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Human Physiology 2 > Unit 2 - Blood Flow & Blood Pressure PART C > Flashcards

Unit 2 - Blood Flow & Blood Pressure PART C Flashcards

1
Q

_____ organs require ________ amounts of blood flow both at rest and as activity changes. As such, the body needs a way to allow for changes in blood flow to different organs.

A

DIFFERENT

DIFFERENT

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2
Q

Most of the blood flow coming out of the left ventricle at rest goes to the ____.

A

LIVER

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3
Q

If cardiac output from the left ventricle is ~5.0 L/min (based on the average resting heart rate of 72 bpm and average stroke volume of 70 mL), then flow rate to the liver is…

Figure 15.12 (page 8)

A

27% x 5.0L/min, which is equal to 1.35L/min.

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4
Q

What is there to note about blood flow to the lungs for ex?

A

Note: Blood flow to the lungs occurs at a rate of 5.0L/min coming from the right ventricle, so the entire volume of the body’s blood passes through the lungs each minute).

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5
Q

At rest, the least amount of blood flow goes where?

A

to the heart (4%) and the skin (5%). These values will increase with increasing activity (walking, running, etc).

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6
Q

Kinda random: The arterioles are the main site of variable resistance in the systemic circulation & contribute…

A

more than 60% of the total resistance to flow in the system

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7
Q

____ _____ to each organ is a function of the pressure gradient in the system and the arteriolar _____.

A

FLOW RATE

RESISTANCE

(F = ∆P/R)

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8
Q

How is blood flow to organs controlled by changing arteriolar resistance?

A
  1. The radius of arterioles leading to different parts of the body can be adjusted independently of one another, allowing for specific changes in blood flow to specific organs.
  2. Smooth muscle surrounding the arteriole can contract (VASOCONSTRICTION) or relax (VASODILATION) to produce changes in resistance and therefore changes in FLOW.
  3. So rate of blood flow to each organ depends on the degree of contraction and relaxation (VASOCONSTRICTION/ VASODILATION) in the arterioles that supply blood to that organ.
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9
Q

Describe figure 15.13, blood flow through individual blood vessels and how it is determined by the vessel’s resistance to flow

A

a. 100 ml flows through 2 blood vessels both at 50 ml

b. Then 100 ml flows through 2 blood vessels, 1 is 20 ml & 1 is 80 ml
- from 50 ml –> 20 ml so resistance increased & flow decreased
- from 50 ml –> 80 ml so resistance decreased & flow increased

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10
Q

Blood flow entering capillary beds of each organ/tissue is further controlled by contraction/relaxation of _________.

A

PRECAPILLARY SPHINCTERS

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11
Q

Precapillary sphincters =

A

bands of smooth muscle at junctions between arterioles and capillaries.

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12
Q

When precapillary sphincters are OPEN (RELAXED), blood flows…

A

into the capillary bed

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13
Q

When precapillary sphincters are CLOSED (CONSTRICTED), blood flows…

A

directly from ARTERIOLE to venule though connecting vessels called METARTERIOLE, and does not enter the capillaries.

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14
Q

What are the 5 kinds of regulation of arteriolar vasodilation/vasoconstriction:

A
  1. Begins with vascular tone
  2. Intrinsic (local) autoregulation mechanisms
    a. Myogenic control
    b. Local Metabolic Control
    c. Non-metabolic chemical mediators
  3. Systemic (extrinsic) mechanisms
    a. Neural Control
    b. Hormonal Control
  4. Example of blood flow control during exercise (local metabolic factors, neural and hormonal control)
  5. Example of blood flow control during severe hemorrhage (blood loss that causes MAP to decrease)
    a. Local Effect (e.g. at brain, or heart)
    b. Sympathetic response
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15
Q

Regulation of arteriolar vasodilation/vasoconstriction:

  1. Begins with VASCULAR TONE:
A

a. State of partial contraction independent of neural signaling and chemical effects (hormones, vasoactive mediators)
b. Baseline constriction of arterioles.

c. Can be modified by external signals to increase or tone
decrease the concentration of cytosolic calcium in smooth muscle cells, which in turn will affect the level of contraction/relaxation of the muscle. (Recall from 2410, increasing cytosolic [Ca2+] increases tension, decreasing cytosolic [Ca2+], decreases tension)

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16
Q

Regulation of arteriolar vasodilation/vasoconstriction:

  1. Intrinsic (local) autoregulation mechanisms:
    a. MYOGENIC CONTROL
A
  • Ability of vascular smooth muscle within vital organs to regulate its tone in response to changes in blood pressure.
  • Increasing blood pressure stretches the smooth muscle in the arteriole.
  • Response to stretch is the opening of mechanically gated (stretch gated) Ca2+ channels in the smooth muscle cell membranes, which allows more Ca2+ to enter the cells (DEPOLARIZES), increasing crossbridge formation and therefore tension.
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17
Q

What are 2 examples of Myogenic control?

A

EXAMPLE 1: when you stand, the arterial pressure and flow in the feet increase. The increase in pressure in the feet causes the arterioles to stretch, allowing more Ca2+ into the cells. In response the smooth muscle contracts, resulting in vasconstriction (increased tone) which reduces flow in the feet.

EXAMPLE 2: When you stand up (from a supine position), the cerebral arterial pressure decreases, which reduces the amount of stretch in the arterioles. In response, smooth muscle relaxes (less stretch, less Ca2+), resulting in vasodilation (decreased tone), which increases blood flow to the brain.

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18
Q

In the absence of autoregulation…

A

an INCREASE in BP INCREASES BF through an arteriole

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19
Q

Regulation of arteriolar vasodilation/vasoconstriction:

  1. Intrinsic (local) autoregulation mechanisms:
    b. LOCAL METABOLIC CONTROL
A
  • Many tissues can control their own blood supply by releasing paracrine signaling molecules in response to changes in the metabolic activity of the tissue.
  • The release of paracrines into the extracellular fluid surrounding the arterioles can stimulate the endothelium of the arterioles to release VASOACTIVE MEDIATORS (e.g. nitric oxide, (NO)) that have direct action on the arteriolar smooth muscle and will initiate either vasoconstriction of vasodilation.
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20
Q

An example of Local Metabolic Control is ACTIVE HYPEREMIA. Describe this

A

E.g.1: Active hyperemia

  • Increase in blood flow to a tissue in response to an increase in tissue activity (metabolism).
  • As the tissue becomes more active, oxygen levels decrease and carbon dioxide levels increase. The effect on arteriolar smooth muscle is to cause relaxation and vasodilation, which increases flow to the organ.

Figure 15.10

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21
Q

An example of Local Metabolic Control is AUTOREGULATION & EXERCISE. Describe this

A
  • Rapidly contracting skeletal (and cardiac) muscle leads to:
    i. Local reductions in O2 levels (hypoxia)
    ii. local increases in CO2,H+,K+, AND ADENOSINE LEVELS (metabolic waste products)
  • Causes vascular endothelial cells to secrete NITRIC OXIDE specifically at these sites.
  • Increased [NO] reduces Ca2+ entry into adjacent smooth muscle cells thereby inducing localized VASODILATION of:
    i. Arterioles – increases blood flow to active tissues
    ii. Precapillary sphincters –increases number of open capillaries inactive
    tissues
  • Result = increased O2 delivery and increased waste removal by blood.
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22
Q

Regulation of arteriolar vasodilation/vasoconstriction:

  1. Intrinsic (local) autoregulation mechanisms:
    c. NON-METABOLIC CHEMCAL MEDIATORS (LIST)
A

i. Endothelin-1
ii. Histamine
ii. Serotonin

23
Q

Endothelin-1 (Non-metabolic chemical mediator)

A
  • Released from arteriolar cells in response to an increase in pressure.
  • Causes VASOCONSTRICTION by opening non-stretch sensitive Ca2+ channels and enhancing Ca2+ release by the sarcoplasmic reticulum in smooth muscle cells.
24
Q

Histamine (Non-metabolic chemical mediator)

A
  • Released by mast cells of the immune system.
  • Causes VASODILATION and plays a role in inflammation.
  • Localized release occurs during allergic reactions (quick onset) or in response to injury or infection (2-8 hr onset) resulting in redness and swelling.
25
Q

Serotonin (Non-metabolic chemical mediator)

A
  • In the blood, serotonin is released from platelets in response to a wound.
  • Causes VASOCONSTRICTION (part of hemostasis known as vascular spasm, the acts to reduce blood flow to the site of the wound).
26
Q

When damaged blood vessels activate platelets, the subsequent serotonin-mediated vasoconstriction helps to…

A

slow blood loss

27
Q

Regulation of arteriolar vasodilation/vasoconstriction:

  1. Intrinsic (local) autoregulation mechanisms:

During autoregulation myogenic and metabolic factors often operate at the ____ ____ to bring about a ____ in blood flow to a tissue/organ.

A

SAME TIME

CHANGE

28
Q

Regulation of arteriolar vasodilation/vasoconstriction:

  1. Intrinsic (local) autoregulation mechanisms:

Example - REACTIVE HYPEREMIA

A
  • An increase in tissue blood flow following a period of
    low perfusion.
  • Reduced flow/pressure, decreases stretch and causes local arteriolar RELAXATION (VASODILATION)
  • VASODILATION also occurs as a result of localized hypoxia and the accumulation of metabolic by- products (since low perfusion means waste removal is not occurring at an optimal level, and must be restored through via an increase in blood flow).
  • Result of vasodilation being triggered by both myogenic and metabolic pathways is RAPID restoration of local cellular conditions to normal
29
Q

Regulation of arteriolar vasodilation/vasoconstriction:

  1. Systemic (extrinsic) mechanisms:
A
  • Signaling from nervous or endocrine systems.
  • Can create body wide changes in blood flow and blood
    pressure (systemic).
  • Extrinsic control of arteriolar radius across multiple organ systems alters Total Peripheral Resistance (TPR) which is also an important regulator of Mean Arterial Pressure (MAP).
30
Q

For SYSTEMIC (EXTRINSIC) MECHANISMS (Regulation of arteriolar vasodilation/vasoconstriction), what is the formula? Describe

A
  • F = ΔP/R ∴ ΔP = F x R; substituting cardiac output for flow, MAP for ΔP and TPR for R we get:
    MAP = CO × TPR
  • So increasing or decreasing TPR by systemic (involving multiple organ system) vasoconstriction or vasodilation will not only change the blood flow in those systems, but will also have a measurable effect on blood pressure (unlike myogenic/metabolic regulatory mechanisms that act locally).
31
Q

If sympathetic release of NE ↓

A

the arterioles DILATE

32
Q

If sympathetic stimulation ↑

A

the arterioles CONSTRICT

33
Q

Regulation of arteriolar vasodilation/vasoconstriction:

  1. Systemic (extrinsic) mechanisms:
    a. NEURAL CONTROL

SYMPATHETIC NEURONS…

A

SYMPATHETIC NEURONS MAINLY release NE, which binds to arteriolar smooth muscle α1-ADRENERGIC RECEPTORS causing VASOCONSTRICTION
- brain arterioles lack α1-adrenergic receptors (as do terminal arterioles), so their radius/diameter is entirely controlled by LOCAL mechanisms (i.e myogenic/metabolic control).

34
Q

What do brain arterioles lack?

A

brain arterioles lack α1-adrenergic receptors (as do terminal arterioles), so their radius/diameter is entirely controlled by LOCAL mechanisms (i.e myogenic/metabolic control).

35
Q

Regulation of arteriolar vasodilation/vasoconstriction:

  1. Systemic (extrinsic) mechanisms:
    a. NEURAL CONTROL

SYMPATHETIC NERVES…

A

SYMPATHETIC NERVES constantly discharge at an intermediate rate (in addition to basal tone); however the firing rate is controlled by the cardiovascular center in the medulla of the brain.

  • increased firing leads to generalized* VASOCONSTICTION (↑ TPR) also causes venoconstriction (constriction of veins).
  • decreased firing leads to generalized VASODILATION (↓ TPR)
36
Q

Regulation of arteriolar vasodilation/vasoconstriction:

  1. Systemic (extrinsic) mechanisms:
    b. HORMONAL CONTROL (LIST)
A

i. Epinephrine
ii. Angiotensin II
iii. Vasopressin (= antidiurectic hormone or ADH)
iv. Atrial Natriuretic Peptide (ANP)

37
Q

Regulation of arteriolar vasodilation/vasoconstriction:

  1. Systemic (extrinsic) mechanisms:
    b. Hormonal Control

i. EPINEPHRINE

A
  • Released from adrenal glands in response to sympathetic stimulation
  • In skin and most abdominal viscera – binds to smooth muscle α1-receptors , reinforcing SNS VASOCONSTRICTION (the ↑ in R diverts blood from nonessential organs (like GI tract, to the skeletal muscles, liver, & heart)
  • In heart, liver and skeletal muscle, it binds with greater affinity to NON-INNERVATED b2-receptors that bind epinephrine with HIGHER affinity
38
Q

What is the result in these tissues from Epinephrine?

A

Result in these tissues is vasodilation, which strengthens local metabolic control mechanisms during exercise.

(such B2-mediated vasodilation enhances BF to the heart, skeletal muscles, & liver, tissues that are active during fight or flight response (liver produces glucose for muscle contraction))

39
Q

What is something to note to remember effects of epinephrine on different organs?

A

Note: to remember effects of epinephrine on different organs – think about which ones need to be active during exercise (fight-or flight). These will have vasodilation via b2-receptors (as well as local control mechanisms). If the organs mainly function for resting and digesting, then the generalized response of vasoconstriction will apply.

40
Q

a-receptors have a ____ affinity for E & don’t respond as strongly to it as they do to ___

A

LOWER

NE

41
Q

Regulation of arteriolar vasodilation/vasoconstriction:

  1. Systemic (extrinsic) mechanisms:
    b. Hormonal Control

ii. ANGIOTENSIN II

A
  • Decreased renal perfusion pressure (e.g. decreased MAP) causes RENIN to be secreted by the kidneys, leading to an increase in blood [angiotensin II].
  • Causes arteriolar VASOCONSTRICTION (increases TPR)
42
Q

Regulation of arteriolar vasodilation/vasoconstriction:

  1. Systemic (extrinsic) mechanisms:
    b. Hormonal Control

iii. VASOPRESSIN (= antidiurectic hormone or ADH)

A
  • Released from posterior pituitary in response to signaling from atrial receptors that are stimulated by a decrease in blood volume (or mean arterial pressure)
  • Causes VASOCONSTRICTION (increases TPR)
43
Q

Regulation of arteriolar vasodilation/vasoconstriction:

  1. Systemic (extrinsic) mechanisms:
    b. Hormonal Control

iv. ATRIAL NATRIURETIC PEPTIDE (ANP)

A
  • Synthesized and released by specialized atrial cells in response to excess stretch in the heart (e.g. increased venous return due to increased blood volume/pressure).
  • Causes RELAXATION of vascular smooth muscle and VASODILATION (decreases TPR)
44
Q

What is something to note about hormones Angiotensin II & Atrial Natriuretic Peptide (ANP)?

A

Hormones ii) to iv) are also closely linked to control of blood volume via their effects on the kidney arterioles.

45
Q

Regulation of arteriolar vasodilation/vasoconstriction:

  1. Example of blood flow control during exercise (local metabolic factors, neural and hormonal control):

Look in notes page 21

A

*Note: local metabolic influences DOMINATE in those muscles that are largely inactive during exercise (i.e. they VASOCONSTRICT)

46
Q

Regulation of arteriolar vasodilation/vasoconstriction:

  1. Example of blood flow control during severe hemorrhage (blood loss that causes MAP to decrease):
    a. LOCAL EFFECT (e.g. at brain, or heart)
A

i. DECREASED ARTERIOLE STRETCH
ii. DECREASED [OXYGEN] & INCREASED [METABOLIC WASTE] AT TISSUES
- Result = dilation of these arterioles; increased blood flow to brain/heart
- Problem: This causes MAP to decrease further, so must combine with:

47
Q

Regulation of arteriolar vasodilation/vasoconstriction:

  1. Example of blood flow control during severe hemorrhage (blood loss that causes MAP to decrease):
    b. SYMPATHETIC RESPONSE
A

i. INCREASED SYMPATHETIC STIMULATION
- NE – VASOCONSTRICTION of smooth in non-essential organs
- E – VASODILATION of skeletal muscle arterioles; however, this is opposed by (dominant) local
metabolic effects
ii. INCREASED PLASMA [VASOPRESSIN] AND [ANGIOTENSION II] – prevents water loss at kidneys (affects volume)
- Result: : INCREASED SMOOTH MUSCLE TONE of MOST arterioles (except brain, heart), and an attempt to preserve if not increase blood volume, thereby increasing MAP TOWARDS pre-hemorrhage values

48
Q

All arterioles receive blood…

A

at the SAME time from the aorta

49
Q

Total BF through ALL the arterioles of the body always =…

A

the CO

50
Q

Flow through individual arterioles in a branching system of arterioles depends on…

A

their R

  • ↑R in an arteriole, the ↓ the BF through it
  • if an arteriole constricts & R↑’s, BF through the arterioles ↓’s
51
Q

Blood is diverted from…

A

↑R arterioles to ↓R arterioles

- blood traveling through the arterioles takes the path of LEAST R

52
Q

In the brain & heart, tissue metabolism is what?

A

the primary factor that determines arteriolar R

53
Q

To avoid unconsciousness & eventually brain damage…

A

cerebral BF is relatively constant under normal circumstances

  • ↑’s in systemic BP trigger myogenic responses that result in VASOCONSTRICTION
  • however, the primary factor that alters BF in the brain is TISSUE METABOLISM
54
Q

Accumulation of CO2 around arterioles acts as what?

A

a VASODILATOR

  • if metabolism in 1 region of the brain ↑’s, oxygen consumption & CO2 production both ↑
  • the CO2 vasodilates arterioles, ↑’ing BF to the active region

Human Physiology 2 (37 decks)

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