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2 main functions of respiratory system
move air into and out of lungs
To ensure that O2 diffuses from the lungs and CO2 moves from blood to the lungs
funtion of alveoli
absorb o2 and secret co2
huge surface area - required to take in enough oxygen into the body and excrete CO2 and accommodate the increased gas exchange which occurs in exercise
respiratory membrane: suited for diffusion of gasses - tissue paper is 15 x thicker
other functions: temporary regulation (panting), Ph regulation, speech and other audible activities, the deep recesses of the lungs are warm and humid, an ideal environment for growth of pathrogens – important to have proper defence system to protect fragile lungs
describe the nasal cavity
lined with olfactory epithelium containing olfactory receptors and pseudo-stratified ciliated columnar epithelium – goblet and cells seromucous glands
The latter secrete water and mucus
Mucus contains lysozymes and defensins
Nasal membrane function
humidify and heat air, secrete mucous – provide defence mechanisms
Nasal conchae function
increase surface area and create turbulent – aid trapping of particles
describe the pharynx and larynx
extends from base of the skull C6 –
3 parts: nasopharynx – air passage with pseudostratified ciliated columnar epithelium, oropharynx, laryngopharynx – common passageway for both food and air – stratified squamous endothelium. Dedicated respiratory tree begins at the larynx – anterior to the laryngopharynx and extends from the 3rd to 6th cervical vertebra
Protective mechanisms of mucous and role of nasal cavity structures
Mucus membranes secrete 1L per day – most is swallowed and in stomach gastric acid kills microorganisms
Mucus contain lysozymes (antibacterial enzyme) and defensins (antimicrobial proteins)
Humidification and warming – humidifies the hair before it reaches lungs – important to protect lining of alveoli from drying out and against irritation from the cold air
Nasal conchae – greatly increase surface area + cause turbulence in nasal cavity – heavier non gaseous particles get trapped against mucous coastes surfaces. Filter, heat and moisten air – important in cold/dry climates
protection against irritants
Nasal sensory epithelium – initiates sneezing
Larynx is very sensitive to anything other than gases and will elecit cough reflex
Carina at the bifurcation of the trachea to the 2 main bronchi – also very sensitive and initiates cough reflex
Irritants also release production of mucous
Spasm of smooth muscle in smaller airways
vocal cords
Sound relies on vibrations of true vocal cords, but also the resonating chambers of the throat and mouth and the position of the toungue
The glottis can close completely (act like spincter) holding air in the lungs when there is a need to increase abdominal pressure e.g on the toilet, or when lifting weights (valsalva manoevre – forced expiration against closed glottis)
Laryngitis – inflammation and swelling of vocal folds – interferes with the vibration of the folds – change in tone – hoarse voice
characteristics of the conducting zone
nose to terminal bronchioles
Conduit for the movement of air to and from the lungs
Contains cilia to move particles in the airways up to the laryngopharynx
Cartilaginous rings or lates at the end of bronchi – hold airways open
As we move down respiratory tree smooth muscle replaces cartilage in bronchioles – this is because gas perfusion can occur, airways can constrict protect
Smooth muscle can contract and close off these small airways
respiratory zone:
where gaseous exchange takes place, consists of the respiratory bronchioles, alveolar ducts and the alveoli
No cilia
No mucous membranes
No cartilage
Lots more smooth muscle + elastic fibres
Alveoli – very thin membrane for gas exchange to occur – risk of bacterial infection as only few defences are available
Dust and asvestos – reach lungs and irritate alveoli – chronic inflamation – scarring and fibrosis of alveoli
differences between conducting and respiratory
. Upper respiratory airways contain mucous secreting goblet cells and a pseudostratified ciliated epithelium – to trap foreign materials
The upper airways contain bands of hyaline cartilage – to keep airways open
As the tubes become smaller and smaller cartilage is replaced by smooth muscle – to promote gas diffusion
The very smallest tubes abd alveoli contain neither smooth muscle nor mucous secreting cells – no obstacles that may reduce gas diffusion
Layers of the trachea and their funtions:
trachea is flexible and mobile.
Mucosa – goblet cells within the ciliated pseudostratified columnar epithelium – thick lamina propria – has rich supply of elastic fibres – allows for stretch of trachea during inspiration
Submucosa – connective tissure layer with seromucous glands – secretes mucus
Adventitia – outermost layer – connective tissue layer reinforced internally by C shaped rings of hyalin cartilage – this keeps trachea patent/ open and attached trachea to surrounding tissue
mucociliary esculator
mucous covered cilia lining of the trachea, bronchi and bronchiols
Cilica bear synchronously and sweep foreign particles trapped in mucus upward toward pharynx, where it is swallowed and digested by gastric juices
What makes escalator movement sluggish – 1. cold air, smoking – cilia covered in tar and semi paralysed
pulmonary blood supply
deoxygenated blood is delivered from the right ventricle via the pulmonary artery that bifurcate repeatedly to become alveolar capillaries
Oxygenated blood is devlived to lung tissues via the bronchial arteries – arise off the aorta and travel along bronchi and bronchioles – retunred to systemic an pulmonary veins via anastomoses
lymphatic system
very good lymphatic system
Serves immune funtion as microoganisms are inhaled
Drains excess fluid from the lungs
Return fluid to subclavian veins
inspiration
active process - contract diaphram inferiorly, use external intercostal muscles to pull the rib cage up and out
Inspiration muscles contract
Throacic cavity volumn increases
Lungs are strecthed; intrapulmonary vomun increases
Intrapolomonary pressure dorps (to – 1mm)
Air gasses flow into the lungs down its pressure gradient until intrapolmonary pressure is 0 (equal o atmospheric pressure)
Changes in anterior – posterior and superuor – inferior dimensions - Ribs are elevated and sternum flares as external intercostal contact. Diaphram moves inferely during contraction
Changes in lateral dimensions – external intercostal contract
Heavy breating assosiated with exertion recruits extra muscle activity e.g sternocleidomastoid, scalnes, pectorals minor – help to lift rib cage
what is boyles law
At a constant temperature pressure of a gas in a closed container varies inversly with its volume
double volumn = halve pressure
P1V1= P2V2
expiration
Inspiration muscles relax
Throacic cavity volumn decreases
Elastic lungs recoil; intrapulmonary vomun decreases
Intrapolomonary pressure rises (to + 1mm)
Air gasses flow out of the lungs down its pressure gradient until intrapolmonary pressure is )
With exertion contraction of abdominal muscles to push diaphragm superiorly, intercostal muscles pull ribs down
pressure in the static chest/ lungs
Asmoshperic pressure Patm 0MMgh (760mm Hg)
Transpulmonary pressure 4 mm Hg (difference between 0 mmHG and – 4mm HG
Intrapleral pressure - -4mm Hg – inside pleural space
Intrapulmonary pressure 0mm Hg – inside alveoli
how is interpleural pressure generated?
the visceral pleara is attched to lungs, and the parietal pleura is attached to chest wall, seperated by a very think layer of fuild
The surface tension of this fluid holds the two pleural layers together
Gladwrap or plastic sheet
Lungs natrual tendency to callaspe (elastic fibres) and the surface tension of the alveoliar fluid, both which tend to collapse the lungs
These forces are opposes by the natural elasticity of the chest wall which creates a force which tents to pull the thorac outwards, enlarging the lungs
When air entres the pleural cavity from the lungs or outside then the seal between the two pleura is broken, the lungs collaspes – atelectasis
pressure during pulmonary ventilation
Intrapulmonary pressure: pressure inside lung decreases as volumn increases during inspiration. Pressure increases during expiration
Intrapleual pressure – plearal cavity pressure becomes more negative as chest will expand during inspiration, returns to intial value as chest wall recoils – negative during both inspiration and expiration
Volumn of breatch: during each breath the pressure gradients move 0.5 litre of air into and out of the lungs
Only 1-2mm change required to create a tidal volumn of 500ml per resting breath
what additional muscles are recruited for forced breathing
forced inspiration - acessory muscles to enlarge thoracic volumn - sternocleidomastoid, scalenes, pectoralis minor.
forced expiration - oblique, transversus abodominal muscles push abdominal viscera superiorly against diaphragm - aided by internal intercoastals
factors influencing efficency of polmonary circulation
Airways resistance caused by friction
Alveolar surface tension
Lung and thoracic wall complisnce
what is airway resistance
resistance caused by friction
very low in healthy lung so that:
very small changes in the pressure gradient allow large changes in the volume of air flowing through the system,
during breathing at rest, the average blood pressyre = 1-2mmHg which allows – 500mL of air to move in and out of the lungs
can change due to conditions such at COPD
minimal in healthy lungs because
Airway diameter in the first part of the conducting zone are large, relative to the low viscosity of air
The terminal bronchioles and alveolar ducts are arranged in parallel and cross-sectional area is large, so resistance is low
where is resistance occur the most and least
greatest - medium sized bronchi
least - after terminal bronchi
alveolar surface tension and the role of surfacant
Alveoli membrane has layer of water of its surface, water generates surface tension at the air-water interface
It creates a subsational force which tends to collapse the alveoli
The surface tension of water incrases with decreasing radius --.> the smaller alveoli tend to collapse and push air into larger ones
Surfactant (phospholipid complex) secreted by the type II alveolar cells is a detergent like substance which reduces surface tension of the alveolar fluid by reducing the force between adjacent water molecules – important to keep alveoli inflated and prevent collapse
The lung is inherently elastic structure. Elastic fibres are stretched during inhalation. Elastic fibres recoil to allow expiration when inspiration ceases
Surfactant inhibits the tendency for alveolar collapse at end of expiration and for small alveoli to collapse into larger spaces
Surfacant is important for the ability to expand the lungd during inspiration in newborn
what is laplaces law
the pressure generated is inversely proportional to the radius of a sphere. A surface tension in the smaller sphere generate higher pressure then in larger sphere. As a result air moves into small sphere to the larger sphere – this causes alveoli to collapse
Surfacatant lowers surface tension more in smaller sphere then in larger sphere – the net result is that pressure in the small and larger speres is similar.
infant respiratory distress syndrome
Premature babies are often born without surfactant, which developes late pregnancy at 32-36 weeks gestation
Alveoli collapse as they take first breth – difficuilt breathing
Unable to inflate alveoli, may collapse into larger alveoli decrease surface area decrease area for gas exchange – baby hypocic and blue (cyanotic)
Treatment: spray natural or synthetic surfacant into airways and the lungs – may use mechanical ventilators or devices that maintain a positive airway pressure throughout the respiratory cycle – prevents alveoli collapsing
complience of respiratory system
In order to expand lungs, respiratory muscles have to overcome – the elastic recoil of the lungs and chest and the alveolar surface tension.
These muscles contract and create the transpulmonary pressure that increase the lung volume during inspiration
For a given change in transpulmonary pressure, the resultant change in lung AP volume AV depends on the “stretchiness” of the lungs and chest wall
The “stretchiness” is called compliance (C) of the lungs/chest
C=AV/AP (in this context, AP = the change in transpulmonary pressure
Respiratory system compliance depends on the “distensibilitiy of the lungs tissure, the chest and alverolar surface tension
Changes in the condition in the lugns and chest will effect total respiratory system compliance and the transpulmonary pressure required to inflate the lungs
If compliance decreases, the respiratory uscles need to generate a larger transpulmonsry pressure to move air nto alveoli
examples: pulmonary fibrosis (excessive connective tissue/scarring in the alveolar walls), absense of adequate amounts of surfacant, aging (ossification of the costal cartilage between sternum and ribs)
Diseases which increase the compliance of the lungs decrease the pressure required to inflate the lung (e.g emphysema)
Respiratory volumns and capacities - graph…
what is obstructive lung disease
airways are narrowed – residual volum, total lung capacity, funtional resisdual capacity – increase values
what is restrictive lung disease
compliance of lungs is decreased, reduced lung volumns esidual volum, total lung capacity, funtional resisdual capacity, vital capacity – decreased values
what is anatomical, alveoli and total dead space
anatomical - air filling the conducting zones (air passages not engaged in respiarotry gas echange – 150ml
Alveolar dead space = inactive alveoli due to collapse or obstruction of mucus
Total dead space = anatomical dead space + alveolar dead space
Atelectasis (lung callapse) and pneumothorax (air in pleural cavity)
Wetglad wrap analogy: the pleurl membranes slip over each other easliy but are difficuilt to pull apart
Lungs are held onto chest wall by visceral membranes ‘stuck’ to parietal; this counters net collapsing force
If a wound allows atmospheric air to seperte the membranes, the intrapleural pressure becomes positive and the force which opposes the collaspung foce is lost (even if lungs are not punctioned)
what is COPD
Chronic obstructive pulmomary disease - decreased ability to force air out of lungs
what is chronic bronchitis
tobacco smoke/air pollution – continual bronchial irritation and inflamation – chronic broncitis (excess mucous productioj, chronic productive cough) -- airways onstruction or air trapping, dyspnea, frquent infection – hypoventilation, hypoxemia, respiratory acidosis
what is emphysema
1 antitrypsin deficiency – breakdown of elastin in connective tissue of the lungs – emphysema – destruction of alveoli walls, loss of lung elacilty -- (Bronchioles collapse during expiration trapping air in lungs) - airways onstruction or air trapping, dyspnoea, frequent infection – hypoventilation, hypoxemia, respiratory acidosis-- (Alveolar capplaries are damaged and increase pulmonary resistance to cause RV hypertrophy)
what is asthma
Chronic inflammatory pulmonary disorder characterised by intermittent, reverisble obstruction of airways - triggered by excercice, allergens
Reversible airway narrowing caused by bronchoconstriction, bronchiolar inflammation, oedema, mucous plugging
Treated with: bronchiodilators in inhalers/ nebulisers and corticosteriods to reduce inflemation of the airways
what influences gas movement across membrane
Exchange of O2 and CO2 at the lungs and in the tissue occurs by simple diffusion
Rate of diffusion is determined by differences in partial pressures of the gas on each side of the membrane
ficks law of diffusion
Describes net rate of diffusion of a gas across a membrane
Rate of diffusion across membranes
Proportional to the differences in partial pressure, the area of the membrane, and the gas solubility
inversely proportional to thickness of membrane and the square root of the molecular weight of the gas
blood pressure x surface area x solubility/thichness of membrane x squarroot of molecular weight of the gas
what is daltons law
in any mixture of gasses the total pressure will be equal to the sum of the partial pressure which each gas generates independtly
what is partial pressure of gas
the pressure excreted by a gas in a mixture so that:
In alveolar aur the partial pressure of O2 is higher than in the venous blood returning to the lungs and the partial pressure of CO2 is lower
In the tissues the partial pressure on O2 is lower then to arterial blood supplying them and the partial pressure of CO2 is higher - oxygen will diffuse from the blood into tissues and CO2 will diffuse from tissues into blood
Capillary blood exchanges O2 and CO2
alveolar gas composition is different to atmospheric air composition because
Gas exchange occurs in the lungs
Air is humidified
Mixing of inspired air with air already in lungs
what happens to partial pressure at altitude
Partial pressure is equivalent to concentration – at altitude concentration of oxygen remains the same but the atmospheric pressure and therefore partial pressure is decrease
At 3000 m elevation atmospheric 523 mmhg – 760 at sea level
If O remains are 21% what would the partial pressure of 02 be – 21% X 523 = 110 mmhg
For summit to Mt Everest – 8880 high – 225 mmhg – PO2 – 48 mmhg - at these altitues O2 tanks are needed
pulmonary and alveolar ventilation rates
Breathing is a tidal process
Tidal volume – vol insp = vol exp
Minute pulmonary ventilation rate – amount of rair brought in and out of respitory system each minute
V = Vt x respiratory frequency
Does not represent the volume of air reaching the respiratory membranes
Anatomical dead space volume – for each 500ml inspired 150ml stays in conducting zone – not contribute to gas exchange
what is alveolar ventilation rate
a measure of the total amount of air reaching alveoli - ‘respiratory zone’
determines gas excahnge because it determines PO2 and PCO2
amount of fresh air reaching alveoli each minute
increasing the depth of breathing enhances the AVR and gas exchange more then raising respiratory rate
vt - vd x F
partial pressures - diagragm
ventilation perfusion coupling
Mismatching these variables is inefficient and will not optimise gas exchange at the respiratory membranes
In working skeletal muscles: tissue )2 levels decrease, and tissue PCO2 increases – hoe are local arterioles likely to response – causes vasodilation to increase blood flow and improve oxygenation – autoregulation by metabolites cause vasodilation
If poorly ventilated with ‘outside air’ they will obtain low )2 levels and Co2 levels with be elevated - how might arterioles respond – vasoconscriction
How is ventilation and perfusion matched to ensure gas ecchange is efficent
What happens if bronchioles is blocked – blood directly to wear oxygen is available – reflex arteriolar vasoconstriction occurs in regions of the lungs where Po2 is low – vasoconstriction directs blood to respiratory membranes where PO2 is high and O2 uptake is more efficient
In alveoli where ventilation is high the high PO2 will dilate the pulmonary arterioles, increasing blood flow into the pulmonary capillaries to improve the pickup of available oxygen
effects CO2 on bronchiolar diameter - bronchiolar smooth muscle is sensitive to changes in CO2
Excess CO2 cause bronchodilation – reduction cause bronchoconstriction
These alter amount of ventilation and perfusion in lung to return V/Q ratio to normal
what is chronic obstructive pulmonary disease
Many poorly ventilated alveoli, extensive arteriolar vasoconstriction, increased pulmonary circulation resistance and pressure, difficult to pump blood out from the right heart against the high pressure in pulmonary arteries, heart enlarges with all the extra work until it fails – RIGHT SIDED HEART FAILURE
what is henrys law
At a constant temperature, the amount of gas that disolved in a liquid is directly proportional to the partial pressure of that gas
A gas with a higher solubility will dissolve in a liquid more readily than a gas with a lower solubility - (if they have the same partial pressure)
Therefore gas disolve in liquid in propotion to their partial pressure and their solbility until equilibrium is reached
Gas exchange takes place between the two phases as long as there is a partial pressure difference between them e.g blood – alveoli
Once equilibrium is reached net gas exchange ceases
If the partial pressure of a gas in a liquid is higher then in the ajacent gas, the disolved gas in the liquid will reeneter the gas
henrys law in relation to carbonated drinks
Removing the cap exposes the liquid inside to a pressure less then what is required to hold the gas in solition; gas escapes and froms bubbles
explain gas solubility
Depends on
Solubility of the gas and the liquid
Temperature of the liquid
Co2 is 20x more soluble in water than oxygen - disolives in water
Nitrogen gas is half as soluble as O2 - almost no NO2 disolves in water
explain what happens if we have high partial pressure - e.g underwater diving
Nitrogen is chemically inert and not a problem – high pressures underwater can cause nitrogen narcosis/ decompression sickness
If the pressure making nitrogen dissolves in the blood it is lowered quickly as the diver repadily acsends, the nitrogen returns to its gaseous state as gas bubbles causing ‘ the bennds’
explain decompresion sickness
Diver experiences excruciating musculoskeletal pain caused by the nitrogen gas bubbles formed in joints, muscles, and bones become disorientated – reseaon for these neural effects are unknown
Treatment: hyperbaric therapy – has pipes that increase pressure inside chamber and slowly decrease pressure , reinstituting compresion and then slow decompression
Hyperbaric therapy- also used to force large amonts of oxygen into the blood by applying oxygen at pressure higher then 760 – anaerobic infections, gangrene, sports injury, CO posioning
explain oxygen transport
O2 is relatively insoluble in water and we could not transport enough in blood if it were only avilbale as a gas disolved in solution
How do we carry oxygen in the blood
Dissolved in plasma – only about 1.5 % of O2 is transported dissolved in the plasma
Bound to heamoglobin in the RBC – 98.5% of O2 is transported from the lungs to the tissues loosly bound to haemoglobin – O2 binding to Hb is rapid and reversible
0.3ml O2/100ml plasma vs 200 O2/100ml blood
oxygen and heamoglobin
oxyhaemoglobin
doxyheamogloin
oxyheamoglobin = HHB
As one O2 molecule is bound, haemoglobins affinity for the other 3 O2 increase
The offloadint or one O2 makes the others easier
oxygen haemoglobin dissociation curve
Lungs hB 100% saturated
In tissue 75% - at rest – during excersise more may be taken
At high Po2 (lungs) a large amount of O2 can bind to HB
At low PO2 (tissues) HB readily releases O2 for it to diffuse to tissues
Altitude - At high Po2 – large changes in PO2 cause only small changes in HB saturation
Excersise – at low Po2 – large changes in Po2 cause large changes in HB saturation – excersise 60% o2 offloaded to tissues compared to 25%
what is the Bohr effect
increased H or PCO2 in tissue decreases hb saturation at the same PO2 – during excersise tissue H and PCO2 levels increases. Oxygen binds less tightly to HB at higher H and PCO2 is released. oxygen unloading is facilitated by changes in the comfirmation of the HB molecule
Increased release of oxygen by the heamoglobin in response to increase H concentrations and Partial pressues
effect of temperature on oxygen binding
during excersise temperature will increase. Oxygen binds less tightly to HB at a higher temperature. Oxygen unloaded is facilitated by changes in the conformation of HB molecules
3 methods of CO2 tranport
Disolved in plasma: 7% is transported dissolved in plasama – Co2 is 20x soluble
Bound to heamoglobin: 20% transported, loosely and reversibly bound to NH2 groups of heamoglobin, not attached to dedicated haem binding sites. Therefore no competition with O2 binding sites. CO2 attaches to hb when PCO2 is relatively high in tissues and detaches when PCO 2 is relatively low in the lungs
Biocarbonate ion HCO# in plasma: 70% is transported as bicarbonate ion (h30 in plasma
CO₂ + H₂O ⇌ H₂CO₃ ⇌ H⁺ + HCO₃⁻
what is carbonic anhydrase
enzyme found in RBC allowing fast conversion of water and carbon dioxide to bicarbonate
graph with CO2 tissues to blood transport
what is the haldane effect
less O2 = more CO2 transport
how is breathing controlled
by neurons and the medulla and pons
what is poutine respiratory centres
– interact with the medullary respiratory centre to smooth the respiratory patterns
what is the medullary respiratory centre
Ventral respiratory group – contains rythme generators whose output drives respiration
Dorsal respitory group intergrates peripheral sensory input and modifies the ryhtmes generated by the VRG
Planic nerve innervates the diaphram
respiratory centres in the brain
stem control breathing with the inputsfrom mechano- and chemoreceptors and higher brain centres
Mophine, heroin and alchol – overdose—ceesation of breathing, inhibits neurons in VRG
Poliomyelitis damages peripheral nerves, sometimes affecting phrenic nere to the diaphragm
PRC – has inputs to the VRG to smooth and fine tunes brealthing , sleep and excersise
describe - neural and chemical control of breathing feedback from receptors to the respiratory centres
Inspiration depth is determined by how many motor units the VRG excites to elicit respiratory muscle comtraction – more muscles = deeper breath
Rate is determined by how long the inspiratory neurons are active
Both influenced by aterioal blood H, CO2 and O2, central and peripheral chemoreceptors
describe - peripheral chemoreceptors
Decreased breathing – increased alveolar PCO2 and decreased PO2
Increased PCO2 – increased formation of H in ateriol blood
Changes detected in peripheral chemoreceptors in the biurcation of the common corotid artery and aortic arch
Respond to decrease O2 increase CO2 increase H
Increase firing rate --- increase flow of formation to respiratory control neurons – increase rate of depth of breathing
describe central chemoreceptors
On the anterior part of the medulla next to th respiratory control centres
Much more senstive than peripheral chemoreceptors
Stim breathing in response to much smaller changes in PCO2
This is the major way breathing is controlled in response to changes in PCO2
Respond to increased H not PCO itself – H changes as a result of changes in the PCO2 in the ateriol blood
H cannot cross BBB but CO2 can
It is the hydrogen ions produced by the carbonic anhydrase reaction which stimuate the central chemoreceptors and stimulate breathing via the medullary neruons
graph on effect of increasing aterial pco2 on venrilation
excersie and ventilation
Ventilation adjust very quickly after initation of excersise
Not dependent on arterial 02 and CO2 changes
Psychological stimuli stimulate respiratory centres
Muscle and joint proprioceptors are activated in exercise and stimulate respiratory centres
Transmit information to respiratory centres in brain to increase breathing and ventilation
This provides more oxygen to the excersising muscles
Details of the mechanism are unclear
describe the inflation reflex
hering breuer reflex - inspiratory center - phrenic nerve - diaphragm contracts -- stretch receptor in lung - vagus nerve
In infants this plays part in regulating the basic ryhtm of breathing preventing over inflation of the lungs – important in adults only when tidal volumn is large – excercise