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Y1 - Cardiovascular > Physiology: Arterial Blood Pressure and its Control (short & long term) > Flashcards

Physiology: Arterial Blood Pressure and its Control (short & long term) Flashcards

1
Q

Define blood pressure

A

The outward hydrostatic pressure exerted by blood on the vessel walls

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2
Q

Define the systolic and diastolic blood pressures

A

Systolic:
- blood pressure exerted on systemic arteries when the heart contracts

Diastolic:
- blood pressure exerted on systemic arteries when the heart relaxes

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3
Q

Define hypertension

A

A Bp > 140/90 mmHg in clinic
or
A daytime average Bp > 135/85 mmHg

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4
Q

Define pulse pressure

A

The difference between the systolic and diastolic blood pressures

(systolic)-(diastolic)

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5
Q

What is the range for a healthy Bp in adults?

A

90/60 to 120/80

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6
Q

Describe how a sphygmomanometer measures Bp

A
  • Cuff pressure is made to completely occlude the artery (cuff pressure > systolic pressure)
  • Pressure is decreased until sound can be heard (1st Korotkoff sound)
  • Sound is due to the turbulent flow of blood through the semi-occluded artery
  • Pressure is decreased further until no sound can be heard (5th Korotkoff sound)
  • Laminar flow restored
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7
Q

What blood pressure is represented by the first Korotkoff sound?

A

The MAX systolic pressure

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8
Q

What blood pressure is represented by the fifth Korotkoff sound?

A

The diastolic Bp

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9
Q

What pressure gradient drives blood through the systemic circulation?

A

The pressure gradient between the right atrium (pressure nearly 0) and the aorta (high pressure)

Thus it is the MAP that drives blood in the systemic circulation

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10
Q

Define mean arterial blood pressure (MAP)?

A

The average arterial blood pressure during a single cardiac cycle

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11
Q

Give the 2 formulae for calculating the MAP from blood pressures

A

MAP = [(2x Diastolic)+(systolic)]/3

MAP = Diastolic + (1/3 Pulse Pressure)

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12
Q

Give the range for a healthy MAP in an adult at rest

A

70 –> 105 mmHg

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13
Q

What is the MAP required to perfuse the vital organs?

A

60 mmHg

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14
Q

Give the formulae for calculating the MAP from cardiac output and systemic vascular resistance

A

MAP = CO x SVR

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15
Q

Define cardiac output

A

The volume of blood being pumped by each ventricle of the heart per minute

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16
Q

Define systemic vascular resistance (SVR)

aka TPR

A

The sum of resistance of all vasculature in the systemic circulation

Mainly from arterioles (~50%)

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17
Q

Give the equation for calculating the cardiac output

A

CO = SV x Heart rate

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18
Q

Define Total Peripheral Resistance (TPR)

A

The sum of resistance of all vasculature in the systemic circulation

The same as systemic vascular resistance

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19
Q

Describe the effect of parasympathetic stimulation of the heart on MAP

A 
Vagal stimulation
-->
heart rate decreases
-->
cardiac output decreases
-->
MAP DECREASES
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20
Q

Describe the effect of sympathetic stimulation of the heart on MAP

A 
Sympathetic stimulation
-->
heart rate increase
-->
cardiac output increase
-->
MAP increase
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21
Q

Describe the effect of sympathetic stimulation of the arterioles on MAP

A 
Sympathetic stimulation
-->
vasoconstriction
-->
SVR increases
-->
MAP increase
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22
Q

Describe the effect of sympathetic stimulation of the veins on MAP

A 
Sympathetic stimulation
-->
vasoconstriction
-->
venous return increases
-->
stroke volume increases
-->
Cardiac output increases
-->
MAP increases
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23
Q

Define postural (orthostatic) hypotension

A
  • Failure of Baroreceptor responses causing a drop in Bp

- Due to gravitational shifts in blood, when moving from horizontal to vertical position

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24
Q

What mechanism manages acute changes in MAP?

A

The baroreceptor reflex

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25
Q

Is the baroreceptor reflex a +ve or -ve feedback mechanism

A

Negative feedback control

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26
Q

Describe a baroreceptor

A
  • Mechanoreceptors
  • Sensory neurons
  • Detect ‘stretch’
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27
Q

Where can baroreceptors be found

A
  • Carotid sinuses (carotid baroreceptors)

- Aortic arch (aortic baroreceptors)

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28
Q

Which nerves innervate the baroreceptors?

A

Carotid baroreceptors:
- glossopharyngeal nerve (cranial nerve IX)

Aortic baroreceptors:
- Vagus nerve (cranial nerve X)

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29
Q

Describe the afferent firing of baroreceptors

A

Usually fire at normal rate

When MAP increases, firing rate increases

When MAP decreases, firing rate decreases

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30
Q

What region of the brain receives the afferent signalling from the baroreceptors?

A

The cardiovascular control centre in the medulla

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31
Q

What is the role of the cardiovascular control centre in the medulla with regards to the baroreceptor reflex?

A
  • Receives afferent signals
  • Relays info to other brain regions
  • Generates vagal outflow to the heart (if needed)
  • Regulates spinal sympathetic neurons
32
Q

What effect can the baroreceptor reflex have on the heart?

A
  • Modify heart rate

- Modify stroke volume

33
Q

What effect can the baroreceptor reflex have on the vasculature?

A

Modify systemic peripheral resistance

34
Q

How is heart rate modified by the baroreceptor reflex?

A

To increase heart rate:
- Sympathetic stimulation

To decrease heart rate:
- Vagal stimulation

35
Q

How is stroke volume modified by the baroreceptor reflex?

A

To increase SV:

  • Sympathetic stimulation of heart
  • Sympathetic stimulation of veins (venoconstriction increases venous return, increasing SV)

To decrease SV:

  • decreased sympathetic stimulation
  • vagal stimulation has little effect
36
Q

How is SVR modified by the baroreceptor reflex?

A

To increase MAP:

  • Increased vasomotor tone
  • Vascular smooth muscle contracts
  • Causing vasoconstriction
  • Increasing SVR

To decrease MAP:

  • decreased vasomotor tone
  • Vascular smooth muscle relaxes
  • Vasodilatation
  • Decreasing SVR
37
Q

What type of vessel accounts for the majority of SVR?

A

Arterioles (~50%)

38
Q

In the baroreceptor reflex what happens to the corrective mechanism after the change in MAP has been corrected?

A

Negative feedback control stops the overcorrection

39
Q

Describe the ‘resetting’ of baroreceptors

A
  • Baroreceptors reset what they consider a normal range
  • Only stimulating a response again if there is an acute deviation from their current normal range
  • Slow changes in MAP can avoid detection of the reflex, and raise its considered normal range
40
Q

Explain why the baroreceptor reflex fails to deal with slow rises in blood pressure

A

The change is to slow to be picked up the the baroreceptors

Slow enough that the baroreceptors reset their considered normal MAP range to match the raised MAP

41
Q

Describe the constriction of vascular smooth muscle at rest

A

They are partially constricted

Due to the vasomotor tone

42
Q

What is the vasomotor tone?

A

The continuous of sympathetic stimulation to vascular smooth muscle

Results in a continuous release or noradrenaline

Can vary in strength to modify vasoconstriction and vasodilation

43
Q

Describe the parasympathetic innervation of arterial smooth muscle

A

There is no significant innervation of arterial smooth muscle

(except in the penis and clitoris)

44
Q

What type of control mechanisms control long-term changes on MAP

A

Hormonal control of blood volume

45
Q

Describe the fluid compartments of the body

A

Intracellular:
- Intracellular fluid

Extracellular:

  • Interstitial fluid
  • blood plasma
46
Q

Describe what happens to the interstitial fluid volume if the blood plasma volume decreases

A

It decreases as compensatory mechanisms shift fluid from the interstitium to the the plasma compartment

47
Q

List the 2 main factors that affect extracellular fluid (ECF) volume

A
  • Water excess/deficit

- Na+ excess/deficit

48
Q

What do hormones regulate in order to control the ECF volume

A

Hormones control the extracellular fluid volume (including Plasma Volume) by regulating the Water and Salt Balance

49
Q

List the hormone systems that regulate ECF volume

A
  • Renin-Angiotensin-Aldosterone system (RAAS)
  • Natriuretic peptides (NPs)
  • Antidiuretic hormone (ADH
    (aka Arginine vasopressin)
50
Q

Describe how aldosterone is produced by the Renin-Angiotensin-Aldosterone System (RAAS)

A
  • Juxtaglomerular cells in the kidneys release renin
  • Renin stimulates the formation of angiotensin I from angiotensinogen
  • Angiotensin I is converted to angiotensin II by the enzyme ‘angiotensin converting enzyme (ACE)’
  • Angiotensin II stimulates the release of aldosterone from the adrenal cortex
51
Q

Where is angiotensinogen produced?

A

The liver

52
Q

Name the enzyme that converts angiotensin I –> angiotensin II

A

Angiotensin converting enzyme (ACE)

53
Q

Where is aldosterone released from?

A

The adrenal cortex

54
Q

Describe the role of angiotensin II in regulating blood pressure

A

1) It causes systemic vasoconstriction, increasing the SVR, thus increasing the MAP
2) Stimulates the release of aldosterone from the adrenal cortex. Increases water and Na+ retention
3) Stimulates thirst. Water intake increases –> plasma volume increases –> MAP increases
4) Stimulates ADH release. Increasing plasma volume

55
Q

Describe the role of aldosterone in regulating blood pressure

A

Aldosterone:

  • Increases Na+ and water reabsorption in the kidneys
  • Decreases Na+ and water excretion
  • Plasma volume increases, thus Bp increases
56
Q

What stimulates the release of renin from the juxtaglomerular cells in the kidneys (starting the RAAS)?

A
  • Low plasma volume and low Bp
  • Decreased [Na+] in the renal tubular fluid
  • stimulation of renal sympathetic nerves
57
Q

Where is Angiotensin converting enzyme (ACE) produced?

A

pulmonary vascular endothelium

58
Q

What is the rate limiting step for RAAS?

A

The secretion of renin from the kidneys

59
Q

Describe the natriuretic peptide control of Bp

A 
Increase Na+ and water excretion in the kidneys
-->
Reducing blood plasma 
-->
BP decrease

Also decrease renin release, decreasing Bp

Also act as vasodilators (decrease SVR, decrease Bp)

60
Q

What causes Natriuretic Peptides to be released?

A
  • Cardiac distension (hypervolemic state)

- Neurohormonal stimuli

61
Q

What inhibits the release of renin from the juxtaglomerular cells in the kidneys?

A

Natriuretic peptides

62
Q

Describe the role of the Natriuretic Peptides

A

To lower blood pressure and plasma volume

Acts as a county-regulatory system for the RAAS

63
Q

Name the 2 types of Natriuretic Peptide released by the heart

A
  • Atrial Natriuretic Peptide (ANP)

- Brain-type Natriuretic Peptide (BNP
aka ventricular-type)

64
Q

Describe Atrial Natriuretic Peptide (ANP)

A
  • 28 amino acid peptide
  • synthesised and stored by atrial myocytes
  • released in due to atrial distension (hypervolemic state)
65
Q

Describe Brain-type Natriuretic Peptide (BNP)

A
  • 32 amino acid peptide

- synthesised by heart ventricles, brain and other organs

66
Q

Describe the synthesis of BNP

A 
Prepro-BNP
-->
Pro-BNP
-->
BNP
67
Q

Describe the role of BNP in diagnosing heart failure

A
  • Serum BNP and NT-pro-BNP can be measured to diagnose heart failure
68
Q

Describe the synthesis and storage of antidiuretic hormone (ADH)

A

ADH is derived from a prohormone precursor that is synthesised in the hypothalamus

  • ADH is stored in the posterior pituitary
69
Q

What is another name for antidiuretic hormone (ADH)

A

vasopressin

70
Q

What stimulates the secretion of ADH from the posterior pituitary?

A

1) increased extracellular fluid osmolality
2) reduced extracellular fluid volume
3) increased plasma osmolality
* (osmolarity increases due to loss of water volume, thus ADH responds to changing water levels)

71
Q

How is plasma osmolarity monitored?

A

By osmoreceptors

  • Mostly in the brain close to the hypothalamus
72
Q

Describe the mechanism of action of ADH

A 
Acts in the kidney tubules to increase water reabsorption
-->
Increases ECF and plasma volumes
-->
Cardiac output increases
-->
Bp increases

Also causes vasoconstriction
–>
Increases SVR and Bp

73
Q

Describe the main role of ADH

A

To regulate plasma and interstitial fluid volumes and osmolarities

74
Q

Describe the main role of RAAS

A

Long term regulation of MAP

75
Q

Why don’t you check both carotid pulses simultaneously?

A

It would generate enough baroreceptor stimulation to cause hypotension that would lead to syncope or presyncope

76
Q

Describe why checking the carotid pulse causes baroreceptor stimulation

A

finger pressure causes partial occlusion of the artery
–>
causes a back pressure
–>
back pressure reaches the carotid sinus, causing it to stretch
–>
The increased stretch is detected by carotid baroreceptors

Y1 - Cardiovascular (19 decks)

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