Lecture 5 - Gas exchange 2 Flashcards
What is the alveolar gas equation?
PiO2 is 150ml
What does an increased ΔA-a mean?
Decreased gas exchange
What are the 3 causes for impaired gas exchange? (increased ΔA-a >10mmHg)
- Impaired diffuson
- Shunt
- Ventilation-perfusion mismatch (V/Q) mismatch
What are the causes of impaired diffusion?
Decreased surface area
Increased thickness
Decreased PAO2 (breathing low O2 mix)
Exercise
For impaired diffusion to cause arterial hypoxema, what % capcity does diffusion have to be ?
At rest impaired diffusion doesn’t start causing an issue until it reaches about 25% of diffusion capacity
There needs to be significant impairment of diffusion before you get a reduction in PaO2 at rest - but problems are more evident in exercise
Responds well to extra O2
Why is CO2 diffusion rarely impaired?
Since its diffusion constant is 23x greater than O2
Describe what a shunt is?
A shunt is when venous blood is return to arterial circulation of the systemic circuit without going through oxygenated areas of the lung
May be anatomical: cardiac defect, bronchial artery blood, myocardial blood via Thebesian veins
May be patholgical: Alveoli full of pus, meaning that when blood passes through parts of pus filled lung it doesn’t get oxygenated since those areas aren’t ventillated (removing a functional chunk of lung but still perfusing it)
Answer these:
whats a shunt?
How does it affect the ΔA-a gradient?
How does it respond to additonal O2?
How can shunt size be calculated?
- Shunted blood is essentially venous blood being returned to the arterial blood, this reduces PaO2
- The ΔA-a gradient is increased by a shunt
- Shunts respond poorly to additional O2
- Shunt size can be calculated from the shunt equation.
What does a shunt refer to?
A shunt refers to venous blood with re-enters the arterial system without going through the ventilated areas of the lung.
This may be either anatomical e.g. thebesian veins, or pathoglical, eg. pneumonia.
How does pneumonia act as a pathological shunt?
Pnemonia causes the alveolar sacrs to fill with pus, and this prevents them from being ventillated. This means that the blood which flows through the pus filled alveoli will not be able to undergo gaseous exchange to become oxygenated.
What is shunted blood, and what does it dilute?
How can it be calculated
How do shunts respond to O2
Shunted blood is essentially venous blood which bypasses the ventilated areas of the lungs, and is drained into the systemic arterial systemic.
Shunted blood dilutes the PaO2, this is why it is never 100mmHg (~95) (Increases the A-a difference)
Shunt size can calculated via the shunt equation - since putting more O2 into alveoli won’t affect whether blood bypasses the lungs or not.
And shunts respond poorly to O2.
This person has pneumonia.
Would this person be hyperventilating?
And how would you calculate the A-a difference?
So, what’s causing the hypoxemia?
No, they are hypoventilating due to elevated CO2.
calc. A-a difference by PAO2-PaO2, for PAO2 calc. it with alveolar gas equation. If A-a is elevated this indicated gas exchange problem.
Hypoxemia is party caused by the pneumonia causing a shunt (when the affected lung is perfused blood isn’t oxygenated), and party due to the hypoventilating (pus filled lungs are harder to inflate)
What are the 5 mechanisms that can cause hypoxemia
- Reduced PB or FiO2
- Hypoventilation
- Impaired diffusion
- Shunt
- Ventilation-perfusion mismatching
What is the PO2 of gas in the alveolus and in the blood leaving it determined by?
What happens when ventilation aren’t matched?
By the ratio of ventilation to perfusion to that alveolus.
E.g. if theres increased Q, then more PO2 will be in the capillary and less in the alveolus. And if V is increased too much, then theres a limit of Q where only so much blood can pass through at a given time to be oxygenated.
They needs to be a balance between them.
Anytime V and Q aren’t matched there will be impaired gas exchange, causing an abnormal A-a gradient
What can cause non-uniform distribution of alveolar ventilation? (i.e more O2 is going to one area of the lung more than another)
- Non-uniform VA may be caused by
- uneven resistance to airflow (e.g. airways collapse, tumor blocking an airway)
-
Non-uniform compliance if different parts of the lung
- Unven compliance may be a result of fibrosis; regional variation in surfactant production; pulmonary congestion or edema; emphysema; atelectasis (collapse of lung tissue; pneumothorax; compression by tumors/cysts
What can cause a non-uniform perfusion of the lung?
- Embolization
- Thrombosis
- Compression of pulmonary vessels by high alveolar pressurs
- tumors
- exudates
- pneumothorax
- destuction or occlusion of pulmonary vessels by various disease processes
- pulmonary vascular hypotension
- collapse or overexpansion of alveoli
Describe how ventilation and perfusion change from top to bottom of the lung, and how this compares with the change in ventilation
Both ventilation and perfusion increase from the apex of the lung to the base.
The change in perfusion from apex to base is greater than that for ventilation.
A distribution of V/Q ratios exist, even in the normal lung.
In relation to V and Q, compare the alveoli between the apex and base
Alveoli at the apex are relatively underperfused (over ventilated), and at the base they are relatively underventilated (over perfused).
At apex the ratio is 3.4, this means that V is much greater than Q.
At the base the ratio is 0.63, meaning that there is much more perfusion than there is ventilation.
Any disease that impairs ventilation will increase a mismatch of what?
V/Q mismatch causes impairment of overal gas exchange, A-a increases
What are the causes of hypoventilation?
- High work of breathing
- decreased compliance
- increased airways resistance
- Damage to chest wall or fatigue/ paralysis of the respiratory muscles
- respiratory depressants - morphine/ barbiturates
- sleep (relative)
In hypoventilation what happens to the:
- PaCO2
- PaO2
- How is hypoxaemia reversible in hypoventilation?
- Hypoventilation always increases PaCO2, since you can’t breathe it out
- decreases PaO2 unless additional O2 is inspired
- Hypoxaemia reversible by adding O2
- can increase O2 concentration of the air that is reaching the lungs, can outweigh affects of there being less air.
What are the 5 mechanisms that cause arterial hypoxemia?
- Reduced FiO2
- Hypoventilation (hypercapnia)
- Impaired diffusion - Worse with exercise, responsive to O2
- Shunt - unresponsive to O2
- Ventilation-perfusion mismatching, commonest gas exchange abnormality - responsive to O2.
What are the two types of respiratory failure? (Arterial hypoxemia)
And below which PaO2 and above which PaCO2 does this occur
Arterial hypoxema occurs when PaO2 is less than 60mmHg, and when PaCO2 is greater than 55mmHg.
-
Type I: PaO2 low, PaCO2 normal.
- Gas exchange problems - V/Q mismatch, shunt (pneumonia, pulmonary oedema)
-
Type II: PaO2 low, PaCO2 high
- ventilatory failure
- e.g. chronic bronchitis, emphysema
Both types may co-exist
What happens to pH in hypercapnia?
What does CO2 exhalation need to match?
pH increases, since elevated CO2 shifts equillibrium to the right to increase H+
CO2 exhalation needs to match CO2 metabolic production rate, if doesn’t hypercapnia results.
But in hyperventilation respiratory alkalosis occurs due to decreased H+.
