ventilation & perfusion Flashcards
what is the importance in ventilation?
what is alveolar ventilation?
what is dead space air?
what volume is in dead space air?
what is alveolar ventilation a major factor for?
1- the importance of alveolar ventilation is the renew air in gas exchange areas
2- alveolar ventilation is defined as the volume of air entering and leaving the alveoli per minute.
3- dead space air is air the is breathed, but never reaches gas exchange areas, instead filling the respiratory pathway.
4_ normally about 150ml.
5- alveolar ventilation is one of the major factors determining O2 and CO2 concentrations in alveoli.
what is the equation for alveolar ventilation rate?
What is a consequence of gas exchange?
As a consequence of gas exchange, the fraction of O2 decreases and the fraction of CO2 increases in the alveolus
What equation is the relationship between O2 and CO2 given?
what is the alveolar air equation?
What does the alveolar air equation describe?
Relationship between the 2 gases is given by alveolar air equation
Alveolar air equation describes ideal case of what PAO2 should be
When will PAO2 = PaO2?
Why will this not happen?
What can PaO2 be affected by?
What is the Alveolar – arterial (A-a) gradient?
What is a typical value for this?
What can a high value indicate?
If there is perfect transport and no venous admixture, PAO2 = PaO2
This will not happen, as deoxygenated blood from bronchiole vessels can be shunted into the pulmonary vein where there is oxygenated blood (this is a normal process)
PaO2 can affected by disease e.g COPD
The Alveolar – arterial (A-a) gradient is the difference between PAO2 and PaO2
It is normally less than 15 mmHg, with higher values indicating problems with exchange
define the term “ventilation -perfusion ratio”
this is a ratio that is used to assess the efficiency and adequacy of the matching of two variables: ventilation and the air that actually reaches the alveoli.
what is the difference in ventilation across the lung
perfusion increases more than ventilation at the base of the lungs.
what are the reasons for the difference in ventilation across the lungs?
because the pleural pressure at the apex is higher than the pleural pressure at the base.
therefore the alveoli will have different expansions.
why do we have the alveolar gas equation?
- as a consequence of gas exchange, fraction of O2 decreases and CO2 increases in alveolus.
So the relationship between the 2 gases will be given by alveolar air equation.
why is ventilation not uniformly distributed in lung?
what is tis due too?
due to the effects of gravity.
- the alveoli at the apex of the lungs are much more expanded than the alveoli at the base of the lung.
- this is due to there being a greater pressure at the apex of the lung in comparison to the base. (pleural pressure decreases as we move from the apex to the base)
so what alveoli gets most of the ventilation are?
- why is this?
the alveoli at the base will receive most of the ventilation air (the alveoli at the apex will receive the least)
- this is because they alveoli at the base are able to expand more because they start of more crushed than the alveoli at the apex.- under inflated alveoli at the base of the lung receive more tidal volume
- overinflated alveoli at the top have a lower compliance and receive less tidal volume.
Describe the 6 steps in the pulmonary circulation.
Why might blood not reach the apex of the lung?
How can this be overcome in exercise?
6 steps in the pulmonary circulation:
1) Pulmonary circulation begins with RA
2) Deoxygenated blood pumped via RV into pulmonary artery
3) Pulmonary artery divides into right and left main artery then enters lung tissue
4) Ends in mesh like network of capillaries where rbc flow single file through alveolus
5) Capillaries drain into pulmonary venules
6) Finally, 2 large pulmonary veins emerge from each lung to empty into LA
Blood may not be able to reach the apex of the lung if the pressure generated by the right ventricle can’t overcome the pressure in the apex of the lung.
This can be overcome during exercise, as the heart pressure increases, meaning blood can be pushed into the apex of the lung
what are the 2 blood supplies of the lungs?
what do pulmonary arteries carry?
what do pulmonary veins carry?
2 blood supplies of the lungs:
1) Pulmonary arteries
2) Bronchial arteries
Pulmonary arteries carry deoxygenated mixed venous blood from right ventricle to alveoli of lungs
Pulmonary veins return oxygenated blood to left atrium
where do bronchial arteries originate from?
what do bronchial arteries supply?
Bronchial arteries branch from aorta and supply oxygenated blood to conducting airways
where is the majority of venous blood drained from the lungs?
what does this lead to?
Bronchial veins exist, but majority of blood drains into pulmonary veins via a shunt
This leads to Venous admixture, where venous blood is going into oxygenated blood
what are 2 ways that pulmonary arterioles differ from systemic arterioles?
1) Less smooth muscle in pulmonary arterioles
- This is because they deal with lower pressures
- This gives arterioles less control over the blood flow going through capillaries
2) There is less autonomic regulation in lung arterioles
- Lung arterioles expand and contract predominantly as a result of production of metabolic substances
- So in this case, it is about PO2 and PCO2 present in different areas
what happens if perfusion is greater than ventilation?
in disease
CO2 increases -> vasodilation of local airway -> airflow increases
O2 decreases -> vasoconstriction of local blood vessels -> blood Flow decreases
what happens if ventilation is greater than perfusion?
co2 decreases -> vasoconstriction of local airways -> airflow decreases
O2 increases -> vasodilation of local blood vessels -> blood flow increases
What are the hydrostatic and colloid osmotic pressure inside pulmonary capillaries and interstitial fluid?
What do these values result in the net pressure being?
Hydrostatic pressure inside pulmonary capillaries is +7mmHg
Hydrostatic pressure inside pulmonary interstitial fluid is -8mmHg
The colloid osmotic (aka oncotic) pressure inside pulmonary capillaries is +28mmHg
The colloid osmotic pressure inside pulmonary interstitial fluid is +14mmHg
These values result in the net pressure being +1 in favour of hydrostatic pressure, meaning some fluid is lost along the length of the pulmonary capillary and drained by the lymphatic system
Why are positive pressures not common in alveoli?
Why is water needed on the alveoli?
Why do alveoli not fill with fluid?
Positive pressures are not common in alveoli, as alveolar walls are extremely thin and alveolar epithelium is weak and can be ruptured by a positive pressure
Water is needed on the surface of alveoli in order to allow for gas exchange
Alveoli don’t fill with fluid as pulmonary capillaries and lymphatics normally maintain a slight negative pressure in interstitial spaces
This allows excess fluid will be sucked back into interstitial space from alveoli
How can pulmonary oedema be caused?
Pulmonary oedema can be caused by the presence of too much fluid in the interstitial spaces around alveoli
This can lead to fluid collecting in the alveolar walls and alveolar spaces of the lungs, which can affect alveolar capacity, and lead to shortness of breath and coughing
why do alveoli not fill with fluid?
- normally pulmonary capillaries and lymphatics maintain a slight negative pressure in interstitial spaces.
- excess fluid will be sucked back into interstitial space from alveoli
- the lymphatics will suck in the excess fluid due to it being a slight negative pressure (this is why it won’t go to the alveoli)
What does the body match in terms of gas exchange?
What will this lead to in terms of perfusion?
The body tries to match ventilation (where air is going) with perfusion (blood flow) to allow for the most efficient gas exchange possible
This will lead to the middle and base of the lung being better perfused than the apex of the lung, as they receive more of the tidal volume
zone 1
1) Zone 1
* Apex of lung under specific conditions
- PA>PPA>PPV
- No blood flow during all portions of the cardiac cycle
- Blood flow doesn’t occur normally, only under conditions such as shock, haemorrhage or positive pressure being put through airways in medical treatments
(there is no blood flow to these alveoli, so does not happen in human under normal circumstances)
zone 2
2) Zone 2
- Apex to mid lung
- PPA>PA>PPV
- Intermittent blood flow only during the pulmonary artery pressure peaks
- Systolic Ppc > Palv (pressure in pulmonary capillary > pressure in alveoli)
- Diastolic Ppc < Palv
- this is because alveolar pressure is less than the pressure on the pulmonary artery. but it will always have a greater pressure than the pressure in the pulmonary vein.
zone 3
continuous blood flow through capillaries because the pressure in the capillaries will always be lower than the pressure in the pulmonary artery and vein.
3) Zone 3
- Mid to lower lung
- PPA>PPV>PA
- Continuous blood flow during entire cardiac output
- Ppc » Palv
- Get distension of pulmonary capillaries
zone 4
peak flow decreases because of the increase in expansion of alveoli at the base.
4) Zone 4
- Extreme base of lung
- PPA>PPV>PA
- Constriction of extra-alveolar vessels
- Peak flow decreases
How does right and left ventricle cardiac output compare?
What are pulmonary arteries not subjected to?
The cardiac output of the RV is the same as the LV (~ 5L/min)
Pulmonary arteries are not subjected to autonomic regulation by any large degree
How is pulmonary artery vasoconstriction/vasodilation regulated?
Why does the body do this?
How does this mechanism compare with systemic circulation?
What is this mechanism thought to involve?
How do we know this is a local response?
Pulmonary artery vasoconstriction/vasodilation is regulated by PO2 and PCO2:
- Areas of low PO2 (hypoxia) or high PCO2 (hypercapnia)
- arteries constrict so that blood is diverted to better oxygenated areas
- mechanism thought to involve inhibition of K channels on smooth muscle cells
The body diverts blood to well ventilated areas, otherwise this would lead to a ventilation-perfusion mismatch, leading to inefficient gas exchange
this is a local response because it remains even after section of autonomic nerves.
what agents are dilators that affect pulmonary vascular resistance?
- increase in pAO2
- decrease in pACO2
- increase in pH
- H2 agonists
- PGI2 (prostacyclin) PGE1
- B adrenergic agonists
- Bradykinin
- theophylline
- Ach
- NO
what agents are constrictors that affect pulmonary vascular resistance?
- decrease in pAO2
- increase in paco2
- decrease in pH
- H1 agonists
- Thromboxane A2, PGF2alpha, PGE2
- A adrenergic agonists
- serotonin
- angiotensin 2
what is the:
- fraction of total lung volume
- Va/Q
- pO2
-pCO2
pH
- Q (L/min)
for the APEX
what is the:
- fraction of total lung volume
- Va/Q
- pO2
-pCO2
pH
- Q (L/min)
for the BASE
what is the:
- fraction of total lung volume
- Va/Q
- pO2
-pCO2
pH
- Q (L/min)
OVERALL
what 3 places can bronchial arteries arise from?
what 3 things do bronchial arteries supply?
1- bronchial arteries arise from aortic arch, thoracic aorta or their branches
2- arteries will supply:
- smooth muscle of airways
- intrapulmonary nerves
- interstitial lung tissue
what 2 ways does venous blood return to the heart from bronchial circulation?
venous blood returns to the heart via:
- true pulmonary veins
- or drains into bronchipulmonavry veins where it mixes with oxygenated blood from alveoli.
How are ventilation and perfusion matched?
How is ventilation-perfusion ratio (V/Q) defined in a single alveolus and the lungs?
Ventilation and perfusion are matched when pulmonary blood flow is proportionally matched to the pulmonary ventilation - greatest efficiency for gas exchange
Ventilation-perfusion ratio (V/Q):
1) In a single alveolus is defined as alveolar ventilation/capillary blood flow
2) In the Lungs is defined as total alveolar ventilation/cardiac output
What does a V/Q ratio of more than 1 mean?
Where might this be found?
What does a V/Q ratio of less than 1 mean?
Where might this be found?
Where is V/Q ratio exactly 1?
How does all of the blood that perfuses through these areas with different V/Q ratios differ in composition?
What is a normal V/Q ratio?
1) If ventilation exceeds perfusion, V/Q ratio > 1
- Found at the apex of the lung
- Well ventilated alveoli which are poorly perfused with blood.
- Blood leaving the alveoli will be low in CO2 (as there is a large concentration gradient, efficiently blown off), but as the haemoglobin is fully saturated, there will not be a significant increase in O2 levels
2) If perfusion exceeds ventilation, V/Q ratio < 1
- Found at the base of the lung
- Poorly ventilated alveoli with a rich blood supply.
- Alveolar air will equilibrate with the blood and the blood will tend towards the same composition as venous, as ↓fresh air is being brought in.
- Low PO2, high PCO2
3) The V/Q ratio is exactly 1 at somewhere in the lungs between rib 3 and 4 (can be seen on intersection of V and Q lines on diagram
- Perfect matching: well ventilated alveoli with a good perfusion of blood.
- Blood will equilibrate with alveolar air and be rich in oxygen and low in CO2
Normal V/Q ratio is 0.85 (4.2L/min / 5L/min)
This value accounts for overall V/Q ratio of the lungs
define arterial hypoxemia?
define hypoxia?
hypoxemia= abnormal Pao2 (if an adult at sea level has a Pao2 less than 80 mmHg, this is considered hypoxaemia)
hypoxia = insufficient O2 delivery to tissues to carry out normal metabolic functions (Pao2 less than 60 mmHg)
what are the 4 major causes of hypoxemia?
- anatomical shunt (perfusion that bypasses the lungs)
- physiological shunt (absent to areas being perfused)
- V/Q mismatch (low ventilation to areas being perfused)
- hypoventilation (under ventilation of lung units)
what 3 factors will stay the same in anatomical shunts?
1- alveolar ventilation
2- distribution of alveolar gas
3- composition of alveolar gas are normal
What is changed in anatomical shunts?
What kind of shunt are anatomical shunts that cause hypoxaemia?
What are the most common causes of anatomical shunts?
What can not be used as a treatment for hypoxaemia caused by anatomical shunts?
In anatomical shunts, the distribution of CO is changed, as some blood now bypasses gas exchange unit
Shunts that cause hypoxaemia are right to left shunts, as deoxygenated blood is moving into oxygenated blood
The most common causes of anatomical shunts are Cyanotic congenital heart diseases e.g atrioseptal defect, where blood moves from right atrium to left atrium, bypassing the lungs
Hypoxemia caused by anatomical shunts cannot be abolished by giving 100% O2
what are the 3 effects of physiological shunts on perfusion and ventilation?
1- if airway is completely blocked, alveoli supplied by that airway will receive no ventilation
2- all ventilation foes to the other lung units
3- perfusion will be equally distributed to both ventilation and non ventilation lung units.
What is the V/Q ratio of a lung unit without ventilation?
A lung unit without ventilation but with perfusion has a V/Q = 0
What is the most common cause of physiological shunts?
What 4 things might this be due to?
Atelectasis (partial collapse or incomplete inflation of the lung) is the most common cause of a physiological shunt
This may be due to may be due to obstruction by
1) Mucous plug
2) Airway oedema
3) Foreign body
4) Tumour
What do most respiratory diseases produce changes in?
How does this affect individual airways?
What will this lead to?
What will vary in this case?
What can be used to treat hypoxaemia caused by V/Q mismatch?
Most respiratory diseases produce changes of varying extent in lungs (e.g. chronic bronchitis, asthma)
So individual airways will have varying degrees of abnormal ventilation, but perfusion will be normally distributed
This results in V/Q mismatching or low V/Q (V/Q < 1)
Alveolar and end capillary gas compositions will vary according to degree of obstruction
Supplemental O2 can be used to treat hypoxaemia caused by V/Q mismatch, as poorly ventilated units will get enriched O2
effects of V/Q mismatch in different regions?
How does hypoventilation affect gas flow to alveoli?
Who is at risk of developing hypoventilation?
Hypoventilation will result in less fresh gas flow to the alveoli
O2 levels in alveoli will decrease (hypoxia)
CO2 levels will increase (hypercapnia) – If ventilation is halved, arterial CO2 will double
Patients with respiratory muscle weakness (e.g. muscular dystrophy or diaphragmatic paralysis) are at risk of hypoventilation
what are the 4 different types of V/Q mismatch?
