bind to B2-adrenergic receptors found on smooth muscle cells of arterioles supplying skeletal muscle, heart and liver
- B2 receptors are couples to Gs protein that activates cAMP
- cAMP causes smooth muscle to relax and vasodilate, so we increase flow to these regions
Contraction _____________ during exercise or stress ( B2)
Decrease
Baroreceptors
- are pressure sensors and essentially nerve endings that express stress activated or mechanically gated channels, so if the wall of a vessel stretches channels will open and the baroreceptors will fire
- tonically active
- higher blood pressure causes more opening of stretch activated channels then increased depolarization and increased firing of AP
Where are baroreceptors located
- in the aorta
- in the carotid artery
The baroreceptor reflex
- ensure sufficient MAP for adequate blood flow to heart and brain
If stimulus is the increase blood pressure what is the sensor and what is happening
- aortic and carotid baroreceptors
- increase in firing of baroreceptors in carotid arteries and aorta
If stimulus is the increase blood pressure what is the integrating center
- all of this is sent to cardiovascular control center in the medulla
If stimulus is the increase blood pressure what is the output signal
- turn up parasympathetic response
- turn down sympathetic response
If stimulus is the increase blood pressure what is the target
- Turning up parasympathetic input (more ACh on muscarinic receptor)
- on SA node it will decrease HR which will decrease cardiac output and decrease MAP - Turning down sympathetic input (less NE on B1 adrenergic receptor)
- decrease HR (B1)
- decrease contractility in ventricular myocytes which will decrease SV, decrease CO and decrease MAP (B1)
- since we decrease contractility, arteriole will vasodilate and resistance of arterioles will decrease, decreasing MAP (A1)
- veins
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Lecture 110
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Lecture 231
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Lecture 320
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Lecture 425
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Lecture 512
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Lecture 618
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lecture 720
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Lecture 814
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lecture 910
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lecture 10/1133
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lecture 1214
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lecture 1321
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lecture 1425
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lecture 1523
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lecture 1626
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lecture 1716
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lecture 1819
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lecture 1917
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lecture 2020
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lecture 2123
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lecture 2222
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Lecture 2329
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lecture 2432
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lecture 2523
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lecture 2617
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lecture 2726
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lecture 2824
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lecture 2919
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lecture 30/3117
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lecture 3223
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Lecture 3338
