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Cardiology > Vascular Physiology > Flashcards

Vascular Physiology Flashcards

1
Q

What is the distribution percentages of blood in circulation?

A

5% - capillaries
65% - veins
30% - arteries/heart

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2
Q

What some mechanisms that increase venous return?

A
  • sympathetic activation

- breathing/ cardiac function (ie. inspiration)

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3
Q

How many layers are there in each vessel?

A

3 layers

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4
Q

What are the three layers of vessels?

A

1) Intima: thin layer separating blood from wall tissue, mostly 1 cell layer of endothelium
2) Media: variably thick smooth muscle layer—thicker in high-pressure arterial vessels
3) Adventitia: connective tissue outer lining of vessel (a.k.a. ‘serosa’); often separated by elastic layers (in arteries and aorta) from media

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5
Q

What happens to the elastins in arteries during systole and diastole?

A

systole - expands with surge

diastole - rebounds when arterial pressure wanes

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6
Q

When endothelium is activated, the mediators released affect which layers?

A

media and adventitia

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7
Q

What is the anti-coagulant milieu of the the vessels?

A

endothelial glycocalyx

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8
Q

What is the difference between cardiac and smooth muscle calcium muscle contraction?

A

calcium contraction of vascular smooth muscle is graded (i.e. the more calcium that’s available the greater the contraction) compared to cardiac muscle where contraction is “on” or “off”.

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9
Q

How is smooth muscle activated?

A
  1. Calcium enters a cell via voltage-gated calcium channels in response to membrane depolarization
  2. Calcium binds to calmodulin, a tetrameric protein, each chain binding one calcium ion. Binding of calcium facilitates binding of further calcium ions in a cooperative manner and calmodulin becomes progressively more activated.
  3. Activated calmodulin activates myosin light chain kinase (MLCK) which phosphorylates serine 19 on the myosin light chains allowing for actin-myosin interaction
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10
Q

Whats the difference between cadherins and integrins?

A

Integrins mediate adhesion between the cell and its extracellular matrix (ECM), and cadherins mediate homotypic adhesion between cells.

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11
Q

Normal resting state involves the release of which chemicals?

A

Vasodilatory factors released
NO
PGI2
EDHF = endothelial dependent hyper-polarizing factor

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12
Q

Activated endothelial state results to the release of which chemicals?

A

vasoconstrictors released
most potent constrictor known is released by endothelium = endothelin
local production of angiotensin II
Thromboxanes, etc.
(inflammation –> histamine & NO –> in some settings actually vaso-dilates)
Glycocalyx lost

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13
Q

What is the endothelial function of NO?

A

highly protective of the vessel, prevents inflammation and atherosclerosis, and important for normal function

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14
Q

What is the most important endothelin?

A

endothelin-1

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15
Q

True or False: endothelin is released also via the activation of other vasocontrictors

A

True: vasoconstrictors (epinephrine, angiotensin II), hypoxia, lipoproteins, thrombin, shear stress

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16
Q

What is the equation for blood pressure?

A

BP = Cardiac output x vascular resistance

Pressure = heart rate x strove volume x vascular resistance

17
Q

What are pressure sensors called?

A

baro-receptors

18
Q

What happens if there is inadequate pressure?

A

sympathetic activation (decrease in parasymp) –> HR up, contractility up, vessel tone up –> CO up, resistance up –> BP up

19
Q

how to calculate mean BP?

A

[SBP + 2(DBP)]/3

20
Q

what is pulse pressure?

A

systole - diastole

21
Q

what is vascular compliance?

A

stretchability of vessels proportional to elasticity (volume change in response to pressure change)

22
Q

Why does pulse pressure increase in aging?

A

loss of elasticity and predominance of rigid collagen –> stiff and less compliant arteries that are unable to maintain BP –> high systole, low diastole

23
Q

How do tissue control flow?

A

resistance

24
Q

Where is most of the resistance found?

A

Arterioles

25
Q

How is resistance regulated at the capillary level?

A

pre-capillary ‘gates’ regulate fine-tuned resistance; flow = pre-capillary sphincters

26
Q

Which organs have low resting tone?

A

low resting tone (sensitive to sympathetics, not to metabolic factors): kidneys, skins, gut

27
Q

What are the 3 main factors to influence resistance?

A 
Nerve endings (ie. noreprinephrine) 
Local chemicals (ie. endothelin-1)
Hormones (chemicals secreted in glands) (ie. epinephrine)
28
Q

Why is there a 20 mm Hg pressure difference between the start and end of capillary?

A

pressure of 20 mm Hg drives fluid into tissue space

Start has high pressure to compel fluid out and low pressure at the end to get waste into

29
Q

What is the pressure from proteins that sucks fluid back in?

A

oncotic/osmotic pressure

30
Q

At the end of capillary what pressure predominates?

A

oncotic pressure greater than BP/hydrostatic

31
Q

What is a pathogenesis of atherosclerosis?

A

starts with endothelial activation / damage (often at sites of turbulence / shear stress)
–> allows entry of ‘bad’ LDL cholesterol & macrophages
–> macrophages ‘eat’ cholesterol –> foam cells
–> accumulation of enough foam cells –> fatty streak (visible on lining of artery)
macrophages die –> free cholesterol pool
other inflammatory cells move in
fibrotic ‘cap’ of matrix + cells seals off core of necrotic (dead) cholesterol pool
= atherosclerotic / cholesterol plaque

as more cholesterol accumulates –> vessel often bulges outward (remodels) –> inner diameter maintained till late = no major stenosis!

  • -> more cholesterol accumulation
  • -> inner diameter (lumen) squeezed = stenosis
  • -> symptoms from vessels slowly blocking
  • -> eventual calcification = ‘hardening of arteries’
32
Q

What is unstable atherosclerosis?

A

fibrous cap often attacked by underlying inflammation or physical stresses

  • -> ‘crack’ in cap; loss of glycocalyx
  • -> blood comes in contact with intensely pro-thrombotic plaque core
  • -> thrombus formation
  • -> risk of instantaneous vessel clot / emboli
  • -> sudden death of down-stream tissue
33
Q

What kind of flow create murmurs and bruit?

A

turbulent flow (aka increased resistance)
Happens in:
-lg vessels
-stenotic and bifurcations

34
Q

What does a narrow pulse pressure mean?

A

low/narrow pulse pressure due to ↓ SV (e.g., congestive heart failure, shock, cardiac tamponade, aortic stenosis)

35
Q

What does a wide pulse pressure mean?

A

High/wide pulse pressure due to ↑ SV (e.g., exercise, hyperthyroidism, aortic regurgitation) or stiff arteries

Cardiology (29 decks)

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