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
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
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
4
Q
What are the exceptions in vascular arrangement?
A
Hypothalamus and pituitary, gut and liver
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
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
7
Q
What determines the flow?
A
Pressure gradient / resistance
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
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
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
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
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
13
Q
Which valves are exist valves and entrance valves
A
Pulmonary and aortic are exit valves, tricuspid and mitral are entrance valves
14
Q
What opens the valves ?
A
Pressure differences, it is passive process
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
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
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
18
Q
What are the two types of cardiac muscle cells ?
A
Non-pacemaker and pacemaker cells
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
20
Q
What are L type Ca2+ channels ?
A
They are long lasting activation channels, they are open by voltage
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
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
23
Q
What are T type Ca2+ ion channels
A
They are transient opening, low voltage activated, have fast voltage dependent inactivation
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
25
How L type Ca2+ channels blockers modulate electrical activity of the heart?
They block the L type channel, less Ca2+ in and so the force of contraction is weaker
26
How cardiac glycosides alter the electrical activity of the heart?
Cardiac glycosides cause build up of Ca2+ ions, and therefore increase the strength of contraction
27
How does temperature affects the electrical activity of heart?
Increase in HR by 10 beats per every degree, in fever the heart rate is higher
28
How does hyperkalemia alter el. activity of heart?
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
29
How does hypokalemia affects el. activity oh heart?
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
30
How does hypercalcemia affect the el. activity of heart?
More Ca2+ can enter the cell, this leads to higher HR and stronger force of contraction
31
How does hypocalcemia affect the el. activity of heart?
There is fewer Ca2+ ions in the plasma, fewer enter the cell, decreases HR and force of contraction
32
How does hypercalcemia affect the el. activity of heart ?
There are more Ca2+ ions in the plasma, more Ca2+ into the cell, increased HR and force of contraction
33
What is sinoatrial node?
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
34
What is annulus fibrosus?
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
35
How does the condition spreads from SA node to AV node?
Via internodal tract, there is also Bachmann's bundle to left atrium
36
What is AV node?
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
37
What are bundle of his and Purkinje fibres?
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
38
What is Bundle of His?
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
39
What are Purkinje fibres?
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
40
What leads does ECG consist of?
Standard limb leads, augmented leads and
41
Name the standard limb leads
SLI (from left arm to right arm), SLII (from left leg to right arm), SLIII (from left leg to left arm)
42
Describe how is ECG recorded
The wave of depolarisation is detected, it passes down to ventricles and then through bodily fluids and to electrodes where it is recoded
43
What is PR interval?
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
44
What is QRS complex interval?
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
45
What is QT interval?
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
46
Describe the parts of the QRS complex
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
47
Explain why depolarisation is positive blip
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
48
In limb leads which has the bigger R wave and why?
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
49
Name the augmented leads
aVR, aVL, aVF
50
What happens to R wave in augmented leads?
aVL has postive R wave, aVL has no R wave and aVR has negative R wave
51
What are pre-cordial leads?
Six leads on the chest, they record what happens on the transverse (horizontal plane), V1-V6
52
What happens to R wave in precordial leads?
R wave is negative in V1 to around V3-4 where it changes to positive, there is R wave progression
53
Name the stages of cardiac cycle
Late diastole, atrial systole, isovolumetric ventricular contraction, ventricular ejection, isovolumetric ventricular relaxation
54
Describe what happens in the late diastole phase
All chambers are relaxed and are filling passively
55
Describe the atrial systole
During the atrial systole the atria contract and force the last amount of blood out to the ventricles
56
Describe the isovolumic ventricular contraction
The ventricles contract and increase the pressure pushing the AV valves closed, there is increased pressure but there is no change to the volume
57
Describe the ventricular ejection phase
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
58
Describe the ventricular isovolumic relaxation phase
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
59
What is the relative duration of systole and diastole in the cardiac cycle?
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
60
Describe the pressure changes in the ventricle during cardiac cycle
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
61
During which part of the cardiac cycle there is rapid change in the pressure in ventricles ?
There are rapid changes to the pressure during isovolumic ventricular contraction and relaxation
62
What is the maximum and minimum pressure in the ventricles?
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
Describe the pressure changes that occur in the aorta
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
What is the minimum and maximum pressure in the aorta and what is dicrotic notch?
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
What is the average pressure and pulse pressure
The average pressure is diastolic pressure plus 1/3 of pulse pressure, pulse pressure is the difference between systolic and diastolic pressure
66
Describe the changes of pressure that occur in atria
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
Describe how the volume of ventricles changes during cardiac cycle
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
What is end diabolic volume ?
Is the the volume of blood in vehicles at the end of diastole, it is around 140 mL
69
What is end systolic volume ?
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
What is stroke volume ?
The amount of blood pumped out during one contraction, it is usually 80 ml
71
What is ejection fraction ?
The fraction between stroke volume and end diastolic volume, in healthy individuals it is about 2/3
72
What is rapid ejection and filling?
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
At what heart rate does the filling phase change?
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
Compare the pressure in the right side of the heart to the left side
Pressure in right side is much smaller than in the left side, it is about 1/5 of the left ventricle
75
What is the pressure in right ventricle?
The systolic pressure is about 15-25 mmHg,diastolic is 0-8 mmHg, which is similar to the pulmonary circulation
76
What is phonocardiogram?
recording of heart sounds during the cardiac cycle
77
What is first heart sound?
First heart sound corresponds to closing of mitral valve and tricuspid valve, caused by turbulent blood flow as the valves close
78
What is second heart sound?
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
What is the third heart sound ?
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
What is fourth heart sound?
Corresponds to active filling phase as atria contracts, not usually heard
81
What are the types of murmur that can be heart?
Systolic, diastolic, murmur throughout the cardiac cycle correspond to septal defect
82
What can regulate heart rate ?
Heart rate can be regulated by neural control
83
What can regulate stroke volume ?
Preload, after load, neural, pathological
84
Describe the Starling's law
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
How is stroke volume regulated by preload?
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
How is stroke volume regulated by afterload?
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
How can the stroke volume regular by neurones?
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
How is stroke volume regulated pathologically ?
Hypercalcemia shifts the cure up and left, hypocalcemia shifts the curve down and right, ischaemia down and right , barbiturates down and right
89
What happens during exercise?
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
Give the equation for cardiac output
CO =SV x TPR
91
What is met arteriole?
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
Name the anti-clotting mechanisms of the endothelium
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
What happens to hydrostatic pressure and oncotic pressure as the blood moves via circulation
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
What is filariasis?
Infection with thread-like parasite, it is tropical disease, blocks the lymphatic system
95
Name the causes that can lead to oedema
Lymphatic obstruction, increased venous pressure, hypoproteinemia, increased permeability
96
What is Darcy's law?
It states that flow is proportional to the pressure difference / resistance
97
What is Poseuille's law?
It states that resistance in proportional to L and viscosity / radius4
98
What is the fundamental equation of cardiovascular system?
MAP = CO x TPR
99
What is MAP?
Diastoloc pressure + 1/3 pulse pressure
100
What are the two main mechanisms for regulating MAP?
Extrinsic and intrinsic mechanism
101
How is the MAP regulated by neural activation?
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
How is the MAP controlled by hormones?
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
Name the 4 components of the intrinsic control
active hyperaemia, pressure autoregulation, reactive hyperaemia, injury response
104
What is active hyperaemia ?
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
What is pressure auto regulation?
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
What is reactive hyperaemia?
It is extreme version of pressure alteration, for example occlusion of blood flow causes accumulation of metabolites and subsequent dilation
107
What is the injury response?
Nociceptive C fibres release substance P that causes mast cells to release histamine, histamine causes vasodilation and increases permeability
108
Why are coronary arteries special?
They have opposite circulation to the systemic, blood flow is stopped during systole and occurs during diastole, also has many beta 2 receptors
109
Why is pulmonary circulation special?
Reduction in O2 leads to contraction and not dilation like in other arterioles
110
Which two circulations show great pressure auto regulation?
Cerebral circulation and renal circulation
111
What is the name of the sounds of blood when measuring BP?
Korotkoff sounds
112
How can be BP measured?
Using sphygmomanometer and stethoscope
113
Describe the Korotkoff sounds
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
What does affect the rise in pressure of blood?
Stroke volume, ejection velocity, elasticity of aorta
115
What does affect the declining pressure of blood?
Total peripheral resistance
116
What happens to BP during exercise?
The systolic pressure increases whereas the diastolic pressure decreases
117
Where is the circulation there is variation in pressure ?
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
What is systemic filling pressure?
It is the difference between pressure in veins and right atrium, it is quite small about 5-20 mm Hg
119
Describe the velocity changes of blood as it flows through systemic circulation
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
Name the 5 factors that affect veins
gravity, skeletal muscle pump, respiratory pump, venomotor tone, systemic filling pressure
121
Describe the effect of gravity on venous system
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
How can be the height go jugular venous collapse be used?
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
What effect does skeletal muscle pump have ?
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
What effect does respiratory pump have?
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
What effect does venomotor tine have?
There is small amout of muscles around the veins, contraction can increase the venous return, but this has only very small effect
126
What effect does systemic filling pressure have?
Pressure created by the heart is transmitted through vascular three, it can create a bigger pressure gradient between atria and veins
127
Why is MAP so important?
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
How is MAP controlled?
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
What monitors MAP?
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
What is arterial baroreflex?
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
What are the nerves involved in firing the action potential in arterial baroreflex?
From aortic arch the signal is sent via vagus nerve, in carotid sinus the signal is sent via glossopharyngeal nerve
132
Where in the brain does the signal from baroreceptors go to?
To medullary cardiovascular centre
133
What is the response to the arterial baroreflex?
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
What other inputs go to medullary cardiovascular centre ?
cardiopulmonary baroreceptors, central chemoreceptors, chemoreceptors in muscle, joint receptors, high centres, but these are all minor inputs compared to the arterial baroreflex
135
Where can be cardiopulmonary baroreceptors found and what do they do?
in the atria, junction of great vessels and atria, ventricular myocardium and in pulmonary vessels, they respond to stretch
136
Where are central chemoreceptors and what do they do?
They are in the brain and respond to the levels of O2 and CO2
137
Where are muscular chemoreceptors and what do they do?
They are in the muscles and respond to metabolites concentration
138
Where are joint receptors and what is their function ?
In joints, they signal when joints move excessively, they signal from them is relatively small
139
What is the function of higher centres ?
It is feed -forward system, they send signals in the anticipation of activity
140
When is the arterial baroreflex important ?
In the posture and when sending up, in Valsalva maneouvre
141
What is Valsalva manoeuvre?
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
What is the role of kidneys?
They excrete waste products, maintain ion balance, pH, osmolarity and plasma volume
143
What happens in the glomerulus in kidneys?
In the glomerulus blood that passes through capillaries gets filtered, almost everything gets filtered except proteins
144
What happens in the proximal convoluted tubule of kidney?
In the proximal convoluted tubule water, ions, nutrients get reabsorbed, toxins are removed and pH of the filtrate is adjusted
145
What happens in the descending loop of henle?
Water leaves the filtrate into interstitial space via aquaporins
146
What happens in the ascending loop of henle?
Ions get reabsorbed into interstitial fluid, it is impermeable to water
147
What happens in the distal convoluted tubule?
Selectively secretes and absorb ions to maintain pH and electrolyte balance
148
What happens in the collecting duct?
Water can leave the filtrate via aquaporins, the amount is determined by the permeability of the collecting duct that can be altered
149
How kidneys can control the MAP?
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
Name the three system that control the permeability of collecting duct
Renin-angiotensin-aldosterone system, antidiuretic hormone, natriuretic hormone
151
Describe the RAAS system
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
What is the role of angiotensin II ?
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
Describe the antidiuretic system
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
Describe the atrial natriuretic peptide system
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
