Phys Lecture 5: Application of Ohm's Law Flashcards

1
Q

Why are our organs arranged in parallel rather than in a series?

A

parallel arrangement allows every organ to recieve adequate perfusion

*if they were in a series, blood flow would decrease successively bc Rparallel < Rseries

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2
Q

WHat is the formula for flow (Q)?

A

Q = P/R

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3
Q

Blood flow is regulated by changing (pressure or resistance). Why?

A

resistance = this allows blood flow to each organ to be regulated independently of e/o; resistance is also easier to change (just have to change the radius of the vessels you want to regulate)

**changing the pressure for the needs of one organ would change the pressure for all the organs = not good

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4
Q

What is the difference between active and reactive hyperemia?

A

active: blood flow increases due to increase in tissue activity/functional need
reactive: blood flow increases due to prior reduction of blood flow

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5
Q

T or F: blood flow is linked to metabolic need

A

T: inc met –> inc Q

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6
Q

What is “blood flow reserve”?

A

When a tissue increases metabolic activity (has greater need for O2), then the resistance will decrease so that blood flow can increase

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7
Q

What happens to blood flow when there is a decrease in O2 saturation (aka oxygen tension)?

A

it will increase (need more blood to get the necessary amt of O2)

*inverse relationship between Q and oxygen tension

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8
Q

Describe what happens to Q when a an artery is clamped shut and then released(i.e. inc R)

A

when the artery is released blood flow will exceed the rate it was prior to the clamping (hyperemia) and will stay higher the longer it was clamped closed/interrupted

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9
Q

T or F: The longer the blood flow is interrupted/ischemia endures, the longer the time interval of reactive hyperemia and more hyperemia there is.

A

T

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10
Q

How does O2 regulate blood flow in active hypermia?

A

inc in metabolism/tissue activity dec O2 –> vasodilatation –> inc Q

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11
Q

How does O2 regulate blood flow in reactive hypermia?

A

dec blood flow decreases O2 –> vasodilatation –> inc Q

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12
Q

What are the 2 hypothetical mechanisms for how O2 levels may influence vascular resistance/radius?

A
  1. low O2 causes dec in VSM metabolism which causes a decrease in the smooth muscle force generation = vascular relaxation (inc flow)
  2. small arteries (<500 microm) may have a yet to be IDed O2 sensing capacity
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13
Q

T or F: A decrease in O2 causes a decrease in R

A

T

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14
Q

What are the important vasodilator metabolites (he said to know these**)?

A
adenosine
ATP, ADP, AMP
CO2
lactic acid
potassium ions (K+)
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15
Q

How do metabolites control blood flow in active hyperemia?

A

Inc tissue activity/metabolism leads to inc in metabolites –> vasodilatation –> inc Q

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16
Q

How do metabolites control blood flow in reactive hyperemia?

A

decreased Q causes metabolites to accumulate –> vasodilation –> inc Q

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17
Q

What is the autoregualtion?

A

the capacity of blood vessels to maintain blood flow despite changes in blood pressure

18
Q

How to blood vessels keep Q constant (autoregulate) when BP increases?

A

they vasoconstrict/increase resistance

Q = P/R

19
Q

How to blood vessels keep Q constant (autoregulate) when BP decreases?

A

they vaspdilate/decrease resistance

Q = P/R

20
Q

Why is there zero blood flow when perfusion pressure is less than 60 mmHg?

A

the vessels collapse bc there is not enough BP to oppose the baseline sympatheic activity

21
Q

Describe autoregualtion via the metabolic mechanism (with inc P)

A

inc pressure causes blood flow to increase –> dec metabolite presence and inc O2 (hyperemia) causes increase in vascular resistance –> dec Q

22
Q

Describe autoregulation via myogenic control.

A

inc P –> vessels stretch –> Ca++ channels are activated and there is an inc in cytoplasmic Ca++ –> inc force in VSM –> vasoconstriction/inc R –> dec Q

23
Q

What are the rapid regulators of vascular resistance?

A
  • local factors: hyperemia (vasodilator metabolites, O2 levels)
  • sympathetic NS: vasoconstrictor fibers + Norepi
  • humoral/circulating factors: epi > norepi released, alpha and beta receptors
24
Q

What is the slow regulation of vascular resistance?

A
  • change in # of vessels per tissue unit

- hypertrophy = decrease in size of vessel lumen

25
T or F: Capillaries are innv with sympathetic nerve fibers
F (but all other blood vessels are)
26
T or F: Cerebral and coronary vasculature is highly innv with symp nerve fibers
F: do not what this bc we cannot afford to have the blood flow to these organs decrease in response to external stimuli--> Brain and heart aways needs blood flow
27
Epi and norepi are released from ___
adrenal medulla
28
Norepi binds ____ receptors and epi binds ____ receptors
alpha | alpha and beta
29
alpha receptors mediate vaso _____ | beta receptors mediate vaso____
constriction | dilation
30
An oligopeptide that constricts both arteries and veins and is involved in the regulation of arterial pressure and plasma volume. Has a direct vasoconstrictor effect on blood vessels. Directs kindeys to decrease urine output
Angiotensin II
31
An oligiopeptide that increases plasma volume by directing kidney to decrease urine output. At high levels, it constricts arteries and veins (particularly in splanchnic area)
vasopressin
32
A polypeptide that increases capillary permeability. Is released by immune cells and will cause edema during inflammation reaction.
bradykinin
33
A biogenic amine that increases capillary permeability. Is released by immune cells and will cause edema during inflammation reaction.
histamine
34
Derived from arachidonic acid, and are mostly vasodilatory but some are vasoconstricting
prostaglandins
35
An oligiopeptide that is mostly released from atrial myocytes (when they are stretched) and will cause kidneys to increase urine output
ANP
36
NO is derived from ____
arginine
37
NO is released in response to ____
shear stress or the presence of ATP
38
NO regulates Q by...
vasodilation in larger vessels and decreasing intracellular Ca++ levels
39
What is rarefaction?
dec number of blood vessels
40
What are examples of well established angiogenic factors?
FGF, VEGF, angiotensin
41
What is "hypertrophic vascular remodeling"?
decreasing the size of vascular lumen to decrease Q