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PMP-101 > Cardiovascular system V - Blood pressure & CVS disease continuum > Flashcards

Cardiovascular system V - Blood pressure & CVS disease continuum Flashcards

1
Q

Blood pressure

A

Pressure exerted on the walls blood vessel (largely referred to Arterial pressure)

Pressure is essential to perfuse all the cells of the entire body (constant & consistent)

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2
Q

What is blood pressure measured in?

A

mmHg

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3
Q

What causes variation in blood pressure>

A
  • Age
  • Pathological conditions
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4
Q

Systolic and Diastolic BP

A

Systolic BP: MAP during heart contraction
Diastolic BP: MAP during heart relaxation

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5
Q

Systemic: 120/80 mmHg, Pulmonary: 25/8 mmHg, Venous: 6-8 mmHg

A

Normally BP is measured as the trend rather a single read

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6
Q

Equation for blood pressure

A

BP= Cardiac output x Peripheral Resistance

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7
Q

Cardiac output equation:

A

Cardiac output = Heart Rate x Stroke volume
= 70/min x 70 ml
= 4900 ml/min = 5L/min

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8
Q

Cardiac output equation:

A

Cardiac output = Heart Rate x Stroke volume
= 70/min x 70 ml
= 4900 ml/min = 5L/min

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9
Q

Blood viscosity can affect:

A

Recollect: Blood Lecture
Polycythaemia: Too much RBC

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10
Q

Regulation of Blood pressure control

A

1) Auto-regulation

2) Neural

3) Hormonal

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11
Q

Auto-regulation

A

Changes in blood flow detected by the local receptors during micro perfusion (recollect micro/capillary perfusion from lec. 2)

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12
Q

Neural

A

Short-term regulation of blood pressure, especially in responses to transient changes in arterial pressure, via baroreflex mechanisms

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13
Q

Hormonal - Long-term regulation of blood pressure

A

Renin-Angiotensin-Aldosterone

Anti-diuretic hormone (ADH; arginine vasopressin)

Atrial natriuretic hormone/peptide/factor

Erythropoietin

Adrenaline/Noradrenaline

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14
Q

Three types of regulation

A

Hypertension/ Normotension/ Hypotension

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15
Q

Brain Stem

A

Medulla & Pons
Cardiovascular control (sympathetic & vagal)
Vasomotor control (sympathetic)

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16
Q

Factors influence neural regulation of BP

A

Higher centre: High & Low

Low O2

Low CO2

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17
Q

Two types of nerves:

A

Vagus nerves
Glossopharyngeal nerves

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18
Q

What type of pressure sensors are located in aortic arch and carotid sinus?

A

Baroreceptors

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19
Q

What are the Baroreceptor pressure sensor role?

A

They are connected by nerve innovations to vasamotor centre

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20
Q

What is the role of the vasomotor centre?

A

Regulate sympathetic and vagus activation and the heart and other tissues

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21
Q

Glossopharyngeal nerves role

A

Connect carotid sinus to cardiovascular centre - regulate blood pressure short-term

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22
Q

What can cause rise in blood pressure?

A

Rise in stress levels

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23
Q

Heart > HIGH blood pressure > ventricle is pumping high amount of blood to aortic arch > what does aortic arch do?

A

Start firing Baroreceptors to the cardiovascular centre in brain stem

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24
Q

What is a high blood pressure?

A

120 - 180 mmHg

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25
Q

Increase in vagal activity will _______ heart rate (vagal innovation)

A

Suppress

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26
Q

What suppresses the sympathetic cardiac activity?

A

adrenaline and nonadrenaline will raise heart rate - AS VAGAL nerve suppresses heart rate these two will work and compliment each other so that contraction reduction and decrease heart rate.

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27
Q

Heart contraction and heart rate low; Heart output=

A

LOW - achieve normal homeostasis - low blood pressure

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28
Q

Suppression for sympathetic activity in the cardiac cells whereas there is a stimulus for the sympathetic activity which comes from…..

A

the vasomotor centre and the vaso-activation which causes vaso-DILATION .

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29
Q

Sympathetic activation at the vascular SMOOTH MUSCLE causes ______

A

Relaxation

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30
Q

the vessel of the smooth muscle tend to dilate which means….

A

The vessels expand (blood vessel becomes larger) more allowing more blood flow through
= blood pressure will DROP

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31
Q

Name for blood vessels dilating?

A

Vasodilitation

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32
Q

In LOW pressure in arteries> Barareceptors firing rates decrease > and cardiovascular centre in brain stem responds….

A

Increase in adrenaline - will increase the heart contraction and heart rate

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33
Q

Name for low blood pressure

A

Low hypotension

34
Q

To get low pressure to normal levels

A

Vagal activity is decresead

= cardiac output is input

35
Q

When cardiac output increases what happens to the blood vessels?

A

The arteries start to narrow - blood pressure will increase as it in constructing blood from flowing

36
Q

Blood vessels narrowing:

A

Vasoconstrition

37
Q

Blood pressure equation =

A

BP = Cardiac output x Peripheral resistance

38
Q

decrease cardiac output = blood pressure…

A

will drop

39
Q

1) Kidney receives a low amount of cardiac output; which mean they receive _____ pressure;

A

LOW

40
Q

2) What senses the pressure in the kidney?

A

Juxtaglomerular (granular cells)

41
Q

3) Juxtaglomerular (granular cells) sends the RENAL HYPERFUSION - low oxygen and they release _____

A

RENIN

42
Q

4) The liver synthesises______ which is a key molecule to regulate blood pressure

A

Angiotensinogen

43
Q

5) Renin converts Angiotensinogen to _________

A

Angiotensin I : cleaved to 8 peptide molecule

44
Q

6) The lungs secretes Angiotensin converting enzyme (ACE), which converts ______ to ______

A

Angiotensin I to Angiotensin II

45
Q

a) function of angiotensin II

A

Its a peptide hormone - act as vaso contrictor

Cause contriction of vascular SMOOTH muslce and cause arterie to contrict / narrow ^ in blood pressure

46
Q

Angiotensin II ^^^ = PR?

A

will increase also because resistance is maintained

47
Q

b) function of angiotensin II

A

act on adrenal cortex to stimulate the aldosterone

48
Q

Aldosterone is the predominant regulator of _______ + ________ homeostasis.

A

Water + Sodium

49
Q

Role of Aldosterone:

A

reabsorption of sodium (help Na/K pump to reabsorb)

50
Q

Sodium reabsorption causes change is OSMOTIC PRESSURE, water will move towards _____

A

the sodium

51
Q

Complete flow diagram from sodium reabsorption to the cardiac output

A

^^Sodium reabsorption > osmotic pressure > water reabsorption > intravascular volume > venous return > venous return > ^^Cardiac output
= BLOOD pressure goes up

52
Q

in high pressure the Juxtaglomerular senses….

A

there is no need for RENIN producjtion which means there is no production of angiotensinogen to angiotensin I

53
Q

High blood pressure causes BP -

A

Go down because the resistance needs to be decreased

54
Q

Prevention of ______ reabsoption with high blood pressure

A

sodium - urine volume will be higher because the water follows the sodium

55
Q

Reduction in intravascular volume = venus return will be ______

A

reduced

56
Q

Frank Starling’s LAW

A

If there is a decrease in the Venus return there is a decrease in the cardiac output

57
Q

Other endocrine hormones modulating BP:

A

a) Antidiuretic Hormone (vasopressin)
b) Atrial Natriuretic Hormone/ Peptide
c) Catecholamines: Adrenaline/Nor-adrenaline
d) Erythropoietin

58
Q

Hypovolemia:

A

Increase in tissue fluid osmolarity (loss of blood volume) trigger ADH release

59
Q

High blood volume and extreme stretching of the cardiac cells trigger_______ release.

A

ANH/ANP release

60
Q

a) Antidiuretic Hormone (vasopressin) roles;

A

ADH is secreted by the cells in the hypothalamus, transported to the posterior pituitary and stored until nervous stimuli.

ADH signals kidneys to reabsorb more water

Prevent the loss of fluids in the urine.

Increase overall fluid levels

ADH constricts peripheral vessels.

Restore blood volume and pressure.

61
Q

b) Atrial Natriuretic Hormone/peptide roles;

A

Secreted by cells in the atria of the heart (B-type ANH by ventricle)

Natriuretic hormones are antagonists to angiotensin II (BLOCKs i)

Prevent aldosterone release

Promotes loss of sodium and water from the kidneys.

Suppress renin, aldosterone, and ADH production and release.

Promotes loss of fluid from the body

Blood volume and blood pressure drop.

Restore blood volume

62
Q

c) Catecholamines: Adrenaline/Nor-adrenaline

A

Released by the adrenal medulla
Enhance and extend the body’s sympathetic activity (“fight-or-flight” response)

Increases
Heart rate
Force of contraction
Vasoconstriction (non essential organs)
Energy mobilisation to liver, muscle and heart

63
Q

d) Erythropoietin

A

Blood flow and/or oxygen levels decrease (Hypoxia).

EPO is released by the kidneys

EPO stimulates the production of erythrocytes within the bone marrow. It is a vasoconstrictor.

Increase
Blood viscosity, resistance, and pressure

Decrease
Blood flow

64
Q

Excersise and vascular homeostasis:

A
  1. Resting
  2. Mild Excercise
  3. Maximised Exercise (Athletes)
65
Q
  1. Resting
A

CO - 5L/min
BP = 120/80

66
Q
  1. Mild Exercise
A

CO - to 20L/min
BP - to 180/85

Increased Blood flow (Vasodilation)

Increased Blood Flow (Vasodilation)

Skeletal muscle (x 2 times)
Heart (x 0.5 time)
Lungs (x 0.5 folds)
Integument System (x 0.2 folds)

Decreased Blood Flow
(Vasoconstriction)
Kidney, Digestive, Reproductive

67
Q
  1. Maximised Exercise (Athletes)
A

CO = ~30L/min
Size and Wt= 500 gms (Increased efficiency)
BP = ~200/90

Increased Blood Flow (Vasodilation)

Skeletal muscle (x 10-20 times)
Heart (x 3 time)
Lungs (x 3 folds)
Integument System (x1 folds)

Decreased Blood Flow
(Vasoconstriction)
Kidney, Digestive &
Reproductive (higher levels)

68
Q

Cerebral Blood Flow is affected or unaffected, Independent (mediated by chemicals locally)????

A

UNaffected

69
Q

Events that can influence factors; hypotension? (opposite for high BP)

A

Stroke volume low/ heart rate low = cardiac output and PR low

70
Q

Factors that cause HYPOtension;

A

HYPOVOLEMIA
Haemorrhage
Dehydration
Diarrhoea
Burns
Diuretics

STRUCTURAL DYSFUNCTIONS
Valves disease
Ischemia
Myopathy
Pulmonary hypertension
Pericardial disease

ARRHYTHMIAS
Sinus bradycardia
AV nodal block
Ventricular fibrillation

SYSTEMATIC VASODILATION
Sepsis
Autonomic dysfunction
Anaphylaxis
Neurogenic

OBSTRUCTION
Pulmonary embolism

71
Q

Symptoms of low hypotension;

A

Light headedness or dizziness
Feeling sick
Blurred vision
Generally feeling weak
Confusion
Fainting

72
Q

Factors that effect on HYPERtension;

A

SODIUM HOMEOSTASIS
Renal disease
Nephropathy
Reduced nephron number
GFR

HORMONAL IMBALANCE
Renin
Angiotensin II
Aldosterone
Erythropoietin
Adrenaline/Noradrenaline

SYSTEMIC VASOCONSTRICTION
Stress
Autonomic dysfunction

STRUCTURAL DYSFUNCTIONS
Obesity
Endothelial dysfunction
Altered cell membrane
Venous constriction

73
Q

Symptoms of HYPERtension;

A

Severeheadaches
Nosebleed
Fatigueor confusion
Visionproblems
Chest pain
Difficulty breathing
Irregular heartbeat
Blood in the urine

74
Q

RISKS of high blood pressure:

A

Heart disease
Heart attacks
Srokes
Heart failure
Peripheral arterial disease
Aortic aneurysms
Kidney disease
Vascular dementia

75
Q

Main complications of persistent high BP in;

A
  1. brain
  2. retina of eye
  3. blood
  4. kidneys
  5. heart
76
Q
  1. High BP brain
A

Cerebrovascular accident (strokes)
Hypertensive encephaolpathy; confusion, headache, convulsion

77
Q
  1. High BP retina of eye
A

Hypertensive retinopathy

78
Q
  1. High BP blood
A

Elevated sugar levels

79
Q
  1. High BP kidneys
A

Hypertensive nerphropathy/ chronic renal failure

80
Q
  1. High BP heart
A

Myocardial infarction (heart attack)
Hypertensive cardiomyopathy; heart failure

PMP-101 (53 decks)

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