Physiology - new Flashcards
define internal respiration
intracellular mechanisms which consume O2 and produce CO2
define external respiration
exchange of O2 and CO2 between the external environment and the cells of the body
outline the four stages of external respiration
- ventilation
- gas exchange between alveoli and blood
- gas transport in the blood
- gas exchange at tissue level
Boyle’s Law
At any constant temperature the pressure exerted by a gas varies inversely with the volume of the gas
how does Boyle’s law influence ventilation
- air must flow down a pressure gradient from atmosphere to intra alveolar space
- before inspiration, intra-alveolar pressure is equivalent to that of atmposphere
- during inspiration, thorax and lungs expand (inc volume), and according to Boyle’s law this means that the pressure decreases (inverse)
which two forces hold the lungs to the thorax
- intrapleural fluid cohesiveness: water molecules in the fluid are attracted together
- negative intrapleural pressure: lungs expand outwards and chest squeezes inwards
how is volume of thorax increased during inspiration
- diaphragm contracts and flattens - inc volume vertically
- external intercostals lift the ribs and move out the sternum
is expiration passive or active
passive
pneumothorax
- traumatic - hole in chest wall, spontaneous - hole in lung wall
- abolishes transmural pressure gradient, lung collapses to unstretched size and chest wall spring outwards
what gives thle ungs their elastic behaviour, and when is this important
- elastic connective tissue and alveolar surface tension
- important during passive expiration
alveolar surface tension
- the attraction between the water molecules at the liquid air interface, resists stretching of the lungs
- if the alveoli were lined with water alone, they would collapse. so surfactant reduces surface tension by interspersing between the water molecules lining the alveoli
- as, according to LaPlace’s law, smaller alveoli are more likely to collapse. the surfactant lowers the surface tension of smaller alveoli more than larger ones, preventing them from collapsing
law of La Place
P = (2T / r)
- smaller alveoli (smaller radius) are more likely to collapse
- P = inward collapsing pressure
- T = surface tension
what is pulmonary surfactant produced by
type II alveoli cells
RDS of newborn
- developing foetal lungs dont synthesize surfactant unti late in pregnancy, so premature babies dont have enough of it
- there is a really high surface tension between alveoli, so babies have to work really hard to overcome it and inflate the lungs
alveolar interdependence
If an alveolus start to collapse the surrounding alveoli are stretched and then recoil exerting expanding forces in the collapsing alveolus to open it
what are the accessory muscles of inspiration
sternocleidomastoid and scalenus - contract during forceful inspiration
what are the muscles of active expiration
internal intercostal muscles and abdominal muscles
FRC
volume of air in lungs at end of normal passive expiration (ERV + RV)
arond 2.2L in young man
VC
maximum volume of air that can be moved out during a single breath following maximal inspiration (IRV + TV+ ERV)
TLC
- maximum volume of air that the lungs can hold (VC + RV)
- average value: 5700ml
when does RV increase
when elastic recoil is lost eg emphysema, old age
why is it not possible to measure TLC by spirometry
RV cannot be measured by spirometry
FVC and FEV1
- FVC is the maximal volume forcibly expelled from lungs following maximal inspiration
- FEV1 volume of air expired in first second of expiration in and FVC
obstructive and restrictive lung diseases and spirometry
- restrictive: decreased chest expansion - dec FVC and therefpre FEV1
- stiff lungs
- eg ILD, scoliosis, neuromuscular disease, marked obesity
- obstructive: usually normal chest expansion, reduction in airflow (normal/dec FVC), dec FEV1
- air remains inside lungs after full expiration
- eg COPD, asthma, bronchiectasis
dynamic airway compression
- during active expiration, rising pleural pressure compresses alveolia and airway. it helps push air out of alveolus, but is not desirable on airway as compresses it. this increases pressure upstream, helping to open the airways downstream
- this causes no problems in people with normal airways, but if there is an obstruction, the driving pressure is lost. there is a fall in airway pressure downstream and results in airway compression
- this is worsened in patients with decreased elastic recoil of lungs
pulmonary compliance
- pulmonary compliance is the lungs ability to stretch - the distensibility of the elastic tissue
- volume changer per unit pressure change across the lungs
- the less compliant the lungs are, the more work is put in
- compliance is decreased in pulmonary fibrosis, oedema, lung collapse, pneumonia, absence of surfactant - greater change in pressure needed per volume
- this can cause SOB on exertion
what pattern on spriometry does decreased pulmonary compliance cause
restrictive
increased pulmonary compliance
- occurs if elastic recoil is lost eg emphysema
- in emphysema the elastic tissue is lost so the lungs dont bounce back after being stretched. this means that the patients have to work harder to get air out of lungs - they dont manage to get all the air out of the lungs so they are hyperinflated
- compliance also increases with age
compare pulmonary and alveolar ventilation
- PV = TV x RR
- volume of air breathed in and out per minute
- AV = (TV - dead space (inspired air remaining in airways)) x RR
- volume of air exchanged between atmosphere and alveoli per minute
- therefore, AV<pv></pv>
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which type of breathing is more advantageous
- deep, slow breathing due to dead space
- as opposed to shallow, rapid breathing
alveolar dead space
ventilated alveoli which are not adequately perfused with blood
in the systemic system, describe the effects of dec O2 and increased CO2
vasodilation
in the pulmonary system, describe the effect of dec O2 and increased CO2
arteries constrict
airway resistance decreases - increase
Dalton’s Law of partial pressures
- the partial pressure of gas in a mixture of gases that dont react with each other is the pressure that gas would exert if it occupied the total volume in the absence of other components
- the total pressure = P1 + P2 etc
- takes into account fractional composition of gas
why is there a difference in partial pressure gradient between Co2 and O2
- CO2 is 20x more soluble in membranes than O2 - the diffusion coefficient
gradient between alveolar and arterial O2
- a small gradient is normal as VQ match is not perfect
- a big gradient indicates a problem with gas exchange in the lungs or right to left shunt
Fick’s law of diffusion
- The amount of gas that moves across a sheet of tissue in unit time is proportional to the area of the sheet but inversely proportional to its thickness
- lungs provide a very large surface area with thin membranes to facilitate effective gas exchange
Henry’s Law
- the amount of a given gas dissolved in a given type and volume of liquid at a constant temperature is proportional to the partial pressure of the gas in equilibrium with the liquid
- this means that if the partial pressure in the gas phase increased, the concentration of the gas in liquid phase would increase proportionally
- eg amount of O2 dissoved in blood is proportional to partial pressure
- PAO2 depends on PiO2 (which depends on atmospheric pressure and water vapour)
what does oxygen delivery to tissues depend on
oxygen delivery index = oxygen content of arterial blood x cardiac index
- cardiac index is CO related to body surface area
what is the oxygen content of arterial blood determined by
- Hb saturation with O2
- concentration of Hb
how does altitude affect partial pressure of inspired oxygen
- as altitude increases, atmospheric pressure decreases
- this means the partial pressure of inspired oxygen decreases, and so does the amount of it dissolved in blood (Henry’s Law)
- acute response: hyperventilation and increased CO
- acute mountain sickness: headache, fatigue, nausea, tachy, dizzy, sleep disturbance, SOB, unconsciousness
how does anaemia impair oxygen delivery to tissues
decreased Hb concentration and hence decreasd O2 content of blood
what is the significance of sigmoid binding at peripheral tissues
- they get a lot of oxygen for a small drop in capillary partial pressure of oxygen (PO2)
what is the significance of sigmoid binding at pulmonary tissues
a moderate fall in alveolar PO2 will not affect oxygen loading much
Bohr effect
- allows the release of oxygen at tissue by their conditions
- CADET face right
- shift to the right of the oxyhaemoglobin dissocation curve
23 DPG
- causes oxygen unloading - shift to right of curve - when there is low oxyhaemoglobin concentrations
- therefore , it is inhibited in high oxyHb concentrations (dont need the O2 unloading)
how does foetal Hb differ
- 2 alpha and 2 gamma subunits (no beta)
- interacts less with 2,3 DPG
- HbF has a higher affinity for oxygen than HbA, allowing O2 transport from mother even in PO2 in the mother is low
- shift to left of curve
how many haem molecules does one Mb molecule bind
1
myoglobin Oxygen binding
- hyperbolic dissociation curve
- myoglobin releases oxygen at a very low PO2 in the skeletal and cardiac muscles, providing a short term storage of O2 for anaerobic conditions
how is most CO2 transported in the blood
as bicarbonate
Haldane effect
- some CO2 is transported as carbamino compounds - combination of CO2 and globin of Hb = carbamino-Hb
- as reduced Hb can bind more CO2 than HbO2 can, removing O2 from Hb increases its ability to pick up CO2 and CO2 generated H+ ions at tissues
chloride shift
- allows bicarbonate to exit the RBC, in exchange for chloride ions
how is breathing rhythm generated
by the Pre-Botzinger complex in the medullary respiratory centre
modified in pons
what gives rise to inspiration
- dorsal neurones fire in bursts - contraction of inspiratory muscles and inspiration
- they stop firing - passive expiration
active expiration during hyperventilation
- this only happens in hyperventilation (too much inspiration)
- the ventral neurones are activated , and these excite the active expiration muscles (abdominal and internal intracostals) to cause active expiration
pneumotaxic centre
- PC stimulation terminates inspiration
- it is stimulated when the dorsal respiratory neurones fire
- without it, apneusis
apneustic centre
prolongs inspiration
how do we guard against hyperinflation
- there are stretch receptors in the walls of the bronchi and bronchioles - Hering-Breuer reflex
- they are only activated at very large TV (eg >1l)
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joint receptors
- impulses from moving limbs reflexly increase breathing
- this may contribute to the increase ventilation during exercise
what do central cehemoreceptors respond to
- the H+ in CSF , partially influenced by CO2 in blood (CO2 can cross the BBB into the CSF)
hypoxic drive
- only stimulated when PO2 falls v low <8kPa (not relevant in normal respiration) - life threatening situations
- hyperventilation and increase elimination of CO2 from body (important in acid base balance)
- sensed by peripheral chemoreceptors (carotid and aortic bodies)
- important in patients with chronic CO2 retention and at high altitudes
- low PO2 in arterial blood directly depresses the central chemoreceptors and the respiratory centre when <60mmHg
name 5 chronic adaptations to high altitudes hypoxia
- inc RBC production - inc O2 carrying capacity of blood
- inc 23 DPG - inc oxygen offloading into tissues
- inc number of capillaries - blood diffuses easier
- inc number of mitochondria - O2 can be used more efficiently
- kidneys conserve acid - dec pH - right shift of curve, inc O2 offlaoding into tissues
H drive of respiration
- stimulates the peripheral chemoreceptors - hyperventilation and increased CO2 elimination
- PC are weakly stimulated by CO2 in arterial blood
