Test 2 week 4 Flashcards

(145 cards)

1
Q

Tissue ____ blood in proportion to its need

A

controls own

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2
Q

What are the tissue needs?

A
  • Delivery of o2 to tissues
  • delivery of nutrients –> glucose, amino acids
  • removal of CO2, hydorgen, and other metabolites from the tissues
  • Maintenance of proper ionic concentrations in tissues
  • transport various hormones and other substances to different tissues
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3
Q

Flow of blood is closely related(proportional) to _______

A

metabolic rate of tissues

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4
Q

What is the difference between flow and perfusion?

A

Flow is volume over time, while perfusion is volume over time over an amount of tissue

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5
Q

Because we do not have the ability to constantly pump the max amount to all organs at the same time…

A

Some organs receive constant amount of blood flow regardless of other organs (the brain), other organs change the amount they receive depending if they are active or inactive depending on the need

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6
Q

Possible regulators of acute control of local blood flow: metabolic control

A
  • O2 demand theory
  • Vasodilatory theory: as metabolism increases, certain substance conc. also increases around the tissue. These metabolisms have different effects on SMC & on endothelium that causes vasodilation
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7
Q

Oxygen demand theory

A

regardless if there is a decrease in O2 or increase in tissue metabolism, there will be a decrease in tissue O2 levels. This leads to relaxation, which leads to vasodilation, which leads to an increase in blood flow

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8
Q

Decrease in O2, is sensed by…

A

precapillary sphincters, which causes then to relax and vasodilate

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9
Q

As oxygyen saturation increases, _____decreases

A

Blood flow

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10
Q

No decrease in O2 levels leads to…

A

sphincter contraction, and decreased blood flow. Blood is then shunted to other areas that needs it

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11
Q

What is reactive hyperemia?

A

The blocking of blood supply for a period of time causes build-up of waste product metabolites that have vasodilatory properties.

Increase in blood flow will be proportional to time of ischemia & how strong it is.

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12
Q

What is active hyperemia?

A

An increase in local metabolism causes rapid diminishing of nutrients and increased release of vasodilatory substances

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13
Q

What does the increased release of vasodilatory substances do?

A

it stimulates endothelium & SMC to vasodilate, hence increasing blood flow

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14
Q

As activity levels increase, so does _____

A

blood flow. Once activity returns to normal, so will blood flow

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15
Q

What are the two components of metabolic autoregulation?

A

Intrinsic and extrinsic components

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16
Q

Intrinsic factors that increase the activity of the muscle produces…

A

vasodilator metabolites that will act on microcirculation to produce vasodilation.

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17
Q

Where is the most resistance found?

A

In the arterioles and microcirculation

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18
Q

What does flow-induced dilation in the extrinsic component do?

A

It increases blood flow & will further increase dilation upstream

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19
Q

Flow- mediation dilation is a good indicator of…?

A

Arterial & endothelial health

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20
Q

How is flow mediation dilation does

A

Use a probe to find the brachial artery, get a baseline video & use it to get the average diameter of the artery, wrap a cuff around it & inflate it to around 200mmHg & leave it for 5 mins, let g of the cuff, resulting in great increase of blood flow & the dilation of the arteries

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21
Q

What type of hyperemia is flow mediation dilation?

A

Reactive hyperemia

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22
Q

What does the pressure curves in flow mediation dilation tell?

A

How fast the blood is flowing and how much blood is flowing. This tells us the function and state of the microcirculaton.

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23
Q

Multiple signaling pathways that determines vascular tone

A

When blood flow increases, it causes shear stress pulling on the endothelium.

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24
Q

What does shear stress and pulling of the endothelium do?

A
  1. stimulates the endothelial cells to open K channels. (hyperpolarizes the cell membrane) At the same time, muscle contraction also stimulates K channels on the SMC to hyperpolarize the SMC membrane, because of metabolites released from muscle & gap junction.
  2. Hyperpolarization transfers to neighboring SMC & endothelial cells via gap junctions.
  3. Hyperpolarization inhibits Ca channels, decrease Ca intracellular conc. in SMC. Contraction depends on Ca.
  4. shear stress on endothelial, stimulates vasodilators (NO), stimulates muscle to relax further.
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25
Exercise wants to vasoconstrict, but the ____ process negotiates this & stronger signals
shear stress and pulling of the endothelium
26
Phosphorylation _____ Ca
decreases
27
What is the role of endothelial cells?
- Vasoconstrictor: norepinephrine increases muscle tone in muscles, and the addition of acetylcholine decreases it - A destroyed endothelium occurs when acetylcholine is added
28
What is the role of NO
it is an endothelial relaxing factor.
29
Endothelial dysfunction is a precursor to...
vascular disease.
30
Acetylcholine is a endothelium ____ factor
dependent relaxing
31
Sodium nitroprusside is an endothelium ____ factor & it directly acts on _____
Independent relaxing factor. Directly acts on SMC regardless of endothelium
32
Autoregulation of Blood Flow in response to BP main views are...
1. Metabolic autoregulation = vasodilatory theory 2. Flow mediated- shear stress 3. Myogenic autoregulation: - Sudden stretch of small blood vessels stimulates Vascular smooth muscle cell (VSMC) contraction via stretch induced depolarization. - When flow increases, so does pressure, leading to increased VSMC contraction, which increases resistance, and therefore decreases flow back to normal. - Opposite happens with decreased flow and pressure. - Metabolic autoregulation overrides myogenic autoregulation – e.g. vigorous exercise.
33
Transmural Pressure and Luminal shear stress | Interact to determine vasomotor tone
- Myogenic autoregulation is governed by VSMC: - ↑ Wall stress (Transmural Pressure x radius) : ++ VSMC contraction - Due to mechanical transduction of voltage operated Ca channels (VOCC). - Contraction of VSMC decreases radius and restores wall stress. • Flow-Mediated Dilation is governed by endothelial cells (EC): - Shear stress: ++ NO bioavailability and ++ hyperpolarization through K+ channels that is transmitted to VSMC via gap junctions.
34
Functional Sympatholysis
- Sympathetic stimulation: vasoconstriction through α1-receptors * SNS is activated during exercise * Exercising muscle need increased blood flow • Metabolic autoregulation (O2 demand and vasodilatory theories) cause vasodilation that is strong enough to override sympathetic stimulation in the exercising musculature • In non-exercising muscles and organs: sympathetic stimulation reduces blood flow to non-exercising organs and shunting blood to exercising organs
35
Role of Autonomic nervous System
- Redistribution of blood flow • Increasing pumping activity of the heart • Rapid control of arterial pressure
36
Sympathetic nervous system is important in control of...
circulation (SA, AV, & heart muscle)
37
Parasympathetic nervous system is important in regulating...
Heart function (SA & AV)
38
Sympathetic nerve fibers innervate all vessels except
capillaries and precapillary sphincters and some | metarterioles
39
Innervation of small arteries and arterioles allow sympathetic nerves to
increase vascular resistance
40
Large veins and the heart are also ____innervated
sympathetically
41
Parasympathetic nervous system is mainly important in control of
heart rate via the vagus nerve
42
Distribution of sympathetic vasoconstrictors are distributed greater in ____ and less potent in ____
- kidneys, gut, spleen, and skin - circulation and the brain
43
The Vasomotor Center (VMC) transmits efferent impulses...
downward through the cord to almost all blood vessels
44
VMC is located bilaterally in the
reticular substance of the | medulla and the lower third of the pons
45
The VMC is composed of what 3 areas
``` vasoconstrictor area (C1), vasodilator area, and sensory area ```
46
Effect of Parasympathetic Outflow
Effect on SA node via vagus nerve (↓HR)
47
Effect of Sympathetic Outflow
- Effect on SA node (↑HR) - Effect on cardiac muscle (↑contractility and SV) - Effect on arterioles (vasoconstriction and ↑TPR) - Effect on veins (venoconstriction and ↑VR)
48
Functions of VMC
- Vasoconstrictor area of VMC transmits signals continuously to sympathetic nerve fibers called: sympathetic vasoconstrictor tone. These impulses maintain partial state of contraction in blood vessels called vasomotor tone • Lateral portions of VMC controls heart activity by increasing heart rate and contractility • Medial portion of VMC transmits signals via vagus nerve to heart to decrease heart rate
49
The neurotransmitter for the vasoconstrictor nerves is
norepinephrine
50
Adrenal medulla secretes epinephrine and norepinephrine which...
constricts blood vessels via alpha adrenergic receptors
51
____can also dilate vessels through a potent β2 receptor
Epinephrine
52
The nervous system via the vasomotor center(VMC) can | increase arterial pressure (AP) within seconds by:
- Constricting almost all arterioles of the body which increases total peripheral resistance (TPR) - Constricting large vessels of the circulation thereby increasing venous return and cardiac output - Directly increases cardiac output by increasing heart rate and contractility
53
Rapid increases in arterial pressure can occur during...
exercise or with fright
54
Reflex Mechanisms for BP Control
1. Baroreceptor Reflex (High-Pressure Baroreceptors) 2. Chemoreceptor Reflex 3. Atrial and Pulmonary Artery Reflex (Low-Pressure Baroreceptors) - Bainbridge Reflex 4. CNS Ischemic response - Cushing Reaction 5. Abdominal Compression Reflex 6. Respiratory Sinus Arrhythmia
55
The baroreceptor reflex: anatomy
- Aortic arch: nerve endings - send through vagus nerve: found at the carotid sinus, which is at the bifurcation of the internal & external carotid artery
56
The 9th & 10th cranial nerves is responsible for sending responses from ____ to ___
high pressure baroreceptors to VMC
57
Baroceptor response to BP
period in time when the carotids are not sensitive to changes of BP ( 60-100_ After 100, increase in pressure = increase in vagal activity & a decrease in sympathetic activity.
58
When the body senses an increase in vagal activity....
a decrease in muscle tone & a decrease in contractility occurs.
59
Baroreflex: buffer function
- Buffers fluctuations in BP - Opposes either increases or decreases in arterial pressure thereby reducing daily variations in arterial pressure. - Unimportant in long term control of arterial pressure because the baroreceptors adapt to BP
60
Baroreceptor response to increase BP
Carotid sinus barorecptors
61
Baroreceptor response to hemorrhage in parasympathetic activity to the heart
Decrease in arterial pressure ---> decreased stretch on carotid sinus baroreceptors --> decreased firing rate of carotid sinus nerve ---> decreased parasympathetic activity to the heart ---> increased heart rate --> increased arterial pressure toward normal
62
Baroreceptor response to hemorrhage in sympathetic activity to the heart and blood vessels
Decrease in arterial pressure ---> decreased stretch on carotid sinus baroreceptors --> decreased firing rate of carotid sinus nerve ---> increased sympathetic activity to heart and blood vessels --> increased heart rate, increased contractility, constriction of arterioles (increased TPR) constriction of veins decreased unstressed volume & increased venous return
63
Chemoreceptors are chemosensitive cells | sensitive to
oxygen lack, CO2 excess, or H ion excess
64
Chemoreceptors are located in
carotid bodies near the carotid bifurcation and on | the arch of the aorta
65
Activation of chemosensitive receptors results in
excitation of the vasomotor | center
66
Chemoreceptors are not stimulated until
pressure falls below 80mmHg
67
flow of chemoreceptor reflex
decreased O2, decreased CO2, decreased pH --> Chemoreceptors --> VMC--> increased sympathetic activity --> BP
68
Low pressure receptors in atria and pulmonary arteries minimize
arterial pressure changes in response to changes in blood volume
69
Increases in blood volume activates low pressure receptors which in turn...
lower arterial pressure
70
Activation of low pressure receptors enhances Na and water by
- Decreasing rate of antidiuretic hormone - Increasing glomerular filtration rate (Renal vasodilation) - Decreasing Na reabsorption
71
The Bainbridge Reflex
↑ atrial pressure --> ↑ HR by ∼75%
72
Stretch receptors in the atria transmit signals to the medulla via
via vagal afferents and | sympathetic efferent signals are transmitted back to ↑HR and contractility.
73
The bainbridge reflex helps prevent...
damming of blood in veins, atria, and pulmonary circulation
74
In respiratory sinus arrythmia, inspiration leads to...
HR accelration
75
In respiratory sinus arrythmia, expiration leads to...
HR decelaration | - spillover from inspiratory center stimulate the VMC as well
76
In respiratory sinus arrythmia, decreased intrathoracic pressure leads to
Increased VR which leads to increased HR in jugular veins
77
CNS ischemic response is activated in response to
cerebral ischemia
78
Reduced cerebral blood flow causes CO2 buildup which stimulates
vasomotor center thereby increasing arterial pressure
79
CNS Ischemic response is one of the most powerful activators of the
sympathetic vasoconstrictor system
80
• CNS Ischemic response is not activated until pressure falls below
60 mmHg; | - Greatest activation occurs at pressures of 15-20mmHg
81
Prolonged CNS ischemia has a
depressant effect on the vasomotor center
82
Effect of changes in blood volume on CO
- Baroreceptor reflex: relieving stretch on high pressure arterial receptors causes tachycardia - Bainbridge reflex: stretching low-pressure atrial receptors causes tachycardia - Cardiac output increases monotonically - Starling's law: decreasing initial fiber length decreases SV. The baroreceptor reflex steepens this response Baroreceptor reflex: increased stretch on high-pressure arterial receptors decreases SV, flattening the starling response
83
Steps in a cushing reaction
- increased CNS pressure - compressed of cerebral arteries - decreased blood flow - ++ cushing reaction --> increased BP - blood flow is restored
84
Baroreceptor/Chemoreceptor stimulation also stimulate
abdominal muscles
85
Abdominal muscle contraction compresses _____ and helps _____
- venous reservoirs | - translocate blood from the abdomen toward the heart, thus increasing VR and CO
86
Effect of fluid volume on BP
- Increased ECF volume --> - Increased hydrostatic in the interstitium --> - Increased capillary reabsorption --> - Increased blood volume --> - Increased mean circulatory filling pressure --> - Increased venous return of blood to the heart --> - - Increased cardiac output (because: frank-starling mechanism, low barorecptor activation, & bainbridge reflex) -> - Autoregulation --> - increased TPR --> - increased arterial pressure (so kidneys receive more blood and excrete more fluid) --> - increased urine output (helps restore ECF and blood fluid levels. Restores blood pressure levels)
87
Importance of Salt (NaCl) in BP regulation
- Pure water is excreted very rapidly but salt is not. 1. ↑ salt in ECF -> ↑ osmolality -> stimulates thirst center -> ↑ water intake to restore normal salt concentration 2. ↑ osmolality -> ++ ADH secretion -> ++ water reabsorption - H2O deficit -> - ↑ ECF osmolarity -> - ↑ ADH secretion (posterior pituitary) -> - Plasma ADH -> - ↑ H2O permeability in distal tubules, collecting ducts - ↑ H2O reabsorption -> - ↓ H2O excreted
88
Urine output is a driving factor that normalizes ___
Cardiac output levels and arterial pressure levels.
89
Renal-Body Fluid System for BP Control
1. when mean arterial pressure ↑ 2. Urine output ↑ 3. Cardiac output ↓
90
What is pressure diuresis?
Increased fluid excretion in result of increased pressure
91
What is pressure natriuresis?
Increased sodium excretion in result of increased pressure
92
With increased arterial pressure
- Flood loss is greater than intake - Blood volume decreases - Decreased blood volume will help drop pressure to equilibrium point (more urine will be excreted to lower BP to equilibrium point)
93
With decreased arterial pressure
- Intake is greater than fluid loss - Blood volume increases - Increased blood volume will help drive pressure back to equilibrium point
94
What is equilibrium point?
point where at renal output curve & water and salt intake curve. This is where BP is located
95
Two- key determinants of long-term arterial pressure
- degree of pressure shift of the renal output (shift to right increases BP) - Level of salt and water intake (increase in water/salt intake, increases BP)
96
Under normal conditions, Chronic renal output curve is much steeper than the...
acute curve
97
Due to the steepness of the chronic renal output...
increased salt intake has small changes on arterial pressure (under normal conditions)
98
Chronic curve is more steep because
``` indirect nervous (SNS activity) and hormonal changes help control BP and collectively enhance efficiency of pressure diuresis and natriuresis ```
99
Sympathetic nervous system baroreceptors hormonal changes allows for
increased water/salt intake without change in BP, but chronic, sustained increases in salt intake associated with kidney & vascular problems
100
Why can’t TPR modulation provide long-term BP control?
- Systemic ↑TPR (except in the kidneys) does not change the equilibrium point for BP control. - As a result, pressure diuresis and natriuresis will ensue until BP is restored to equilibrium. - If TPR of renal artery is ↑, this can shift the renal output curve to the right. Note that this shift in BP is due to a change in renal vascular resistance not TPR. (exception is when TPR ↑ in renal artery)
101
Reduction in kidney mass (function) and drinking saline solution causes ___
↑ BP because inability to regulate fluids
102
The Renin-Angiotensin-Aldosterone System | RAAS
- Renal arteries detect drop in BP - Then they secrete renin (enzyme) - Renin + renin substrate produce angiotensin I - Angiotensin I, circulates in blood until reaching lung endothelium and converts to angiotensin II
103
Angiotensin II characteristics
- strong vasoconstrictor: increases TPR & normalizes BP - stimulates thirst centers - stimulates sodium & water retention - stimulates kidneys to produce aldosterone
104
What is aldosterone?
Hormone that stimulates water retention
105
ACE inhibitors block ____ to decrease ___
RAAS system to decrease BP
106
Role of RAAS in maintaining BP during high salt intake
- increased salt intake -> - increased extracellular volume -> - increased AP -> - decreased renin and angiotensin -> - decreased renal retention of salt and water -> - return of extracellular volume almost to normal -> - return of arterial pressure almost to normal
107
Increase in concentration of RAAS activity results in...
injection of Ang II, and increased Na intake caused large increase in BP. - normally, increase in salt would inhibit renin secretion (Ang II)
108
Decrease in conc. of RAAS activity results in...
Ang II inhibited by ACE blocker
109
Effect of renal artery stenosis on BP
1. Early rise in mean arterial pressure (MAP) due to the vasoconstricting effects of the RAAS system. 2. Renin secretion is normalized because renal artery BP is normalized. 3. Second rise in MAP is due to Na+ and water retention activity of the RAAS system
110
Renin secretion increased because...
kidneys think whole body pressure decreased and increase continues until kidney senses normal pressure at renal artery (not anywhere else)
111
Cooperative roles of ADH and aldosterone
- Water loss-> - Decreases BP-> - Causes the kidney to secrete Ang II & stimulates secretion of ADH & aldosterone -> - Hold on to Na and H2O, to restore BP
112
In integrated BP control systems, become activated within a few seconds
CNS, Baroreceptors, and Chemoreceptors are activated
113
In integrated BP control systems, activated within a few minutes
Stress relaxation, capillary fluid shift, RAAS system
114
In integrated BP control systems, activated within hours or days
Renal- blood volume pressure control
115
Factors that cause a shift in pressure natriuresis
Increased Na intake, obesity, insulin resistance, dysfunction of natriuretic hormones, endothelial ddysfunction, and increased RAAS system
116
It is important to monitor vitals especially ___ before and after exercise
BP
117
Obesity may contribute to hypertension through the following
1. ↑ Cardiac Output 2. ↓ Baroreceptor sensitivity -> ↑ SNS activity 3. ↑ RAAS activity 4. Impairment of renal pressure natriuresis 5. Adipocyte dysfunction -> ++ inflammatory . mediators -> ++ vascular remodeling and endothelial dysfunction (#1 factor)
118
When you eat food high in fat, BP ____. Stimulation of _____ caused normal BP & lower HR
- increases | - baroreceptors
119
Exercise has shown to promote the following
1. ↑ NO bioavailability(Nitric oxide; strong vasodilator, restores endothelial) 2. ↓ Arterial stiffness (compliant arteries, ↑ baroreceptor sensitivity) 3. ↑ Baroreceptor sensitivity 4. ↓ RAAS overactivity 5. ↓ Excessive SNS activity 6. ↑ Weight loss
120
What is cardiac index?
basically the same as cardiac output, but standardizes it to a certain surface area
121
The greater the O2 consumption (VO2), the greater the...
CO
122
The pressure in the right atrium gives us an idea of...
- the pumping of the heart | - what is going on in the venous circulation
123
Hypereffective heart is one where
- nervous stimulation - SNS activation - PNS inhibition - cardiac hypertrophy
124
Hypoeffective heart is one where
- ↑ BP - Pathologies of HR or rhythm - Valvular heart disease - HF: heart failure
125
Without nervous control, dinitrophenol (a vasodilator) is unable to ___
correct vasodilation by increasing CO
126
Factors that can alter external pressure on CO
``` 1. Cyclical changes during respiration (more pronounced during heavy breathing) 2. Breathing against –ve pressures 3. Positive pressure breathing 4. Opening the rib cage 5. Cardiac tamponade ```
127
The heart is in the thorax, & the intrathoracic pressure is ___
negative.
128
Any factors that is going to increase intrathoracic pressure will shift the CO curve to the ____, also will increase ____. Making it harder to push blood into the heart
Right. | Right atrial pressure
129
Mean systemic filling will ___ venous return
Increase
130
Blood volume is ___ proportional to mean systemis filling pressure
Directly
131
A decrease in intrapleural pressure will make the right atrial pressure more ____ & making it ____
negative. Hypoeffective
132
An increase in intrapleural pressure will make the right atrial pressure more ____ & making it ____
Positive. Hypereffective
133
What is mean systemic filling pressure(MSFP)?
The pressure in the circulation once no blood is flowing into or out of the heart. Blood is at equilibrium between the venous & arterial side.
134
Decreasing resistance typically will ____ blood volume
increase
135
Increase in resistance will ____ venous return
decrease
136
Increase in blood volume through transfusion, shifts the venous return curve to the ____, ____ CO
right. | Increasing
137
SNS stimulation shifts the CO curve to the ____, increasing CO
left
138
When TPR is increased, the CO or VR curve moves ___
down
139
When TPR is decreased, the CO or VR curve moves
up
140
What happens in response to exercise?
1. ↑MSFP 2. ↑Effectiveness of CO 3. ↓External pressure (heavy breathing)
141
There is an increase in MSFP during exercise, because..?
Exercise causes SNS stimulation that will cause vasoconstriction to non-exercising muscles. Shifts blood from venous to arterial system
142
What is hemorrhage?
loss of blood volume
143
Cardiovascular response to erect posture
When we stand up, our BP drops. This is as a result of blood in veins
144
If you take a BP while laying down, it'll be ____ than when sitting
higher
145
If you take a BP while sitting down, it'll be ____ than when standing
higher