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Cardiovascular > Phys Lecture 5: Application of Ohm's Law > Flashcards

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
Q

T or F: Capillaries are innv with sympathetic nerve fibers

A

F (but all other blood vessels are)

26
Q

T or F: Cerebral and coronary vasculature is highly innv with symp nerve fibers

A

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
Q

Epi and norepi are released from ___

A

adrenal medulla

28
Q

Norepi binds ____ receptors and epi binds ____ receptors

A

alpha

alpha and beta

29
Q

alpha receptors mediate vaso _____

beta receptors mediate vaso____

A

constriction

dilation

30
Q

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

A

Angiotensin II

31
Q

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)

A

vasopressin

32
Q

A polypeptide that increases capillary permeability. Is released by immune cells and will cause edema during inflammation reaction.

A

bradykinin

33
Q

A biogenic amine that increases capillary permeability. Is released by immune cells and will cause edema during inflammation reaction.

A

histamine

34
Q

Derived from arachidonic acid, and are mostly vasodilatory but some are vasoconstricting

A

prostaglandins

35
Q

An oligiopeptide that is mostly released from atrial myocytes (when they are stretched) and will cause kidneys to increase urine output

A

ANP

36
Q

NO is derived from ____

A

arginine

37
Q

NO is released in response to ____

A

shear stress or the presence of ATP

38
Q

NO regulates Q by…

A

vasodilation in larger vessels and decreasing intracellular Ca++ levels

39
Q

What is rarefaction?

A

dec number of blood vessels

40
Q

What are examples of well established angiogenic factors?

A

FGF, VEGF, angiotensin

41
Q

What is “hypertrophic vascular remodeling”?

A

decreasing the size of vascular lumen to decrease Q

Cardiovascular (31 decks)

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