07-11-22 - Pulmonary Circulation, Ventilation/Perfusion Matching Flashcards
Learning outcomes
- Define the term “ventilation-perfusion ratio”
- Describe the differences in ventilation across the lung
- Explain the reasons for the differences in ventilation across the lung
- Describe the differences in perfusion across the lung
- Explain the reasons for the variation in lung perfusion
- Define the term “alveolar dead space”
- Define the term “transmural pressure”
- Describe the mechanisms for actively altering lung perfusion
- Recognise how the V/Q ratio varies across the different lung regions
- Recognise what the average V/Q ratio is for the lung
Lung structure diagram
What is the importance of ventilation?
What is alveolar ventilation?
What is dead space air?
What volume is dead space air?
How is alveolar ventilation rate (VA) calculated (in picture)?
What is alveolar ventilation a major factor for?
- The Importance of pulmonary ventilation is to renew air in gas exchange areas
- Alveolar ventilation (A) is defined as the volume of air entering and leaving the alveoli per minute
- Dead space air is air that is breathed, but never reaches gas exchange areas, instead filling respiratory passages (e.g. nose, pharynx, trachea) Normally about 150ml
- Alveolar ventilation is one of major factors determining O2 and CO2 concentrations in alveoli
What is a consequence of gas exchange?
What equation is the relationship between O2 and CO2 given?
What is the alveolar air equation (in picture)?
What does the alveolar air equation describe?
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?
- As a consequence of gas exchange, the fraction of O2 decreases and the fraction of CO2 increases in the alveolus
- Relationship between the 2 gases is given by alveolar air equation
- Alveolar air equation describes ideal case of what PAO2 should be
- 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
How is ventilation distributed in the lung?
Why is this?
How do pleural pressures compare at different parts of the lungs?
How does this change with inspiration?
Why is this?
How is alveolar inflation different in different parts of the lungs?
How does this affect compliance and tidal volume received at different parts of the lung?
Why does all of this occur?
What does it help?
When does all of this occur?
How can it be changed?
- Ventilation is not uniformly distributed in lung due to effects of gravity
- Pleural pressure is less (more negative) at apex than base of lung, with pleural pressure decreasing further with inspiration
- This is due to the effects of gravity
- Alveoli in the apex of the lungs are more inflated than in the base of the lungs
- This is due to the lung being interconnected and the effects of gravity pulling the upper alveoli down, leading them to be more inflated
- This leads to the overinflated (expanded) alveoli at top having a lower compliance and receiving less of tidal volume
- Alveoli at the base/middle of the lung are less inflated due to the weight of the lung compressing them
- This leads to the underinflated (smaller) alveoli at base/middle of the lung being more compliant and receiving more of the tidal volume
- This all occurs due to the interconnection of the lung tissue, which helps to maintain patency of airways
- All of this occurs during quiet breathing
- During exercise, we need to increase respiratory rate
- The increased pressures generated by the heart will overcome this ventilation issue, and more air will be directed to the apex of the lung as the middle and base of the lung become full
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?
Where do bronchial arteries originate from?
What do bronchial arteries supply?
Where is a majority of venous blood drained from the lungs?
What does this lead to?
- 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
- Bronchial arteries branch from aorta and supply oxygenated blood to conducting airways
- 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 pulmonary arterioles differ from systemic arterioles?
- 2 ways 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 are the hydrostatic and colloid osmotic pressure inside pulmonary capillaries and interstitial fluid?
What do these values result in the net pressure being?
Why are positive pressures not common in alveoli?
Why is water needed on the alveoli?
Why do alveoli not fill with fluid?
How can pulmonary oedema be caused?
- 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
- 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
- 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
What does the body match in terms of gas exchange?
What will this lead to in terms of perfusion?
When will pulmonary capillaries be opened?
What are the 4 different zones of pulmonary flow of the lung?
Where is each zone located?
How do pressures in the alveoli, pulmonary artery, and pulmonary vein compare in each zone?
What is blood flow like through each zone?
- 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
- PA = Alveolar pressure
- PPA = Pulmonary artery pressure
- PPV = Pulmonary vein pressure
- Pulmonary capillaries be opened when the PPA and PPV can overcome the PA
- 4 different zones of pulmonary flow of the lung:
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
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
3) Zone 3
* Mid to lower lung
* PPA>PPV>PA
* Continuous blood flow during entire cardiac output
* Ppc » Palv
* Get distension of pulmonary capillaries
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?
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?
- 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
- Pulmonary artery vasoconstriction/vasodilation is regulated by PO2 and PCO2
- Areas of low PO2 (hypoxia) or high PCO2 (hypercapnia) constrict so that blood is diverted to better oxygenated areas
- The body diverts blood to well ventilated areas, otherwise this would lead to a ventilation-perfusion mismatch, leading to inefficient gas exchange
- This is the opposite effect from that seen in systemic circulation
- This mechanism thought to involve inhibition of K channels on smooth muscle cells
- This is a local response, as it remains even after the cutting of autonomic nerves
What are 11 vasodilators for pulmonary circulation?
What are 10 vasoconstrictors for pulmonary circulation?
What 3 places can bronchial arteries arise from?
What 3 things do bronchial arteries supply?
What 2 ways does venous blood return to heart from bronchial circulation?
- 3 places can bronchial arteries arise from:
1) Aortic arch
2) Thoracic aorta
3) Their branches - 3 things bronchial arteries supply?
1) Smooth muscle of airways
2) Intrapulmonary nerves
3) Interstitial lung tissue - 2 ways venous blood returns to heart from bronchial circulation:
1) True bronchial veins
2) Draining into bronchopulmonary veins where it mixes with oxygenated blood from alveoli (venous admixture)
How are ventilation and perfusion matched?
How is ventilation-perfusion ratio (V/Q) defined in a single alveolus and the lungs?
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?
- 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
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
What are the differences between the apex and base of the lung in:
* Fraction of total lung volume
* VA/Q
* PO2 (mmHg)
* PCO2 (mmHg)
* pH
* Q (L/min)
What is the point of this table?
What makes up the missing values?
- The point of this table is to show the 2 extremes – the base and the apex of the lung
- The missing values are made up by the middle of the lung, which isn’t accounted for in this table
What is arterial hypoxaemia?
What is hypoxia?
What are PaO2 values associated with each?
What should pulmonary vein partial pressures be equal to?
What should happen to pulmonary artery blood?
What is the 2-compartment lung model used for?
What are 4 major causes of hypoxemia?
- Arterial hypoxemia is abnormal PaO2 (if an adult at sea level has a PaO2 of less than 80 mmHg, this is considered hypoxaemia)
- Hypoxia is insufficient O2 delivery to tissues to carry out normal metabolic functions (PaO2 less than 60 mmHg)
- Pulmonary vein blood partial pressures should be equal to what is breathed in at the alveoli
- The CO2 should be removed and O2 replenished in the pulmonary artery blood
- The 2-compartment lung model is useful way to examine V/Q relationships
- 4 major causes of hypoxaemia:
1) Anatomical shunt (perfusion that bypasses lung)
2) Physiological shunt (absent ventilation to areas being perfused)
3) V/Q mismatching (low ventilation to areas being perfused)
4) Hypoventilation (underventilation of lung units)
What 3 factors are the normal in anatomical shunts?
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?
- 3 factors that are the same in anatomical shunts:
1) Alveolar ventilation
2) Distribution of alveolar gas
3) Composition of alveolar gas are normal - 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 3 effects of physiological shunts on perfusion and ventilation?
What is the V/Q ratio of a lung unit without ventilation?
What is the most common cause of physiological shunts?
What 4 things might this be due to?
- 3 effects of physiological shunts on perfusion and ventilation:
1) If airway completely blocked, alveoli supplied by that airway will receive no ventilation
2) All ventilation goes to other lung units
3) Perfusion will be equally distributed to both ventilated and non-ventilated lung units
- A lung unit without ventilation but with perfusion has a V/Q = 0
- 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
What are the 4 different types of V/Q mismatching?
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
