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guyton - unit questions > Unit IV (14-24) - The circulation > Flashcards

Unit IV (14-24) - The circulation Flashcards

1
Q

What is the effect of vasodilation on peripheral vascular resistance?

A

Decreased peripheral vascular resistance

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2
Q 
Increase in which of the following most likely stimulates growth of vessels in a solid tumor? 
A. Plasma glucose concentration
B. Growth hormone
C. Vascular endothelial growth factor
D. Tissue oxygen concentration
A

C. VEGF

Ch. 17 p.209-210

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3
Q

How is the velocity of blood flow calculated?

A

v=F/A

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4
Q

What is the average functional pressure in most vascular beds?

A

17mmHg

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5
Q

What is Ohm’s law?

A

F = pressure change / resistance

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6
Q

How is the tendency for turbulent blood flow measured? How is it calculated? At what level does turbulent flow occur?

A

Reynolds’ number
Re = v x diameter x density / viscosity
200-400 (branches)
2000 (everywhere)

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7
Q

What is conductance?
How is it calculated?

A

Measure of blood flow through a vessel for a given pressure difference
C = 1/R

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8
Q

What is Poiseuille’s law?

A

F = (pi x pressure change x radius^4)/(8 x viscosity x length)

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9
Q

Does arterial pressure affect blood flow? Why?

A

No. Increase in AP initiates compensatory increase in vascular resistance, reduction initiates decreased VR - blood flow autoregulation

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10
Q

How is vascular wall tension calculated?

A

Laplace law
T = pressure change x (r/wall thickness)

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11
Q

What physical force is most important for development and adaption of the vascular system?

A

Shear stress

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12
Q

How is vascular distensibility calculated?

A

VS = increase in volume / (increase in pressure x original volume)

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13
Q

How does the distensibility of veins and arteries differ?

A

Veins 8x more distensible than arteries

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14
Q

How is vascular compliance calculated?

A

Vascular compliance = increase in volume / increase in pressure

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15
Q

How can pulse pressure be calculated?

A

PP = stroke volume / arterial compliance

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16
Q

What is normal RAP?

A

0mmHg

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17
Q

What could cause a RAP of 20-30?

A

CHF
Massive transfusion

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18
Q

What are the constituents of the intestitium?

A

Collagen fibre bundles
Proteoglycan filaments

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19
Q

What is the normal % of free fluid in the interstitium?

A

<1%

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20
Q

What are the theories that explain acute control of tissue blood flow?

A

Vasodilator theory - adenosine, CO2, ADP, histamine, K+, H+ - cause dilation of met arterioles and pre-capillary sphincters
Oxygen demand theory - oxygen required for muscle contraction, O2 deficiency = muscle relaxation

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21
Q

What are the two theories that explain auto regulation of blood flow during changes in arterial pressure?

A

Metabolic theory - vasodilators washed out => vasoconstriction
Myogenic theory - stretch induced vascular depolarisation and contraction

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22
Q

How is acute blood flow regulation different in the brain?

A

CO2 concentration and H+ play prominent roles in addition to O2

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23
Q

What is the most important endothelial derived vasodilator?

A

Nitric oxide (NO)

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24
Q

How is NO produced?

A

By endothelial-derived nitric oxide synthase, from arginine and O2

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25
Q

What is the half life of NO?

A

6 seconds

26
Q

How does NO cause vasodilation?

A

Activates guanylate cyclases in vascular smooth muscle - converts cGTP => cGMP - activates cGMP-dependent protein synthase

27
Q

What stimulates NO production?

A

Shear stress
AngII

28
Q

What is the mechanism of action of sildenafil?

A

PDE-5 inhibitor
PDE degrades cGMP, inhibition prolongs action of NO

29
Q

What is the main locally produced vasoconstrictor? What stimulates its production?

A

Endothelin
Released from damaged endothelium

30
Q

What are the 4 vascular growth factors?

A

VEGF
FGF
PDGF
Angiogenin

31
Q

What determines the vascularity of a tissue?

A

Its maximum blood flow need

32
Q

What are the humoral vasoconstrictors? Where are they secreted?

A

Norepinephrine
Epinephrine
SNS activation - from nerve endings and adrenal medullae

Angiotensin II - RAAS activation
Vasopressin (ADH) - posterior pituitary

33
Q

What are the humoral vasodilators? Where are they secreted?

A

Bradykinin - produced from alpha2-globulins in plasma by kalikrein - activated by maceration of blood and tissue inflammation
Histamine - mast cells in damaged tissue

34
Q

What are the effects of increased concentrations of the following on vascular tone?
a - Ca
b - K
c - Mg
d - H+
e - Acetate/citrate
f - CO2

A

a - vasoconstriction
b - vasodilation
c - vasodilation (+++)
d - vasodilation
e - vasodilation
f - vasodilation (marked in brain)

35
Q

Describe the anatomy of the SNS

A

Sympathetic vasomotor nerves leave the spinal cord through all thoracic and first 2 lumbar spinal nerves, pass into sympathetic chains.
Pass to sympathetic nerves and peripheral portions of spinal nerves

36
Q

Describe the structure of the vasomotor centre?

A
  1. Vasoconstrictor area (acts on all levels of the spinal cord)
  2. Vasodilator area (inhibits VCA)
  3. Sensory area (input from vagus/GP nerves - controls VCA and VDA)
37
Q

What is the sympathetic vasoconstrictor neurotransmitter? Where does it act?

A

NEpi
Alpha-adrenergic-r of vascular SM

38
Q

How does SNS activation affect the circulation?

A

1 - arterioles contracted => ^TPR => ^ABP
2 - veins constricted => ^SV
3 - direct adrenergic stimulation of heart

39
Q

Where are baroreceptors found?

A

Carotid arteries and aortic arch

40
Q

How are signals transmitted from the different baroreceptors?

A

Carotid arteries => Hering’s nerves => GP nerves => nucleus tractus solatarius (brainstem)
Aortic arch => vagus nerve => NTS (medulla)

41
Q

What is the effect of baroreceptor stimulation?

A

Inhibits vasoconstrictor centre
Excites vagal parasympathetic centre

Causes vasodilation, decreased HR and force of contraction

42
Q

Are baroreceptors important in long term regulation of arterial pressure?

A

No - reset after 1-2 mins
However, may influence sympathetic nerve activity of the kidneys

43
Q

Where are the chemoreceptors?

A

Carotid and aortic arch

44
Q

What activates the chemoreceptors?

A

Low O2, high CO2/H+

45
Q

When are the chemoreceptors important?

A

At lower pressures than baroreceptors

46
Q

How do the atrial and pulmonary artery reflexes affect arterial pressure?

A

Low pressure receptors
Minimise arterial blood pressure change after blood loss

47
Q

What is the volume reflex?

A

Stretch of atria activates low pressure atrial receptors => reduced renal sympathetic nerve activity => decreased tubular reabsorption and afferent arteriole dilation
Signals also transmitted to hypothalamus to reduce ADH
Results in increased fluid loss

48
Q

What is the Bainbridge reflex?

A

Atrial pressure increase = increased HR

49
Q

What is the CNS ischaemic response?

A

When blood flow to brain reduced enough to cause ischaemia, vasoconstrictor centre becomes strongly excited
Increase in BP
Vasoconstriction so intense some peripheral vessels totally occluded

50
Q

How does anaemia impact cardiac output?

A

Anaemia => peripheral vasodilation + reduced blood viscosity => reduced TPR => increased CO

51
Q

What factors influence venous return?

A

RAP
Degree of filling of the systemic circulation
Resistance to blood flow between peripheral and RA

52
Q

What factors increase mean circulatory filling pressure?

A

Increased blood volume
SNS stimulation

53
Q

What is the formula for calculating venous return?

A

VR = Pdf - PRA / RVR

54
Q

Which blood vessel receptors are associated with vasodilation and vasoconstriction?

A

Alpha - constriction
Beta - dilation

55
Q

Following cardiac infarction, what 4 factors contribute to the risk of fibrillation?

A

1 - potassium depletion and accumulation in the ECF - increases irritability
2 - ischameia causes injury current
3 - SNS stimulation
4 - ventricular dilation => circus movements

56
Q

What is the MOA of digitalis?

A

Increase calcium in muscle fibres by inhibition of Na-K ATPase = ^Intracellular Na = slowing of Na-Ca exchanger

57
Q

What 4 effects do SNS stimulation have on fluid balance?

A

1 - Constriction of renal afferent arteriole = water retention
2 - Activation of alpha-adrenergeric receptors on tubular epithelial cells => na/H2O retention
3 - stimulation of renin release
4 - Stimulation of ADH release

58
Q

Where are a) ANP and b) BNP released from?
What are their effects?

A

a - atria
b - ventricles
Increase na excretion

59
Q

What are the 3 stages of circulatory shock?

A

1 - nonprogressive
2 - progressive
3 - irreversible

60
Q

What mechanisms engage in nonprogressive shock?

A

Baroreceptor reflex
CNS ischaemic response
Reverse stress relaxation of the circulatory system
RAAS activation
ADH secretion
Increased epinephrine and norepinephrine secretion

61
Q

In which kinds of shock is sympathomimetic therapy valuable?

A

Neurogenic and anaphylactic

guyton - unit questions (14 decks)

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