Cardiovascular system - Cell Biology Semester 2
Why is the cardiovascular system good
It has a large surface area and this is good for the movement of oxygen for efficiency diffusion
For unicellular diffusion is sufficient for oxygen, metabolism and waste tranfer but are dependent on surface area
In multicellular there are system that allow there to be differentiation and better efficiency in types of cells with defined tasks so then better function
What are the advanatge and disadvnatge of specialised systems
Advantages: There is specialisation that improve function and efficicency, there is a defined internal environment that is better for homeostatic control, there will also be more growth
Disadvantage - Specialisation can cause complecity and so more energy costs, there will be cellular competition for resources, cells that are remote from the external environemnt may be slow to respond to change, there is slow diffusion of gases and require pressure gradients
Why is diffusion bad over long distances
This is due to diffusion is slow over larger distances over multiple cell layers so is too slow to provide o2 and remove co2 waste
What is used for movement of substances over long distances
There is the use of bulk flow for the adding of o2 and removal of co2 and waste
It is the movement of fluid down a pressure gradient and diffusion is the movement of molecules down a concentration gradient
What are the differences between bulk flow and diffusion
Bulk flow is pressure gradient dependent and diffusion is concentration gradient
Bulk flow will move the whole solution and diffusion there is movement dependent on solute concentration differnce through the solvent
Bulk flow is rapid and diffusion is slow
Bulk flow needs energy and diffusion is passive and bulk flow is altered by pressure changes due to gravity and then diffusion is altered by solvent, temp, surface area, and gradient
Bulk flow is needed for long distance and diffusion for cellular level
What was the first evolution of the Cardiovascular system
The first CV system used partially open system which then means that the fluid moving out of the vessels and tubes with regions of puming muscles in the tubes
There was a chordate anscestor that had a notochord but not vertabrate column, there were also some aortic arches between the central aorta, which was unpaired and sat more in the ventral plane than dorsal aorta
It is open systen so had sinuses, and there was paired dorsal aorta as well as unpaired dorsal aorta
What was the CV system of the lancelets
It was a closed system and there was muscle pumping in the aortic regions
There was no heart or chambers as well as no valves or true gills
There was a tube all the way through the lancelets and it is always fluid filled
There is also gas exchange all over the epidermis
What was the CV system of the hagfish
There was a basic vertabrate with internal gills with cutaneous respiration meaning can survive in very hypoxic conditions
There are areas of circulatory system that have sinuses in the tissues
There is gas exchange over the skin and so can survive in low o2 areas
There are multiple hearts but the main brachial heart is similar to mamalian heart that send blood to the gills and there are secondary hearts that pump blood back to the main heart
What is the structure of the hagfish brachial heart
There are 2 chambers made of 3 layers- endocardium, epicardium and myocardium
There is defined organisation of pumping due to valves for one way flow of blood
There is a pacemaker region and is alterations in the venous output that respond to ANP/ANF and catecholamines
There is low blood pressure so no need for high oxyegn level so not a refined repiratory system so then no need for a seperation of systemic and repiratory low pressure systems
What is the CV system of fishes
There is a single circuit that has 2 chambered hearts so a single atrium and ventricle
This can happen due to gills have pressure againts it due to fluid water that they are in
What is the CV system of the amphibians
There is a dual circuit with a 3 chambered heart with 2 atria and 1 ventricle
There is a direct laminar flow in the ventricle due to even blood flow from the atria and this mean the sides dont mix and so deoxygenated blood go up to the skin for gas exchange and then oxygenated blood go to the tissues
What is the CV system of the reptiles
There is a dual circuit with 3 chambers heart with 2 atria and a partial septum in the ventricle for partial seperation
There is little mixing of oxugenated and deoxygenated blood in the heart so blood go to necassary tissue dependent on o2 partial pressure
Some of the oxygenated blood can bypass the lung and go back to systemic system to lower pressure in the lung capillary to limit aerobic respiration
What is the CV system in the mammals
There is a dual circuit and a 4 chamberd heart made of a high pressure systemic system and low pressure pulmonary circuit
There are 4 chamber for high metabolic rate so efficient o2 transfer
The lungs interact with air to cause low hydrostatic pressure and so diffusion is slow so need seperation between air and blood vessel to be thin and strong, and also need a lower blood pressure to prevent fluid enter the lungs or thickening of the vessel wall
The general tissue vascular bed is larger and need to control the flow
This means this will need a higher blood pressure in tissues
This means need 2 sperate vascular circuits of one at high blood pressure and one at low blood pressure
The heart will generate blood pressure increase due to generating force
The systemic system will control the flow of blood by creating resistance
When does the mammalian heart develop
It is the first organ developed in the heart and is the final cause of death when it stops beating
There are valves to stop to backflow of blood and the human heart developed starts with 2 parrallel tubes that form left and right side of the heart with an atrium and ventricle either side in a logical world
How does the mammal heart actually develop in the foetus
There are 2 parrallel tubes that fuse together to make primitive heart region to form common heart space that has 2 inflows from bottom and 2 outflow from the top
The inflow enter 1 primitive atrium at bottom of heart and after this then there is differential grwoth when ventricel grow down and push atria up to one side above it so ventricle sit below atria
The atria is then able to grow out into to 2 inflow vessesl so then inflow and outflow both at the top of the heart in both left and right side
What happens to the heart during development
There is the pinching of the central regions to then seperate the atrial and ventricle region and an ingress occur to make the cushions
2 septa grow down to the cushions in atrium to form a right and left atria only to leave a small passage that is closed after birth
A full septum grow up form lowest part of the ventricle to make left and right ones and setum continue to grow into outflow passage to make aorta and pulmonary artey
At the splitting of the atria and ventricle there is formation of AV valves and out outflow vessel splitting there is semi lunar valves made
What are the end results after the mammal heart fully develops
The left hand side will be much thicker than the right due to working with oxygenated blood so a higher blood pressure caused by the high pressure systemic system and then low pressure pulmonary system on the right side of the heart due to being deoxygenated blood
How does blood flow through the heart
There is deoxygenated blood enter in the vena cava and enter right atrium that then force AV valve to open and deoxygenated blood flow to right ventricle and AV valve shut and semi lunar valve open for blood to leave to the lungs via the pulmonary artery
Then oxyegnated blood enter left atrium via pulmonary vein and force open semi lunar valve to enter left ventricle foroicing open the AV valve and shutting the semi lunar valve then the oxygenated blood leave for the body via aorta
What are the cardiomycocytes
The cardiac muscle is similar to skeletal as it is striated so there is commonality between how actin and myosin are arranged
They cardiac mucsles are involuntary so dont rely on hormones or nerves lime smooth muscle that is myogenic
What is the structure of thr cardiomycoytes
There is sliding filament contraction, there are small binucleated cells that have central nucleus with branching cells in a strong network
There are no stem cells
There is automatic contraction with the action potential having a long plateu and a long latent period
There are t tubule invaginations the sarcolemma are larger than in skeletal muscles
There are diads rather than triads of T tubules intrercating with SR and the Ca2+ ion propagtae further into the cells and there are many mitochondria
What is the enery use by the cardiomyoctytes
Cardiac function has a high energy demand and so 30% of the cell is made up of mitochondria
90% of the energy requirements is met by the oxidative phosphorylation so a large consumption of oxygen for the heart to beat 60-70 times per min
The oxygen consumption by myocardium s 20 x higher than that of skeletal muscle at rest
There are many capillaries and myoglobin and the heart density is 2-8 times higher than that of skeletal muscle
Cardiomyocytes maintain high level of oxygen extraction from the blood
But due to having no stem cells it may mean then due to excess exercise the muscles get bigger and so then overrun ability to get oxygen to those cells so then they don’t get enough o2 often found in cyclists
What is the action potential pattern for cardiomyocytes
There is a prolonged action potential up to 200 mseconds
There are slow activated volatge gated Ca2+ channels so a longer action potential so then longer contractions
How is the action potential generated in cardiac muscles
It is generated by the influx of Na+ in gap junctions through the intercalated disks, the Na+ channels are volatge gated and open, they then close and fats K+ channels open, leading to the opening of Ca2+ channels and the closure of the fast K+, the Ca2+ channels then close and slow K+ channels open to then return to resting potential
What is contraction coupling
This is where volatge gated Ca2+ ion channel L type opne in the action potential
Then there are RyR receptors are Ca2+ activated Ca2+ channels in the ER and cause a calcium spark in the SERCA
The Ca2+ is then used to cause muscle conteaction of the heart and are then removed from the ER by Ca2+ pumps that are ATP dependent and pull Ca2+ back to the SR
Na+ antiport transporters system lined with Na/K ATPase as well as Sarcoplasmic reticulum calcium pumps - SERCA in the ER as well as Ca2+ uniport in the mitochondria
What happens when calcium enter Sarcoplasm
The calcium will bind to the cardiac tropomysoin and cause a conformational change that will move the tropomysoin away from the myosin actin binding site on the actin, this will then cause the formation of myosin actin cross bridges to then allow muscle contraction by sliding filiament theory
What is the muscle banding pattern in the heart
There is the banding pattern in the cardiac muscles due to the mysoin and actin, this means when there is contraction it will elad to greater overlap between filaments and so H and I band change width during contraction but sarcolemma length stay the same and M line stay the same
What are the thin filaments of muscle in the heart
Actin- thin filaments of 2 stranda that are arranged in an alpha helix formation of G actin that can turn to F actin with a + and - end
Tropomyosin is a double helix that will lie between groves of the actin and in the resting state will block the binding of myosin
Troponin- Made of 3 subunits that sit along the actin at intervals: TnT will tie the actin and tropomyosin molecules, TnI will inhibit ATPase in actin myosin interaction, TnC bind calcium ions to regulate contractile process pulling the tropomysoin from the myosin binding site
What is the structure of myosin
It is made of 2 heavy chains that have a tail in an alpha helix dimer and also the globular head sites for the myosin ATPase activity and actin binding
There are 4 light chains that are needed for regulatory of the myosin function
There is thick filament assmebly due to binding of many indiviudals myosin molecules together that have multiple heads branching out
what is the complete sarcomere
The I and H band change during contraction
The light filaments are attached at the Z line and held play by the actin
There is think filaments that regulate where the Z lines are protected in regards to each other in the sarcolemma
The myosin filament will be held in place by protein called obscurin on the M line
Sarcolemma can then interact with outside of the cell via desmosomes and intergalted disks as well as the plasma membrane by anchorin and dystrophin that intercat with sarcoglycans and dystroglycans
What are the stages of contraction
S1- The calcium will bind to the troponin and cause the conformational change by pulling the troponin T and tropomyosin to expose the mysoin binding site on the actin
S2- There is release of ADP + Pi from myosin to induce the power stroke and cause myosin head to pivot and pull the actin to cause contraction
S3- This will expose the ATP binding and a new ATP molecule will bind to myosin head
S4- Cause the head to then detach from the actin and ATP is hydrolysed to impart energy for cocking and reattachement if Ca2+is present
If there is no ATP then remain at S2 and there is constant myosin actin binding to cause rigomorsis
What is the refractory period
This is the state after a response to the stimulu where the same stimuli lead to no response, this is due to in cardiac muscles the voltage gated Na+ and Ca2_+ channels have refreactory periods where they wont open immediatle
In an absolute refractory period there can be no action potential generated but in a relative refractory period there may be a new action potential if there is a greater new stimuli
What are the effects of the refractory period - Tetanus
In skeletal muscles there are relative refractory periods but this is much shorter in cardiac muscles and this can lead to if a rapid large stimuli summation of the muscles that then may develop to incomplete tetanus and then to full tetanus if the stimuli keep growing
What are the effects of the refractory period - action potential length
There is a longer action potential in the cardiac muscles it means that summation and tetanus cant occur, this is a good thing due to the needed time of relaxtion between the action potentials to allow cardiac filling in the heart and to prevent the heart muscle from tiring and so ATP can be regenerated
What does no tetany mean for the heart
It will result in there being greater ability to increase the strength of the beat and this is done by adding more pressure by filiing the heart with more blood
What is the Frank Starling law
This is where the greater the initial length of the sarcomere then the greater the force of the contraction and so a greater blood volume pumped out
Can increase the length of the sarcomere by adding more fluid to the heart and the length is variable due to no bone to fix to and so is directly dependent on the volume of blood in the heart for the length
What type of muscle is the heart
The heart is a myogenic muscle due to activity not controlled by the nerves and it is autonomous but the rate can be altered by nerves
How does the overall heart have 1 beat
The are some cardiac muscles that may have different inherent beats but if they come into contact then gap junctions are made and the quicker cell will dominate the other cells and they both end up beating at the faster rate, the fastest cell will decide the overall heart rate but there may be smaller groups of differing beats at the same time
How is tje heart rate controlled and coordinated
Due to the latent period and the gap junctions the beating becomes coordinated with the action potentials spreading from 1 cell to another and so then all cells end up having same beat
There is an inherent pacemaker and coordinated pattern of contraction
If the beating of the cells arent the same then heart will fail to pump blood as the blood pumping will be uneven = Fibrillation
How is the heart beating order of process
Atrial contraction when the ventricle are relaxed and blood is pushed down through the AV valves in atrial systole
Then the ventricle will contract and close AV valves and opne semi lunar valves and blood will pump out in ventricle systole
Then both will atria and ventricle will relax to allow heart to refill during diastole
How is the regulation of the heart beat achieved
There is electrical seperation of atrial and ventricle functional syncitia and physical seperation of the atrial and ventricular chamber due
There are neuromyocardial cells that initiate and conduct impulses as well pacemakers that set frequency of heart beats
Conducting cells - give a coordinated beat as the bottom of ventricle contract before the walls of the ventricle
The strenght of the beat is controlled by: Degree of blood filling, resistance of peripheral vasculature and nervous control
What are the 2 functional syncytia in the heart
There is the atrial and ventricle syncytia that are electrically seperated from each other
There are fibrous heart skeleton formed between the atria and ventricle made of dense irregular connective tissue
This skeleton is to provide a rigid framework for the attachment of cardiac muscle as well as anchoring the heart valves by forming rings of attachement points
It will also help to form endocardial cushions and seperate the atria and ventricle physically and electrically and also give insulation so then impusles dont randomly spread through the heart
What are the AV valves
The AV valves are formed of tricupsid and mitral valves, these valves are made of conective tissue and large amounts of collagen and elastic fibres
They are held in placr by chordae tissue that are strands of connective tissue that bind distal parts of the valve to the heart wall and are vital for valve structure
What are neuromyocardial cells
These cells will initiate and conduct the cardiac impulses
What does the pacemaker of the heart do
There is a pacemaker located in the sino atrial node that will set the heart beat frequency and it is an oval shaped mass below the epicardial surface4 in the right atrium near the vena cava
It will bgeat 60-100 x per min ans cause impulses to spread along cardiac muscle fibres of the atria and along the internodal tracts to a 2nd node
What does the nodal cells do
These are small poorly striated compared to myocardial cell
They have connective tissue surrounding them to seperate the, from the muscle insulated by collagen
As you get older there is more collagen laid down and so the heart signals wont escape from the muscle causing failure of the heart so more collagen laid down
How is the action potential passed around the heart
It will come from the SA node and be passed down internodal tracts to then spread along the Right atrium to the atriventriocular node
This then will cause the action potential to slow to allow atrium to beat before the ventricle contracst as the action potential is passed down conducting fibres in the bundle of his beofre finishing at the Perkinje fibres
The heart apex beat beofre the heart walls
What are the Purkinje fibres
They are the inner venctricular wall beneath the endocardium and are large specialised conducting tissue larger than the cardiomyocytes and with few myofibrils and large mitochondria number
They will conduct act6ion potentials quicker due to being large to then allow synchronised contraction of the ventricles
Carry the action potential through the heart
What is the overall conducting system of the heart
It is initiated by the pacemaker at 60-100 beat/min and then conduction will spread along the muscle fibres of the atria and the internodal tracts and bachmanns bundle
The impusle is then carried to the ventricles acorss firbous skeletonn at the Atrioventricular node and passed the interventricular wall by the bundle of his that then divide to purkinje fibres
How are the apsects of the conducting system adapted
The AV and SA nodal cells are modified cardiac muscle cells and so work at a 4x faster rate to normal heart cells
The AV bundle and Purkinje fibres are modified cardiac cells as well
Where do the parasympathetic nerve supply and sympathetic nerve supply end
They both will terminate at the SA and AV nodes
What cells arde found in the heart wall
There are muscle cells, excitory pacemaker and conducting cells, endothelium cells, fibroblasts, axons and epithelium cells that line the wall of the heart
Where are Purkinje fibres found
They are just beneath the endocardium layer and are able to conduct the AP quicker than the myocytes so along with refractory period allows there to be syncchronised contraction of the ventricles
What is the epicardium
This is the site of the coronary vessels, myocardium and the epicardium
It is made of loose tissue with both autonomic and adipose tissue
It is comtinuoos with the pericardium and covered by the simple epithelium that secrete lubricating fluid to allow heart to move as without this lubricant the heart would stick to the chest
What is the order that action potential go through the heart
It will start in the Sino atrial node, to then go to the atriums that then will pass to the AV node to then spread to the purkimje fibres and then finally the action potential will pass to the ventricles
How are muscle cells and purkinje fibres similar
This is due to have a similar action potential but in the atrial muscle the Ca2+ ingress is much shorter so then result in the shorter systole
The longer action potential that then the longer the refractory period and this will cause the diastole
How are the action potential of the nodes similar to the rest of the heart
Due to less stable resting potential so then there will be more permeable to Na+ and closer the threshold
There is Na leaking and this is called the funny currents due to the HCN channel and causes the instability
There will be gradual lead to the threshold so then T and L Ca2+ channels open to cause action potential that is then stopped by the K+ channels to return the node to resting potential
What does the ECG measure
Will measure the change in potential over the membrane during the action potential and resting potential of the heart, but it is not a measure of the AP but the AP will cause it
What causes the ECG and potential change
It is the potential difference over time that cause the summated vectoral flow of the charge at the skin surface caused by heart AP to then change the convection currents running + --> -
The current will only run when there is a difference in potential difference between the electrodes
The overall ECG reading is the vector component of the direct6ion of the lead flow between the electrodes
The leads and wires are the tracing between the 2 electrodes
What is the electrocardiogram showing
It is a graphic reading of the chaneg in the heart of the total electromotive forces of the heart
The signal is related to the size of the potential differnce, the page the lead is in so the line between the 2 electrodes , the vectored summation of the current due to multiple heart cells and the direction of the charge in relation to the electrodes
What is the Lead number 1
It will run from a + electrode on the left arm to a - electrode on the chest or wrist as it makes no difference as both will pick uo the same signal in resting indiviudal as main charge change is due to the heart
What is the typical ECG reading
The chart will be ste to 10mm- 1mV and there are 5 main waves that will be seen on the chart
P waves are caused by the atrial depolarisation
Q wave are due to the initial depolarisatio of the heart wall
R waves are due to the inner part of the ventricle depolarising
S wave is when the main part of the body is depolarsing in the heart
T wave is for the repolarisation of the heart
There may be very rare U waves caused from the depolarising of the purkinje fibres
What happens in the heart to cause the ECG waves
The depolarsiation spread over the atrial surface from the SA node and the vector is downward and left so = P wave
The atria will contract and the electrical passageway only cross at AV node which slow the passage of P-Q waves
Q wave is formed due to the summation of the atrial polarisation wave and the interventricular wall depolarisation wave
R wave is formed due to inner wall of the ventricle depolarise
S wave is from outer ventricle wall depolarise
The the ventricle will contract and then there is repolarisation from apex of the heart to the base of the heart = T wave
How do you extend an ECG beyond 1 lead
A single pair of electrodes can give electrical activity in 1 axis but it can be extended by doing 3 leads:
Right arm to left arm , Right arm to left foot or left arm to left leg
The size of wave may then change depending on the lead angle as well as angle of deflection and vector and summation of AP
Using the 3 leads will give heart rates and together show transmission defects where waves have been lost such as AV node fail on different new axis
What is Eindhoven triangle
Is where all 3 leads all give a rise to a different R wave
What is eindhoven law
The difference between the vector and the potential difference of each of the leads is =
Lead 1- Potential difference on lefr arm - potential difference on right arm
Lead 2- Potential difference on left leg - Potential difference on right arm
Lead 3 - Potential difference on right leg - Potential difference on left arm
Lead 1 + Lead 3 = potential difference on left leg - potential difference on right arm = lead 2
What is the electrical axis of the ventricle
Can calculate the angle of depolarisation for the total ventricel using the angle caused by the summated depolarisation in any 2 leads
Need to use triganometry
Can calculate a vector sum of the 2 leads total summated values of the waves involved
Why can we double up leads
It can be useful to use lead positions and double them up by joining them together and feed them together to a new location
Join the 2 arm currents together in a new position of the middle of the chest which will = an augemented lead and then can use this to compare to the potential difference of the left leg and S wave is running vertical now
Why do we triple up some leads
Can join together the 2 arm and the left leg into 1 treble lead and the feed to voltmeter and then use another moving electrode in another voltmeter that move across the chest so multiple different planes of info on the ECG
What do valves do
Give an efficient one way flow of blood and failure will lead to cardiac function and they are passive so open in response to pressure changes in the heart chambers
What do all the waves of the ECH cause in the heart
P wave will start and this means the atria will contract and push blood to the ventricle so force the AV valve open
Then the Q wave where the wall of the ventricle start to depolarise and then the ventricle starts to contract
Initially the Aortic Valve is closed and so then increase the pressure due to ventricle contraction so that there is greater pressure in ventricle so then force the Valve open
The go to T wave where get relaxation and repolarisation of the
ventricle so then the AV valve close and heart will relax
What is sinus
These are related to changes at the SA node and are generally parasympathetic causes
There are 2 types:
Sinus tachucardia where the Heart rate is 130 at a regular rhythm and due to shock, anxiety or fever
Sinus Brachycardis where the heart rate is 50 at regular rhythm in fit athletes, but also hypothermia and Carotid sinus syndrome
What are the changes in the electrical axis of the ventricle
The heights of the QRS ventricular complex can be used to define the ventricular axis
The angle of the summated vector of heart depolarisation is between +90 - -30
There however may be a left sided deviation leading to:
<-30
Deep breathing via expiration and Obesity
There may be aortic valve stenosis or regurgitation
There also may be right sided deviation leading to :
>+90
Deep breathing via inspiration and may be from standing up tall
Right sided hypertrophy
Pulmonary hypertension
Pulmonary valve stenosis or regurgitation
What is fibrillation ECG
atrial = Irregular rhythm, 90bpm, There are chaotic P waves and no P-Q interval time
Ventricular = Chaotic rhythm and heart rate and also then an absent P wave, P-Q interval amd mo QRS waves either = This is lethal due to no cardiac output during it
What is the peripheral system
The blood vessels are organised into 3 concentric layers called the intima, media and the adventitia and these are present in all blood vessels except capillaries
What is the Tunica intima
The tunica intima is the most inner layers and is mainly endotheelium that line lumen of the vessel, there are 3 layers called squamous endothelium then the basal lamina and then the subendothelial layers
In arteries there are internal elastic fibres in the subendothelila layer
What is the tunica media
This is the middle layer of the 3 layers and is made of smooth muscle and elastic fibres
There is circumferential smooth muscle layer and elastin between the smooth muscles in thicker artiers
There is external elastic membrane to seperate the media and adventitia
What is the tunica adventitita
This is the outer most layer and is made of collagen fibres
There are longitudinal colleganous tissue that is thin in arteries and thicker in veins
In larger artiers and veins there are vessles that supply blood to the cells of the wall and a network of autonomic nerve to control smooth muscle
What is the role of endothelium
This is for selective permeabilty of molecules - allow small lipid soluble to enter via diffusion and others need transport pathway
Non thrombogenic barrier - Prevent blood clotting between platelets and subendothelial tissue
Modulation of blood flow and resistance - Effect on smooth muscle by secretionof vasoconstrictors and dilators to regulate lumen width
Immune response regulation - Control the interaction of neutrophils. Lymphocytes and monocytes with the endothelial surface that have selectins that attach to carbohydrate groups on white blood cells and modify them
Hormonal synthesis - Regulate growth factor by hormone synthesis
What is the structure of blood vessels
There are thick walls in arteries to resist the high blood pressure and also elastic walls in the arterioles to allow expansion and retain BP at diastole, to prevent aneuryssm
In veins there are thin walls to allow distension and also have muscles to increase venous return of blood back to the heart and valves where needed as well
As vessels get smaller there becomes less muscle
What are arterioles
These are the major point of majore pressure drop due to their being very high resistance for blood flow and so there is les muscle here due to smaller vessel
What do venules and smaller veins do
These are a major reserve for blood and will decide how much will be bought back to the heart, the smooth muscle is to resist the pressure of the blood coming out of the heart
When the blood vessel cant cope with the pressure it will burst and cause an aneurysm due to the weakening of the smooth and elastic wall in the venules
What is the normal blood pressures
In the systemic system it is around 120/80 mg/Hg this is due to the elasticty of the arterial vessels so there is diastolic pressure so there is some flow even at diastole
You can measure the flow of the blood as 80=1M and 120=1.6M so then show the pressure of the aorta between 1-1.6M above the heart and this will be enough to overcome resistance
In the capillary there is pressure of 10.5-22.5 mmHg and so due to the elasticity of the arterial system there is no beat in these vessels and the flow is dependent on the opening of the capillary bed
In the Pulmonary system it is 15/8mmHG which mean about flow of 0.35M as the lungs are a low resistance system due to a lack of tissue in the capillaries, due to the need for thin walls due to gas exchange so is under low pressure to avoid them bursting
What are the pressure and volume changes in the heart
The heart generate the force for the blood pressure and circulation will control blood flow bases in vessel resistance
The greatest pressure drop in the systemic arterioles as well as small pressure drop in capillaries due to fluid leaving capillary bed
There is very low pressure in the venous system before enter pulmonary side with still low pressure
The amount of blood going through the system is same no matter what vessel you are in but amount of blood in each tube is different
The blood volume leaving right side = Volume of blood leaving the left side of the heart
What is the blood flow in the aorta
330mm/s and in surrounding capillary is 0.3mm/s so 1000x less
The capillary length is around 0.3-1mm so then blood is in them for enough time for gas echange to take times = 1-3 seconds in the capillary
What are the 3 types of circulation
Pulmonary is where blood flow from right ventricle to lung to left atria under low pressure and resistance
Systemic peripheral the blood flow from left ventricle to capillary bed to right atria under high pressure and varying resistance due to changing tissues
Cardiac system the blood flow from left ventricle to aorta to coronary artery to cardiac muscle to then right atria under high pressure
How is the cardiac circulation different
In normal conditon the blood enter the tissue at systole when heart beat is the strongest but in the heart the blood vessel go between muscle cells so enter at diastoole when heart is relaxed so the vessels not blocked by contraction so need diastolic blood pressure
There is also poor collateral blood flow in brain and heart so this means if the vessel cant get blood to the tissue then it will die due to no other way to get blood to these tissues = clot or stroke
In the heart there are few stem cells so damage is hard to be repaired so have to sue infarctions using fibrose tissue but no cells can be regenerated = loss of function
How is blood returned to the heart via veins
The large veins will have very low resistance and pressure but the venous pressure dependent on location its highest in legs and lowest in head when standing due to mercury collect at bottom due to gravity
The venous pump is surrounded by extravascular muscles that compress veins to squeeze blood through to make low pressure blood flow
There are valves to stop backflow and direct blood back to the heart and the venous retuen will need muscle activity, due to am artery found next to vein the pulse is enough to cause contraction of extravascular muscle to force blood back to heart
What happens if person stands still for long time
There will be pooling of blood at the bottom of the legs due to gravity and also no extravascular pumping, there will also be swelling due to capillaries increasing causing fluid to leak into tissue space - very extreme on the plane
Valves can fail and get varicose veins where not all blood is pumped to the heart
How does hydrostatic pressure cause extravascularisation
There is greater hydrostatic pressure in tissues when standing upright and also loss of pressure in the capillaries due to leak out to capillary bed
This means that system is not completely closed system as some leaking of extra vascular fluid so there needs to be retrieval system for this leaking fluid
This can be done by lymphatic vessel to return extravascular fluid back to the circulatory system
Why are lymphatics needed to retrun fluid to the blood
The lymphatics will return the fluid from tissue to the blood stream by first the lymphatic capillaries that are blind ended so have 1 opening and the other end just close
These capillaries are overlapping endothelial cells as well as a continuous basal lamina that is highly permeable for returning fluid
These capillaries then drain to the lymphatic vessels that will fuse to form right lymphatic trunk and the thoracic duct that then empty into the jugular and subclavian veins above the heart as there is a pressure of 0 or negative to atmospheric pressure so makes it easy to return the fluid to the blood
The lymphatic vessels have valves that prevent the backflow of the blood but there is no central pump so the fluid is driven by the compression of the adjacent skeletal muscles
Before the fluid is returned to the blood it is exposed to the immune system in lymph nodes to remove any pathogens and prevent them returning to the blood
The blockage of major lymph vessels will lead to the build up of extracellular fluid and will cause tissue swelling
Why does CVS system need to be regulated
Running of the CVS is extreme energy expensive due to the need to supply sufficient nutrients to then remove waste from metabolising cells as well to match tissue demand to perfusion demand
It can be controlled in a whole body way:
-This is done by regulating: circulating blood volume, Autonomic nervous system to effect blood flow to areas when stressed, circulatory response in the when can increase HB by sending more blood back to heart
Can also be done in local way in different regions at different times
This can be done by tissue Ph change as well as change NO regulators concentrations
How is the CVS regulated
Overall volume control
This can be done by ADH, renin , ANF-angiotensin and aldosterone levels in the endocrine system and the kidneys
Control of local blood flow
At resting Cardiac output can increase from 5l per min to 35L per kin depending on environment and stress and this needs regulations
More related to returning blood to the heart and also the regulation of loss of fluid by leaking and how it return to the pump to then go back to the blood
What is cardiac output
The sum of the local blood flow to the tissues and it depends on venous return as the heart only pump what it receives
If tissues are active then the metabolism will increase by 20x so then same increase in demand for oxygen and glucose but the heart output can only increase by 6x and the O2 release from a given volume of blood only go up 3x and then other nutrients are also needed
This means it is not possible to then simply increase blood flow to meet the demand so the regulation flow is specific to certain tissues that need O2 at the certain time
How is there local blood flow regulation
Micro vessels that monitor O2 and nutrient level as well as Co2 and waste production as well as regulating the flow into a tissue via precapillary sphincters so then alter the return of blood to the heart by changing resistance to let more of less blood to a region
The heart will automatically respond to the sum of all these= Frank Starling Law
What are the main regulators of blood flow
Vasodilators acting on the pre capillary sphincter such as ADP,AMP, Histamine and K+ and H+
Can also have a lack of oxygen and nutrients so sphincters will open up
These will cause
Active Hyperaemia when there is greater blood flow to a tissue during localised work
Can also cause reactive hyperaemic that is caused after a block of blood flow to a specific region
What does No signalling do for CVS
Cause overall smooth muscle contraction due to:
O2 + Arginine with eNOS hormone --> NO + Citrluine
The NO made then will go to GTP --> cGMP that then will cause relaxtion