Cardiovascular physiology 2 Flashcards

1
Q

What is the heart rate set by ?

A

The pacemaker cells

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2
Q

What can be used to speed up or slow down the heart rate ?

A

The sympathetic and parasympathetic nervous system

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3
Q

How does the sympathetic NS affect HR ?

A

The sympathetic nervous system works in two ways, the sympathetic nerves releases noradrenaline and the adrenal medulla releases adrenaline. Noradrenaline and adrenaline act on the B1 receptors in the SA node and increase the rate of the pacemaker potentials

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4
Q

How does the parasympathetic NS affect HR ?

A

The parasympathetic nervous system decreases the heart rate when the vagus nerve releases AcH which acts on muscarinic receptors on the SA node.

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5
Q

What is stroke volume ?

A

the volume of blood pumped out by the heart in one beat

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6
Q

What is starlings law?

A

Starlings law states that the energy of a contraction (tension) is proportional to the initial length of the cardiac muscle fibre

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7
Q

How does starlings law apply to the control of our heart?

A

The greater the tension the greater the stoke volume. The lengths of the cardiac muscles fibres is determined by the volume of blood in the ventricles. The relationship can be seen in the graph. To a certain point the longer the fibres the greater the tension however after a certain point this is no longer the case.

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8
Q

How can stoke volume be regulated by the sympathetic NS?

A

The stoke volume can be regulated by adrenaline and noraadrenaline released by the sympathetic NS and adrenal medulla. The noradrenaline and adrenaline acts on B1 receptors and cause a stronger and shorter contraction. It also increases contractility (an inotropic effect).

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9
Q

How can stoke volume be regulated by the parasympathetic NS?

A

The parasympathetic pathway has very little effect because the vagus does not innervate the ventricular muscle.

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10
Q

What is the afterload ?

A

the load against which the muscle contracts

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11
Q

The larger the … the larger the afterload

A

the resistance in the vascular system

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12
Q

When happens to the stroke volume when the afterload increases

A

The larger the resistance in the vascular system the larger the load against which the muscle contracts and the higher the required ventricular pressure for the aortic valve to open (remember that happens when the aortic pressure is less than the ventricular pressure). The resistance in the system can be controlled by the arterioles. If there is a large afterload then there will be less ‘energy’ to eject blood and so there is an decrease in stroke volume.

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13
Q

What is the preload ?

A

how full the ventricles are before the contraction starts

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14
Q

What is the preload affected by ?

A

the state of the contracted venules/veins

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15
Q

What is another name for the volume of blood in the heart?

A

end diastolic volume.

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16
Q

What is contractility ?

A

How strong a contraction is

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17
Q

What affects the contractility ?

A

The sympathetic system

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18
Q

EQUATION: Cardiac output =

A

Heart rate x stroke volume

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19
Q

How do you get from an increased vagal tone and increased in sympathetic tone to a reduced in afterload ?

A

An decrease in vagal tone (activity) and an increase in sympathetic tone (activity) causes an increase in HR and contractility (inotropic effect). Here is an decrease in length of systole. Sympathetic system works on the veins causes an increases venous return, and this maintains preload. The sympathetic system works on the arteries and causes a reduction in resistance and therefore a reduction in afterload.

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20
Q

By what mechanisms is venous return controlled ?

A
Pressure 
Gravity 
Skeletal muscle pump 
Respiratory pump 
Venomotor tone
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21
Q

How does pressure affect the venous return ?

A

Pressure falls as you move through the vascular tree. There is a small drop in pressure between the arteries, a large drop into the arterioles and it then continues to fall until it is back in the heart. The pressure different through the system is what drives the movement on blood.

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22
Q

How does gravity affect venous return ?

A

Always pulling downwards

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23
Q

How does the skeletal muscle pump affect venous return ?

A

The skeletal muscle pump increases the movement of venous blood back to the heart. It occurs where there is a rhythmic contraction of skeletal muscles in the legs i.e. when you are exercising. A lack of skeletal muscle pump use can cause a DVT.

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24
Q

How does the respiratory pump affect venous return ?

A

The respiratory pump also increases venous return. An increase in respiratory rate and depth increases venous return and EDV. This is because inspiration causes a decrease in alveolar pressure adding to the pressure gradient and pulling blood up towards the lungs.

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25
Q

How does the venomotor tone affect the venous return?

A

The venomotor tone is the contraction of the smooth muscle which surrounds the veins and venules. This increases capacitance and EDV.

26
Q

What is blood flow ?

A

Flow is the volume and velocity of the blood passing a point. Flow is greatest in the large vessels where blood is passing through the smallest cumulative diameter and therefore blood must move faster.

27
Q

Altering the flow will

A

alter the peripheral resistance.

28
Q

How can blood flow be controlled ?

A

Flow can be controlled using local (intrinsic) mechanisms as well as central (extrinsic) mechanisms.

29
Q

What is the aim of local methods ?

A

Local mechanisms ensure the needs of individual tissues are met

30
Q

What is the aim of central methods ?

A

ensure that the peripheral resistance is well controlled.

31
Q

What are the names of some of the local control systems of blood ?

A

Autoregulation
Active (metabolic) hyperaemia
Reactive hyperaemia
Skin scratching

32
Q

What is autoregulation ?

A

Autoregulation is an example of a local control. Autoregulation is carried out in the heart, brain and kidney. This is when a decrease in perfusion causes vasodilation in order to being more blood to the area. Vasodilation is caused by the release of molecules like EDRF from the endothelial cells.

33
Q

What is active hyperaemia ?

A

Active (metabolic) hyperaemia is vasodilation which occurs when supply of blood does not meet the demand. Here the cells detect an increase of ions which are moving into the cell and this triggers the release of molecules such as EDRF which cause vasodilation and therefore dilute the ions found in the blood.

34
Q

What is reactive hyperaemia ?

A

Reactive hyperaemia is an increase flow of blood to an area after a period of occlusion. Injury response that is another local control

35
Q

What is the skin scratching pathways

A

is an increase flow of blood to an area after a period of occlusion. Injury response that is another local control. Scratching the skin causes C-fibres to stimulate substance P which causing mast cells to release histamine. This increases arterial radius, flow and permeability.

36
Q

How is the blood flow controlled centrally ?

A

Sympathetic nerves

37
Q

How is the blood flow in the body controlled centrally ?

A

Sympathetic nerves release noradrenaline which binds to A1 receptors causing vasoconstriction, decreasing flow and increase total peripheral resistance. The adrenal medulla can also release adrenaline which acts on A1 and causes vasoconstriction. Adrenaline and noradrenaline in skeletal and cardiac muscle can also act on B2 to causes vasodilation

38
Q

How is the blood flow in the coronary circulation controlled centrally ?

A

shows great active hyperaemia as its blood supply is cut off every time the heart contracts . It has lots of B2 receptors which cancel out the sympathetic vasoconstriction and cause vasodilation.

39
Q

How is the blood flow in the renal and cerebral circulation controlled centrally ?

A

heart contracts. It has lots of B2 receptors which cancel out the sympathetic vasoconstriction and cause vasodilation. Cerebral circulation and renal circulation show great pressure autoregulation

40
Q

How is the blood flow in the renal and pulmonary circulation controlled centrally ?

A

In the pulmonary circulation a decreased ventilation causes vasoconstriction to prevent more blood from going to an area which cant oxygenate blood.

41
Q

What mechanisms are used to help prevent clotting in the wrong places at the wrong time ?

A
  • The endothelium stops the blood contacting collagen. This stops platelets from binding to the collagen.
  • The endothelium produces prostacyclin and nitric oxide. This stop other platelets from binding on to other platelets which are bound to the collagen.
  • The endothelium produced tissue factors pathway inhibitors which stop thrombin production.
  • The endothelium expresses thrombomodulin which binds to thrombin and inactivates it.
  • The endothelium expresses heparin which also inactivates thrombin
  • The endothelium secretes tissue plasminogen activator which converts to plasmin and digests clots.
42
Q

What is MAP ?

A

mean arterial pressure

43
Q

Why is MAP important to control of blood ?

A

MAP is the driving force for movement of blood and therefore it is very important to control it.

44
Q

How is MAP controlled in the short term?

A

through baroreflexes

45
Q

Explain baroreflexes

A

Baroreflexes are found in the aortic arch and carotid sinus. They are stretch reflexes, then there is an increase is MAP they are stretched and send signals to the brain. Aortic signals are sent via the vagus nerve and carotid sinus signals are sent through the glossopharyngeal nerve. The signal is processed in the brain and assed to the parasympathetic signals in the vagus nerve which act on the SA node and decrease the heart rate. If there is a decrease in MAP then the brain sends signals to the SA node through the sympathetic nerves to increase the HR. Sympathetic nerves cause increased stoke volume and blood vessel constriction.

46
Q

How is MAP controlled in the long term ?

A

kidneys.

47
Q

How does the kidneys control BP ?

A

They control plasma volume

48
Q

Describe how the kidneys alter plasma volume

A

In the kidneys water follows salt. In low blood pressure there will be a lower osmolarity in the blood then in the kidneys. Therefore there will be an increase re-absorption of salt and an increased re-absorption of water which will increase blood volume and pressure. In high blood pressure there will be a higher osmolarity in the blood than in the kidneys. Therefore there will be an decreased re-absorption of salt and a decreased re-absorption of water which will decrease blood volume and pressure. The further along the collecting duct of the kidney the greater the osmotic gradient.

49
Q

Name three mechanisms by which the kidneys control of BP is altered

A

Renin-Angiotensin-Aldosterone system
ADH
ANP And BNP

50
Q

How is renin released ?

A

. Sympathetic nerves act on the juxtaglomerular apparatus and induce the secretion of Renin from juxtaglomerular cells in the kidneys.

51
Q

How is renin converted to angiotensin II ?

A

Renin is converted to inactive angiotensinogen and then into angiotensin I. The angiotensin converting enzyme (ACE) then converts angiotensin I to Angiotensin II.

52
Q

How does angiotensin II reduce BP ?

A
  • Stimulates release of aldosterone which increases N2+ reabsorption
  • Stimulates the release of ADH which increases water permeability
  • Causes vasoconstriction
53
Q

How is ADH released?

A

ADH is produced by the hypothalamus and released from the posterior pituitary gland.

54
Q

What does ADH stand for ?

A

antidiuretic factor / hormone

55
Q

What triggers the release of ADH ?

A

The release of ADH is triggered by a number of things including,

  • A decreased blood volume
  • increases osmolarity
  • increased interstitial fluid
  • Increased presence of circulating angiotensin II
56
Q

What does ADH do ?

A

ADH increases the water permeability of the collecting duct, reducing diuresis (urine excretion) and increasing plasma volume.

ADH also causes vasoconstriction which also increased MAP.

57
Q

What does ANP and BNP stand for ?

A

The atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP)

58
Q

Where is ANP and BNP produced and released ?

A

myocardial cells in the atria and venticules respectively

59
Q

What causes the release of ANP and BNP ?

A

be increased tension in the ventricles which triggers the secretion of ANP and BNP

60
Q

What do ANP AND BNP do ?

A

increase excretion of Na+,
inhibit renin release
act on medullary CV centres to reduce BP.

61
Q

What is the Valsalva manoeuvre?

A

The control of blood vessels can be seen in the Valsalva manoeuvre. The Valsalva manoeuvre is a method of reducing heart rate and blood pressure in the short term. It is the forced expiration against a closed glottis or ‘bearing down’.

62
Q

How does the Valsalva manoeuvre work?

A

This action increases thoracic pressure which increases the blood pressure (1). Increased blood pressure reduces filling pressure from the veins and therefore reduced venous return, end diastolic volume, stroke volume, cardiac output, and mean arterial pressure (2). Reduced MAP is detected by the baroreceptors which increase cardiac output and peripheral resistance which starts to increase blood pressure (3). As the end of the manoeuvre the venous return is restored and so stroke volume is increased however the effects of the baroreceptors has not worn off and so the blood pressure decreases further (4). The venous return is then restored and so the stoke volume increase but the reflex effects have not worn off (5). By (6 eventually everything is back to normal).