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PBL SEM 2 > PBL 6 - control of BP > Flashcards

PBL 6 - control of BP Flashcards

1
Q

what is the equation for BP?

A

blood pressure = CO x total peripheral resistance

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2
Q

what is cardiac output?

A

the volume of blood expelled by the heart per minute

varied to meet the demands of the body

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3
Q

what is the equation for cardiac output?

A

CO = SV x HR

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4
Q

what is stroke volume?

A

the volume of blood ejected per beat

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5
Q

what is the equation for stroke volume?

A

SV = end diastolic volume - end systolic volume

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6
Q

what 3 things is stroke volume affected by?

A
  1. preload
  2. contractility
  3. afterload
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7
Q

what is preload?

A

the tension in the cardiac myocytes before they contract

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8
Q

what happens if you increase the stretch in cardiac myocytes?

A

more forceful contraction

— the more you stretch them, the greater the tension, the more forceful the contraction

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9
Q

what is preload dependent on?

A

venous return

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10
Q

how does venous return affect preload?

A

the more blood that comes back to the heart, the more the ventricles will stretch, therefore more contraction force

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11
Q

what is contractility?

A

the contraction force of the myocardium for a given preload

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12
Q

what increases the contraction force for a given preload?

A

adrenaline

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13
Q

what is afterload?

A

the BP in the aorta and pulmonary trunk

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14
Q

how does afterload affect SV?

A

the greater the afterload/pressure, the harder is it for the LV to reach that pressure — increased afterload reduces SV

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15
Q

what things increase HR?

A
  • adrenaline and noradrenaline
  • increase in temperature
  • thyroid hormone
  • caffeine
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16
Q

what things decrease HR?

A
  • acetylcholine
  • decrease in temp
  • intense visceral pain
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17
Q

what is total peripheral resistance?

A

the total pressure in the peripheral vessels

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18
Q

what 3 things affect TPR and how do they alter BP?

A
  1. viscosity of the blood — relatively stable so wouldn’t really use to alter resistance or BP
  2. blood vessel length — remains unchanged so wouldn’t really use to alter resistance or BP
  3. blood vessel radius — can easily be changed so regularly used to alter BP
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19
Q

what is vessel radius determined by?

A

the SNS

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20
Q

bloods vessels are maintained in what state?

A

a state of partial vasoconstriction

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21
Q

what does the maintenance of partial vasoconstriction of blood vessels provide?

A

sympathetic tone — a sympathetic nerve fibre is continuously partially constricting the vessel

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22
Q

what happens if you stop sending impulses through the sympathetic nerve fibre for a blood vessel?

A

vessel will dilate (this is a good way of rapidly changing the radius)

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23
Q

where does the control of vessel radius come from?

A

the vasomotor centre in the medulla oblongata

24
Q

what are 4 different sensors used in the neurohormonal control of BP?

A
  • baroreceptors
  • chemoreceptors
  • volume receptors
  • osmoreceptors
25
Q

these sensors send what kind of fibres to the CNS?

A

afferent nerve fibres

26
Q

the areas in the brain/CNS send what type of fibres to the periphery to bring about changes?

A

efferent nerve fibres

27
Q

where does the CNS send impulses to to bring about changes?

A
  • heart
  • blood vessels
  • kidneys
28
Q

what is the aim of maintaining this peripheral arterial BP?

A

to ensure the arterial blood pressure is adequate for oxygen perfusion

29
Q

describe the neural component of BP control

A
  • autonomic nervous system
  • directly influences the heart and blood vessels
  • short-term mechanism
30
Q

describe the humoral component of BP control

A
  • circulating factors/hormones
  • directly influence heart and blood vessels or alter blood volume
  • intermediate and long-term mechanisms
31
Q

describe baroreceptors

A
  • mechanical/stretch receptors

- at bifurcation of common carotid artery (carotid sinus) and the arch of the aorta (aortic sinus)

32
Q

via what nerve do impulses travel from the carotid and aortic sinuses?

A
  • carotid = glossopharyngeal nerve

- aortic = vagus nerve

33
Q

where is the afferent information for the carotid and aortic sinuses taken to?

A

the nucelus solitarius in the brain stem = a collection of sensory neurons

34
Q

what does the nucleus solitarius modulate the activity of?

A

the cardiovascular centres

35
Q

describe the cardiovascular centres

A

3 groups of cells

1 + 2 = groups of sympathetic neurons on the medulla

3 = dorsal motor nucleus of the vagus and the nucleus ambiguus in the brain stem

  1. vasomotor centre — causes vasoconstriction of peripheral vessels
  2. cardiac accelerator centre — increases HR and force of contraction
  3. cardiac inhibitor centre — involved with the vagus nerve and slowing down the HR (vagus nerve has vagal tone to slow down the HR under normal circumstances)

pressor centre = upper part of medulla oblongata
depressor centre = lower part of medulla oblongata

36
Q

how can the receptors be altered?

A

sensitivity can be altered — eg. long term hypertension - baroreceptors have been set at a higher level

37
Q

how does an increase in BP affect the baroreceptors?

A

increased BP —> sinuses are stretched —> increase firing rate to cardiac and vasomotor centres

38
Q

what is the effect of increased firing rate to the cardiac and vasomotor centres?

A
  1. stimulates cardioinhibitory centre — increases PNS activity to SA node — decreases HR
  2. inhibits cardioaccelerator and vasomotor centres — decreases SNS activity — decreases HR and vasodilation
39
Q

how does haemorrhage affect BP?

A

causes fall in BP

40
Q

what does haemorrhage result in?

A
  • vasoconstriction (look pale)
  • increased force of contraction
  • increased HR
41
Q

what happens if blood volume is not replaced after haemorrhage?

A
  • venous return continues to fall
  • decreased EDV
  • HR increases — systole cannot shorten therefore diastole shortens — fill heart during diastole — decreased filling time — EDV decreases even more — decreased force of contraction (starling’s law of the heart) — decreased SV/CO/BP
42
Q

describe the valsalva manoeuvre

A

= forced expiration against a closed glottis

  • increases in intrathoracic pressure increases compression of the vena cava
  • slow down VR — decrease EDV — decrease CO — decrease BP
  • baroreceptors decrease output

increase force of contraction/HR/total peripheral resistance

43
Q

what do chemoreceptors detect?

A

chemical changes in the blood

44
Q

what are catecholamines?

A

adrenaline and noradrenaline — released by the SNS

45
Q

what factors are part of the humoral control of BP?

A
  • catecholamines
  • RAAS
  • Atrial Natriuretic Peptide (ANP)
  • Antidiuretic Hormone (ADH) / Arginine Vasopressin (AVP)
46
Q

what releases catecholamines and when are they released?

A
  • release by the adrenal medulla
  • produced by chromaffin cells
  • released during stress, exercise, blood loss, emotion, excitement, pain
  • 80% adrenaline and 20% noradrenaline
47
Q

what is the effect of catecholamines on a1 vascular smooth muscle?

A

vasoconstriction

48
Q

what is the effect of catecholamines on a2 presynaptic membrane?

A

negative feedback

49
Q

what is the effect of catecholamines on B1 SA node and cardiac muscle?

A

increase HR and contraction force

50
Q

what is the effect of catecholamines on b2 vascular smooth muscle in heart and skeletal muscles?

A

vasodilator (to increase blood supply to the heart to increase HR)

51
Q

what is the effect of catecholamines on b2 airway smooth muscle?

A

bronchodilator

52
Q

what is the effect of catecholamines on B3 adipocytes?

A

lipolysis

53
Q

what is RAAS stimulated by?

A
  • a decrease in renal perfusion pressure:

less blood flowing through the kidneys causes a drop in pressure in the kidneys — triggers the system

  • also stimulated by sympathetic stimulation
  • also stimulated by decrease in sodium delivery to the distal tubule
54
Q

briefly describe the RAAS

A
  • renin released from juxtaglomerular cells
  • renin acts on angiotensinogen and inverts it to angiotensin 1
  • ACE (angiotensin converting enzyme) converts angiotensin 1 to angiotensin 2
55
Q

describe some of the effects of angiotensin 2

A
  1. acts on adrenal cortex to bring about aldosterone secretion — reabsorbed Na and water (increases blood volume)
  2. acts on release of ADH to bring about water reabsorption
  3. makes you thirsty — drink more

all of these increase blood volume and at high doses is also a vasoconstrictor (increase total peripheral resistance) —> increase BP

56
Q

describe atrial natriuretic peptide (ANP)

A
  • released by cells in the atria
  • responds to atrial stretch, sympathetic stimulation, angiotensin 2 (high levels)
  • acts on kidneys to increase glomerular filtration rate, natriuresis, diuresis — increase urinary output
  • decrease renin and aldosterone release
  • these all decrease blood volume, CO and BP

= COUNTER-REGULATORY SYSTEM FOR THE RAAS

57
Q

describe ADH

A
  • made by hypothalamus, stored and secreted by posterior pituitary
  • stimulated by increase in plasma osmolarity, angiotensin 2, sympathetic stimulation, stretch receptors (atria and veins)
  • leads to water reabsorption in the collecting duct (not sodium)
  • increases blood volume and BP
  • also causes vasoconstriction when the levels are very high

concentrated blood = increase levels of ADH - increase fluid

PBL SEM 2 (44 decks)

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