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Systems Phys 2022 > Peripheral Circulation > Flashcards

Peripheral Circulation Flashcards

1
Q

What is the relationship between pressure, flow, and resistance:

A

Flow = (PA-PV)/R

PA → arterial pressure

PV → venous pressure

R → resistance

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2
Q

Define: Autoregulation of Blood Flow

A

The intrinsic ability of an organ to maintain blood flow constant despite changes in perfusion pressure

as pressure increases, you get a proportional rise in resistance

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3
Q

What organs does autoregulation occur in?

A

Brain, Kidney, Heart

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4
Q

How does vascular smooth muscle respond to stretching?

A

by contracting (increasing resistance)

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5
Q

What range of pressures does autoregulation occur in?

A

between 60 - 140 mmHg

when pressure increases here, flow is maintained constant

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6
Q

Do endothelial cells influence autoregulation?

A

no

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7
Q

Define: Hyperemia

A

increased blood flow

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8
Q

Define: Active Hyperemia

A

During a period of increased metabolic rate (using a muscle), blood flow will increase to muscle being used during the period of metabolic activity and will stop when activity is stopped

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9
Q

What is responsible for active hyperemia?

A

metabolites

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10
Q

Define: Reactive hyperemia

A

increase in blood flow that occurs after a period of reduced or arrested blood flow

block blood flow and then restore causes increase in blood flow due to metabolites that build up

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11
Q

What does hyperemia depend on?

A

how long the blood flow was limited

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12
Q

What type of control predominates in the cardiovascular system?

A

local control over central control

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13
Q

What is the function of endothelial cells in vascular smooth muscle?

A

They function in the control of constriction and dilation

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14
Q

In the organ/tissue bath experiment, what happened before rubbing?

A

endothelial lining was intact

NE caused constriction

ACh caused relaxation

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15
Q

In the organ/tissue bath experiment, what happened after rubbing?

A

The endothelial layer was disrupted.

NE caused constriction

ACh also caused constriction

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16
Q

What is EDRF?

A

endothelium derived relaxing factor

Nitric Oxide released from endothelium to relax muscle

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17
Q

What can the endothelium release?

A

vasodilators and constrictors

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18
Q

Define: Endothelial Sheer Stress (ESS)

A

force caused by blood flowing past stationary cell on a vessel wall

changes at dif points in the vasculature

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19
Q

What part of the endothelial cell does ESS rapidly activate?

A

signal transduction and gene expression

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20
Q

How does ESS work?

A

endothelial cells can sense a change in sheer stress and it effects the gene expression in the cell

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21
Q

Define: Atherosclerosis

A

Beginning of is likely caused by ESS

can lead to blockage of coronary arteries and heart attacks

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22
Q

What influences the vascular smooth muscle?

A

endothelium and local tissue metabolites

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23
Q

How do NO and endothelin occur in a normal cell?

A

More Nitric Oxide than endothelin

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24
Q

How do NO and endothelin occur in a damaged cell?

A

more endothelin less nitric oxide

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25
Q

What does endothelial damage result in?

A

nicotine

HTN

aging

ischemia

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26
Q

Define: Humoral Mediators

A

circulating mediators that can effect vascular function

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27
Q

Humoral mediator → Vasodilators

A

Eicosanoids (Arachidonic acid) → PGI2, PGE 2, PGD 2

Atrial natriuretic peptide

Kinins (bradykinin)

Adenosine

Nitric Oxide → Endothlium-derived hyperpolarizing Factor (EDHF)

Histamine

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28
Q

Humoral Mediators → Vasoconstrictors

A

Eicosanoids (arachidonic acid) → TxA2, PGF2α, LTC4, LTD4, LTE4

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29
Q

What is the mechanism of membrane phospholipids?

A

Phospholipase A2 cleaves arachidonic acid from membrane phospholipid

Free arachidonic acid is added on by enzymes

CycloOxygenase can metabolize arachidonic acid and form prostoglandins

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30
Q

What activates Phospholipase A2?

A

Nerve stimulation

31
Q

What inhibits Phospholipase?

32
Q

What vasodilators are produced when cyclooxygenase metabolizes arachidonic acid?

A

PGI2

PGE2

PGD2

33
Q

What vasoconstrictors are produced when cyclooxygenase metabolizes arachidonic acid?

34
Q

Define: Lipoxygenase

A

metabolizes arachidonic acid and produces leukotrienes

35
Q

Define: Leukotrienes

A

vasoconstrictors

LTC4, LTD4, LTE4

produced when lipoxygenases are metabolized by arachidonic

36
Q

Define: Renin

A

controlling enzyme for production of angiotensin II

released by decreased blood flow to kidneys or increased sympathetic stimulation

37
Q

Where is Renin stored?

A

the kidneys

38
Q

How does Renin work?

A

Renin cleaves angiotensiogen → forms Angiotensin I NH2 → Kininase II converts Angiotensin I to angiotensin II (strong vasoconstrictor)

39
Q

What does Angiotensin II do?

A

causes constriction of peripheral vasculature and an increase in blood pressure

40
Q

Where is bradykinin produced?

A

near the sweat glands

41
Q

When is ANF (ANP - Atrial Natriatric Peptide) released?

A

When atria or ventricles are significantly stressed

42
Q

What is ANF (ANP - Atrial Natriatric Peptide)?

A

vasodilator

promotes sodium excretion

43
Q

What does adenosine do?

A

it links tissue oxygen levels with increasing blood flow to the heart

important to the heart oxygen demand and supply

44
Q

What process occurs when metabolic activity in the cell increases and ATP stores decrease?

A

More ADP & AMP present → AMP accumulates but cant cross membrane → 5’ nucleotidase dephosphorylates → adenosine diffuses out of the cell → adenosine interacts with receptors on vascular smooth muscle and causes vasodilation → increases blood flow→ deliver more oxygen→cardiac muscle cells can make ATP

45
Q

What is the main function of adenosine?

A

oxygen supply and demand

46
Q

What determines how constricted or dilated the vasculature is?

A

the relative amount of vasoconstrictors vs. vasodilators present

47
Q

Where does the heart receive innervation from?

A

sympathetic and parasympathetic

48
Q

What is continuously released from the sympathetic nervous system?

49
Q

What happens if you inhibit the sympathetic tone by total spinal anesthesia?

A

it blocks all the sympathetic fibers innervating vascular smooth muscle → BP drops

50
Q

What would occur in the baroreceptors if BP increased?

A

increase in stretch in the aortic arch and carotid sinus →causes increased firing in parasympathetic, decreased sympathetic tone to heart → release less NE → slope of prepotential would flatten → decrease HR

51
Q

When BP increases and sympathetic tone decreases….

A

less NE is released → less NE binds to α1 receptors → HR decreases, SV decreases → CO decreases → vascular smooth muscle in arterioles dilates → BP decreases

52
Q

When BP increases and parasympathetic tone increases….

A

release of ACh increases → opens K+ channels → flattens slope of prepotential → HR and SV decrease

53
Q

What is on the afferent side of the cardiovascular system?

A

Carotid-sinus pressoreceptors

Aortic pressoreceptors

aortic body

carotid body

carotid sinus nerve

vagus

54
Q

What is on the efferent side of the cardiovascular system?

A

Vagus

sinus node

sympathetic chain

55
Q

What does the Nucleus Tractus Solitarius (in medulla) stimulate when BP is increased?

A

Cardiac decelerator (parasympathetic)

56
Q

What does the Nucleus Tractus Solitarius (in medulla) inhibit when BP is increased?

A

Cardiac accelerator (sympathetic)

Vasoconstrictor (sympathetic)

57
Q

What does the cardiac decelerator of the parasympathetic nervous system inhibit when BP is increased?

A

sinoatrial node (heart)

58
Q

What do the cardiac accelerator and vasoconstrictors o the sympathetic nervous system stimulate when BP is increased?

A

Arterioles and veins (blood vessels)

SA Node and contractility (heart)

59
Q

What would the baroreceptors do if you lost 2L of blood?

A

Increase sympathetic firing to veins → venoconstrict → reduce compliance → raise pressure on venous side of system → force more blood into right atrium → increase preload → increase venous return → increase HR and SV→ increase CO→ decrease compliance → raise resistance → increase BP →decrease parasympathetic firing

60
Q

When is parasympathetic firing reduced?

A

When BP drops and you need to raise it

61
Q

When is sympathetic firing reduced?

A

When BP increases and you need to drop it

62
Q

What would happen to Renin and angiotensin II if sympathetic firing increased in the kidney?

A

they would increase

63
Q

What do the baroreceptors do?

A

keep BP constant

good at preventing abrupt changes in BP

64
Q

Why can baroreceptors not prevent HTN?

A

b/c they regulate pressure from a certain set point, but the set point can change

it isn’t good at setting BP at an absolute pressure

65
Q

What happens to BP when you lose Baroreceptor function?

A

regulation of BP is lost

66
Q

What does the Nucleus Tractus Solitarius (in medulla) stimulate when BP is decreased?

A

Cardiac decelerator (parasympathetic) → inhibits SA node

Cardiac accelerator and Vasoconstrictor (sympathetic) → stimulate Arterioles and veins (blood vessels) and SA Node and contractility (heart)

67
Q

If your patient was given an unknown drug that caused the BP to increase, but reduced peripheral resistance, what did the drug do to the CO?

A

stimulate it

68
Q

In response to a decrease in mean arterial blood pressure, the baroreceptor reflex mediates which of the following effects?

A. a decline in ventricular contractility

B. tachycardia and increased LV SV

C. bradycardia and increased LV afterload

D. increase in the firing rate of cranial nerve X innervating the heart

E. an increase in the firing in cranial nerve IX

A

B. tachycardia and increased LV SV

69
Q

Upon assuming an upright posture, after lying quietly for several hours, the compensatory respond of the baroreceptor control system regulating arterial blood pressure will involve which of the following?

A. decreased sympathetic postganglionic nerve activity

B. decreased venoconstriction

C. increased firing in the carotid sinus nerve

D. increased heart rate

C. decreased CO

A

D. increased HR

70
Q

Carotid sinus massage is sometimes used to stop supra ventricular tachycardia (rapid rhythms which originate above the ventricles). Which of the following is most likely explanation for the effectiveness of this maneuver?

A. It increases sympathetic discharge to the SA node

B. It decreases vagal discharge to the SA node

C. It increases vagal discharge to the conducting tissue between the atria and the ventricles

D. It increases the refractory period of the ventricular myocardium

E. It reduces the conduction velocity around the reentry loop

A

C. It increases vagal discharge to the conducting tissue between the atria and the ventricles

71
Q

Mitral valve stenosis would be associated with:

A. low aortic diastolic pressure and a diastolic murmur
B. elevated left ventricular pressure and a systolic murmur
C. elevated left atrial pressure and a systolic murmur
D. elevated left atrial pressure and a diastolic murmur
E. elevated aortic pressure and no murmur

A

D. elevated left atrial pressure and a diastolic murmur

72
Q

The sinoatrial (SA) node is the pacemaker for the heart because:

A. is the most richly innervated structure in the heart

B. is the only structure in the heart capable of generating action potentials

C. has the shortest absolute refractory period of all myocardial cells

D. has the highest rate of automatic discharge
E. is the cardiac cell that is least sensitive to catecholamines

A

D. has the highest rate of automatic discharge

73
Q

An increased afterload (i.e., increased aortic pressure) on the
ventricle would be expected to have which of the following
effects on the heart?

A. Increase heart rate
B. Decrease preload reserve
C. Decrease left ventricular end-systolic volume
D. Decrease left ventricular end-diastolic volume
E. All of the above

A

B. Decrease preload reserve

74
Q

Which of the following is/are CORRECT concerning the
effect of catecholamines on myocardial cells?

A. they promote the phosphorylation of phospholamban, thereby enhancing the rate of relaxation of the myocardial cell

B. they inhibit the sarcolemmal Na+-K+ pump resulting in a reduced Na+-Ca++ exchange and an increased cytosolic Ca++ concentration

C. they reduce the influx of extracellular Ca++ via voltage- dependent Ca++ channels in the sarcolemma

D. they inhibit Ca++ reuptake into the sarcoplasmic reticulum resulting in an elevated cytosolic Ca++

E. Two of the above
F. None of the above

A

A. they promote the phosphorylation of phospholamban, thereby enhancing the rate of relaxation of the myocardial cell

D. they inhibit Ca++ reuptake into the sarcoplasmic reticulum resulting in an elevated cytosolic Ca++

E. Two of the above

Systems Phys 2022 (25 decks)

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