Respiratory physiology - ventilation and perfusion Flashcards
Does there have to be a pressure gradient for air to be drawn into the lungs
yes
how is respiratory Air flow determined
by the pressure difference between the mouth and the alveoli ( in the lungs)
has to be a difference either increase p1 or decrease p2
flow results from either an upstream rise ( positive pressure breathing) or a downstream fall in pressure ( negative pressure breathing)
what is positive pressure breathing
increase P1 at the mouth - creating positive pressure in relation to the lungs therefore forcing air in
assisted breathing
what is negative pressure breathing
Decrease P2 relative to the atmosphere so you create gradient drawing air in
what is normal ATM
750mmHg
when you increase the pressure inside the lungs to create gradient and force air out
what is happening
expiration
Pip
inter pleural pressure ( intrathoracic pressure)
Palv
Alveolar pressure - pressure inside the alveoli
Ptp
transpulmoanry pressure (Palv-Pip=Ptp)
Patm
atmospheric pressure - pressure around us
what happens in the mechanism of inspiration
inspiratory muscles contract
diaphragm goes flat
ribs up and out increasing thoracic cavity size
what process
alveolar vol increase
Palv decrease
difference in pressure between alveolar and atm
inspriaotry muscles contract sp Pip more negative so increase difference
Inspiration
what happens in the mechanism of expiration
what happens to Ptp
inspiratory muscles relax , chest wall decreases and goes down so the space between the two membranes decrease so Pip less negative so decrease ptp
what to fibres are used in expiration in elastic recoils
elastin - twice its size
collagen fibres - 2/3 and retain
As we know outer alveoli are affected by the change in inter pleural pressure - this in turn effects the next alveoli along the chain until it reaches the inner depth - what is this called
alveolar interdependence
In a pneumothorax the pleural seal is broken - what does this mean
negative pressure cannot be generated as ventilation is ineffective , lung collapses - alveoli recoil layers can’t hold
Resistance
resistance of respiratory tract to airflow during inspiration and expiration( predominantly expiration)
Affected by diameter of airways
compliance
Measure of ability of the lungs to stretch and expand ( distensibility of elastic tissue)
what is an obstructive disorder
increasing resistance going from a large entry point to small entry point - reduced diameter
what is a restrictive disease
when the ability of expansion s reduced such as fibrosis as thicker lung tissue so have a lower compliance
what is the conduction zone
conducts air breathed in that is filtered warmed and moistened by the lungs
if radius is reduced by half what would the resistance be - knowing that r^4
16
is resistance predominately an expiratory problem
yes
what happens in emphysema
Destruction of the alveolar walls → large air spaces that are not cleared of air on exhalation ( air trapping)
Reduced elastic fibres as a result of destruction which then leads to a reduced elastic recoil
Characteristic “barrel chest”
Decreased gas exchange leads to reduced oxygen diffusion so reduced oxygen levels in the blood - blood vessels also destroyed with destruction of alveolar walls
Even mild exercise can cause breathlessness
what can cause emphysema
farmers lungs
consistent exposure of irritants - smoke, dust chemicals and irritants and that roofs
what causes the genetic version of emphysema
alpha 1 antitrypsin deficiency
Principle Causes of COPD
emphysema and chronic bronchitis
what cells secrete surfactant
type 2 alveolar cells - lipoprotein
what does surfactant do
Lowers surface tension
- increases compliance
- less forces trying to bring the alveoli in making breathing easier
Improves work of breathing
ventilation of alveoli is
4-6L/min
pulmonary blood flow of alveoli
Co= 4-6L/min
Hr - beats per min
SV is volume of blood ejected duringg each ventricular contraction
CO- amount of blood pumped through circulatory system in one minute
where is the greater ventilation and perfusion occur
at the bottom of the lung
does regional V/Q vary and does it have a high impact on gas exchange
yes and no
what is it called when no ventilation can reach area but pulmonary arterial blood can
shunt
breathe in something
when a pulmonary embolism occurs ( travels from somewhere else) and gets lodged you still have ventilation but no perfusion what is this called
alveolar dead space
Stages involved in supply of oxygen and removal of carbon dioxide
Ventilation - gas exchange between atmosphere and alveoli
External respiration - oxygen and carbon dioxide transfer between alveoli and blood
Internal respiration - oxygen and carbon dioxide transfer between blood and tissue
Gas transport - oxygen and carbon dioxide carried in blood between alveoli and tissues
Cellular respiration - oxygen utilization and carbon dioxide production by tissues
what is external respiration
oxygen and Co2 transfer occurs between alveoli and the blood
what is internal respiration
oxygen and CO2 transfer is between the blood and the tissues
In the upper division of the respiratory tree tidal flow is generated by what 1-16 ( conducting airways)
respiratory muscles
in alveoli where respiratory exchange occurs and lower division of the respiratory tree 17-32 how is air moved
passive diffusion driven by partial pressure gradients
daltons law
how gases move down their conc gradient by diffusion
henrys law
how the solubility of a gas relates to its diffusion
in daltons law gases move from a higher partial pressure to a lower partial pressure
ATM 750mmHg
PO2 is 157mmHg
where does this occur
between alveoli and capillaries
then later on between blood and tissue cells
also atmosphere and lungs
partial pressure in solution =
partial pressure in gas phase
in external respiration - deoxygenated blood goes to oxygenated blood and the diffusion of gas is an independent process
Alveolar air is P02 105mmHg
PCO2 = 40mmHg
what is the partial pressure of oxygen and carbon dioxide in deoxygenated blood coming towards alveoli
PO2 = 40mmHg PCO2 = 45mmHg
in internal respiration exchange occurs between systemic capillaries and tissue cells - Oxygen-deoxy
As we know oxygenated blood is PO2=100mmHg
PCO2 = 40mmHg
coming from the alveoli
what is its levels in tissue cells
PO2=40mmHg
PCO2 = 45mmHg
solubility of oxygen in plasma is low only 1.5% what carries oxygen to form Hb-O2
oxyhemoglobin
How do we measure the partial pressure of oxygen
measure the oxygen dissolved in plasma - not carried by Hb
Hb is a globin protein made of 4 polypeptides - 2 alpha and 2 beta - it has 4 haemolytic groups which has a porphyrin ring what ion is at the centre attached by 2 bonds ( 1st bond joins with oxygen molecule )
Fe2+
binding is reversible
when fully saturated how many oxygen molecule does Hb carry
4
on a O2 -Hb saturation curve which - Indicates that the saturation of Hb depends on the PO2
High PO2 → high saturation of HB from oxyhB
Low PO2 → low saturation of Hb ( Hb + O2)
this sigmoidal curve shows that the initial binding is difficult due to finding it but after a conformational change the next 2 can join - why is binding of the last oxygen so hard
full saturation is hard as oxygen has to find the last group
how much oxygen can 1g of Hb hold
1.34ml
At level of pulmonary capillaries what is the level of the partial pressure of O2
02 high partial pressur e of oxygen - most bound to HB
At level of peripheral capillaries Is partial pressure of O2 low or high and why is this beneficial to the tissue?
partial pressure of oxygen is low, saturation of Hb flals rapidly - beneficial for tissue as allows cells to tke up unload O2
in tissues that need more O2 the local environment moves the Hb-O2 curve to the right aidning unloading of O2
true or false
true
what two products increase as a result of tissue metabolism
lactic acid and carbon dioxide
carbonic acid is the product of water and carbon dioxide
produces what
proton and HCO3-
decerases O2 carrying capacity
what side does the curve shift to in Bohr effect as tissue environment
right
so Hb is less saturated and gives up oxygen more easily
what side does the Bohr effect curve shift in the lungs and why
left
Hb can more easily bind to molecules of oxygen so more saturated - low Co2 conc environment
In the foetus at the level of the umbilical vein which way does the Hb-O2 curve shift and why
Up and to the left
oxygen saturation in the placenta is very low compared to maternal blood
Fetus has more Hb than adult and fatal Hb has a higher affinity for oxygen
How Is fatal blood more adapted to get oxygen
higher affinity for oxygen
More Hb than adult
in anaemia what happens to the saturation( PO2 ) and content of the blood
the saturation is not affected so the Hb present will still be effectively saturated
content of Hb in blood is halved
what does PO2 measure
dissolved oxygen
Co2 is 25x more soluble than O2 in plasma - but still needs transport systems
Carried in 3 forms
Dissolved in plasma
Bicarbonate -generated in RBC
Carbamino compounds - generated in RBC
as Co2 content increases the PCO2 increases
In RBC water and CO2 form bicarbonate and move out the cell to maintain electrochemical balance
how do chloride ions move into the cell and HCO3- out
chloride shift
buffer effect
what is the purpose of the chloride shift
exchange of ions that takes place in RBC in order to ensure that no build up of electric change takes place during gas exchange
Co2 can also bind to amino groups to from carbamino compound to take up more Co2 from the tissues
what is produced from both this and bicarbonate process that needs to be buffered
protons
what is the Haldane effect
the lower the amount of oxyHb the higher capacity of blood to carry Co2
In peripheral tissues Hb give up O2 so increases affinity for CO2 increases so has a greater Co2 carriage
However in the lungs Hb binds to O2 so affinity for Co2 decreases so allows removal of it from blood as Hb given up CO2
true or false
true
frequency of ventilation is controlled by rthymic activity of autonomic neurones in respiratory centre found where
medulla
what nerves are involved
phrenic and intercostal nerves
central chemoreceptors respond to PCO2and mechanoreceptors in muscles and joints all stimulate respiration in response to exercise.
what to peripheral chemoreceptors and baroreceptors do
what cranial nerves control motor autonomic function of peripheral chemoreceptors
Baroreceptors stimulate respiration in response to hypotension
Peripheral chemoreceptors ( in aortic and carotid bodies) respond to decreased PO2 , metabolic acidosis
9,10
CO2 is the main controller of ventilation - how does this work
central chemoreceptors respond to this. The higher the partial pressure of CO2 in blood the more acidic CSF becomes ( BBB) driving up ventilation lowing the partial pressure
dependent variable
the effect - the one you are measuring
on Y axis
independent variable
the one you change
Hyperventilation leads to lower levels of CO2 also called ?
Hypocapnia
Hypoventilation increases level of Co2 also called what
Hypercapnia
pleural reflection
where the pleura changes direction
visceral pleura( around lungs) is continuation of parietal pleura true or false
true
medial mediastinum contains the heart true or false
true
function of intercostal muscles
hold ribs in place and assist In inspiration
An 8 year old boy comes into the GP with his mother. His mother explains that he gets SOB quite often and sometimes when he breathes out he makes a strange sound.
What is the most likely dx?
asthma
obstructive
wheeze
tests vital-graph and peak flow
- You’re on ward and a really educated patient comes in and tells you that he has an alpha 1 anti trypsin deficiency. What on earth does this mean?
- He’s got an autoimmune condition
- Gas exchange can’t take place in the alveoli
- He has a neurotransmitter problem
- He is suffering from hyperinflation of the lungs
- He will have peripheral neuropathy
4
Alpha 1 antitrypsin usually stops elastin in the lungs being broken down by proteases.
Therefore a deficiency means elastin is broken down and so lungs can’t inflate and come down and stuff –hyperinflation!
