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
Increase in vagal activity will _______ heart rate (vagal innovation)
Suppress
26
What suppresses the sympathetic cardiac activity?
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.
27
Heart contraction and heart rate low; Heart output=
LOW - achieve normal homeostasis - low blood pressure
28
Suppression for sympathetic activity in the cardiac cells whereas there is a stimulus for the sympathetic activity which comes from.....
the vasomotor centre and the vaso-activation which causes vaso-DILATION .
29
Sympathetic activation at the vascular SMOOTH MUSCLE causes ______
Relaxation
30
the vessel of the smooth muscle tend to dilate which means....
The vessels expand (blood vessel becomes larger) more allowing more blood flow through = blood pressure will DROP
31
Name for blood vessels dilating?
Vasodilitation
32
In LOW pressure in arteries> Barareceptors firing rates decrease > and cardiovascular centre in brain stem responds....
Increase in adrenaline - will increase the heart contraction and heart rate
33
Name for low blood pressure
Low hypotension
34
To get low pressure to normal levels
Vagal activity is decresead = cardiac output is input
35
When cardiac output increases what happens to the blood vessels?
The arteries start to narrow - blood pressure will increase as it in constructing blood from flowing
36
Blood vessels narrowing:
Vasoconstrition
37
Blood pressure equation =
BP = Cardiac output x Peripheral resistance
38
decrease cardiac output = blood pressure...
will drop
39
1) Kidney receives a low amount of cardiac output; which mean they receive _____ pressure;
LOW
40
2) What senses the pressure in the kidney?
Juxtaglomerular (granular cells)
41
3) Juxtaglomerular (granular cells) sends the RENAL HYPERFUSION - low oxygen and they release _____
RENIN
42
4) The liver synthesises______ which is a key molecule to regulate blood pressure
Angiotensinogen
43
5) Renin converts Angiotensinogen to _________
Angiotensin I : cleaved to 8 peptide molecule
44
6) The lungs secretes Angiotensin converting enzyme (ACE), which converts ______ to ______
Angiotensin I to Angiotensin II
45
a) function of angiotensin II
Its a peptide hormone - act as vaso contrictor Cause contriction of vascular SMOOTH muslce and cause arterie to contrict / narrow ^ in blood pressure
46
Angiotensin II ^^^ = PR?
will increase also because resistance is maintained
47
b) function of angiotensin II
act on adrenal cortex to stimulate the aldosterone
48
Aldosterone is the predominant regulator of _______ + ________ homeostasis.
Water + Sodium
49
Role of Aldosterone:
reabsorption of sodium (help Na/K pump to reabsorb)
50
Sodium reabsorption causes change is OSMOTIC PRESSURE, water will move towards _____
the sodium
51
Complete flow diagram from sodium reabsorption to the cardiac output
^^Sodium reabsorption > osmotic pressure > water reabsorption > intravascular volume > venous return > venous return > ^^Cardiac output = BLOOD pressure goes up
52
in high pressure the Juxtaglomerular senses....
there is no need for RENIN producjtion which means there is no production of angiotensinogen to angiotensin I
53
High blood pressure causes BP -
Go down because the resistance needs to be decreased
54
Prevention of ______ reabsoption with high blood pressure
sodium - urine volume will be higher because the water follows the sodium
55
Reduction in intravascular volume = venus return will be ______
reduced
56
Frank Starling's LAW
If there is a decrease in the Venus return there is a decrease in the cardiac output
57
Other endocrine hormones modulating BP:
a) Antidiuretic Hormone (vasopressin) b) Atrial Natriuretic Hormone/ Peptide c) Catecholamines: Adrenaline/Nor-adrenaline d) Erythropoietin
58
Hypovolemia:
Increase in tissue fluid osmolarity (loss of blood volume)  trigger ADH release
59
High blood volume and extreme stretching of the cardiac cells trigger_______ release.
ANH/ANP release
60
a) Antidiuretic Hormone (vasopressin) roles;
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
b) Atrial Natriuretic Hormone/peptide roles;
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
c) Catecholamines: Adrenaline/Nor-adrenaline
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
d) Erythropoietin
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
Excersise and vascular homeostasis:
1. Resting 2. Mild Excercise 3. Maximised Exercise (Athletes)
65
1. Resting
CO - 5L/min BP = 120/80
66
2. Mild Exercise
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
3. Maximised Exercise (Athletes)
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
Cerebral Blood Flow is affected or unaffected, Independent (mediated by chemicals locally)????
UNaffected
69
Events that can influence factors; hypotension? (opposite for high BP)
Stroke volume low/ heart rate low = cardiac output and PR low
70
Factors that cause HYPOtension;
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
Symptoms of low hypotension;
Light headedness or dizziness Feeling sick Blurred vision Generally feeling weak Confusion Fainting
72
Factors that effect on HYPERtension;
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
Symptoms of HYPERtension;
Severe headaches Nosebleed Fatigue or confusion Vision problems Chest pain Difficulty breathing Irregular heartbeat Blood in the urine
74
RISKS of high blood pressure:
Heart disease Heart attacks Srokes Heart failure Peripheral arterial disease Aortic aneurysms Kidney disease Vascular dementia
75
Main complications of persistent high BP in;
1. brain 2. retina of eye 3. blood 4. kidneys 5. heart
76
1. High BP brain
Cerebrovascular accident (strokes) Hypertensive encephaolpathy; confusion, headache, convulsion
77
2. High BP retina of eye
Hypertensive retinopathy
78
3. High BP blood
Elevated sugar levels
79
4. High BP kidneys
Hypertensive nerphropathy/ chronic renal failure
80
5. High BP heart
Myocardial infarction (heart attack) Hypertensive cardiomyopathy; heart failure