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Ventilation Perfusion Matching- Dean 02/25/11

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cc c **know 4 causes
1.c 
oventilation
2.c Im
airment of diffusion
3.c Intra
ulmonar shunting (R-L shunting)
4.c V/Q mismatching
1. 
oventilation- Alveolar ventilation lower than relative metabolic
demands. Due to over- anesthesia, narcotics, neuromuscular disorders (weak so no

um
ing action), lung diseases(reduced ventilation in
arts)

2. Diffusion im
airment- think Fick eq. Increased thickness will decrease

diffusion. Due to: fibrosis, sarcoidosis-c
 
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, asbestosis ( 

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, edemac

3. Intra
ulmonar shunting(venous admixture)- Alveoli not vec ntilated. igh

CO2 blood b
asses lung and mixes with the O2 rich blood so get mixed
venous and arterial blood. Cannot be fixed with
ure O2. Due to airwa
blockage (mucus), lung diseases (bronchos
asm, alveolar edema)

4.Ventilation/Perfusion Mismatching ± Low PO2 and high CO2 in that area of

lung due to low gas exchange. Low PO2 relative to blood flow so low
V/Q. Normal value= 1.
***This is the most common cause of h
oxemia in
atients with lung
diseases. When in doubt, answe is V/Q mismatch‰c

Ventilation/Pefusion Ratio (V/Q): The
ressures of gases(O2 and CO2)

in the blood blood de
ends on the V/Q ratio and not on the individual
amount of
erfusion and ventilation.

Effect of Altering V/Q Ratio on PO2 and PCO2:

-
c- value is 1. The PO2 becomes 100 mm g and
PCO2 becomes 40 mm g in the blood and in the aveloli after equilibrium is reached.
c- The V/Q ratio is decreased b obstructing ventilation. Alveolar gas will be the same as
the deox genated arterial blood with PO2 = 40 and PCO2 = 45.

c The V/Q ratio is increased b obstructing blood flow. Alveolar gas will be the same as
the inhaled air so PO2 = 150 and PCO2 = 0.

The left correlates to low V/Q and match

the blood- PO2 = 40 and PCO2 = 45.
The right correlates to high V/Q with
PO2/CO2 values matching air- PO2 = 150
and PCO2 = 0.

In an u
right lung, the a
ex has a

high V/Q ratio and there fore has a high
PO2, low PCO2,. The base has
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a low V/Q ratio and there for has a low PO2, high PCO2. The base also has more ventilation and more

erfusion than the a
ex. But the slo
es at which Q and V change are different and therefore the rate are
different. The rate of change of
erfusion is much greater than the rate of change of ventilation (more of a
slo
e) because fluid is heav than blood so it
ools at the base more.

V/Q inequalit in normal lungs results in de
ression of arterial PO2. A-a gradient is due to V/Q mismatch
and anatomical shunting. It is normall around 10 mm g.
Low V/Q units -5 mmg
Anatomical shunting- 5 mmg. ±S stemic venous blood mixes with s stemic arterial blood.
- bronchial circulation ‰
ulmonar vein ‰ s stemic arterial blood (now with a lower O2)
-coronar circulation ‰ thebesian veins ‰ L ventricle and atrium(now goes to the bod )
Large A-a difference and V/Q mismatch =main cause of h
oxmia. A-a gradient increases with age and
lung diseases. **
eri
heral chemorece
tor res
ond to O2, CO2, and
 while central chemorce
tors are
more sensitive to CO2.
Effect of V/Q Inequalit on O2 & CO2 Exchange in Diseased Lungs- low V/Q units increase in number‰
PO2 decreases and the PCO2 increases‰ stimulates chemorece
tors ‰ increase alveolar ventilation‰ CO2
back to normal BUT O2 will remain low.

ow is an increase in ventilation to lungs with V/Q inequalit effective at reducing the PCO2 of arterial
blood but ineffective at raising its PO2? Can be ex
lained b the sha
es of the O2 and CO2 dissociation
curves.

O2 Exam
le- Alveolus A has no ventilation due to a shunt. Alveolus B is normal. The blood from both of
these alveoli is mixing together to lower the PO2. 
erventilation is caused due to
eri
heral can onl
affect alveolus B. But alveoli B is l ing on the
latau stage of the O2 dissociation curve so increase
ventilation does not make a huge difference. Therefore the mixed bloods are still h
oxic even though
ventilation was increased. The increase from alveolus B is so small that is cannot
ull the mixture u
even
though Alveolus A sits on the stee

art of the curve.
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CO2 Exam
le: Alveolus A has no ventilation, alveolus B is normal. A small change makes a big difference
due to the linear curve. So CO2 is more readil com
ensated for.

Increase in ventilation to normal or high V/Q units can com
ensate for low or zero V/Q units and return
arterial CO2 to normal (or below), but cannot return O2 to normal.Because of the trans
ort characteristics of
O2 and CO2 in the blood, as  cc
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Elevated arterial CO2 is observed onl when alveolar ventilation is severel im
aired (h
oventilation)
so high CO2 is not an issue unless there are lots of shunts in lung.

oxic vasoconstriction occurs when there is low amount of PO2 in the alveolus. It is beneficial in
earl to middle stages of lung disease because it redirects blood flow from
oorl ventilated area to a better
ventilated area. But
ulmonar vascular resistance increases eventuall leading to right side heart failure.
Low alveolar CO2 will cause constriction of airwa smooth muscle. This is useful when there is a
blocked arter and no blood getting to the alveolus. It com
ensates for a high V/Q b constricted the smooth
muscle in the alveolus and redirecting air to areas with more blood flow.
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1.c Pure O2 will not fix
a.c 
oventilation
b.c Im
airment of diffusion
c.c Intra
ulmonar shunting (R-L shunting)
d.c V/Q mismatching

2.c Most common cause of h
oxemia

a.c 
oventilation
b.c Im
airment of diffusion
c.c Intra
ulmonar shunting (R-L shunting)
d.c V/Q mismatching

1. C 2. D

Objectives: Discuss changes in lung function that can lead to low O2 in s stemic arterial blood (h
oxemia).
Ex
lain regional gas exchange in normal lungs. Describe how V/Q mismatching can lead to arterial h
oxemia
and onl minor changes in arterial CO2.