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Cardiovascular system > Cardiovascular physiology > Flashcards

Cardiovascular physiology Flashcards

1
Q

What is the function of cardiovascular system?

A

Transport of O2, CO2, nutrients, metabolites, hormones and heat around the body

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2
Q

What is the arrangement of the chambers in the heart and what is the significance?

A

In series, the same amount of blood is pumped by the right and left side

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3
Q

What is the arrangement of vascular bed and what is the significance?

A

They are in parallel, this enables all tissues to get oxygenated blood and allows ability to redirect blood, there are some exceptions in liver and hypothalamus and pituitary

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4
Q

What are the exceptions in vascular arrangement?

A

Hypothalamus and pituitary, gut and liver

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5
Q

What is the distribution of blood to organs at rest?

A

At rest most blood goes to abdomen, then kidneys, muscles, brain, other, skin, heart

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6
Q

Is cardiac output proportional to the O2 consumption?

A

Yes in most organs, it is not in kidneys and skin where the O2 consumption is lower, and brain where it is bigger

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7
Q

What determines the flow?

A

Pressure gradient / resistance

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8
Q

Describe the properties of elastic arteries

A

They have wide lumen, thick wall with lot of elastic fibres, the wall is elastic and damps the pressure changes, reduce the peak pressure as the pressure in diastole is increased by elastic recoil, the stored energy in the walls is released

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9
Q

Describe the properties of muscular arteries

A

They have wide lumen, strong thick wall with many muscle cells and non-elastic, can withstand pressure variations, low resistance conduit

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10
Q

Describe the properties of arterioles

A

They have narrow lumen, thick contractile wall, resistance vessels, contraction varies the resistance and allows regulation of blood flow

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11
Q

Describe the properties of capillaries

A

They are exchange vessels, very narrow lumen, thin one cell wall, allows diffusion, have large surface area

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12
Q

Describe the properties of venules and veins

A

They have wide lumen, distensible wall with some smooth muscle, low resistance reservoir, they can be squashed by external forces, they are capacitance vessels and can store a lot of blood

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13
Q

Which valves are exist valves and entrance valves

A

Pulmonary and aortic are exit valves, tricuspid and mitral are entrance valves

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14
Q

What opens the valves ?

A

Pressure differences, it is passive process

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15
Q

What is the difference between action potential in skeletal muscles and cardiac muscles and why?

A

In cardiac muscles it is a lot longer, it lasts 250 ms, in skeletal only 2 ms, a lot of Ca2+ enter the cardiac muscles regulating the strength of contraction, there is also long refractory period meaning no tetanic contraction can occur

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16
Q

How is the strength of contraction regulated in cardiac muscle cells?

A

By varying the amount of Ca2+ ions that can enter in

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17
Q

How does the shape of action potential vary in cardiac muscles ?

A

It is not a sharp peak, there is rapid depolarisation, plateau phase and gradual slower repolarisation

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18
Q

What are the two types of cardiac muscle cells ?

A

Non-pacemaker and pacemaker cells

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19
Q

Describe the action potential in non-pacemaker cells

A

These cells have stable resting membrane potential, resting membrane has high permeability to K+ions , depolarisation is caused by opening of Na+ ion channels, sharp rise in potential, then there is plateau phase caused by slow opening of L type Ca2+ ion channels and decreased permeability to K+, after repolarisation phase follows with Ca2+ channels closing and K+ channels opening

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20
Q

What are L type Ca2+ channels ?

A

They are long lasting activation channels, they are open by voltage

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21
Q

How is Ca2+ released from sarcoplasmic reticulum in cardiac cells?

A

In cardiac cells it is calcium induced calcium release, initiated by entry of Ca2+ through voltage gated channels

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22
Q

Describe the action potential in pacemaker cells

A

In pacemaker cells the resting membrane potential is not stable, there is pre-potential or pacemaker potential, during the pacemaker potential there is gradual closure of K+ ion channels, early increase in Na+ permeability and late increase in Ca2+ permeability as T type Ca2+ channels open, the depolarisation of the cells is caused by influx of Ca2+ ions and L type of Ca2+ channels open, the depolarisation is caused by increased permeability to K+ and Na+ channels, this occurs automatically and explains the autorhythmicity

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23
Q

What are T type Ca2+ ion channels

A

They are transient opening, low voltage activated, have fast voltage dependent inactivation

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24
Q

What can modulate electrical activity?

A

Sympathetic and parasympathetic system, cardiac glycosides, drugs such as L type Ca2+ channels blockers, temperature, levels of K+ and Ca2+ in plasma

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25
Q

How L type Ca2+ channels blockers modulate electrical activity of the heart?

A

They block the L type channel, less Ca2+ in and so the force of contraction is weaker

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26
Q

How cardiac glycosides alter the electrical activity of the heart?

A

Cardiac glycosides cause build up of Ca2+ ions, and therefore increase the strength of contraction

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27
Q

How does temperature affects the electrical activity of heart?

A

Increase in HR by 10 beats per every degree, in fever the heart rate is higher

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28
Q

How does hyperkalemia alter el. activity of heart?

A

High K+ levels in plasma decrease K+ gradient and the so resting potential is higher, this causes spontaneous firing of action potential that is uncoordinated, can lead to fibrillation and heart block

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29
Q

How does hypokalemia affects el. activity oh heart?

A

The resting potential is reduced as the K+ gradient is increased, it is harder to trigger action potential, it can lead to fibrillation and heart block

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30
Q

How does hypercalcemia affect the el. activity of heart?

A

More Ca2+ can enter the cell, this leads to higher HR and stronger force of contraction

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31
Q

How does hypocalcemia affect the el. activity of heart?

A

There is fewer Ca2+ ions in the plasma, fewer enter the cell, decreases HR and force of contraction

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32
Q

How does hypercalcemia affect the el. activity of heart ?

A

There are more Ca2+ ions in the plasma, more Ca2+ into the cell, increased HR and force of contraction

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33
Q

What is sinoatrial node?

A

Fastest pacemaker cells in the heart, set the rhythm for the whole heart if healthy, wave of depolarisation spreads across the atria at speed of 0.5 m/s

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34
Q

What is annulus fibrosus?

A

Annulus fibrosus is a part of fibrosus skeleton, it is non-condition insulator between atria and ventricles, it is connective tissue without any gap junctions

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35
Q

How does the condition spreads from SA node to AV node?

A

Via internodal tract, there is also Bachmann’s bundle to left atrium

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36
Q

What is AV node?

A

It is atrioventricular node, conducts the signal from SA node to the ventricles, it is delay box, it delays the condition by 0.05 m/s

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37
Q

What are bundle of his and Purkinje fibres?

A

It is a rapid conduction system for the ventricles, make sure the contraction occurs from the bottom to top, speed of signal is 5 m/s

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38
Q

What is Bundle of His?

A

Collection of heart muscles that are specialised for condition of depolarisation, carry signal from AV node to the apex of the heart, splints into right and left bundle branch, they then split to smaller Purkinje fibres that carry the conduction up to the ventricle muscles

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39
Q

What are Purkinje fibres?

A

Special fibres that are larger than myocytes but with fewer myofibrils and many mitochondria, they arise from bundle of his, found in subendocardial connective tissue

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40
Q

What leads does ECG consist of?

A

Standard limb leads, augmented leads and

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41
Q

Name the standard limb leads

A

SLI (from left arm to right arm), SLII (from left leg to right arm), SLIII (from left leg to left arm)

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42
Q

Describe how is ECG recorded

A

The wave of depolarisation is detected, it passes down to ventricles and then through bodily fluids and to electrodes where it is recoded

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43
Q

What is PR interval?

A

The duration between P wave and QRS complex, the time it takes from atrial depolarisation to the ventricular depolarisation, the duration should be from 0.12-0.2 s

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44
Q

What is QRS complex interval?

A

The time it takes for the whole ventricle to depolarise, it is the interval from the start of QRS complex to the end, normally about 0.08 s, it shows how well Bundle of His and Purkinje fibres are working

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45
Q

What is QT interval?

A

The time it takes for the ventricles to depolarise and repolarise, it is the interval form the start of QRS complex to the end of T wave, it depends on the heart rate, it should be about 0.42 s at 60 bpm

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46
Q

Describe the parts of the QRS complex

A

Q wave is small negative blip produced by the depolarisation spreading across the septum from left to right, R wave is big sharp blip corresponding the depolarisation from endocardium to epicardium, since the bulk of ventricle depolarise towards the left leg it is positive signal, the S wave it a small negative blip corresponding to the depolarisation of the upper parts of the inter ventricular septum depolarise away from the left leg

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47
Q

Explain why depolarisation is positive blip

A

The action potential in endocardium is longer, the repolarisation occurs from epicardium to endocardium, so the direction is opposite to depolarisation, cells depolarise at different times and so the peak is smaller and broader

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48
Q

In limb leads which has the bigger R wave and why?

A

SLII has the bigger R wave, direction of depolarisation is almost identical to the direction of recording, than SLIII and SLI based on the increasing angle of recording to the depolarisation

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49
Q

Name the augmented leads

A

aVR, aVL, aVF

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50
Q

What happens to R wave in augmented leads?

A

aVL has postive R wave, aVL has no R wave and aVR has negative R wave

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51
Q

What are pre-cordial leads?

A

Six leads on the chest, they record what happens on the transverse (horizontal plane), V1-V6

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52
Q

What happens to R wave in precordial leads?

A

R wave is negative in V1 to around V3-4 where it changes to positive, there is R wave progression

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53
Q

Name the stages of cardiac cycle

A

Late diastole, atrial systole, isovolumetric ventricular contraction, ventricular ejection, isovolumetric ventricular relaxation

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54
Q

Describe what happens in the late diastole phase

A

All chambers are relaxed and are filling passively

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55
Q

Describe the atrial systole

A

During the atrial systole the atria contract and force the last amount of blood out to the ventricles

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56
Q

Describe the isovolumic ventricular contraction

A

The ventricles contract and increase the pressure pushing the AV valves closed, there is increased pressure but there is no change to the volume

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57
Q

Describe the ventricular ejection phase

A

As the ventricles continue to contract the pressure inside ventricles continue to rise and eventually the semilunar valves open leading to ejection of the blood

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58
Q

Describe the ventricular isovolumic relaxation phase

A

As the ventricles stop to contract the pressure drops and the semilunar valves close, the ventricles stop to contract and relax, the pressure is dropping but there is no change to volume until the AV valves open

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59
Q

What is the relative duration of systole and diastole in the cardiac cycle?

A

Systole is 1/3 of a cycle, diastole is 2/3 of a cycle, but as the heart rate goes up the systole takes up proportionally more and more time of the cardiac cycle

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60
Q

Describe the pressure changes in the ventricle during cardiac cycle

A

The pressure in ventricles is low during the diastole, there is slight increase in the pressure as the atria contract pushing the last amount of blood into ventricle, the rise is the same as in atria, then the ventricles start to contract and the pressure rises and AV valves close, then there is rapid increase in the pressure during isovolumic phase as the ventricles are interacting until the semilunar valves open, the blood is ejected from the heart but the pressure keeps increasing further until the ventricles stop contracting, then the pressure starts to decrease until semilunar valves close, then again there is rapid drop in the pressure during isovolumic relaxation until AV valves open again

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61
Q

During which part of the cardiac cycle there is rapid change in the pressure in ventricles ?

A

There are rapid changes to the pressure during isovolumic ventricular contraction and relaxation

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62
Q

What is the maximum and minimum pressure in the ventricles?

A

The maximum pressure is the same as systolic pressure in the arteries, so about 120 mmHg normally, but the lowest pressure is near 0 mmHg, not the diastolic pressure

63
Q

Describe the pressure changes that occur in the aorta

A

The pressure is very high even in diastole and the energy from walls is released, the pressure in the diastole keeps dropping until aortic valve opens and the pressure keeps increasing following the ventricles reaching the peak and then falling down as ventricles stop contracting, as the aortic valve close there is further small increase called dicrotic notch in the pressure which is followed by gradual deuces during the diastole

64
Q

What is the minimum and maximum pressure in the aorta and what is dicrotic notch?

A

The minimum pressure is the diastolic pressure about 80 mmHg, the maximum pressure is the systolic pressure so 120 mmHg, the dicrotic notch is the increase in the aortic pressure as the aortic valve closed caused by elastic recoil of the aorta

65
Q

What is the average pressure and pulse pressure

A

The average pressure is diastolic pressure plus 1/3 of pulse pressure, pulse pressure is the difference between systolic and diastolic pressure

66
Q

Describe the changes of pressure that occur in atria

A

There are three valves in the atria, first a wave is due to atrial contraction, second c wave occurs between the time AV valve closes and the semilunar valve opens, it occurs because the AV valve is floppy and pushes slightly to the atria, the third wave v is caused by the blood flowing into the atria but the AV valves are still closed, the blood accumulates there increasing the pressure until the AV valve opens again

67
Q

Describe how the volume of ventricles changes during cardiac cycle

A

Volume of ventricles increases slightly during the atrial systole, then during the isovolumic contraction it stays the same, after the semilunar valves open there is rapid decrease that gradually slows down as the blood is ejected, then again it remains constant during isocolumic relaxation, rapid increase due to initial rapid filling phase with gradual slowing down of increase until again atria contracts

68
Q

What is end diabolic volume ?

A

Is the the volume of blood in vehicles at the end of diastole, it is around 140 mL

69
Q

What is end systolic volume ?

A

The amount of blood left in ventricles after systole, it is usually around 60 ml, meaning there is some reserve in the heart, not all blood is pumped out

70
Q

What is stroke volume ?

A

The amount of blood pumped out during one contraction, it is usually 80 ml

71
Q

What is ejection fraction ?

A

The fraction between stroke volume and end diastolic volume, in healthy individuals it is about 2/3

72
Q

What is rapid ejection and filling?

A

The majority of the blood is ejected or filled in the 1/3 of the ejection and filling phase respective, the rest if slow ejection and filling

73
Q

At what heart rate does the filling phase change?

A

The rapid filling phase changes if the heart rate is above 150 bpm, below this rate changes if heart rate does not change much the end diastolic volume

74
Q

Compare the pressure in the right side of the heart to the left side

A

Pressure in right side is much smaller than in the left side, it is about 1/5 of the left ventricle

75
Q

What is the pressure in right ventricle?

A

The systolic pressure is about 15-25 mmHg,diastolic is 0-8 mmHg, which is similar to the pulmonary circulation

76
Q

What is phonocardiogram?

A

recording of heart sounds during the cardiac cycle

77
Q

What is first heart sound?

A

First heart sound corresponds to closing of mitral valve and tricuspid valve, caused by turbulent blood flow as the valves close

78
Q

What is second heart sound?

A

Second heart sound corresponds to the closure of aortic and pulmonary valves, it is caused again by turbulent blood flow as the valves close

79
Q

What is the third heart sound ?

A

It is caused by rapid filling phase and mixing of the blood, not usually heard, but can be heard if ventricles contain a lot of blood at the end of systole

80
Q

What is fourth heart sound?

A

Corresponds to active filling phase as atria contracts, not usually heard

81
Q

What are the types of murmur that can be heart?

A

Systolic, diastolic, murmur throughout the cardiac cycle correspond to septal defect

82
Q

What can regulate heart rate ?

A

Heart rate can be regulated by neural control

83
Q

What can regulate stroke volume ?

A

Preload, after load, neural, pathological

84
Q

Describe the Starling’s law

A

The energy of contraction is proportional to the initial length of cardiac muscle fibre, there is optimal length with the maximum number of cross bridges formed, therefore it is affected by preload, the stroke volume increases, it reaches plateau and then decreases again

85
Q

How is stroke volume regulated by preload?

A

Increasing preload stretches heart muscle causing stronger contraction, the preload can be increased by increased end diastolic volume, it is increased by increasing venous return. Venous return can be increased by venous constriction, action of skeletal muscles and respiratory pumps

86
Q

How is stroke volume regulated by afterload?

A

Afterload is the load against which heart muscle has to contract against, it is set by mean arteriolar pressure, MAO is affected by peripheral resistance, bigger the MAO the more energy is wasted to build enough pressure, less strong contraction

87
Q

How can the stroke volume regular by neurones?

A

There are also beta 1 receptors on the myocytes, so activating sympathetic nervous system allows more Ca2+ ions in causing stronger contraction, but it is shorter, this shifts the Starling curve up and to the left, parasympathetic system has little effect

88
Q

How is stroke volume regulated pathologically ?

A

Hypercalcemia shifts the cure up and left, hypocalcemia shifts the curve down and right, ischaemia down and right , barbiturates down and right

89
Q

What happens during exercise?

A

The HR is increased by reduction of vagal activation and increase in sympathetic activation, also contractility increased by sympathetic activation -inotropic effect (more Ca2+ in) and quicker re-uptake, there is also increased preload by venoconstriction, skeletal muscle and respiratory pump, the after load is reduced as the blood is redirected to where it is needed, there is more dilation than constriction, all these cause increase in the cardiac output

90
Q

Give the equation for cardiac output

A

CO =SV x TPR

91
Q

What is met arteriole?

A

Type of arterioles, have smooth muscle cells scattered around and they from pre capillary sphincter regulating the blood flow, it connects arterioles to capillary bed

92
Q

Name the anti-clotting mechanisms of the endothelium

A

Endothelium provides barriers between platelets and collagen, prostacyclins and NO inhibit platelets aggregation, tissue factor pathway inhibitor stops thrombin production, express thrombomodulin that binds and inactivates thrombin, expresses heparin tha also inactivates thrombin, secretes tissue plasminogen activator that causes production of plasmin that can digest the clot

93
Q

What happens to hydrostatic pressure and oncotic pressure as the blood moves via circulation

A

Hydrostatic pressure decreases going from arterioles to venules, but the oncotic pressure increases, there is net filtration based on the overall balance between the two gradients

94
Q

What is filariasis?

A

Infection with thread-like parasite, it is tropical disease, blocks the lymphatic system

95
Q

Name the causes that can lead to oedema

A

Lymphatic obstruction, increased venous pressure, hypoproteinemia, increased permeability

96
Q

What is Darcy’s law?

A

It states that flow is proportional to the pressure difference / resistance

97
Q

What is Poseuille’s law?

A

It states that resistance in proportional to L and viscosity / radius4

98
Q

What is the fundamental equation of cardiovascular system?

A

MAP = CO x TPR

99
Q

What is MAP?

A

Diastoloc pressure + 1/3 pulse pressure

100
Q

What are the two main mechanisms for regulating MAP?

A

Extrinsic and intrinsic mechanism

101
Q

How is the MAP regulated by neural activation?

A

Sympathetic system releases noradrenaline and adrenaline that acts on alpha 1 receptors on smooth muscle in arteries causing constriction and therefore increasing TPR, but there in some tissues such as skeletal and cardiac musicals arterioles also have beta 2 receptor that causes vasodilation, parasympathetic has very little effect as there is no innervation to the arterioles

102
Q

How is the MAP controlled by hormones?

A

Vasopressin and angiotensin II are released in response to low blood volume and cause arteriolar constriction increasing the TPR, atrial natriuretic hormone (atria) and brain natriuretic hormone (ventricles) are released as a response to high blood volume and cause arteriolar dilation reducing the TPR

103
Q

Name the 4 components of the intrinsic control

A

active hyperaemia, pressure autoregulation, reactive hyperaemia, injury response

104
Q

What is active hyperaemia ?

A

Increased concentration of metabolites causes local vasodilation, there is increased metabolic activity and this increases the concentration of metabolites, it is detected by the endothelium of blood vessels and they release endothelium derived relaxing factor or NO that cause relaxation of smooth muscles and therefore dilation, EDRF and NO are paracrine acting

105
Q

What is pressure auto regulation?

A

If the MAP is reduced the blood flow is reduced as there is no driving force, this again leads to accumulation of metabolites and causes vasodilation by the same mechanism

106
Q

What is reactive hyperaemia?

A

It is extreme version of pressure alteration, for example occlusion of blood flow causes accumulation of metabolites and subsequent dilation

107
Q

What is the injury response?

A

Nociceptive C fibres release substance P that causes mast cells to release histamine, histamine causes vasodilation and increases permeability

108
Q

Why are coronary arteries special?

A

They have opposite circulation to the systemic, blood flow is stopped during systole and occurs during diastole, also has many beta 2 receptors

109
Q

Why is pulmonary circulation special?

A

Reduction in O2 leads to contraction and not dilation like in other arterioles

110
Q

Which two circulations show great pressure auto regulation?

A

Cerebral circulation and renal circulation

111
Q

What is the name of the sounds of blood when measuring BP?

A

Korotkoff sounds

112
Q

How can be BP measured?

A

Using sphygmomanometer and stethoscope

113
Q

Describe the Korotkoff sounds

A

When the pressure is above systolic no sound can be heart as no blood flows thought artery, as the pressure decreases tapping sound can be heard when the pressure is around systolic, artery is constricted but small amount of blood can lead though causing turbulent flow, as the pressure continue to drop the constriction is getting smaller and more blood can flow though giving rise to muffled sound, when the pressure is equal to the diastolic pressure there is no longer constrictor, the blood flow is laminar and the muffled sound disappear,

114
Q

What does affect the rise in pressure of blood?

A

Stroke volume, ejection velocity, elasticity of aorta

115
Q

What does affect the declining pressure of blood?

A

Total peripheral resistance

116
Q

What happens to BP during exercise?

A

The systolic pressure increases whereas the diastolic pressure decreases

117
Q

Where is the circulation there is variation in pressure ?

A

In ventricles pressure varies greatly (from 120 to near 0), in arteries the pressure varies from around 120 to 80, in arterioles the variation decreases, the pressure drops from 90 to 40, in capillaries, veins, venules there is no variation, there is only gradual decline in the pressure

118
Q

What is systemic filling pressure?

A

It is the difference between pressure in veins and right atrium, it is quite small about 5-20 mm Hg

119
Q

Describe the velocity changes of blood as it flows through systemic circulation

A

The velocity is related to the surface area, flow must be the same but the velocity varies, velocity is the highest in aorta as it has smallest surface area, then arteries, the velocity is the lowest in the capillaries, increases slightly again in veins

120
Q

Name the 5 factors that affect veins

A

gravity, skeletal muscle pump, respiratory pump, venomotor tone, systemic filling pressure

121
Q

Describe the effect of gravity on venous system

A

Gravity causes pooling of blood in veins as they are distensible, on standing in legs 80 mmHg is added, in head -20 mmHg, the venous return is reduced and therefore the end diastolic volume is reduced leading to lower stroke volume and can cause orthostatic postural hypotension, the driving force of blood from arterial site to venous site is not affected as the same thing happens in both arteries and veins

122
Q

How can be the height go jugular venous collapse be used?

A

It can be used to estimate central venous pressure, if the pressure in the heart is lower the JVP is lower, if the pressure in heart is higher the venous collapse is higher

123
Q

What effect does skeletal muscle pump have ?

A

It pumps the blood up towards the heart, valves prevent back-flow, rhythmic exercise increase the venous return and therefore stroke volume, static exercise with sustained muscle contraction stops blood from getting back to the heart, if is bad for the heart

124
Q

What effect does respiratory pump have?

A

Respiration causes negative pressure in the thorax and positive pressure in the abdomen, there is bigger pressure gradient and more blood is sucked to the heart, more frequent and deeper breathing allows increase in the venous return and therefore stroke volume

125
Q

What effect does venomotor tine have?

A

There is small amout of muscles around the veins, contraction can increase the venous return, but this has only very small effect

126
Q

What effect does systemic filling pressure have?

A

Pressure created by the heart is transmitted through vascular three, it can create a bigger pressure gradient between atria and veins

127
Q

Why is MAP so important?

A

MAP is the driving force the pushes the blood around in the systemic circulation, when it is too low it leads to syncope, when it is too high hypertension results

128
Q

How is MAP controlled?

A

Control is via altering the CO and TPR, CO is controlled by HR and SV, HR is controlled by nervous system, SV is controlled by preload, after load, nervous system and pathologically, TPR is controlled by radius which is controlled extrinsically (vasopressin, angiotensin II, sympathetic system, BNP, ANP) and intrinsically (active hyperaemia, reactive hyperaemia, pressure auto regulation and response to injury)

129
Q

What monitors MAP?

A

MAP is monitored by baroreceptors in the carotid sinus in the neck and in the arch of aorta, increase in MAP stretches the wall and activated the stretch receptors

130
Q

What is arterial baroreflex?

A

Reflex system that monitors the MAP and keeps in in the correct range, if the pressure is lower there is reduced firing of action potential by baroreceptors, if the pressure is hight there is more stretch and baroreceptors firing increases in frequency, there is set value which is about 80-90 mmHg, frequency of firing is compared to this set value, in medullary cardiovascular centre, the firing rate against the MAP has sigmoid shape, it helps to control MAP in the short term

131
Q

What are the nerves involved in firing the action potential in arterial baroreflex?

A

From aortic arch the signal is sent via vagus nerve, in carotid sinus the signal is sent via glossopharyngeal nerve

132
Q

Where in the brain does the signal from baroreceptors go to?

A

To medullary cardiovascular centre

133
Q

What is the response to the arterial baroreflex?

A

Parasympathetic system activation reduces the HR by hyper polarising myocytes and therefore reducing SV, activation of sympathetic system increases HR, force of contraction and decreases duration of contraction increasing SV, also cause vasoconstriction and increase TPR

134
Q

What other inputs go to medullary cardiovascular centre ?

A

cardiopulmonary baroreceptors, central chemoreceptors, chemoreceptors in muscle, joint receptors, high centres, but these are all minor inputs compared to the arterial baroreflex

135
Q

Where can be cardiopulmonary baroreceptors found and what do they do?

A

in the atria, junction of great vessels and atria, ventricular myocardium and in pulmonary vessels, they respond to stretch

136
Q

Where are central chemoreceptors and what do they do?

A

They are in the brain and respond to the levels of O2 and CO2

137
Q

Where are muscular chemoreceptors and what do they do?

A

They are in the muscles and respond to metabolites concentration

138
Q

Where are joint receptors and what is their function ?

A

In joints, they signal when joints move excessively, they signal from them is relatively small

139
Q

What is the function of higher centres ?

A

It is feed -forward system, they send signals in the anticipation of activity

140
Q

When is the arterial baroreflex important ?

A

In the posture and when sending up, in Valsalva maneouvre

141
Q

What is Valsalva manoeuvre?

A

It is forced expiration against closed glottis, important in defaecation, there is increased pressure in the thorax which gets transmitted to the vessels and MAP increases, next the MAP falls as the venous return causes decrease in CO, the decrease in MAP is detected by baroreceptors and sympathetic system activation increases the pressure, when the manoeuvre is stopped the thoracic pressure increases and it is transferred to the aorta and the MAP drops, there is again normal venous return but the MAP keeps increasing as the baroreflex response is not worn off

142
Q

What is the role of kidneys?

A

They excrete waste products, maintain ion balance, pH, osmolarity and plasma volume

143
Q

What happens in the glomerulus in kidneys?

A

In the glomerulus blood that passes through capillaries gets filtered, almost everything gets filtered except proteins

144
Q

What happens in the proximal convoluted tubule of kidney?

A

In the proximal convoluted tubule water, ions, nutrients get reabsorbed, toxins are removed and pH of the filtrate is adjusted

145
Q

What happens in the descending loop of henle?

A

Water leaves the filtrate into interstitial space via aquaporins

146
Q

What happens in the ascending loop of henle?

A

Ions get reabsorbed into interstitial fluid, it is impermeable to water

147
Q

What happens in the distal convoluted tubule?

A

Selectively secretes and absorb ions to maintain pH and electrolyte balance

148
Q

What happens in the collecting duct?

A

Water can leave the filtrate via aquaporins, the amount is determined by the permeability of the collecting duct that can be altered

149
Q

How kidneys can control the MAP?

A

Kidneys control volume of plasma, if the collecting duct is very permeable the plasma volume is bigger and MAP increases, if the permeability of the collecting duct is decreased little water get reabsorbed and therefore the MAP decreases

150
Q

Name the three system that control the permeability of collecting duct

A

Renin-angiotensin-aldosterone system, antidiuretic hormone, natriuretic hormone

151
Q

Describe the RAAS system

A

Renin is released from juxtaglomerular cells as a result of sympathetic innervation, decreased distension of afferent arterioles and reduced delivery of Na+/Cl- in the glomerulus that is signalled by macula densa, all three mechanisms get activated by reduced MAP, renin converts angiotensinogen to angiotensin I, which is converted by angiotensin converting enzyme to angiotensin II

152
Q

What is the role of angiotensin II ?

A

Angiotensin II stimulates aldosterone released from adrenal cortex, aldosterone cases more Na+ channels in the kidneys, more slats are reabsorbed and therefore more water is reabsorbed into interstitial fluid, this increases the MAP. Angiotensin II also causes increased release of ADH from pituitary that increase the permeability of the collecting duct and increase the reabsorption of water again increasing the MAP. Angiotensin II also causes vasoconstriction and therefore increase TPR

153
Q

Describe the antidiuretic system

A

Antidiuretic hormone is produced in the hypothalamus and is secreted from the pituitary gland, it is secreted as a response to decreased blood volume sensed by cardiopulmonary baroreceptors, increase of osmolarity of the interstitial fluid sensed by chemoreceptors in the hypothalamus and circulating angiotensin II, it increases permeability of the collecting duct and vasoconstriction

154
Q

Describe the atrial natriuretic peptide system

A

It is produced and excreted by myocytes of the atria, it is triggered by increased distention of atria, it increases excretion of Na+ and therefore water excretion too, it also inhibits renin, acts on medullary cardiovascular centre to reduce MAP

Cardiovascular system (18 decks)

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