Blood pressure Flashcards

1
Q

What is the normal BP for a dog/cat at rest?

A

120/80

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2
Q

How should blood pressure be calculated?

A

Take 3 readings and taken an average

- remember to take stress into account

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3
Q

What is the potential impact of a persistently high BP?

A
  • Afterload on the ventricles is high
  • More force is needed to overcomethe pressure in the arteries
  • Increased heart workload
  • Can lead to muscle thickening
  • Backwards heart failure
  • Damage to kidneys
  • Eyes can be impacted
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4
Q

What is the potenital impact of a persistantly low BP?

A
  • Leads to low perfusion of tissues
  • Exercise intolerance and muscle wastage
  • Reduced urine production
  • Reduced filtration of blood
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5
Q

What is the equation for cardiac output?

A

SV x HR

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6
Q

What is the equation for aortic pressure (Pa)?

A

Pa = CO x TPR

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7
Q

What factors influence stroke volume?

A

EDVV and ESVV

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8
Q

What is the equation for SV?

A

SV = EDVV - ESVV

The volume of blood ejected into the circulation by one ‘stroke’ or contraction of the ventricle

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9
Q

What is the pathological effect of a high heart rate?

A

CO is reduced because EDVV is reduced so there isnt enough time for diastolic filling

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10
Q

What is the physiological effect of a high heart rate?

A

Sympathetic nervous system will shorten systole to allow more time for diastolic filling
- faster conduction of APs

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11
Q

What are the 2 main intrinsic mechanisms to control local blood flow?

A
  • Metabolic autoregulation

- Paracrine control

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12
Q

What is metabolic autoregulation?

A

Increase in metabolic rate increases blood flow to tissues

  • Increased production of CO2, K+, and lactic acid
  • Causes vasodilation
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13
Q

What is paracrine control?

A

Locally acting hormones that lead to vasodilation e.g. nitric oxide

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14
Q

What are the 2 extrinsic mechanisms that preserve flow to essential tissues?

A
  • Baroreflex

- RAAS

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15
Q

What is the baroreflex?

A
  • First to kick in when theres decreased blood pressure
  • Decreases CO and vasoconstriction to try and balance BP
  • Doesn’t change overall volume of blood
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16
Q

What is the RAAS?

A

Can replace lost fluid volume

  • Vasoconstriction
  • ADH
  • Thirst centres in hypothalamus
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17
Q

Where are baroreceptors located?

A

In the aortic arch and carotid sinuses

18
Q

Where do baroreceptors send input and where does the output of that go?

A

To the CV centre in the medulla oblongata which sends outputs via the ANS

19
Q

What are the main actions of the ANS in the baroreflex?

A
  • Drop in BP = increased sympathetic NS
  • Increased HR and contractility = increased SV
  • Vasoconstriction of non-essential tissues
20
Q

Which receptors are involved in the sympathetic NS, which response are they involved in?

A

Adrenergic - α1 α2 β1 β2

- fight or flight

21
Q

Where are the different adrenergic receptors located in the body and what does stimulation of each of them cause?

A

α1 α2 = found in blood vessels, stimulation causes vasoconstriction
β1 = in cardiomyocytes and nodal tissue, stimulation causes increased contractility and HR
β2 = In the coronary arteries, stimulation causes vasodilation

22
Q

Which receptors are a part of the rest and digest response?

A

Cholinergic = M2 and M3

23
Q

Where are cholinergic receptors found and what does stimulation of each of them cause?

A
M2 = in cardiac tissue, causes decreased contractility and HR
M3 = on blood vessels, leads to vasodilation
24
Q

What is the role of nitric oxide in the control of blood flow?

A
  • Released from endothelial cells when there is an increase in the speed of blood flow
  • part of the parasympathetic NS
  • causes vasodilation
25
Q

What is first released in the RAAS and where is it released from?

A

Renin - from the liver in response to a decrease in BP

26
Q

What is the effect on renin, within the RAAS?

A
  • Causes angiotensinogen to be converted to angiotensin I
27
Q

What then happens to angiotensin 1?

A

An enzyme in the lungs called ACE converts angiotensin I to angiotensin II

28
Q

What is the role of angiotensin II?

A
  • causes vasocontriction (increases BP) and release of aldosterone
29
Q

What is the role of aldosterone?

A
  • Causes the kidney to conserve sodium and water which increases the blood volume
  • Increases thirst
30
Q

How does angiotensin II also act on the pituitary gland?

A

Causes it to release antidiuretic hormone which causes the kidneys to conserve water, increasing blood volume and further vasoconstriction

31
Q

Where is aldosterone produced?

A

Adrenal gland

32
Q

Which organ is central to long term regulation of BP?

A

The Kidney

33
Q

Which part of the kidney leads to activation of the RAAS?

A

The afferent arteriole detects changes in BP within the vessel, which leads to activation of the RAAS

34
Q

What is pressure naatriuresis?

A

Kidney pressure changes affect sodium (and water) excretion

35
Q

Which cells in DCT activate the RAAS?

A

Macula densa cells in the DCT sense reductions in sodium causing activation of the RAAS

36
Q

Give the key points of how the ANS controls blood volume

A

Alpha 1/2 –> vasoconstriction & venoconstriction –> effectively increasing central blood volume & preload

37
Q

How does a change in blood vessel diameter affect BP?

A

Causes a change in TPR, which affects the pressure of the atria, which changes the blood pressure

38
Q

How do you increase heart rate and contractility at a cellular level?

A

β1 adrenoreceptor on nodal tissue and cardiac myocytes binds adrenaline/noradrenaline
- leads to formation of cAMP

39
Q

What is the function of cAMP?

A

Activates PK-A which phosphorylates Ca channels causing an influx of Ca, which leads to contraction

40
Q

How can vascular smooth muscle be made to contract - i.e. what are the stimuli?

A
  • Stretch
  • Electrical stimulus
  • Chemical stimulus
41
Q

How do these stimuli on vascular smooth muscle lead to contraction?

A
  • Stimuli causes increased cellular calcium ions
  • these activate myosin light chain kinase
  • MLC phosphorylation causes cross bridge formation
  • leads to muscle contraction