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Cardio > Blood pressure > Flashcards

Blood pressure Flashcards

1
Q

What is the short-term regulation of MAP controlled by?

A

baroreceptors

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2
Q

What is the aim of negative feedback?

A

to minimise any disturbance to a controlled variable (MAP)

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3
Q

Where are the baroreceptors?

A

carotid sinus - base of internal carotid artery

arch of the aorta

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4
Q

Via which cranial nerve do each baroreceptors send signals?

A

carotids - CN IX (glossopharyngeal)

aortic - CN X (vagus)

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5
Q

What is the normal change in circulation when a healthy person stands?

A 
venous return decrease
MAP decreases (slowly)
baroreceptors fire at reduced rate
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6
Q

What causes increased HR and SV when a healthy person stands?

A

reduced vagal tone to heart - sympathetic tone increases

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7
Q

How does postural hypotension occur?

A

failure of baroreceptors to respond to gravitational shifts in blood when moving from horizontal to vertical

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8
Q

What happens when the baroreceptors don’t respond to the gravitational shift of blood to feet?

A

Vagal activity increases (instead of sympathetic);
HR decreases so CO and SV does too.
Decreased sympathetic constrictor tone increases vasodilatation which reduces BP

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9
Q

How is BP regulated long-term?

A

By controlling extracellular fluid volume (ECFV)

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10
Q

ECFV = ?

A

Plasma volume (PV) + Interstitial Fluid Volume (IFV)

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11
Q

What happens if PV falls?

A

compensator mechanisms shift fluid from interstitial compartment into plasma compartment

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12
Q

What is the role of interstitial fluid?

A

bathes cells and acts as go between the blood and body cells

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13
Q

Which 2 basic factors affect ECFV?

A

Water excess / deficit

Sodium excess / deficit

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14
Q

Which hormones regulate ECFV by regulating the water and salt balance in our bodies?

A 
Aldosterone (RAAS)
Natriuretic peptides (NPs)
Antidiuretic hormone (ADH)
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15
Q

What is the role of RAAS?

A

regulation of plasma volume and SVR and therefore, MAP

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16
Q

Where is renin released from?

A

granular cells of the juxtaglomerular apparatus

17
Q

What does renin stimulate?

A

secretion of angiotensin I

18
Q

Which plasma globulin is secreted by the liver and forms angiotensin I?

A

angiotensinogen

19
Q

Which enzyme allows angiotensin I -> angiotensin II, and where is it produced?

A

ACE (angiotensin converting enzyme)

lung vascular endothelium

20
Q

What does angiotensin II stimulate?

A

Aldosterone release
Systemic vasoconstriction - increases SVR
Thirst
ADH release

21
Q

Where is aldosterone released from?

A

adrenal cortex

22
Q

Where does aldosterone act upon? And what does it cause?

A

the kidneys to increase sodium and water retention -> increased plasma volume

23
Q

Which physiological conditions stimulate RAAS?

A

Renal artery hypotension
Stimulation of renal sympathetic nerves
Decreased Na+ in renal tubular fluid

24
Q

Decreased Na+ concentration in renal tubular fluid is detected by?

A

macula densa - specialised cells of kidney tubules

25
Q

What is the juxtaglomerular apparatus?

A

a region comprising:
macula densa
extra-glomerular mesangial cells
granular cells

26
Q

What are natriuretic peptides?

A

peptide hormones synthesised by heart

27
Q

NPs are released in response to ?

A

cardiac distension or neurohormonal stimuli

28
Q

How do NPs affect BP?

A

vasodilators - decrease SVR and BP

29
Q

What are NPs in relation to RAAS?

A

a counter-regulatory system for RAAS

30
Q

What are the 2 types of NPs released by the heart?

A

Brain type Natriuretic Peptide (BNP)

Atrial Natriuretic Peptide (ANP)

31
Q

Which NP is released in response to hypervolaemic states?

A

ANP (atrial distension)

32
Q

What is the role of ADH?

A

acts on kidney tubules to increase absorption of water (conserve water)

33
Q

What stimulates the secretion of ADH?

A

reduced ECFV

increased ECF osmolality

34
Q

What is plasma osmolality?

A

indicates relative solute-water balance - monitored by osmoreceptors

i.e. increased plasma osmolality = not enough water

35
Q

What is the effect of ADH release?

A

increased reabsorption of water
concentrated urine
increased ECFV and PV
increased CO and BP

36
Q

What is the effect of ADH in patients in hypovolaemic shock?

A

exaggerated vasoconstriction

increases SVR and BP

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