V/Q Relationships/Mismatch Flashcards
Causes of non-uniform ventilation may result from
Collapsed airway (eg. emphysema)
Bronchochonstriction (eg. asthma)
Inflammation (eg. bronchitis)
Compression of airways by tumours, cyst, oedema
Non-uniform compliance (eg. fibrosis or regional variations in surfactant production).
Causes of non-uniform perfusion may result from
Embolism or thrombosis
Compression of pulmonary vessels by high alveolar pressures, tumours, oedema, pneumothorax etc.
Vascular destruction or occlusion of pulmonary vessels by various diseases.
Pulmonary vascular hypotension.
Collapse/over-expansion of alveoli.
Can low PO2 in unverventilated regions be compensated for by normal/over-ventilated regions?
No.
Hb saturation may decrease with low PO2. Hb saturation cannot increase more than 100% (98% normal). Therefore, areas with low PO2 cannot be compensated for by regions with better ventilation. Low V/Q alveoli may cause widened A-a gradient, just like a shunt.
Can low PCO2 in underventilated regions be compensatured for by normal/over-ventilated regions?
Yes.
Linear dissociation curve.
Strong almost linear relationship with ventilation.
Therefore well ventilated areas can compensate for under ventilated areas by resulting in near normal [CO2].
Hypoxemia
Low arterial oxygen (<80mmHg).
Causes of hypoxemia
Many respirtaory diseases are characterised by low PaO2.
There may be a number of causes:
- hypoventilation
- shunt
- V/Q mismatch
- diffusion impairment (rare cause)
What test can you perform in addition to ABG values, to determine the cause of hypoxemia?
The response to breathing 100% oxygen (for approximately 15 minutes) on A-a DO2 may help to determine the cause of hypoxemia.
Check diffusion capacity using carbon monoxide.
Cause of the normal (4-10mmHg) difference between alveolar and arterial PO2.
Due to:
- Venous admixture
- Normal differences in V/Q between apex and base
Hypoventilation
E.g. due to depression of the medullary respiratory centre by drugs (opioids).
Increase in PACO2 and decrease in PAO2.
A-a DO2 remains close to normal as both alveolar and arterial oxygen decrease uniformly.
Breathing 100% oxygen will eliminate hypoxemia.
Intrapulmonary shunt
As blood passes through the pulmonary circulation, a very small portion may perfuse regions that are not ventilated so it remains only partially oxygenated.
High VQ ratio is similar to shunt.
Extrapulmonary shunt
‘Normal shunt’ venous (deoxygenated) blood from the Thebesian veins and bronchial circulations.
Abnormal vascular connection between pulmonary artery and vein (pulmonary arteriovenous fistula) or defects between right and left sides of the heart.
Extrapulmonary shunt/ R-L shunt affect on PPs
A-a DO2 increases.
PaO2 remains low relative to PAO2, when breathing 100% oxygen.
PACO2 is often normal, due to compensatory increase in ventilation to expire CO2.
V/Q mismatch - low VQ ratio
Under ventilated alveoli.
Low PAO2 –> low PaO2. (alveoli with adequate VQ ratio, or over ventilated alveoli are unable to compensate for the drop).
Greater A-a DO2 develops.
Breathing 100% oxygen may improve hypoxemia.
PCO2 may be high, normal or low depending on whether changes in ventilation have been stimulated.
V/Q mismatch - high VQ ratio
Under perfused.
High PAO2 –> low PaO2 due to:
- Minimal exchange due to low/no perfusion
- Alveoli with adequate V/Q ratio, or over ventilated alveoli are unable to compensate for the drop.
Greater A-a DO2 develops.
Breathing 100% oxygen will not improve hypoxemia.
PCO2 may be high, normal or low depending on whether changes in ventilation have been stimulated.
Diffusion impairment
Prevents O2 passing into the blood.
Not usually present at rest, but may appear during exercise, or at altitude.
CO2 diffuses more easily, and diffusion abnormalities do not usually alter CO2 elimination. PACO2 may often be reduced, as ventilation will be increased due to the hypoxemia.
A greater A-a DO2 will develop.
Breathing 100% oxygen will eliminate hypoxemia.
Measure diffusing capacity using CO (very soluble in blood).
