Regulation of the Cardiovascular system 2 Flashcards

1
Q

What is perfusion?

A
  • the flow of blood through a tissue
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2
Q

adequate tissue perfusion is essential to maintain its nutritive demands - what does too much perfusion or too little perfusion do to a tissue?

A
  • Too little = hypoxia (doesn’t receive oxygen), impaired metabolism leading to necrosis (irreversible death of tissue)
  • Too much = capillary/endothelial damage, fluid exudation (fluid leaking)
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3
Q

What is flow through a tube driven by?

A
  • flow through a tube is driven by pressure, and opposed resistance
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4
Q

If the tube is an artery pressure and resistance would be described as what?

A
  • pressure = systemic arterial blood pressure
  • resistance = resistance of a vessel
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5
Q

What is systemic arterial pressure a major determinant of?

A
  • major determinant of perfusion pressure, driving tissue perfusion
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6
Q

What would you have to do to maintain tissue perfusion?

A
  • control arterial pressure
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7
Q

Perfusion pressure and arterial control can be described as either of two things - what are these?

A
  • hypertension (high blood pressure)
  • hypotension (low blood pressure)
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8
Q

Normal arterial pressure is continuously variable - what factors contribute to this?

A
  • age
  • physiological status
  • species and breed
  • systole and diastole
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9
Q

What is systolic arterial pressure (SAP)?

A
  • peak pressure in the arteries when the left ventricle is ejecting blood during systole
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10
Q

What is diastolic arterial pressure (DAP)?

A
  • residual pressure in the arteries when the left ventricle is filling during diastole
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11
Q

What does MAP stand for?

A
  • Mean arterial pressure
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12
Q

Why is pulse pressure never in the middle of a graph?

A
  • not quite in the middle as the heart spends more time relaxed more than it does contracting
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13
Q

What determines mean arterial pressure?

A
  • cardiac output
  • systemic vascular resistance
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14
Q

What is the equation for mean arterial pressure (MAP)?

A
  • MAP = cardiac output x systemic vascular resistance
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15
Q

What can we do in order to maintain adequate perfusion?

A
  • change cardiac output and or change vascular resistance
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16
Q

If cardiac output remains constant what happens to arterial pressure?

A
  • arterial pressure can rise or fall as resistance increases or decreases
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17
Q

What is arterial blood pressure controlled by?

A
  • controlled by negative feedback
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18
Q

There are both short-term and long-term feedback mechanisms for arterial pressure - what is the short term mechanism?

A
  • short term is rapid via baroreceptor regulation
  • ANS
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19
Q

What is the long term mechanism for control of arterial pressure?

A
  • long term is slower and via circulating fluid volume
  • anti-diuretic hormone AKA vasopressin
  • renin-angiotensin-aldosterone-system
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20
Q

Cardiovascular reflexes are ultimately directed at regulation of arterial pressure - how do we regulate this?

A
  • heart rate and force (contractility)
  • tone of resistance vessels (arterioles)
  • volume of capacitance vessels (e.g., veins)
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21
Q

Short term control of arterial pressure is a function of what?

A
  • of the cardiovascular system
22
Q

What does long term control of arterial pressure include?

A
  • fluid balance
  • renal system
23
Q

What do cardiovascular reflexes require in terms of pressure?

A
  • sensors (ability to monitor pressure)
  • integrating centre (assess correctness of pressure)
  • effectors (mechanisms to return pressure to correct level
24
Q

What are baroreceptors?

A
  • they are sensors
  • non-encapsulated nerve endings
25
Q

Where are baroceptors found?

A
  • in the adventitial layer of arteries
  • aortic arch and carotid sinus
26
Q

What do baroreceptors serve as?

A
  • serve as mechanoreceptors
  • increasing firing rate in response to pressure
27
Q

Central axons terminate where?

A
  • in the medulla oblongata (cardiovascular centres)
28
Q

How does the autonomic output get to effector organs?

A
  • sympathetic to heart and vessels
  • parasympathetic to heart
29
Q

What does increased blood pressure do to baroreceptor firing rate?

A
  • increases firing rate
30
Q

What does decreases blood pressure do to baroreceptor firing rate?

A
  • decreases firing rate
31
Q

What happens when there is an increased rise in blood pressure?

A
  1. acute rise in blood pressure
  2. increased baroreceptor discharge
  3. goes to brainstem
  4. this increases vagal output which decreases heart rate
    and at the same time
  5. this decreases sympathetic output meaning there is less calcium coming into cells which decreases, contractility (SV), heart rate and arteriolar tone
  6. all of these actions decrease blood pressure
32
Q

How fast do baroreceptors act?

A
  • Act extremely fast, within seconds providing pressure buffering for shot/acute changes
33
Q

What happens to baroreceptors after longer altered pressure?

A
  • there is evidence for resetting of baroreceptors
34
Q

What type of information do baroreceptors relay?

A
  • information on blood pressure that is relative to the individual set point (not an index of absolute pressure)
35
Q

Principle long-term mechanism of blood pressure regulation are via what?

A
  • via kidneys through plasma volume
36
Q

Describe how the kidneys and plasma volume increases arterial pressure:

A
  1. Increase plasma circulating volume
  2. increased preload (Starlings Law)
  3. increased cardiac output
  4. increases mean arterial pressure
37
Q

What does RAAS stand for?

A
  • The Renin-Aldosterone System
38
Q

What is the RAAS system?

A
  • A hormone system regulating fluid balance and blood pressure
39
Q

What is the first step in RAAS?

A
  • the release of the enzyme renin
40
Q

What do triggers for renin release include?

A
  • reduced perfusion of kidney
  • sympathetic stimulation
41
Q

As an enzyme what does renin do?

A
  • renin cleaves a precursor protein (angiotensinogen) into angiotensin 1
42
Q

What happens after angiotensinogen is cleaved into angiotensin 1?

A
  • Angiotensin 1 is then converted to angiotensin 2 by an enzyme angiotensin converting enzyme and this mainly happens in lungs
43
Q

Angiotensin 2 binds to receptors around the body and has many effects what are these?

A
  • Vasoconstriction (increases SVR)
  • Na+ reabsorption in kidney (increases CO/preload)
  • increases sympathetic activity (increases HR and SV)
  • releases anti-diuretic hormone (increases CO/preload)
  • release aldosterone (more Na reabsorption)
44
Q

What does the renin-angiotensin-aldosterone axis provide?

A
  • immediate, potent control of MAP via angiotensin 2
  • slower, prolonged regulation of MAP via volume control (aldosterone + ADH)
45
Q

Other long term control mechanism include volume receptors - What are atrial receptors?

A
  • they are found in the heart and are low-pressure baroreceptors that act as volume receptors
46
Q

When volume receptors detect high volume detected as stretch it leads to what?

A
  • inhibition of sympathetic pathways leading to renal vasodilation (diuresis)
  • inhibition of ADH/vasopressin
  • other effects via atrial natriuretic peptide (ANP)
47
Q

Increase in blood volume leads to stimulation of atrial volume receptors
What are the two responses to this?

A
  • inhibit sympathetic vasoconstrictor pathways to kidneys leading to diuresis
    or
  • reflex inhibition of ADH/vasopressin from posterior pituitary gland
48
Q

What do the two responses to increased blood volume lead to?

A
  • decreased volume
  • decreased central venous pressure
  • decreased stroke volume
  • decreased cardiac output
  • decreased arterial pressure
49
Q

What is acute haemorrhage?

A
  • blood loss
50
Q

What are the two acute cardiovascular reflexes?

A
  1. Baroreceptor reflexes
  2. atrial volume receptors
51
Q

What controls longer term restoration of volume?