Circulation Phys Flashcards

1
Q

Circulation

  • 2 functions
  • 2 circuits
A
  1. pick up nutrients and deliver to tissues
  2. pick up waste and deliver for excretion
  • pulmonary and systemic circuit
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2
Q

Define flow

A

volume per unit of time

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3
Q

hemodynamics definition

A

physics of blood flow

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4
Q

What two things are blood flow dependent on

A

resistance

pressure

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5
Q

What is blood flow directly proportional to?

A

pressure divided by resistance

  • flow proportionate to pressure
  • flow is inversely proportionate to resistance

Q = (P1-P2)/R
P1 is arterial pressure
P2 is venule pressure

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6
Q

normal blood flow is called

A

laminar

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7
Q

How does blood flow near the lamina

A

slowly or not at all

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8
Q

Where does blood flow fastest in the vessel

A

center

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9
Q

probability of turbulence is related to what two things

A
  • diameter of vessel

- viscosity of fluid

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10
Q

what happens to blood flow at vessel branches

A
  • interrupted laminar flow

- increased likelihood of atherosclerotic plaque formation

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11
Q

What is a Bruit

A

auscultation of the sound of turbulent blood beyond a site of constriction

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12
Q

why is turbulence of blood bad

A

creates damage to tissues

  • tissues really want to be repaired
  • repair = plaque
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13
Q

shear stress define

A

frictional force placed on the vessel wall

  • dependent on the area
  • shear stress = force/area
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14
Q

What happens after acceptable amount fo stress of vessel wall is exceeded

A

vessel deforms or changes

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15
Q

how is shear stress detected?

A

endothelium has stress detectors which activate factors that cause repair (plaque formation)
- normal to develop plaque all through life, just a normal response to damage

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16
Q

5 factors that cause shear stress

A
  1. growth factor
  2. CAM (cell adhesion molecule - an adhesion molecule)
  3. NOS (nitrous oxide synthase - leads to platelet aggregation
  4. ACE - vasoconstriction
  5. Tissue factor/thrombomodulin - procoagulation
  • increase these flair signals, increase repair, increase plaque formation
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17
Q

Define blood velocity

A

displacement per unit of time

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18
Q

What is blood velocity proportional to

A

flow/area

- bigger diameter, faster flow, greater velocity

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19
Q

what does flow equal

A

(area)(velocity)

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20
Q

Velocity in

  • aorta
  • capillaries
  • veins
  • vena cava
A
  • high
  • slow
  • speeding up
  • even faster but not as fast as aorta
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21
Q

Plasma and blood viscosity

A

plasma: 1.8X viscosity of water
blood: 3-4X viscosity of water

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22
Q

effects of small vs. large changes in viscosity of blood

- examples of increased and decreased viscosity siutaitons

A
  • small has very little effect, large change can make a difference
  • severe anemia - decrease viscosity
  • polycythemia - viscous blood
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23
Q

Resistance determined by

A
  • vascular resistance (blood vessel radius)

- viscosity of blood (less of an effect than radius)

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24
Q

Which of the two resistance factors can be easily modified

A

vascular resistance - change artery diameter

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25
in what situation can blood viscosity affect circulation
very high hematocrit
26
What would happen if capillaries lose too much intraluminal pressure?
will collapse if blood pressure in vessel drops below critical closing pressure
27
what two things help regulate pressure in capillaries?
- arterioles - pre-capillary sphincters **not smooth muscle bc capillaries don't have it!
28
Law of LaPlace
tension in the wall of a cylinder is directly proportional to the pressure across the wall and the radius
29
Do larger arteries withstand more or less wall tension than other vessels?
MORE
30
What do larger arteries have to protect them from high pressure
- thicker - layer of CT, provides a sort of tunic * preventing aneurysm
31
What physical property of capillaries help prevent rupture
small size
32
Where in the vascular system is the majority of blood
veins (54%)
33
High pressure portion of circulatory system - name - three types
resistance vessels - aorta - arteries - arterioles
34
Low pressure portion of the circulatory system - name - three types
Capacitance vessels - veins - venules - capillaries
35
Blood pressure reminder
- when cuff is inflated, stops arterial blood flow, no sound - when released enough to let blood through, it's turbulent so hear Korotkoff sounds - once artery is no longer compressed, no more turbulence, no more sounds
36
Pulse pressure - def - what does it represent
- diff between systolic and diastolic pressure | - represents the force the heart generates each time it contracts
37
What do both pulse pressure and systolic pressure represent
gauge of "arterial age"
38
What is risk in men with pulse pressure of 70 mmHg or greater
triples heart attack risk vs. pulse pressure of 50 mmHg or less
39
Wide pulse pressure - when normal - when abnormal
- exercise | - heart dz, HTN, ateriosclerosis
40
Narrow pulse pressure - define % - 3 ex
- <25% systolic pressure | - aortic stenosis, cardiac tamponade, heart failure
41
What happens to both systolic and diastolic pressure as age
increases even in absence of HTN, pulse pressure will remain teh same
42
What happens as age and arteries become more resistant
Diastolic pressure can decrease in an effort to reduce effects of afterload
43
Mean arterial pressure - define - what does it mean
- average pressure during cardiac cycle | - relates to adequate perfusion of tissues
44
How to calc mean arterial pressure
diastolic pressure + 1/3 pulse pressure
45
Greater than what mean arterial pressure will sustain organs
>70 mmHg | normally between 65-110 mmHg
46
How does gravity affect arterial pressure
- return to the heart from below (IVC) requires more pressure bc of gravity - pressure in arteries below heart is increased compared to those above heart
47
Capillary pressure - arterial end - venous end - transit time from a to v
- arterial: 32 mmHg - venous: 15 mmHg - 1-2 seconds * blood flows across capillary bc it's pushed from arterial side and pulled from venous side
48
How do gases cross membranes
diffusion down pressure gradient
49
what is the name of the forces that affect filtration in capillaries
Starling Forces
50
Starling forces are what two pressures
- Hydrostatic pressure | - Oncotic pressure
51
Hydrostatic pressure
- aka osmotic pressure | - causes water and solutes to flow from high to low pressur
52
Oncotic pressure
- aka colloid pressure - water is drawn to area of higher colloid concentration - blood has more protein than interstitial fluid, draws fluid into blood from interstitial
53
Filtration at the arterial end of capillary
- strong hydrostatic pressure (32 mmHg) - osmotic pressure of 22 mmHg - net pressure is out of blood (10 mmHg)
54
Filtration at the venous end of capillary
- weaker hydrostatic pressure (15 mmHg) - osmotic pressure 22 mmHg - net pressure into blood (-7 mmHg)
55
Venous pressure - gravity affects - velocity
- gravity increases pressure below the heart | - velocity is slower than arteries due to larger radius
56
pressure of great veins vs. aorta
great veins: 10 cm/s | aorta: 40 cm/s
57
why does venous return to the heart require aid (3)
lower pressure gravity slowed velocity
58
What three factors aid venous return to the heart
- heart - thoracic pump - muscle pump
59
How does the heart aid venous return
- during ventricular systole, atrial pressure decreases | - sucks blood into atria
60
How does the thoracic pump aid venous return
- during inspiration create negative intrathoracic pressure - positive abdominal pressure due to compression of abdominal organs by diaphragm - pressure gradient between infra- and supradiaphragmatic parts of IVC - pulls blood toward right atrium!
61
How does muscle pump aid venous return
- rhythmic contraction of skeletal muscle in limbs propels blood toward heart - venous valves prevent retrograde flow
62
sympathetic and parasympathetic supply to majority of vasculature
sympathetic only!
63
Describe overview of SNS innervation
- SNS adrenergic fibers terminate on vascular smooth muscle | - mediates vasoconstriction via alpha adrenergic receptors
64
What four types of tissue does parasympathetic system have vascular control
- erectile tissue - salivary glands - some facial vessels - uterine vessels
65
Three types of adrenergic receptors found in blood vessels
- alpha 1 (constriction) - alpha 2 (constriction) - beta 2 (dilation) alphas are majority
66
2 types of adrenergic receptors found in heart
- beta 1 (tachycardia, increased contractility) | - alpha 1 (increased contractility)
67
Alpha 1 receptor effects in vascular system
- vasoconstriction - increased peripheral resistance - increased bp
68
alpha 2 receptor effects in vascular system
- inhibition of NE release | - inhibition of acetylcholine release
69
beta 1 receptor effects in vascular system
- tachycardia - increased myocardial contractility - increased renin release
70
beta 2 receptor effects in vascular system
- vasodilation | - slightly decreased peripheral resistance
71
SNS stimulation of the heart sends what neurotransmitter to B1 cells
NE
72
where are B1 cells located in heart
- SA node - AV node - His and Perkinje fibers - atrial and ventricular contractile tissue
73
what is stimulated via SNS in cards
- heart rate - rate of transmission of conductive tissue - force of ventricular contraction
74
other term for heart rate
chronotropy
75
other term for rate of transmission of conductive tissue
dromotropy
76
other term for ventricular contraction
ionotropy
77
What nerve does the PNS use to innervate the heart
Vagus nerve
78
PNS stimulation via vagus nerve - via what type of receptors - 3 termination locations
- Ach to muscarinic receptors 1. SA node 2. AV node 3. Atrial muscle
79
Affect of PNS on cardio system
decreased: - hr - rate through AV node - atrial contractility - SNS activity - inhibits NE release from SNS
80
What part of brain controls sympathetic affects on cardiovascular system
RVLM Rostral ventrolateral medulla
81
How do axons of RVLM project
- via thoracolumbar tract (IML) - activate pregan SNS nerves (motor) - post gang fibers go to heart
82
2 things that directly stimulate the RVLM
- CO2 | - hypoxia
83
effect of vasoconstriction on afterload
- increases by increasing blood pressure | - also increases venous return which increases CO
84
What part of the brain controls parasympathetic input to the heart
nucleus ambiguus in the medulla | - then dorsal motor nucleus of vagus nerve
85
What type of neurons are in the nucleus ambiguus
cholinergic preganglionic parasympathetic neurons - cardioinhibitory
86
PNS vs. SNS | - what is primary means of BP control
SNS | - constricts arterioles and increases chronotropic and inotropic input
87
What is the parasympathetic systems's main role in regulating the cardiovascular system
- inhibit the SNS - vs. directly dial down functions of the system - cannot vasodilate directly
88
what stimulates the PNS in the nucleus ambiguus
increase in blood pressure
89
Two types of receptors that help dictate neural control of cardio system
- baroreceptors | - peripheral chemoreceptors
90
Baroreceptors - measure what - located where
- stretch receptors - carotid sinus - aortic arch - cardiopulmonary receptors: atrial walls and pulmonary circulation sites
91
what stimulates baroreceptors
distention
92
Neural path from baroreceptors
- afferent to medulla (sensory) - caudalventrolateral medulla (CVLM) to inhibit RVLM (if bp is high, reduces SNS control) - nucleus of tracts solitaires (NTS): excites vagal motor neurons * high bp inhibit SNS * low bp increase SNS
93
Two peripheral chemoreceptors
- carotid body | - aortic body
94
What do the peripheral chemoreceptors respond to (3)
- decreased pO2 - increased pCO2 - increased pH
95
Effect of chemoreceptor stimulation
- increased vagal activity to stimulate ventilation - increase O2 - increase catecholamine release from adrenal cortex to increase hr and cause vascoconstriction
96
10 things that accelerate HR
1. decrease activity of arterial baroreceptors (down bp) 2. increased activity of atrial stretch receptors (less venous return) 3. inspiration 4. excitement - YAY 5. anger 6. painful stimuli 7. hypoxia 8. exercise 9. thyroid hormones 10. fever
97
5 things slow heart rate
1. increased activity of baroreceptors (higher bp) 2. expiration 3. grief 4. stimulation of pain fibers in trigeminal nerve 5. increased intracranial pressure
98
Theory for local auto regulation of vasodilation
Metabolic theory of auto regulation - metabolites accumulate in active tissue - act as vasodilators - get increased flow to active tissue via dilation
99
Vasodilator metabolites
1. decreased O2 2. increased CO2 3. lactate 4. histamine 5. adenosine 6. prostacyclin 7. bradykinin 8. NO
100
where is lactate found
skeletal tissue
101
histamine affect on vessels
increases capillary permeability
102
Adenosine
- not naturally made i body - anti-arrhythmic agent - vasodilates cardiac arterioles - inhibits NE release
103
prostacyclin
- produced by endothelial cells - pro-inflammation - vasodilation (so tissue can get what it needs)
104
kinins
- inflammation mediators - vasodilation - bradykinin stimulates NO - vasodilation = vascular permeability - relaxes smooth muscle
105
NO
- converted from arginine in response to vasodilators such as bradykinin - diffuses from endothelial cells - vasodilation via relaxation of blood vessel smooth muscle
106
circulating vasodilators
- ANP and BNP | - natriuretic hormones
107
ANP
A type natriuretic peptide | - secreted by atrial myoctyes in response to high blood volume
108
BNP
B type natriuretic peptide | - secreted by ventricles in response to excessive stretching of cardiomyocytes
109
ANP and BNP two overall effects
1. decreased bp via volume change | 2. vasodilation of vessels
110
ANP and BNP affect on kidneys
decreased sodium retention - water follows, decreases blood pressure
111
ANP and BNP affect on vessel diameter
vasodilation
112
myogenic theory of autoregulation
an intrinsic contractile response of smooth muscle to stretch - as pressure increases, vessel walls distend - increased wall tension stimulates vasoconstriction to reduce the radius (Law of LaPlace - wall tension proportionate to radius) - maintains blood pressure and blood flow
113
Local endothelial vasoconstrictive secretions
Endothelin-1 - potent mediator of vasoconstriction - might be increased in HTN
114
3 Systemic circulating vascoconstrictors
- Angiotensin II - Vasopressin (ADH) - Epinephrine
115
Angiotensin II process
- Angiotensinogen made by liver all the time - Kidney detects decrease in perfusion, releases renin - Renin converts angiotensinogen into angiotensin I - ACE (increased by renin) converts angiotensin I to angiotensin II
116
What does production of angiotensin II cause
- vasoconstriction, increase in blood pressure - directly increases SNS activity = increased epi release - kidney retains water = increased blood volume/pressure
117
ADH - where synthesized - where stored and released - type of hormone
- synth by hypothalamus - stored/released by posterior pituitary - peptide hormone
118
Action of ADH
1. constricts smooth muscle 2. increases blood volume * increased blood volume, peripheral resistance, and blood pressure
119
how does ADH increase blood volume
- acts on kidney, causes water reabsorption
120
Epinephrine - where produced - what tissues does it affect - what does it cause
- produced by SNS in adrenal medulla - effects most tissues - constriction = inc. hr and cardiac output - increases renin production by kidney
121
List of things that cause vasoconstriction
1. SNS innervation 2. myogenic autoregulation 3. endothelial secretion of endothelin-1 4. Angiotensin II (potent) 5. vasopressin (ADH) 6. circulatory epinephrine