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BMS 130 > cardiovascular : blood vessels > Flashcards

cardiovascular : blood vessels Flashcards

1
Q

what is the correlational relationship b/w blood flow and pressure gradient

A

blood flow= change in pressure (gradient) / Resistance

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2
Q

what does the blood flow depend on

A

PRESSURE GRADIENT!!!!!

-does not matter what the overall pressure is just the diference between the pressure at the end/beginning

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3
Q

what is resistance

how does it connect to the flow?

A

measure of hindrance to blood flow through a vessel

Increased resistance means harder to pas blood and a slower flow

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4
Q

what factors impact resistance ??

A
  • blood viscosity (more erythrocytes= more friction between molecules- more resistance)
  • vessel length (longer= more resistance)
  • vessel diameter (smaller = more resistance)
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5
Q

what lines vessel walls ?

A

endothelium / endothelial cells. surrounded by smooth muscle and connective tissue

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6
Q

what are the two types of arterial connective tissue fibers and their purspoe

A

collagen- tensile strength

-elastin- elasticity

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7
Q

how much blood enters arterioles from ventricular systole?

A

1/3 of the volume! the other 2/3 stay in arteries

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8
Q

what happens right at the end of ventricular systole -> diastole to the arteries

A

-blood flows in -> pressure increases in arteries->arteries expand -> (aortic valve closes for diastole and allows ) elastic recoil -> increase pressure -> blood enters arterioles

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9
Q

what is blood pressure

A

force exerted by blood on the vessel wall!!

  • depends on volume of blood contained within the vessel and compliance or distensibility of the vessel wallls
  • fluctuates in relation to ventricular systole and diastole
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10
Q

how does sphygmomanometer measure bp and what sounds does it make

A
  • indirect measurement - inflatable cuff and a pressure gauge
  • pressure is transferred from cuff to BRACHIAL ARTERY
  • stethescope placed over brachial artery on inside of elbow- Korotkoff sounds are created by pressure of cuff on brachial artery (like turbulent flow)
  • first reading at absence of sound is diastole
  • no sound is systolic
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11
Q

what is the main driving force fo rblood flow through the cardiovascular system

A

mean arterial pressure

diastolic pressure + 1/3 pulse pressure

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12
Q

what establishes the pressure gradient

A

pressure in arterioles (vs arteries)

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13
Q

what is in the arteriole wlal

A

little elastic ct, thick layer of smooth muscle
contraction= decrease in radius = increase in resistance = decrease in flow
(precision in control)

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14
Q

what is the blood flow rate vs blood flow velocity

A

blood flow rate : blood volume passing a particular vessel in a period of time

blood flow velocity: blood volume passing total cross section area of all vessels at that given level of the circulatory system

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15
Q

how do blood flow rate and velocity vary in capillaries

A

velocity DROPS , but flow rate REMAINS THE SAME!!

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16
Q

how does cardiac output compare to volume of blood in any level of the cardiac system

A

must be equal

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17
Q

what does the maximum amount of blood received depend on

A

number and caliber of arterioles supplying that aarea

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18
Q

what are the 2 types of control over arteriolar vasoconstriction and dilation

A

intrinsic (local)- distribution of cardiac output to specific tissues - using left arm, etc

extrinsic (global) – pressure regulation

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19
Q

what 5 factors produce relaxation of arteriolar smooth muscle under INTRINSIC control?

A
  • decrease in O2
  • adenosine release
  • increase in co2
  • increase in acidity
  • k+ (release from contracting skeletal muscles- causes hyperpolarization and relaxation in vessels muscles)
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20
Q

what of the two types of control do endothelial cells provifde? what are their vasoactive factors? and what does each do (3 of them )

A

INTRINSIC CONTROL - line BV’s and chambers of the heart

  • Nitric oxide - potent vasodilator
  • endothelin - potent vasoconstrictor
  • vascular endothelial growth factor (VEGF) - stimulates new vessel growth (angiogenesis)
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21
Q

what is active hyperemia

A

intrinsic control type
increasd blood flow in response to enhanced tissue activity (local factors of an organ act on the supplying arteriole)

-increased local metabolic activity

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22
Q

what is reactive hyperemia

A

intrinsic control type
-increase blood flow post-occlusion (blocking of vessel)

-local blockage of blood supply

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23
Q

what is sympathetic extrinsic control

A

EXTRINSIC CONTROL!!!!!!

  • increased sympathetic activity results in generalized arteriolar vasoconstriction
  • vasoconstriction and higher BP in response to sympathetic stimulation is immediately followed with vasodilation of vessels supplying tissues that need more blood!! OVERRIDE
  • Tissues with lower blood demands during sympathetic response will not override the sympathetic constrictor effect and will receive less bloood

(the decreased blood flow to all tissues and increase in pressure causes a driving force for blood to flow to all tissues)

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24
Q

where does blood supply decrease during exercise

A

digestive system, liver, kidneys, and bone

-cardiac output increases but to these it DECREASES

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25
Q

how does blood flow to brain change with cardiac output changes

A

DOES NOT CHANGE

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26
Q

what mediates sympathetic effects on vessels

extrinsic

A

sympathetic vasoconstriction is mediated by norepinephrine activity on alpha 1 adrenergic receptors!!!!

-brain arterioles LACK alpha 1 which is why we dont impact the brain! blood flow must be constant to the brain

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27
Q

where is the cardiovascular control center

A

medulla! integration center for blood pressure regulation

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28
Q

what does the hypothalamus do for vascular control

A

some control- blood flow to skin for temperature

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29
Q

what four hormones are involved in vascular control and what they do

A

(extrinsic)

  • epinephrine and norepinephrine (norepinephrine-vasoconstriction/reinforce sympathetic . epinephrine- both vasoconstriction and vasodilation but preference for beta 2 vasodilation!! – the things that need it )
  • vasopressin and angiotensin : fluid balance - impact blood pressure through water retention; slower acting
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30
Q

what organs for vaso control have beta 2 receptors

A

skeletal muscles and heart (and more)

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31
Q

what organs have alpha 1 and not beta 2

A

digestive organs and kidneys

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32
Q

what do vasopressin and angiotensin II do for vessels

A

they result in vasoconstriction
-vasopressin -> water retention. angiotensin 2 is part of renin angiotensin-aldosterone system and regulates salt balance (promotes salt conservation during urine formation)

-conservation of salt = water retention. the water retentive effect of these hormones causes increase in blood volume and an INCREASE in blood pressure!!!!!!!

33
Q

`what impact does histamine have on blood vessels

A

DILATES arterioles!! pathologically

-does not NORMALLY participate in controlling blood flow

34
Q

where is histamine stored

A

mast cells and basophils - released during injury and acts as a paracrine, promotes relaxation of arteriolar smooth muscle

35
Q

what impacts INTRINSIC control

A
  • heat/cold application (therapeutic)
  • response to shear stress - compensates for changes in longitudinal force of blood flow
  • myogenic responses to stretch (autoregulation)
  • histamine release (injuries and allergic responses)
36
Q

what impacts extrinsic control

A
  • vasopressin – vasoconstrictor effect
  • angiotensin II (salt/water retention)-vasoconstrictor effect
  • epinephrine and norepinephrine
37
Q

how do hydrophilic molecules pass the capillary wall

A

pores!! single layer of endothelium

38
Q

how many precapillary sphincters are open for restin muscles

A

10%

–blood flows thru available cap beds or metarteriole (thoroughfare channel, anastome- passage)

39
Q

how does bulk flow occur

A

at capillaryes; distribution of fluid between plasma and interstitial fluid

-through pores - fluid and electrolytes fusion of vesicles to form pores, between endothelial cells,

40
Q

what increases diffusion (3 things)

A
  • minimize distance for diffusion
  • maximize surface area
  • minimize blood flow velocity
41
Q

what are features of capillary pores - what can pass, how big are they?

A
  • fluid filled pores- permit SMALL WATER SOLUBLE SUBSTANCES
  • present in most capillaries
  • size varies between organs!!
  • in the brain the endothelial cells are held by tight junction and there are No pores

-PROTEINS can sometimes pass in discontinous capillaries

42
Q

what are the 3 types of capillaries

A
  • continous : basement mem intact, tight junctions- proteins can sometimes pass
  • sinusoid (discontinuous) : may haveINCOMPLETE BASEMENT MEMBRANE
  • fenestrated : basement mem intact. some pores,some tight junctions
43
Q

what is bulk flow important for

A
  • protein free plasma filters out of capillary and mixes w interstitial fluid and reabsorbed - important for ECF distribution between interstitial fluid and plasma -
  • HELPS MAINTAIN ARTERIAL BLOOD PRESSURE - keeps plasma volume constant.
  • if plasma volume goes down, blood pressure goes down.
  • dpends on ultrafiltration and reabsorption
44
Q

what is ultrafiltration

A

responsible for bulk flow near the arterial end of capillary!! hydrostatic pressure imparted by heart drives fluid out of capillary mostly thru pores, while plasma proteins are retained within vessels- FILTRATION- protein free plasma

-as you go along capillaries, protein amount stays constant but fluid loss to interstitial fluid, so protein concentration increases

pressure inside cap is higher than inward driving pressure

45
Q

what drives bulk flow at arterial side

A

ultrafiltration

-pressure inside capillary is greater than the inward driving pressure so it leaves (hydrostatic pressure)

46
Q

what drives bulk flow at arterial side

A

osmotic pressure – reabsorption! (pressure inside cap is less than inward driving pressure)

47
Q

what are the net results of capillary/interstitial fluid exchange
-how is it compensated for

A

net loss of fluid in the plasma and a net gain in the interstitial fluid!!

  • ultrafiltration is about 11 mm hg at eginning of caps and reabsorption is like 9 mmm hg at end of caps
  • comprensation = lymph vessels converge into lymphatic ducts- drains into subclavian veins
48
Q

what is feature of lymphatic vessels

A

has free overlapping edges; create a one way valve like opening in the vessel wall

-forced to close valves by fluid pressure in lymph vessel

49
Q

how does lymph move in lymphatic vessels

A

far from capillaries depends on smooth muscle in vessel wal to generate pressure to move it towards the heart. stretching of the lymphatic vessel stretches smooth muscles which stimulates smooth muscle contraction, increasing pressure and pushing lymph forward.

-contraction of skeletal muscles also aids movement of lymph. lymphatic valces found within vessel prevent the backflow of lymph as the vessels is squeezed by smooth or skeletal

50
Q

lymph system function

A
  • return filtered fluid that wasnt reabsorbed
  • defense against disease
  • transport of absorbed fat (from digestion- fatty partcles too large to get into the blood)
  • return of filtered protein- small amount of plasma protein leave most capillaries during filtration cant be reabsorbed into capillary
51
Q

what causes edema

A

edema= swelling due to excess interstitial fluid

  • reduced concentration of plasma proteins
  • increased permeability of capillary walls (high BP/hydrostatic or disease)
  • increased venous pressure
  • blockage of lymph vessels
52
Q

what can cause a decrease in plasma protein (3 things)

A
  • kidney disease: loss of plasma protein in urine
  • liver disease: reduced synthesis of plasma proteins
  • diet deficient in protein

(–> edema)

53
Q

what causes blood to pool in capillaries

A

increaesd VENOUS pressure!! because flow is dependent on pressure gradient!! makes it harder for blood to flow out of capillaries and into veins

need a higher hydrostatic pressure to restore pressure gradient here (working against osmotic pressure- reabsorption of fluid is reduced??)

-can also cause edema bc it wont go into veins?

54
Q

what happens with blockage of lymph vessels

A

edema can occur with lymph vessels blocked.
-net flow is usually to interstitial (as we know) so basically w blocked lymph we get fluid that cant return to the circulatory system. also plasma proteins usually go to lymph, so they are stuck too and that makes osmotic pressure where more fluid wants to go out. reduces reabsorption

55
Q

what are the veins that capillaries drain into called

A

venules

56
Q

how does connective tissue of veins compare to arteries

A

more collagen fibers, and less elastin fibers (less elastic)

57
Q

how much blood does the vein system carry vs the rest of the cardio system

A

more than 60% at rest!!! big storage capacity aka it moves sloowww

58
Q

what are feature of vein valves

A

large veins have them

  • 2 to 3 cm intervals
  • one way obv
  • prevents back movement
59
Q

what can it lead to when valves dont function? what happens with it?

A

varicose veins-swollen and twisted - blue (doesnt impact cardiac output) bc homeostatic effects can compensate by increasing total circulation volume.
complications: formation of clots and pain. legs w/prolonged sitting or standing

60
Q

what is the skeletal muscle pump sequence for veins

A

skeletal muscle contraction -> venous compression -> increased venous pressure -> decreased venous capacity

61
Q

what is the respiratory pump?

A

respiratory activity causes pressure in chest cavity (5 mm) hg less than atmospheric pressure

  • external pressure within limbs and abdomen are normal
  • –> this creates a pressure gradient where blood moves from lower veins to the chest – this promotes venous return!!!! helps w flow back to the heart
62
Q

what is cardiac suction?

A

while the heart is resting during diastole, expansion of the ventricles creates a negative pressure- cardiac suction!! this gradient enhances venous return and allows passive flow of blood into the ventricles

63
Q

how does sympathetic activity relate to venous return? whats the overall result on cardiac output?

A

symp stimulation produces venous vasoconstriction
- increased venous pressure causes a pressure gradient!!!

  • this increases flow, and the change in resistance isnt significant
  • diameter of venous lumen is really large so vasoconstriction increases pressure. increased venous return and increased cardiac output!!!
64
Q

what two things does blood flow to any organ depend on

A

mean arterial pressure and degree of vasoconstriction..

65
Q

how does the system compensate for arterioles of one organ dilating?

A

arterioles of another must constrict to maintain adequate pressure. and the adequate pressure will bring blood to vasodilated vessels
– but still there is an inadequate suppy of blood so there could be a situtaion where arterioles are dilated without adequate blood volume and bp goes down–> lightheadedness or fainting!

66
Q

what receptors monitor mean arteriole pressure

A

baroreceptors

67
Q

what is the baroreceptor reflex

-where is it?

A

short term mechanism- regulates cardiac output and total peripheral resistance

  • in Carotid sinus!! sends signals to cardiovascular control center in the medulla
  • alters activity of autonomic nervous system to return mean arterial pressure to normal
  • like with orthostatic hypertension (laying in supine, blood pressure decreases and arterioles relax, volume of blood in veins increases- when go stand the vesels are still dilated and blood pressure is insufficient for required blood flow since vessels are dilated. etc, temporarily low o2 to brain…
68
Q

how does the baroreceptor reflex react

A

carotid sinus continuously generates action potentials. the rate of firing set the standard fequency for baseline mean arterial pressure. as the mean arterial presure increases the frequency of action potentials increases above the normal frequency. this starts a signaling process which leads to dilation of arterioles to decrease blood pressure. in situtaion where mean arteril blod pressure decreases– the frequency fo action potentials geenerated by carotid sinus decreases and it signals arterioles to contract (sends signal to medulla cardiovascular control system)

69
Q

what is normal systolic /diastolic

A

systolic: less than 120
diastolic: less than 80

70
Q

what is elevated systolic / diastolic

A

systolic: 120-129
diastolic: less than 80

71
Q

what is high blood pressure - STAGE 1 hypertension? systolic/diastolic

A

systolic: 130-139
diastolic: 80-89

72
Q

what is high blood pressure STAGE 2 hypertension s/d

A

s; 140 or higher

d; 90 or higher

73
Q

what is hypertensive crisis s/d

A

s; higher than 180
diastolic ; higher than 120

CONSULT DOCTOR NOW

74
Q

what are the most common hypertensions

A

primary 90%

secondary -10%

75
Q

how can reduced bloodflow to kidneys cause secondary hypertension

A

-reduced blood flow to kidneys -> increased blood volume to compensate for reduced renal blood flow. angiotensin II=vasoconstrictor ! and uptake of salt causes more water reabsorption..

76
Q

how does pheochromocytoma cause secondary hypertension

A

this is an adrenal medullary tumor that secretes excessive epinephrine and norepinephrine.
-results in increaes in cardiac output and generalized peripheral vasoconstriction

77
Q

what is primary hypertension? what causes it/what increases risk

A

unknown cause
genetic disposition- increases with obesity, stress, smokking and dietary habits

  • defects in salt management by kidneys can also cause it.. genetic variations in angiotensinogen (precursor for angiotensin II)
  • excessive salt intake (salt retains water- more blood volume)
  • diets low in fruits and veggies, dairy (low K and ca)
78
Q

what is the recommended sodium intake for anyone with high bp or at risk? everyone else?h

A

risk or high: 3.8 g nacl

everyone else - 5.8 g nacl

79
Q

what are hypertension complications

A
  • heart (increased workload, pump against increased resistance)
  • damaged blood vessels
  • congestive heart failure
  • stroke
  • heart attack
  • renal failure

BMS 130 (3 decks)

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