RESPIRATORY SYSTEM - topic 6 & 7

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84 Terms

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2 main functions of respiratory system

  1. move air into and out of lungs

  2. To ensure that O2 diffuses from the lungs and CO2 moves from blood to the lungs

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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

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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

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Nasal membrane function

humidify and heat air, secrete mucous – provide defence mechanisms

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Nasal conchae function

increase surface area and create turbulent – aid trapping of particles  

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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

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Protective mechanisms of mucous and role of nasal cavity structures

  1. Mucus membranes secrete 1L per day – most is swallowed and in stomach gastric acid kills microorganisms  

  1. Mucus contain lysozymes (antibacterial enzyme) and defensins (antimicrobial proteins) 

  1. 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  

  1. 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 

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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  

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vocal cords

  1. Sound relies on vibrations of true vocal cords, but also the resonating chambers of the throat and mouth and the position of the toungue  

  1. 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)  

  1. Laryngitis – inflammation and swelling of vocal folds – interferes with the vibration of the folds – change in tone – hoarse voice  

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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  

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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  

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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

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Layers of the trachea and their funtions:

trachea is flexible and mobile.

  1. 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  

  1. Submucosa – connective tissure layer with seromucous glands – secretes mucus  

  1. 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  

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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  

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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  

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lymphatic system

very good lymphatic system

  • Serves immune funtion as microoganisms are inhaled 

  • Drains excess fluid from the lungs  

  • Return fluid to subclavian veins  

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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

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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

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expiration

  1. Inspiration muscles relax  

  1. Throacic cavity volumn decreases  

  1. Elastic lungs recoil; intrapulmonary vomun decreases 

  1. Intrapolomonary pressure rises (to + 1mm) 

  1. 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

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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  

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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  

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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  

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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

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factors influencing efficency of polmonary circulation

  • Airways resistance caused by friction 

  • Alveolar surface tension 

  • Lung and thoracic wall complisnce  

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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   

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where is resistance occur the most and least

greatest - medium sized bronchi

least - after terminal bronchi

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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

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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. 

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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  

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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)

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Respiratory volumns and capacities - graph…

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what is obstructive lung disease

airways are narrowed – residual volum, total lung capacity, funtional resisdual capacity – increase values 

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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  

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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  

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Atelectasis (lung callapse) and pneumothorax (air in pleural cavity)  

  1. Wetglad wrap analogy: the pleurl membranes slip over each other easliy but are difficuilt to pull apart  

  1. Lungs are held onto chest wall by visceral membranes ‘stuck’ to parietal; this counters net collapsing force  

  1. 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)  

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what is COPD

Chronic obstructive pulmomary disease - decreased ability to force air out of lungs

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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

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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)

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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

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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  

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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

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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  

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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

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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  

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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  

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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

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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

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partial pressures - diagragm

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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  

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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 

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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

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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

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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 

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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

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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’  

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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

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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  

  1. Dissolved in plasma – only about 1.5 % of O2 is transported dissolved in the plasma  

  1. 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  

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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

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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%

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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   

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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  

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3 methods of CO2 tranport

  1. Disolved in plasma: 7% is transported dissolved in plasama – Co2 is 20x soluble 

  1. 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 

  1. Biocarbonate ion HCO# in plasma: 70% is transported as bicarbonate ion (h30 in plasma  

CO₂ + H₂O ⇌ H₂CO₃ ⇌ H⁺ + HCO₃⁻ 

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what is carbonic anhydrase

enzyme found in RBC allowing fast conversion of water and carbon dioxide to bicarbonate  

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graph with CO2 tissues to blood transport

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what is the haldane effect

less O2 = more CO2 transport

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how is breathing controlled

by neurons and the medulla and pons

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what is poutine respiratory centres

– interact with the medullary respiratory centre to smooth the respiratory patterns  

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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  

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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  

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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  

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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

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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  

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graph on effect of increasing aterial pco2 on venrilation

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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  

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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

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