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Physiology Winter 2012 > Physiology 12.12.12 Peripheral Circulation (Hawkins) > Flashcards

Physiology 12.12.12 Peripheral Circulation (Hawkins) Flashcards

1
Q

What is the CO of adults at rest

A

5.4 L/min

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2
Q

What is avg blood flow for body weight 70kg

A

7.7 ml/min per 100 g of tissue

However, BF varies greatly between tissues

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3
Q

Which organs receive the most Blood flow(mml/min)

A

Liver>Muscle>Kidney > Brain

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4
Q

Do brain and kidney receive proprotionate BF as predicted to their weights?

A

NO!

BF accts for only 0.5% of body weight for 20% CO, brain acts of only 2% of body weight for 14% CO

GI, Spleen, Liver (splanchnic bed) acct fr 2-3% body wieght but receive 25% CO at rest

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5
Q

Which organ receives the most Blood flow (ml/min/100gm)

A

Kindey

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6
Q

Does brain use the same amt of BF all day long?

A

Yes!

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7
Q

Does heart use same amt of BF all day long?

A

NO! Uses more blood during exercise

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8
Q

What is BF at rest? Max CO? Max Dilation?

A

BF rest = 5 L/min

Max CO = 20L/min

Max dilation = 38 L/min

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9
Q

What is Max dilation?

A

If all tissues were being perfused at the same time

This is more than the heart can delvier so has to be regulated

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10
Q

Describe the mechanims of BF distribution as the reservoir and faucet

A

High-presure reservoir function is served by the arterial system

Arterial BP is generated by the heart’s pumping action

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11
Q

Vascular or Arteriole Tone. What causes it?

A

Arterioles, if not all, vascular beds are partially constricted at any given moment.

This is referred to as vascular tone, and is caused by continuous sympathetic stimulation as well as myogenic contration

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12
Q

How/when does blood flow in beds increase?

A

by dilating its arterioles in response to metabolic needs

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13
Q

How does the sympathetic NS innervate teh heart? Through what receptors?

What does it do to CO

A

SNS innervates and stimulates both the chronotropic (rate) and inotropic (contractility) effects on heart medaited by B-1 adreneric receptors, increasing CO under most conditions

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14
Q

How does Symp NS affect Large Arteries? Whch receptors?

A

Mediated through the alpha-1 receptors

Makes arteries LESS COMPLIANT (stiffer)

Causes an immaterial reduction in diameter (not htat big fo a change in radii)

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15
Q

What does Sympathetic NS do to Veins (large)

A

Densely innervated by Sympathetic NS

Mediated by alpha-1 R

Makes much less compliant (stiffer)- like vena cava

Increase Central and Peripheral Venous Pressure

Sends Venous Return to heart and Right Atrium!!!!

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16
Q

How much blood do the veins usually contain?

A

2/3 of the blood supply

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17
Q

How does the Sympathetic NS affect Arterioles? Resistance? BF? Capillary Hydrostatic P? Total Peripheral P? MAP?

A

Densely innervated by SNS

Mediated through alpha-1 receptors
**PRIMARY MECHANISMS OF SNS On PERIPHERAL CVS

Arterioles contract (reduce diameter)

  • Resistance to flow increases (constant P)
  • BF decreases (at constant pressure)

-Capillary pressure may drop, which favors REABSORPTION

Total peripheral resistance may increase

MAP Incerease

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18
Q

What is the affect of Sympathetic NS on Adrenal Meduall

A

Adrenal Medulla releases Epi (80%) and NE (20%)

Essentially a peripheral ganglion on SNS

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19
Q

What does circulating Epi do to cardiac receptors

A

B-1 receptors

Causes positive inotropic and chronotropic effect

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20
Q

What does high doses of Epi bind to?

A

alpha-1 R in peripheral vesels and mimics effects of sympathtic stiumaltion (This is PREFERRED) and B-2 is masked

Binds to beta-2 receptors in Skeletal muscle arterioles

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21
Q

What does low doses of epinephrine pereferentially bidn to?

A

B-2 receptors and produces VASODILATION

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22
Q

What are sympathetic cholinergic fibers? What do they innervate

A

Limited to Sweat glands and Arterioles of muscles

Release ACh- Muscarinic R

  • Dilation of Arterioles
  • increase sweating

Little effect on conrol of BP or Flow to other tissues

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23
Q

Role of Parasympathetic NS - how doees it control heart rate

A

Controls heart rate through INHIBITION (SA node, AV node)

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24
Q

PS on arteries, veins, arterioles

A

PNS does NOT innervate arteries, veins, or arterioles throughout the body, and therefore, has no material efefct on BP by this mechanism

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25
Q

What does PNS innervate

A

Genital Organs, Bladder, Colon

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26
Q

What are some molecules (in addtion to Epi and NE) that affect vascular system (3)

A

Angiotensin II

Vasopressin

Histamine

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27
Q

What is the affect of Histamine. Which side of capillary is most affected

A

Increases capillary Permeability

Mast cells and basophils; leaks into tissue, Decrease oncotic P – >fluid goes OUT of capillary

Most affected are on Venous side; His causes endothelial cells to separate and thus to create discrete intercellular gaps

Plasma escapes through gaps and into intersitium

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28
Q

Is the effect of Histamine great?

A

No! only minor

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29
Q

Affect of Angiotensin II

A

Strong Vasoconstrictor

peptide hormone that cuases BV to cconstrict and increase BP

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30
Q

What is precursor of Angiotensin

A

Globulin that is produced constitutively and released to circulation mainly by the liver

31
Q

What converts Angitensinogen to Angiotensin I

A

Renin form kidneys

32
Q

What converts Angiotensin I to Angiotensin II?

A

ACE- angeiotensin-converting enzyme pirmarly through ACE activity within teh kidney

33
Q

What is the affect of Vasopressin

A

AKA Antidiuretic hormone, ADH is a homrone repsonsible for increasing water reabsorption by kidney

COnserves Vascular volume

34
Q

What are ways of Local Regulation of BF

A
  1. Autoregulation
  2. Active Hyperemia (metabolic regulation)
  3. Reactive Hyperemia (Metabolic Regulation)
35
Q

What is Autoregulation?

A

intrinsic action of SM

36
Q

How is BF regulated by metabolites

A

Involve changes in tissue BF that can be demonstarted in teh absence of Sympathetic input or humeral agents

This leads to conclusion that local factors can control tissue BF directly

37
Q

What is active hyperemia?

A

Blod flow is comensurate with tissue need for energy) Sk muscles BF increases with exercise! The magnitiude of increase in tissue BF is commensurate with the O2 consumption of the tissue.

Increased metabolism creates byproducts that are vasodilators

38
Q

What are vasodilators that are created as byproducts to increased metabolism

A

CO2, H, K, lactate, adenosine

Local arterioles respond by dilating

39
Q

What is Reactive Hyperemia

A

Blood flow is restricted temporarily and tehnt ehre is an increase when vessels are open afterwords’’

The magnitude of hypermia occurring parallels the extend of BF deprivation during the occlusion

40
Q

What is the mechanism behind active and reactive hypermia?

A

Related to metabolic changes in the tissue.

Tissue metabolism consumes O2 and feuls (glucose, FA, etc), produces CO2, and releases K and H, Lactic Acid, Adenosine,etc

In teh absence of adequate BF, ions and metabolites accumulate.

41
Q

What does low O2 content do?

A

hypoxia can produce vasodilation

In absence of adqueate BF (due to elevated metabolism or occlued BF) , these metaboltes accumulate resulting in vasodilation

When BF restored, vessels dilate ad flow is elvated until metabolites have been washed out.

42
Q

What are various metabolites resp for metabolic regulation

A 
Lactic acid
H
Adenosine
NO (endothelial-derived releasing factor)
K+
43
Q

What does it mean to have myogenic autoregulation of blood flow

A

In many tissue beds (kidney), blood flow does NOT change much despite the large changes in Arterial Pressure

Kidney retains a nearly constant BF over a broad range of arterial pressures (90-180 mmHg)

44
Q

What does the alteration in arterial pressure have a direct effect on?

A

on teh resistance of renal arterioles

Reducing arterial Pressure also Reduces vascular resistance –> maintaining BF near constatn

Increase in Pressure in renal artery increases Renal Vascular Resistance

45
Q

Describe how Myogenic autoregulation works in kidney

A

Kindey’s BF greatly exceeds its metabolic need.

An increase in stretch of arterial SM, (by Inc Arterial P) has the effect of causing Contraction of the SM –> producing an increase in vascular resistance, thereby minimizing an increase in BF

46
Q

Describe local regualation of kindey

A

Almost exclusively MYOGENIC REGULATION

BF is near constant between Pa of 90-180 mmHg

47
Q

Local regulation of Brain and Heart

A

Almost exclusively METABOLIC REGULATION

48
Q

Local regulation of Skeletal Muscle

A

Combines both mechanism

Under Strong Sympathetic Control, but as energy demand increases,metabolic regulation predominates

49
Q

Describe the control of arterial pressure

A

Arterial system is a hihg-pressure reservoir of Blood from which the tissues can draw on demand

There is a limit to the quanitty of flow that can be supplied from this sytem, yet heart and arterial sys can supply sufficient BF to tissues over a wide range of dmeands

50
Q

What is the Arterial Baroreceptor Reflex

A

Single most important mechanism for short-term control of ARTERIAL Pressure

51
Q

Where are pressure receptors for Baroreceptors located. Where does afferent run? Where does integration occyr. Efferent?

A

Located in Carotid arteries and Aortic Arch

afferent neurons running to CN medulla

Integration occurs in the medulla.

Efferent pahtway fo refelx involve bot PS and SYmp

52
Q

Describe how Arteria BaroR Reflex works

A

Rise in Arterial P == Inc neural input to medulla –> Increase in PS activity (through vagus) and decrese in sympt

REDUCE ARTERIAL PRESSURE

53
Q

What is the EFFERENT pathway of the Arterial BaroR Reflex

A

Symp and PS

PS = heart slow

Symp = increase heart rate and contractility and arteriolar constriction

54
Q

Describe the CNS integration of BaroR Reflex.

Where do axons synapse?

What kind of synapse (excitatory or inh) what NT

A

Input from Pressure Receptors (AP) ascend to the medulla, via axons of teh glossopharyngeal and vagus nerves, bilaterally

Axons synapse in two bilateral nuclei (NTS) in teh medualla–> excitatory synapse that employs GLUTAMATE (though tehe are both inh and exc from other palce)

55
Q

Where does NTS neurons send axons to?

A

bilateral vagal nuclei and the midline cardiovascular center

56
Q

What do AP coming form NTS stimulate?

A

Vagal nuclei

esp Dorsal Vagal Nucleus and Nucleus Ambiguus

These inc PS output via vagal nerves

57
Q

What do Efferent AP from NTS influence?

A

medullary sympathetic pacemaker region located in teh RVLM via innervation of the CVLM

58
Q

What does stimulation of NTS inhibit?

A

activity of SymP NS

59
Q

ARTERIAL BAROR REFLEX

Which is more sensitsive? Carotid BaroR or Aortic Arch R?

A

Baroreceptors respond more strongly to changing (pulsatile pressure) than to constant pressure

BaroR response parallels mean pressure within a limited range

Carotid baroR are more sensitive to change than aortic arch R

60
Q

Does BaroR reflex respond rapidly wihin a single pulse?

A

Yes

61
Q

Hypothalamic Regions

Inc in temperatue

A

Integrat heart rate and BP in response to emotion-evoking situations

Also elevation of Temperature of anterior hypothalamus eleicits signals taht depress CV center –> actviatind vas mechanisms of heat loss (vasodilation and sweating)

62
Q

How does output of hypothalamus affect baroR reflex?

A

By acting on the NTS nuclei

63
Q

What kind of receptors are those that monitor arterial pressure?

Where are they located

A

Stretch Receeptors

Located in teh wall of Aortic Arch and Carotid sinus that are stimualted by stretch

64
Q

Where are Carotid Sinuses Located

A

both sides of neck near bifurcation of the internal and external carotid arteries

65
Q

When are AP initiatied

A

when nerve endings are stretched, such as woudl happen as arterial pressure rises

THis stimualtes vagal nuclei and increases PS output

66
Q

What are Cardiopulmonary BaroReceptors and what are the function?

A

Stretch receptors respond to absolute pressure in the atria and pulmonary veins.

They discharge at lower pressures than teh arterial baroreceptors, on reaching the brain, the impulses initiate a similar response

Elevated cardiopulmonary pressure inhibits sympathetic output

67
Q

Wher eare Cardiopulmonary Reflexes located

A

in the walls of heart (atria, ventricles),

Great Vessels (vena cava)

and lungs

Respond like baroreceptors but at lower pressures;

Capable of adapting to sustained pressures

68
Q

What are Peripheral ChemoReceptors.

What happens duing asphyxia

A

Located in Carotid and Aortic Bodies

Main function is with REspiration

Responds to :
Increased PaCO2
Increased H+
Decreased PaO2

By stimulating Sympathetic System (Inc BP and Vasoconstriction)

69
Q

When baroreceptors and peripheral chemoreceptors are stimualted, whicih predominates?

A

Baroreceptors

70
Q

What is the Brainbridge reflex

A

An increased stretch of Right Atrium can sometimes increase Heart Rate when HR is SLOW

71
Q

What mediates Bainbridge reflex

A

Vagal Afferents from heart to CV center

and Sympathetic efferents to teh heart

72
Q

What is the main mehcanism for maintaining a uniform cardiac output on both sides of heart?

A

Frank-Sterling Mechanism

73
Q

What is unusual about transplanted hearts, which do not hav ea Bainbridge reflex

A

Shows no imbalance

74
Q

Where is the location of the best possible sites for monitoring and controlling arterial pressure

A

IN aortic arch

and right and left internal carotid arteries 3

Physiology Winter 2012 (10 decks)

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