Respiratory System - Cell Biology Semester 2
What is cellular respiration - Biochem definition
This is the process in which nutrients are converted to useful energy in a cell and is the main oxidation process of living cells where chemical energy from organic substances is released by metabolism involving the consumption of o2 and liberation of co2 and water
What is the Physiology defintion of cell respiration
The process by which an organism will exchange gases with its environment to then control the level of gases in our tissues by:
The movement of o2/co2 out of lungs by ventilation- regulation of breathing
The movement of o2/co2 across alveolar and endothelial membrane
Tranfer of o2/co2 in blood to our tissue so the regulating of molecule transfer
Movement of o2/co2 across endothelial and cell membrane to the mitochondria
What are the roles of the respiratory system
It is used for gas exchange, regulation of blood tissue pH by altering co2 levels
Voice production due to movement of air passed the vocal folds
Olfaction when smell occurs due to airborne molecules drawn to the nasal cavity
Protection against pathogens by preventing entry or removing them from respiratory system, the lungs have more macrophages that any other organ
How is the respiratory system divided in 2 halves
The upper respiratory system is everything that is above the jugular notch and then everything from half way down the chest is the lower respiratory system
What is the nose used for
It is an external nose that has an internal nasal cavity that will act as a passageway for the air and will clean the air due to hairs and turbulence
It will also humidify the air and warm the air and contains nerves for sense of smell called olfactory receptors at the back of the nasal cavity
Why can breathing hurt on a cold day
This is due to there being more breathing with the mouth so then the air wont be humidified and warmed up so more cold air will enter the lungs and cause the drying out of the epithelial cells
There will also be turbulence that removes particles from the air but this will also be missed out
What are the 4 main sinuses
These are holes in the bounding of the skull called the frontal sinus, maxillary sinus, sphenoid sinus and the ethmoid sinus
There role is to act as a resonance chamber andn act as crumple zone to stop brain damage. There is also a potential relation to the immune system as well as defintialy warming the air and mostly important for resonance
What is the pharnyx
After the air pass through the nose it will enter the pharnyx
There are 3 main regions= Nasopharnxy then the oropharnxy and then the laryngopharnyx
Food material can hypothetically end up here and go to trachea and go down the wrong way
The region is very innervated due to larger number of nerve endings so very uncomfortable
What does the larynx do
It is formed from 9 cartilages and the main 3 important ones are: Thryoid cartilage, epiglottis cartilage and the cricoid cartilage
The main job is too make sure there is always an open passageway through the trachea so make sure it always stays open
The epiglottis and ventricular carti;age will fold to prvent swallowed material moving to larnyx, when swallowing the larnyx close to prevent food from entering
There are also vocal cords that are the primary source of sound
What makes up the conducting zone and the respoiratory zone
In the upper respiratory system and the trachiobrachial tree in the lower respiratory system make up the conducting zone
The rest of the lower respiratory system makes up the respiratory zone for gas exchange to take place
What is the trachiobrachial tree
This is part of the conducting zone as there are traches that branch to terminal bronchioles that have cilia for debris removal
It is also the passageway for the air movement and for this to happen need limited resistance and turbulunece
There is cartilage that will hold it open and smooth muscle control the diameter and some smaller bronchioles length
There will be no gas exchange but gas flow so need laminar air flow by increasing the cross sectional area but this increases dead space so lung have to work harder to bring in air
How is there branching of the airways
In humans there is branching of the trachea to them primary bronchuc to then secondary bronchus to the terminal bronchus before reaching respiratory bronchus
The cross sectional area get larger as get further down
There is is much thinner squamous epithelium in respiratory bronchus compared tp ciliated stratified epithelium in other bronchus
The respiratory duct is a passage to all alveoli from the respiatory bronchus
What does pseudo stratified mucosal epithelium do
This is in the conducting zone of the respiratory tract and lines it by sitting on top of the basement membrane
There are many goblet cells making mucus with mucisn that are glycosylated proteins so are sticky so sit on aqueous mucus and particles in the air stick to it
There are also cilia and will beat in defined orientation so then material is bought up from the lungs to be removed by trachea
What is turbulence bad
It will increase resistance so more work to breathe but also goof as particles are pushed to 1 side and interact with mucus layers and at every branch point there is more turbulence so then larger particles picked up
At each branch there are high immune cells and lymphocyte numbers to remove unwanted particles picked up in mucus
What is the respiratory zone
This is made up of the respiratory bronchioles to the alveoli pathway as well as the site for gas exchange to happen
What is the structure of the alveoli
There is a good blood supply due to pulmonary artery bringing in blood as well extensive capillary bed and the pulmnoary vein takes oxyegnated blood away
There is elastic fibre mass and fluid loss so large number of lymphatic vessels
The conducting tubules have their own vascular supply from right side of the heart and their veins drain to left heart side and so a slight drop in oxygenated blood between pulmonary vein and aorta
What are the 4 types of cells in the alveoli
Type 1 cells line the alveolar and major gas exchange surface
Blood vessels of endothelial cells
Type 2 cells to make surfactent
Macrophage cells
The walls are very thin to allow max amount of gas exchange and all these cells combined are called the respiratory membrane
What is the exchange surface of the alveoli
There is fused basemement membrane of type 1 and 2 cells
The distance for gas exchange is 50-100 m2 and distance the gas moces is 1 micron
The red blood cells touch the endothelial membrane as they move so take 1ms for o2 to pass across
There is very larger surface area to Volume ratio
In the lungs when blood passes it become 100% saturdated
How do lungs stay in place in the chest
The lungs free float in our chest due to only being attached at the trachea and some blood vessels near the heart but it only placed againt the ribs and diaphragm
This is due to the partial vacuum caused by the negative partial pressure in the intra pleural space, the pleural is a fine membrane that line the lungs calle the visceral pleura and also line the wall of the chest on the rib cage or diaphragm
There is the continual transfer of fluid from lymphatic channels maintain a – pressure between the visceral surface of the lung and the parietal pleural surface of thoracic cavity and so means if change the size of the thoracic cavity change the size of the lungs
What is inspiration
The volume of the chest will change at rest when breathing due to contraction of diaphragm causing thoracic volume to increase so lung volumue get larger when breathing in as abdominal contents are pushed down by a relaxed abdomen
When there is forced breathing the rib The movement of the ribs due to external intercostal muscles that pull the ribs away wards and upwards
Also the movement of the sternum that move chest outwards
Both increase chest volume and lung volume when doing exercise
What is expiration
Where the diaphragm relaxes and so abdomen contents arent pushed down as diaphragm moves up and also there is elastic recoil of the ribs so they move inwards as external intercostal muscles relax and so then lower lung volume
Contraction of internal intercostal muscles during forced expiration along with rectus muscles force the chest down
What is the difference of inspiration vs expiration
Inspiration has contraction of diaphragm and external intercostal muscles and expiration they relax
Inspiration abdomen content pushed down ansd get bucket hand movement in ribs aand pump handle movement in the sternum
Expiration get elastic recoil of diaphragm, lung tissues and ribs and greater surface tension
What is ventilation
The movement of the air that is induced by volume changes and hence pressure changes in the lung compartment and the air will move from high pressure down to a low pressure area- it is inversely related to the volume
What are the pressures in the lung
Pleural pressure is the pressure of the interpleural space and is always slightly negative
Alveolar pressure is the pressure inside the lung alveoli
Transpulmonary = alveolar pressure - pleural pressure and is the measure of the force that distend the alveoli
What are the pressure changes caused by inspiration
S1= Barometric air pressure is equal to alveolar pressure and tjere is no movement of air
S2= Increase in thoracic volume due to diaphragm contracst and moves downwards so decrease in alveolar pressure and so barometric air pressure is greater and air move down the pressure gradient into the lungs - Inspiration
S3= Expiration begings and the diaphragm relaxes so decrease in thoracic volume so then increase in alveolar pressure so then it is now greater than barometric air presssure so then air moves out of the lungs
Why is there changing alveolar pressure at inspiration
The pleural pressure at the beginning of inspiration is -5 and the during the normal inspiration it will go to there is expansion of the chest cavity as chest pulls outwards and at maximal inspiration the pressure is -7.5 so some pressure go to the alveolar during inspiration
Due to always being negative there is loss of integrity of chest walls and this lead to pneumothorax air entering chest cavity and lung collapse from the chest wall to the upstretched size and then eventually the mediastinum collapse so then other lung collapse as well so that’s why punctured lung has to be treated immediately
What is the complience of the lungs
This is the ease in which the lungs and the thorax move
This is due to the expansion/contraction of volume change / unit change in transpulmonary pressure
For a normal adult = 200mls of air / 1 cm H20 TPP A lower compliance will mean the lungs and thorax are harder to expand and so a greater TPP change needed for a given volume of air and this can be caused by Pulmonary fibrosis or Pulmonary oedema
What lung effect alters the inhiliation complience
There are elastic fibres as well as the surface tension between the air and the lining of the alveoli
The surface tension causes the greatest effect on complience of the lungs
How to prove surface tension causes the greatest effect on complience
This can be proved due to filling lungs with water and then seeing the force needed to expand the lung
In a fluid filled lung there is only the need to overcome elastic fibres forces less than the pleural pressure needed to inflate to the lung by 0.5 L at 1cmH20 compared to the air filled lungs need to overcome the surface tension as well and this mean 3cm H20 pleural pressure
Where is the greatest pressure found in the alveolus
There is greater pressure found in smaller alveoli and when the alveoli is at equlibrium then the pressure is = to the force pushing it down and so the constriction pressure is greater in smaller alveoli than larger ones proved by La Place equation
= P= 2T/r
This cause the alveoli to disappear due to the larger constriction force and so all the air will eventually end up in the larger alveoli due to no smaller ones can survive and function due to to much pressure
What is surfactant
This is a surface active agent in water that will greatky reduce the surface tension of water made by type 2 cells in the lungs by breaking the hydrogen bonds in the semi- crystalline structure of water droplets
They are usually a mixture of lipid and protein especially phospolipids that are amiphillic
How is surfactant made by type 2 cells
It is made in type 2 cells that have high microvilli levels on them and are formed first into lamellar bodies that are secreted by the Golgi
These bodies are then packed to tubular myelin that is released by exocyotisis to be called surfactant and this is regulated by the increase in tidal volume
It will reduce the pressure and so smaller alveoli wont become so small and some air will saty in them and so pressure between small and large alveoli becomes the same
What happens to surfactant when the alveoli contracts
There will be an increase in pressure and so the surfactant concentration will increase and so will inhibit the surface tension and maitain the all the smaller alveoli and the complete lung structure
What are the roles of surfactant
Reduce the amount of work during inspiration due to greater compliance as there is less surface tension
Stabilise the alveoli and reduce their tension to keep them dry and stop pulmonary oedema
Needed for lung expansion during birth, but in premature birth there can be respiratory disease due to type2 cells only develop at 7 months so less surfactant is made combined with smaller weaker
What is respiratory rate and Minute ventilation + Anatomic dead space and Alveolar ventilation rate
RR is the number of breathes per minute
MV is the amount of air moved into and out of the lungs per minuete = Tidal Volume x Respiratory Rate
Dead space = Part od the respiratory system where gas exchange wont take place In the conducting zone
Alveolar ventilation rate = Volume of air per minute entering area of respiratory system where gas exchange will take place
How can Alveolar vent rate change
At a higher tidal volume there is a greater AV rate and vice versa
It can also be increased by fewer deep breathes than many shallow breathes
An increase in dead space will reduce rate
What are the problems with dead space
When using a snorkel has to be a limited length due to act as dead space so if too long then just breathe in the eair that you breathe out and run out of o2
If under anaesthesia then large dead space increase so given modified air and higher level of o2 in your lungs and forced breathing as well
What is partial pressure
This is the pressure that is exerted by each type of gas in a mixture and Dalton law state total pressure = sum of all partial pressure
In the lungs the air is h20 saturated so also water vapoir in the air that adds a partial pressure and when air enter tracheas it is humidifed so then partial pressures of other gases drop
What happens to partial pressure in the alveoli
There is co2 production here so partial pressure of co2 increase and partial pressure of o2 will drop, water vapour stay the same
When we breathe out it is a mixture of the alveolar air and air that has remained in the conducting tissue as well
What is the changing partial pressure of o2 and co2 in the alveoli
By breathing deeper and faster it wont change as you are limited of volume of the lung so will alter alveolar ventrilation rate
Are able to bring the partial pressure of co2 down to near 0 but not 0 but o2 is very limited in partial pressure changes
Increase o2 use and co2 production by increasing excersise and a greater demand for o2 for respiration and so more co2 produced - Co2 drives demand for more respiration that o2
Can also change the partial pressure of oxygen around by gaining altitude so less o2 in the air
What is the response to extreme low o2 levels
Aortic and carotid bodies that are both o2 sensors tell the medulla to send signals to the heart to say more oxygen is needed so then a greater cardiac output and it will be bias to fill essential organs like brain with o2 where they thne can have to much fluid = oedema as well as more brain pumping in the brain so it swells and sometimjes csan push out of the head
What alters the rate of gas exchange
This is shown by ficks law = Diffusion coefficient= K soluble/ Mwt
The rate is dependent on differnce in partial pressures on both side, the surface area it is crossing, it is inversely related to a square the distance it has to travel as well the diffusion coefficient
What is the diffusion coefficient in water
The crossing of lipid membrane for has is not limiting step due to the high gas solubility the membrane
The movement of gas is limited when moving through water due to:
Water has greater fluid level that gas needs to move across so more distance between RBC and endothelial,layers gets larger
What does the diffusion distance do
The rate of transfer of alveolar air to plasma depend on distance
The respiratory membrane is made of endothelial and epithelila cells, basememt membrane, surfactant and connective tissue
In a healthy lung this distance is minimised to max diffusion rate but gets larger when ill
The red blood cell touches capillary walls and forces its way through due to biconcave shape
Where does area diffusion occur
The rate of diffusion is dependent on area of the membrane that is available for gas exchange
The larger then the greater the rate - smoking cause emphysema that lower area due to alveolar sceptre loss and also fewer squamous cells
What are the partial pressure changes in the alveolar
In Pulmonary arterioles pp of O2= 40, co2= 45
Inspired air at nose pp o2= 159 , co2-0.3
Alveolus o2= 104, co2=40
Exhaled air o2= 120, co2= 27
Pulmonary venules o2=104, co2=40
Systemic arterioles - o2-95 , co2, 40
Systemic venules - o2=40 , co2- 45
Why is there a drop in partial pressure on left side of the heart
This is due a small amout of leaching that place so a lower partial pressure of o2 in systemic arterioles compared to pulmonary venules. From the systemic venules to pulmonary arterioles there is no partial pressure change due to no leaching from right side of the heart
How long does blood take to equilibriate
It takes about 1 second for the blood to equilobriate with the alevolar gase, this is due to 0.8 seconds spent in the pulmonary cap and then 0.2 seconds of equilibration
What is pulmonary perfusion
This is where can increase the oxygen carriage to the tissue by increasing the blood flow.
There is 450ml of blood in lungs at any time when resting and 50-70 ml in the alveolar capillaries when resting
What does pulmonary perfusion effect
Increasing blood flow during excersie does not alter the o2 saturation of the blood compared to resting lung but there will be 3x as much blood passing through the lung per second, so then more oxygenated blood will be ciruclating in the body than at rest
What does increasing the blood pressure effect
A greater blood pressure will reduce the amout of time blood spends in the capillaries so then get more o2 round the body to feed more tissues during excersise
The speed of blood through transit through the pulmonary capillaries will increase but still get max o2 uptake
Collapsed vessels in the lungs open to then allow greater alveolar perfusion and vessels also dilate
How is the pulmonary vascular system compliant
In the pulmonary capillaries the pressure is 7 mm/hg compared to systemic where it is 25 mm.hg
The pulmonary blood flow can increase from 6-24 L/min and in some athletes again to 40L/min due to the vessels have recruited and distended so the speed of blood will increase and this will lower resistance in the pulmonary bed
This causes lung blood volume and alvolar capillary volume to increase by 2-3x
What are the regulated factors that determine o2/co2 transfer
Rate of alveolar ventilation and blood flow ( Perfusion)
Why is a ventilation- perfusion match balance needed
This is due to not all of the lungs are eqaully ventialled and perfused, at the top of the lungs there is high ventilation but low perfusion and at the bottom of the lungs there is high perfusion and low ventialtion so need to balance these to max the gas transfer in the lungs
The ventialtion perfusion ratio = 0.8
What are the normal gas partial pressures if breathing normally
The partial pressure of o2 is 100 and the partial pressure of co2 is 40 and this will help to lead to the ventialtion perfsuion ratio of 0.8 due to a normal blood circulation and breathing as well
What happens if breathing becomes impaired
Then there will be lower ventialtion but the blood flow will remain the same and so there is no gas exchange in the area of the lungh where the ventialtion is affected, this mean the partial pressures in the blood stay the same as before gas exchange at 40 o2 and 45 co2 and the ventialtion perfusion ratio is 0
How can the lungs adapt the blood flow
They can do this so the area of the lung with best ventialtion at a time get the best perfusion as well by hyperoxic vasoconsriction of the surrounding alveoli
What are the pulmonary and systemic response to hypoxia when o2 pressure
There will be a decrease in blood flow to that alveolar, this is due to the oxygen sensitive K channels in smooth muscles of pulmonary arterioles
At low o2 partial pressure the K+ channel close but Na+ channels stay open and will depolarise it to cause partial closure of the arterioles
Opposiet happen in systemic circulation in response to hypoxia and important in pulmonary to match perfusion and ventialtion
If there is no o2 movement over an area these vessels are closed off and the blood redirected to better ventilated alveoli and then able to match blood flow to gas exchange and minimse dead space
What are the 2 types of dead space in the lungs
Anatomical dead space – The volume of the respiratory tract involve din conducting gas but not the in the transfer of blood
Physiological dead space – The portion of the tidal volume not participating in gas exchange with the pulmonary capillary blood
What will hypoxic vasoconstriction allow
The ventialtiona and perfusion to match and minimise the alveolar dead space so will reduce the deoxygenated blood returning from the lung because it passes through unventilated area of the lungs
What is Henrys Law
The concentration of a gas in liquid is determined by the its partial pressure and its solubility = C = PP x Solubility
How much oxygen does haemoglobin carry
Oxygen is poorly soluble due to HB in the red blood cells as 1g of HB carry 1.3 mls of o2 when saturated
How is Hb harmful
HB on its own in free solution is toxic due to the amount of iron in its structure, and also in free solution it will form a precipitate that then go the Kidney and cause harm so thats why HB is needed to be carried in red blood cells
How does HB saturation change depending on blood type in body
200mls of o2 is carried at 100% HB saturation in arterial blood byt then only 150mls of 02 at 75% HB saturation is carried back to the lungs in venous blood
This means that 50mls of o2 are taken up by tissue in the body per litre of blood flow
The resting cardiac output os 6L/min so in 1 min there is 300mls of o2 taken out the blood to be used by tissues
How does HB colour change
HB when it is deoxygenated it has a blue colour and then if add oxygen to make oxyhaemoglobin it will become red in colour, there are 4o2 molecules per HB molecules in the red blood cells
This is due to the tetramer shape of the HB
What does Amly Nitrate do to blood
It will oxidise blood and cause a ferrous response that will go to ferric, this will only happen however if haemolysis occurs
Amyl Nitrate can be used as antidote for cyanide due to act as oxidant to indcue formation of methemoglobin that go to methehaemoglobin that cause the cyanide to change to ceynomethoglobin removing the cyanide from the cells
what is the oxygen saturation curve
Oxygen is transported in the HB and is dissovlved in blood plasma and the oxygen HB saturation curve is non linear and shows the oxygen dissociation curce that HB is completly saturated when a partial pressure of over 80 mmHG is bound
How does oxygen bind to HB
There will be binding of 1 o2 molecule that then will induce a conformational change in the 3 remaining active sites that then will change their o2 affinity and make it easier for o2 to bind to them
It will bind to the haem group that has a ring structure called porphyrin ring made of 4 pyrol groups and this will be stabilised by the hisitidine amino acid
When o2 binds it causes the 4 molecules in HB to rotate against each other and this will then increase in the binding affinity for o2 as they go from a tense state to a relaxed state to then allow o2 binding
How does the S shape of the o2 dissociation curve help
This is due to it allows in the lungs there to be high affinity for maximum o2 binding and then in the tissue at low o2 partial pressure it allows o2 unloading into the tissues
How can o2 affinity be modified
It can be regulated due to the histidine ring that can pick up protons and act as a buffer for Ph change if more protons and thsi will then cause + ions in thr HB to effect HB overall and lower the affinity for the o2
As pH gets larger the affinity get larger and Ph drops then less affinity , this is a shift to the right of the curve is due to more acidic body means more H+ and more co2 present
This is called the Bohr effect
What will cause a shift in the dissociation curve
There are more acidic conditons, a greater temperature and a higher partial pressure of o2
How does o2 affinity change under high excersise
Due to the lower partial pressures of o2 will drop under excersise to as low at 15mmHG of o2 and so 75% of o2 available will be released by HB but due to the Bohr effect then can be up to 85% of o2 is released to HB for the muscle to use
Can also increase the cardiac output by 7x and get up to 25x increase in o2 related to active muscles
However due to more vessel constriction then limit the blood supply and hence o2 supply will need an o2 resevoir called myoglobin
What is myoglobin
It is a monomer so doesnt have any allosteric affinity and also has a greater affinoty for o2 that most due to being a monomer
What does 2,3 bisphosphoglycerate do the dissociation curve
It will cause the curve to shift to the right
In prolonged hypoxia there is more glycolysis anerobically so then there is greater 2,3 bisphosphoglycerate formed leading to increase in blood
It is a strong – charge and bind to HB and reduce allosteric retention so that then stabilise the low affinity HB and oush it more towards the fixed state and so less likely to pick up o2 from the lungs
This then all lead to greater o2 release in tissues
What are the 4 things that change HB affinity for o2
H+ concentration, temperature, 2,3bisphosphoglyceraste concentration and CO
Why do foetus always have good perfusion and ventilation
The HB there wont bind to 2,3 DPG so then it will alwasy be inthe relaxed state so have a higher affinity for o2 even when partial pressure of o2 in the placenta is low so always good perfusion and ventialtion
How much co2 will enter HB
24% of the co2 will bind to the HB amino protein group to form HgB.Co2
70% will interact with water and carbonic acic will be produced at a slow rate so need the enzyme carbon anhydrase to speed this up
The carbonic acid is then broken down to bicarbonate ions that leave the red blood cells via chlorine biacrbonate ion transporter to the blood plasma
What is the Haldane effect
The central peptide of oxyhaemoglobin in the lung is a stronger acid that HB in the tissue and there can be a swap of these 2 molecules can cause the doubling of co2 release in the lungs
How does the Haldane effect take place
The HB is a weaker acid and so allows H+ to bind to it in the tissue and then in the lungs the oxyhaemoglobin is much stronger acid so releases H+ ions
These protons will react with caramino group on the N terminus of HB and cause co2 displacement
There is then greater acidity causing bicarbonate ions to from carbonic acid that then will dissociate with water present to then form co2 that is then released to the alveoli
In the lungs there is more oxyhaemoglobin and so will cause more co2 loss from the blood and the opposite will occur in tissue as dexoxygenated blood will carry more co2 back to be released
How is CO2 transported in the blood
If there is more plasma co2 then lower blood pH and cause repsiratory acidosis that causes increase in respiration to drive off co2 = plasma pH regulate breathing
In tissue capillaries co2 combine with water in red blood cell to form carbonic acid that then dissociate to bicarbonate ion that leave RBC and proton that react with HB
In lungs the oxyHB form a stronger acid so release proton that combine with bicarbonate ion to make carbonic acid that dissociate to co2 that then leave blood to alveoli to be released
If there is greater plasma co2 then lower blood pH = respiraotry acidosis that will increase respiration rate
What are ventillation pattern
Thesre are normally auntonomic through the CNS respiratory centres on the medulla of the brain and upper brain stem, there is limited voluntary override and doesnt have intrinsic pacemaker like the heart
Ventialltion rate will be controlled by blood level of co2 rather and than 02 and is directly related to metabolic rate
What are the respiratory centres
There are several groups of neurons located bilatterally in the medualla oblongata and pons
Dorsal Respiratory = Cause inspiration
Ventral respiratory = Modify expriation and inspiration
Pneumotaxic centre = modify the rate and depth of breathing
Apneustic centre = If act unchecked will cause continual inspiration with no stop
These all get input from local centres on brain stem and respond to pH change in the blood on brain stejm surface, there are also peripheral nerves like cranial nerve 9,10 that relate to stress and oxygen tension and input from higher brain allow talking and swallowing
How does normal inspiration take place
The dorsal respiratory group are active causing the inspiratory muscle to contract and inspiration occur, then the DRG are inhibited so the muscles then relax so no inspiration asnd expiration will take place
What happens if cut high in the brain stem
Then due to the majority of breathing controlled by DRG at resting state, then if cut the brain stem high up will stilll breathe normally if the DRG is still intact as we dont need the other groups as much. When the DRG is seperated the DRG causes spontaeneous burst from neurons that have intirinsic repetitive potential so keep the cycle of breathing going
What are the basics of rhythmic breathing
During inspiration the activity of the inspiratory neurones in DRG increase steadily upwards until they stop as the inspiration shut off point where it will end, and then expiration occurs due to elastic recoil of the lungs
What happens when cut higher in brain stem to leave apneustic centre as normal
If there are normal inputs from peripheral nerves like the vagal and glossopharyngeal nerves then the breathing remain normal but if these are stopped the get pneumotaxic breathing so there is no inspiration cut off
The apneustic centre is regulated by vagal inputs from the lug streching as well as pneumotaxic centre
What is the pneumotaxic centre
It is loctated high in the pons and regulate the inspiratory area by controlling through the apneustic centre directlty onto the DRG- it will time the inspiration cut off point in the resting state
When there are stronger pneumotaxic signals then get shorter inspiration as swtich will cut off sooner and if get weaker signals then get longer cut off point so deeper breathing
Overall it can limit the length of the inspiration and change the rate of breathing
What does the ventral respiratory group do
It will modify the inspiration and expiration however it will only be used during excersise so doesnt play a role when at rest
During excerise there is stimualtion of the neurons in the ventral group that cause stronger inspiration and also stimualtion of other neurons that cause more forced expiration at excersise
It also play a role in sending signal to abdomen muscles
What do respiratory centres overall help with
The basic rhythmkic breathing by the DRG
Regulatory effects by pneuomtaxic and apneustic centres
What are the regulatory centres regaulted by inputs wise
Central medullar chemoreceptors - effect the venous system of the heart
Peripheralo sensory signal via vagal and glossopharnygeal nerves to centres = they are strech receptors in chest that prevent breathing in too much and are o2 sensitive
Voluntary cortical factors - talking, swallowing, excersise
What are the central medulla chemoreceptors
They are the most important control for the respiratory centres and work as co2 can leave throughy blood brain barrier unlike carbonbate ions so there are more co2 in cerebral fluid that combine with water to form hydrogen carbonate that dissociate to make H+ ions that bind to the central chemoreceptors and tirgger control of the respiratory control centre and cause more ventialtion
As more H+ then more acidic cerebral fluid that has main effect on the chemoreceptor in triggering them
Co2 has potent but indirect effect due to need to undergo 2 stages to form H+ ions
What is the Herring Breuer reflex
These are stretch receptors in the chest wall, bronchi ,and they lie over smooth muscle and send impulses to the brain to terminate inspiration
They act as protective reflex to prevent over expansio of the lung and coordinate the apneustic and pneumotaxic centres
In infants they regulate basic breathing rhythm as their breathing is strech regulated not co2 regulated
What are peripheral chemoreceptors
These monitor the o2 concentrations but are only used when very low o2 partial pressure as the HB deliver normal amount of o2 if alveolar Ppo2 is >80mmHG so rhen small o2 changes wont change ventialtion so o2 receptors dont need to be sensitive unlike co2 receptors
The oxygen sensors are carotid and aortic bodies located where therev is greatest blood flow in the body so bathed in arterial blood
They have glomus and gilial cells that make dopamine when o2 is low to increase breathing rate and also increase heart rate and blood flow to get more o2 round the body with the greater breathing rate so more gas transfer at the lungs
How do oxygen sensors work
They are able to respond to low o2 by closing K+ channels to cause depolarisation and activation of volatge dependent ca2+ channels that cause ca2+ influx to allow exocytosis of dopamine that increase afferent chemosensory fibres in the vagus signalling to medulla respiratory centres
Type 1 glomus type 2 glial cells allow K+ channels to close and Na enter to depolarise cell similar o2 sensort to that in smooth muscle in lung vessel
How to increase input to respiratory centres overall
Higher centres of the brain, meduallary chemoreceptors for lower pH and increase co2, Carotid and aortic bodies for low o2, Proprioreceptors in muscles, sensory receptors for pain
How to decrease input to respiratory centres
Herring breuer reflex for when lung is too streched during inspiration, higher brain centres
What are the dangers of modifying respiratory centres - Ondine curse
Ondine’s curse = This is congenital central hypoventilation syndromke where there is a defect in the brain stem/ vagal inputs / or the central chemoreceptors so unable to regulate like normal
What is shallow water blackout - dmager of respiratory modfying
Hyperventillating before jumping in water will reduce co2 PP and increase blood PH so less respiratory drive as central chemoreceptor signals drop
Swimming underwater lowers pp o2 so now even though in hypoxic don’t feel need to breathe due to the low co2 after hyperventilating before entering water so then pass out from hypoxia and drown
This is all down due to co2 is the control for the respiratory drive
What is Co2 binding to HB- Danger of modifying respiratory centres
Blood o2 is les in CO poisoning due to more CO bound to HB so then loess oxyhaemoglobin as CO has same binding curve and binds in same way to HB as o2
Due to still not lower arterial blood o2 then don’t get feedback mechanism via carotid and aortic bodies to then increase respiration rate doesn’t happen so then get co2 being unloaded at tissues and not o2