Ventilation and Perfusion Relationships Flashcards
Definition of shunt effect
When gases can diffuse across the alveoli and capillary but there is no ventilation
Definition of dead space
When gases can enter and exit the alveoli but cannot diffuse across to the capillary
Definition of atelectasis
Collapse of the lung, results in the loss of volume for ventilation and gas exchange
Describe the relationship between ventilation and perfusion
What is the value for normal alveolar ventilation
What is the value for normal pulmonary perfusion
V/P roughy equals 1 at the alveolar capillary level
Alveolar ventilation = 5250ml/min
Pulmonary blood flow = 5000ml/min
Describe the 2 normal R => L shunts
- bronchial veins
- thebesian veins
Bronchial veins
-Thoracic aorta => bronchial artery => bronchial veins => pulmonary veins and azygos system
Thebesian veins
-Drain LV => pulmonary veins
Describe these abnormal R => L shunts
- Atelectasis
- Consolidation
- Fallot’s Tetralogy
- Ventricular septal defects
Atelectasis
-collapsed lung => no gas exchange in that region
Consolidation
-fluid filled => no gas exchange
Fallot’s Tetralogy
- ventricular septal defect
- right ventricular hypertrophy
- overarching aorta
- pulmonary stenosis => more blood enters L deoxygenated
Ventricular septal defect
- initially, L => R shunt
- increased pulmonary flow => RV hypertrophy
- R => L shunt
Describe this abnormal L => R shunt
-atrial septal defect
Atrial septal defect
-no effect on PaCO2, PaO2
Direction of blood flow dependent on pressures of both atria
How would you calculate the output of O2 and CO2 in shunts
O2 cont = (% of shunt blood x O2 cont here) + (% of non shunt blood x O2 content here)
CO2 cont = (% of shunt blood x CO2 cont here) + (% of non shunt blood x O2 content here)
Describe the O2 and CO2 dissociation curves
How does small changes in gas content affect PP?
O2 = sigmoid curve
Small decrease in O2 content=> small decrease in PO2 => huge decrease in SaO2
CO2 = linear
Small decrease in CO2 content => small decrease in PCO2
What would happen if you increase ventilation in a R => L shunt
- what happens initially
- what does this results in
- how does this effect CO2
- how does this effect O2
Initially
- PaCO2 is high => decreased pH
- PaO2 is low
Results in
-chemoreceptors detect increased acidity => ventilation increased
CO2 effects
-PaCO2 decreases as more CO2 blown off
O2 effects
- shunted blood does not pass lungs => no effect
- non shunt blood already saturated as much as possible => no effect
- PaO2 stays low
Not addressing the issues with perfusion, no changes in oxygenation
What happens in alveolar hypoventilation
- describe PO2 and PCO2
- describe the renal compensation that occurs
Initially
- PaCO2 high => could lead to CO2 narcosis => respiratory acidosis
- PaO2 is low
Renal compensation if a CO2 retainer
- low pH restored by using up HCO3
- pH restored but PCO2 still too high
Describe normal VQ mismatching
- How does V and Q change as you go down the lung
- What is the normal value for VQ
Both ventilation and perfusion are increased at the base of the lungs due to the effects of gravity.
The effect on perfusion is greater => ratio increases
Perfusion is better than ventilation at base
Ventilation is better than perfusion at apex
What can cause abnormal VQ mismatching and what are the consequences
- VQ too high
- VQ too low
VQ too high
-pulmonary embolism/dead space => hypoxia
VQ too low
-shunt effect/blocked airway => hypoxia
What happens when you increase ventilation in a dead space
- how does PO2, PCO2 start
- why does ventilation increase
- what are the effects on CO2, O2
Initially, low ratio
- good flow, poor vent
- low PO2 and O2
- high PCO2 and CO2
Results in
-increased ventilation due to increased acidity
Effects on CO2
-more CO2 blown off => normal/low
Effects on O2
-underventilated regions get more ventilation => PO2 improves
What happens when you add more O2 rich PiO2 in VQ mismatching
Improvement in under ventilated lungs
No change in R => L shunt as extra O2 cannot reach all blood