4.3 - Circulation Flashcards
What is tissue fluid?
- is the watery fluid that surrounds individual cells and creates their environment
- it is formed from blood plasma at the arteriole end of the capillaries
- it is made from substances that leaves blood plasma
- it contains: glucose, amino acids, ions and oxygen
- unlike blood, tissue fluid does not contain blood cells or big proteins as they are too large to be pushed through the capillary walls
- in capillary beds substances move out of the capillaries into the tissue fluid by ‘pressure filtration’
What is the purpose of tissue fluid?
- is how materials are exchanged between blood and cells
- cells take in oxygen and nutrients like amino acids and glucose from the tissue fluid and release metabolic waste into the tissue fluid.
- essential for the efficient exchange of materials
How is tissue fluid formed?
as blood passes through capillaries some plasma leaks out through gaps in the walls of the capillary to surround the cells of the body - this results in the formation of tissue fluid. (high hydrostatic pressure forces the fluid out of the capillaries at the arteriole end)
What does the formation of tissue fluid depend on?
- the volume of liquid that leaves that plasma to form tissue fluid depends on two opposing forces:
1) Hydrostatic pressure
This is the pressure exerted by a fluid eg. blood. High hydrostatic pressure develops in the arteriole end of the capillary due to the heart-pumping
2) Oncotic pressure
This is the osmotic pressure exerted by plasma proteins within a blood vessel
It is the tendency for water to move into the capillaries.
(plasma proteins lower the water potential within the blood vessel, causing water to move into the blood vessel by osmosis)
high hydrostatic pressure than oncotic pressure means that the fluid is forced out of the capillaries
when oncotic pressure is greater than hydrostatic pressure fluid moves back into the capillaries
Why does the pressure change from the arteriole end to the venous end?
The hydrostatic pressure is high at the arteriole end due to the heart pumping and the oncotic pressure is less than the hydrostatic. At the venous end, the oncotic pressure remains but is greater than the hydrostatic pressure due to the loss of fluid and increase in plasma proteins. This lowers the water potential so the fluid will move into the capillaries. This pressure and fluid movement change is needed as we need constant movements of substances and substances like O2 in this fluid need to be replenished.
What are the stages of tissue fluid formation?
1) Blood in the arteriolar end of capillary has high hydrostatic pressure, meaning it has a high water potential
2) Because it has a lot of water, it also has lots of dissolved ions and small molecules like oxygen, glucose and amino acids
3) These molecules, including water, are small enough to be forced out of the capillary lining because of this pressure.
4) This is called ‘ultrafiltration’ as only small molecules are forced out of the capillaries. Cells and proteins remain in the blood as they are too large to cross the membrane.
5) By the time blood arrives at the venous end of the capillary, the blood has lost some water and ions, so has a reduced hydrostatic pressure.
6) Due to fluid loss, and an increasing concentration of plasma proteins (which don’t leave capillaries as they are too large), the water potential at the venule end of the capillary is lower than the water potential in the tissue fluid.
7) This means that some water re-enters the capillaries from the tissue fluid at the venule end by osmosis.
8) 90% re-enters the capillaries at the venule end of the capillary bed. 10% is extra fluid and will get returned to the blood through the lymphatic system
Explain the formation of lymph
1) Some tissue fluid that is not reabsorbed by the capillaries at the venule end, enters the lymph vessels. Once inside, this fluid is called ‘lymph’
2) The lymph vessels are separate from the circulatory system as they have closed ends and large pores that allow large molecules to pass through.
3) Larger molecules that are not able to pass through the capillary wall enter the lymphatic system as lymph as small valves in the vessel walls are the entry point to the lymphatic system
4) The liquid moves along the larger vessels of this system by compression caused by body movements. Valves prevent any backflow.
5) The lymph eventually reenters the circulatory system in the chest cavity in the subclavian veins.
Purpose of lymph
- If any plasma proteins that have escaped from the blood are returned to the blood via the lymph capillaries as if any plasma proteins were not removed from the tissue fluid they could lower the water potential of the tissue fluid and prevent the reabsorption of water into the blood in capillaries.
- after digestion lipids are transported from the intestines to the bloodstream by the lymph system
Movement of the lymph
3 main ways:
1) Hydrostatic pressure of the tissue fluid leaving the capillaries
2) Contraction of body muscles squeezes the lymph vessels. Valves ensure the fluid inside them moves away from the tissues towards the heart.
3) Enlargement of the thorax during breathing reduced the pressure in the thorax, drawing lymph into this region, away from the tissues.
Compare and contrast the transport of fluid in a vein with its transport in a lymph vessel
Similarities:
- both have low pressure
- both have valves
- both use muscle squeezing to move fluid
Differences:
- faster flow in vein
- heart causes mass flow in vein
- flow to heart in vein but to glands in lymph
High blood pressure leads to an accumulation of tissue fluid. Explain how?
High blood pressure = high hydrostatic pressure
This increases outward pressure from arterial end of capillary and reduces inward pressure at venule end of capillary
so more tissue fluid is formed and less tissue fluid is reabsorbed, which causes the accumulation.
This accumulation causes swelling. Can cause oedema.
What is the structure of Haemoglobin?
- a large globular protein with a quaternary structure
- made up of 4 polypeptide chains (globin part) ( 2 alpha and 2 beta chains)
- Each chain has a haem group so 4 haem groups (prosthetic group, doesn’t have amino acids but is part of protein)
- Haem group contains iron ions and gives Hb it’s red colour
- Haem is necessary as the iron ion can attract and hold an oxygen molecule as it is said to have a high affinity for O2
- Haem allows O2 to reversibly bind (load and unload)
- As each haem group can hold 1 oxygen molecule, each Hb can carry 4 oxygen molecules (8 oxygen atoms)
What is the function of Haemoglobin
- is responsible for binding with oxygen in the lungs and transporting the oxygen to the tissue to be used in aerobic metabolic pathways
- The existence of iron (II) ion in the prosthetic haem group allows oxygen to reversibly bind + has high affinity for O2
- oxygen loads onto Hb in the lungs (alveoli) where there’s a high pO2
- HbO8 is formed and this is a reversible reaction
- Oxygen released (unloaded) where it needed respiring tissues where pO2 is low
Why is O2 not carried around the body in the plasma?
- As oxygen is not very soluble in water and Hb is, oxygen can be carried more efficiently around the body when bound to the Hb
Hb’s affinity for oxygen
- Hb usually has a high affinity for oxygen
- however affinity for oxygen varies depending on it’s condition
One condition is ‘Partial Pressure of oxygen’ (pO2) = the concentration of oxygen
- oxygen loads onto Hb to form HbO8 in high pO2 like in alveolus
- HbO8 unloads its oxygen where there’s low pO2 like in respiring tissue as they use up O2
Oxygen Dissociation Curves for Adult Hb
- in a sigmoid shape (s-shape) due to cooperative binding
- Due to the shape of the haemoglobin, it is difficult for the first oxygen molecules to bind to the haemoglobin. This means that binding of the first oxygen occurs slowly explaining the relatively shallow curve at the bottom left corner of the graph.
- After the first oxygen molecule binds to Hb, it alters the conformation of Hb making subsequent binding easier, allowing the Hb to be saturated quicker. This explains the steeper part of the curve in the middle of the graph
- As the Hb molecule approaches saturation it takes longer for the fourth O2 molecule to bind due to the shortage of remaining binding sites which explains the leveling off of the curve in the top right corner of the graph.
What is cooperative binding?
- when the first O2 molecule binds with the Hb, alters the conformation of the Hb which makes subsequent binding easier and allows Hb to be saturated
What is Foetal Haemoglobin?
- has a slightly different composition to adult Hb. Foetal has 2 gamma and 2 alpha chains
- it has a higher affinity for oxygen (so oxygen dissociation graph for foetal Hb shifts to the left)
- foetal Hb is almost completely gone by 6 month postnatally
Why does foetal Hb be needed?
- since it has a higher affinity for oxygen than adult Hb
- this is vital as it allows the foetus to load oxygen from its mother’s blood at the placenta
- at the placenta there is low pO2 as some of the oxygen is used up by the mother’s body so the oxygen unloads at the placenta at a low pO2
- to ensure the foetus has enough oxygen to survive, its Hb has to have a higher affinity for oxygen so it takes up enough oxygen
- If its Hb had the same affinity for oxygen as adult Hb its blood wouldn’t be saturated enough
- to O2 delivery from mother to foetus there is a counter-current exchange so the maternal and foetus blood runs in opposite directions.
Explain why the foetal haemoglobin
curve is to the left of the adult haemoglobin curve?
1) at the placenta there is low pO2
2) Adult HbO8 will unload O2 in a low pO2 (placenta)
3) Foetal Hb has a higher affinity for oxygen
4) Foetal Hb is still able to load some oxygen at lower pO2 (placenta), unlike adult Hb who can’t load as much O2 at lower pO2
What is the structure of myoglobin?
- a globular protein
- consisted of a single polypeptide chain
- consists of alpha-helices in their secondary structure
- has only one haem group meaning it can only bind 1 oxygen molecule
- found in muscle tissue
What is the function of myoglobin?
- it stores oxygen in muscles for use during periods of high demand
- binds oxygen strongly and releases it only at very low oxygen levels
Myoglobin’s affinity for O2
Has a higher O2 affinity than Hb so when blood reaches muscle tissue, O2 is transferred from HbO8 to myoglobin
What is the oxygen dissociation graph for myoglobin?
- lies to the extreme left in a hyperbolic shape as there is no cooperative binding
Explain why deep diving mammals have very high concentrations of myoglobin in muscles?
Allows it to store lots of oxygen in muscles so they can dive for longer amounts of time as more O2 = allows respiration = more muscles contraction
Similarities between myoglobin and haemoglobin
- the both are globular proteins that are water-soluble and function in oxygen transport or storage
- Both contain a haem group which includes an iron (II) ion capable of binding to oxygen
- both play roles in oxygen management
1. myoglobin: stored oxygen in muscle tissues
2. haemoglobin: transports oxygen from lungs to tissues - both primarily consists of alpha-helices in their secondary structure
Differences between myoglobin and haemoglobin
- Hb consists of 4 polypeptide chains whereas myoglobin only has one
- Hb can bind up to 4 oxygen molecules, whereas myoglobin can only bind 1 oxygen molecule
- Hb: Oxygen affinity increases when one oxygen binds as the oxygen binding is cooperative, myoglobin has no cooperative binding as it is a monomer
- Hb is found in red blood cells (erythrocytes), myoglobin is found in muscle tissue
What is the Bohr Effect?
1) where tissues, like muscles, are contracting and so respiring more = more CO2
2) CO2 combines with water inside of red blood cells producing carbonic acid. . This reaction is catalysed by enzyme carbonic anhydrase (reversible reaction and reaction is reversed when the blood reaches the capillary network surrounding the alveoli in lungs)
3) This acid immediately dissociates to produce H+ and HCO3-
4) HCO3- ions diffuse out of red blood cells into plasma. As a result of all these negative ions leaving the red blood cells, the red blood cells develop a positive charge. To maintain electroneutrality, chlorine ions diffuse into the red blood cells from the plasma. This is called ‘chlorine shift’
5) H+ ions compete for spaces taken up by O2 inside the red blood cell and cause the HbO8 to dissociate and release some of the oxygen it’s carrying. This is exactly what’s required if CO2 is in the blood as it means cells are respiring and in need of oxygen.
6) When CO2 is present, H+ ions displaces the oxygen attached to Hb to produce haemoglobinic acid (HHb). This prevents the H+ ions collecting and causing a fall in pH and the blood becoming acidic. Therefore, Hb acts as a buffer.
7) While this is happening oxyhaemoglobin unloads O2 and this O2 is released into blood plasma
When does Bohr effect occur?
When the pCO2 high….
- Hb less efficient at binding with oxygen because H+ is complete in the place of oxygen
- Hb much more efficient at releasing O2 dissociation because muscle have high O2 demand
What is the Bohr effect due to?
Due to the presence of CO2 but due to the presence of H+
CO2 is transported in three main ways to the lungs..
1) 5% is dissolved directly into the plasma
2) 10% is combined with Hb to form the compound carbaminohemoglobin
3) 85% is transported in the form of hydogencarbonate ions in the plasma
What does blood clotting do?
Prevents excess blood loss
Prevents pathogens from entering via the cut/ wound
What are the two key chemicals involved in blood clotting?
1) Serotonin: smooth muscle of the blood vessels contract, which narrows the blood vessel which cuts off the blood flow to that area
2) Thromboplastin: enzyme causing the cascading effects that lead to formation of a clot.
Explain the blood clotting process
Platelets (thrombocytes) —releases—> enzyme thromboplastin, which only gets released when wound occurs ——> this enzyme converts prothrombin (soluble protein + inactive enzyme) —– (main factor: thromboplastin/side factors: vitamin K, calcium ions and factor 8 required)—-> into thrombin (enzyme) —-> thrombin converts fibrinogen (soluble blood protein) into fibrins (insoluble fibres) —–> these fibrins and trapped cells form the blood clot
Explain the roles of each events leading to blood clots
Injury: exposes collagen fibres to blood and platelets stick onto these collagen fibres
Release of chemicals from platelets: makes the surrounding platelets sticky
Clumping of platelets at the wound site: forms an emergency protection against blood loss and invasion of pathogens, this clump is called ‘platelet plug’
Formation of fibrin clot: reinforces the seal and traps blood cells
What is the role of clotting factors in the formation of the clot?
It catalyses the conversion of prothrombin to thrombin.
Why are these clotting factors not normally present in the plasma?
Because they only happen in the tissue cells of the one being damaged otherwise they will not be produced.
Why does internal bleeding from tears or puncturing of blood vessels occur?
Happens due to high blood pressure.
What is the structure of the heart?
- is a muscular pump
- the right-hand side of the heart pumps deoxygenated blood to the lungs
- the left-hand side of the heart pumps oxygenated blood to the rest of the body
- CHAMBERS:
2 atria (collect blood from the body and lungs)
2 ventricles (pump blood to body and lungs) - VALVES:
atrioventricular valves (between atria and ventricles + bicuspid valve on left and tricuspid on right)
semi-lunar valves (between ventricles and arteries + aortic valve on the left and pulmonary valve on right) - BLOOD VESSELS:
vena cava (inferior and superior) feeds into the right atrium and returns deoxygenated blood from the body
pulmonary artery connects to the right ventricle and sends deoxygenated to the lungs
pulmonary vein feeds into the left atrium and returns oxygenated blood from the lungs
aorta extends from the left ventricle and sends oxygenated blood around the body. - located in the chest cavity
- protected in the chest cavity by the pericardium (tough and fibrous sac)
What are the roles of the valves in the heart and how do they work?
Roles:
- to prevent backflow of the blood by opening and closing due to pressure differences
How do they work?
- they are forced open when the pressure of blood behind them is greater than the pressure in front of them
- they are forced close when the pressure of blood in front of them is greater than the pressure behind them
What is the cardiac cycle?
- is an ongoing sequence of contraction and relaxation of the atria and ventricles that keeps blood continuously circulating through the body
- control of the basic heartbeat is therefore myogenic as the heart can generate its own beat without outside stimulation
Explaining what the cardiac cycle is?
- it is a sequence of events that make up a single heartbeat
- the cardiac cycle is repeated about 72 times per minute
- includes periods of heart muscle contraction and relaxation
- another follows one cardiac cycle in a continuous process (no gaps between cycles where blood stops flowing)
- the contraction of the muscles in the wall of the heart reduces the volume of the heart chambers and increases the pressure of the blood within that chamber
-when the pressure within a chamber exceeds that in the next chamber, the valves are forced open and blood moved through - when the muscles in the wall of the heart relax they recoil which increases the volume of the chamber and decreases the pressure so that the valves close
What are the three stages of the cardiac cycle?
1) Atrial systole
2) Ventricular systole
3) Cardiac diastole
Explain atrial systole
- ventricles are relaxed
- blood under low pressure flows into the left and right atria from the pulmonary veins and vena cava
- this increases the pressure of the blood against the atrioventricular valves (bicuspid and tricuspid)
- as a result atrioventricular valves open
- semilunar valves are closed (so no blood can be pumped to the lungs or body at this stage)
- blood begins to leak into the ventricles
- atria then contracts which forces more blood into the the ventricle
(atrial systole = atria contracts)
Explain ventricular systole
- atria relax
- ventricles contract from the base of the heart upwards
- this increases the pressure in the ventricles (pressure becomes higher than the pressure in the atria)
- this forced the atrioventricular valves to close (preventing backflow to the atria) - producing the first heart sound ‘lub’
- contraction of the papillary muscles pulls heart tendons preventing the valve from being inverted
- this high pressure in the ventricles forces open the semi-lunar valves
- blood can now flow under high pressure into the pulmonary artery (to the lungs) and the aorta (to the body)
Explain Cardiac Diastole?
- Walls of atria and ventricles both relax (elastic recoil)
- higher pressure in the pulmonary artery and aorta which causes semi-lunar valves to close (preventing backflow)
- Atria fills with blood increasing pressure due to the higher pressure in vena cava and pulmonary vein
- ventricles continue to relax, and their pressure falls below the pressure in the atria
- atrioventricular valves open
- blood flows passively without being pushed by atrial contraction into the ventricles from the atria
- the atria contract and the phases begins again
Explain myogenic stimulation of the heart
- it means that the heart can contract without any input from the nervous system, and the signal for cardiac compression is raised within the heart tissue itself
How heart action is initiated and coordinated?
- the heartbeat is initiated by a group of specialised muscle cells in the right atrium = ‘sinoatrial node’
- sinoatrial node acts as a pacemaker
- SAN is a group of cardiac muscle cells connected to nerve endings which form part of the involuntary nervous system, these nerves can alter the basic rhythm of the heart in line with the body’s requirements.
- SA node triggers roughly 60-100 cardiac contractions per minute (normal sinus rhythm)
- if the SA node fails, a secondary pacemaker (AV node) may maintain cardiac contractions at roughly 40-60 bpm
- If both fail, a final tertiary pacemaker (Bundle of His) may coordinate contractions at a constant rate of roughly 30-40 bpm
Electrical conduction of a heartbeat
- SA node sends a wave of electrical activity to the atrial walls (depolarisation)
- this impulse directly caused the left and right atria to contract which initiates the heartbeat
- A band of non-conducting collagen tissue (atrioventricular septum) prevents the waves of electrical activity from being passed from the atria to the muscles
- The only conducting route for the impulse to the ventricles is via the atrioventricular node
- there is a delay of approx 0.15s in conduction from SAN to AVN, meaning the atrial systole is completed before ventricular systole begins
- AV node is connected to a strand of modified cardiac fibres called the bundle of His
- The bundle of His splits into two branches which carry the impulse on into finer branches of cardiac fibres called the purkyne tissue
- the finer fibres of purkyne tissue carry the electrical impulse down the septum and through the ventricles
- this impulse causes both the ventricles to contract from the base upwards (ventricular systole)
- ventricles contract 0.20s after the atria contract giving sufficient time for blood to be fully squeezed into ventricles from the atria before they start to contract
What is the structure of cardiac muscle
- It is myogenic so does not require external stimulation
- composed of branching fibres allowing rapid spread of electrical impulses across the muscle
- this ensures that all parts of an atrium or ventricle contract at the same time
- the cross connections give strength and help to resist tearing when muscles contract.
- has a rich blood supply to provide O2 and glucose for inspiration and to remove CO2
- once the cardiac muscle has started to contract it cannot respond to a second stimulus until it begins to relax - this period is called the ‘absolute refractory period’
- this period allows it to recover fully without becoming fatigued even when contracting rapidly so it is impossible to develop an oxygen debt or a state of sustained contraction called ‘tetanus’
