Ch. 5 Ventilation – Perfusion Relationships
Review V/Q mismatch animation
Oxygen Transport from Air to Tissues
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P ATM = 760 mm Hg
PH20 = 47 mm Hg
Pnormal air ~-> 713 mm Hg (760-47)
FIO2 (fraction of inspired oxygen) = .21 or 21%
PIO2 = 150 mm Hg
Since flow is dependent on the change in pressure the inspired oxygen pressure must be
significantly higher than the pressure in the alveoli
Mouth PO2 = 150 mm Hg
PAO2 = 100 mm Hg (pressure of alveolar oxygen)
PtissuesO2 = ~ 40 mm Hg (i.e. pressure of venous blood (( remember RBC’s are still ¾ saturated w/
O2 upon return to the pulmonary cap’s))
What determines pressure gradient?
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Removal of O2 by pulmonary capillary blood
 Largely determined by O2 consumption in tissues
 Once rbc reaches tissue, O2 leaves rbc d/t very low pressure in mitochondria (1
mm Hg)
o Continual replenishment by alveolar ventilation (continued inspiratory flow)
 Primary determinant of PO2
o Fluctuation of PO2 b/t inspi and expi is only 3 mm Hg, i.e. after expi – PAO2 = 97 mm Hg
o Any decrease in PO2 results in lower PtissueO2 (also why impaired gas exchange results in
rise of PCO2)
Four Causes of Hypoxemia
o Hypoventilation
o Diffusion limitation
o Shunt
o Ventilation – Perfusion inequality
Hypoventilation
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If the alveolar ventilation is abnormally low, the alveolar PO2 falls and PCO2 rises
Causes of hypoventilation:
o Drugs – i.e. morphine, barbiturates – depress medulla  lower inspiratory drive
o Trauma to chest wall (rib fx)
o High resitance to breathing (i.e. asthma attack  constriction of conducting airways)
o PCO2 = (VentilationCO2 / Ventilation alveolar) x K
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This means if you decrease alveolar ventilation by ½:
 PCO2 is doubled
 Thus, PCO2 is inversely proportional to VAO2 (Ch. 2)
Alveolar Gas Equation
o PAO2 = PIO2 – (PACO2/R)
o R = 0.8 for most U.S. diets, appx. O.7 for high fat diet (dependent on CO2 production via
glycolytic pathway)
o PACO2 is normally determined by ABG
o Thus:
o PIO2 = FIO2 x (PATM – PH2O)
o PAO2= .21x(713mmHg) - (PACO2 / 0.8)
Thus during Hypoventilation – a reduction of PAO2 and PaO2 occurs
o Except if person is given oxygen through mask
Hypoventilation
o Always increases the PCO2
o Decreases the PO2 unless additional O2 is inspired
o Hypoxemia is easy to reverse by adding O2
Hyperventilation
o Drives down PaCO2
o Large reserves of CO2 in body via H2CO3 – so takes a longer time for blood PO2/CO2
ratio to balance
Diffusion
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With 100 PAO2 mm Hg and 100 PaO2 mm Hg – (ideal conditions)
o Blood passes alveoli with oxygen content of 18.73 mL O2/dL blood
o Little difference occurs as long as ratio of ventilation/perfusion is proportional  i.e.
1/1  5/5
Shunt
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Means that blood that enters the arterial system essentially bypasses the lungs
o Natural shunts: Thebesian veins, pulmonary veins, pulmonary arterio-venous fistula, or
atrial septal defect
Depresses the arterial PO2
Total amt. of O2 leaving the system is the total flow (Q(dot)T) times the concentration of arterial
blood (Cao2)—(normal CaO2 ~ 18.73 ml/dL of blood)
QT x CaO2 – must be equal to the sum of the amts. Of O2 in the shunted blood
o O2 in shunted blood = Q(dot)S x CV(line)O2; and end-capillary blood (Q(dot)T – Q(dot)S x
Cc’O2
o QS/QT = Cc’O2 – CaO2 / CC’O2 – CVlineO2
o Total blood flow (normally 5L/min) x O2 concentration in arterial blood (normally 18.73
ml/dL) = sum of amounts of O2 in shunted blood and end capillary blood
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Hypoxemia cannot be abolished by giving pt 100% O2 to breathe
 b/c shunted blood bypasses ventilated alveoli
 some O2 added to capillary blood by diffusion, but only to plasma – Hb is usually
saturated (except if cause CO poisoning, sickle cell etc)
 Could worsen hypoxia b/c increasing the alveolar pressure excessively could
further compress capillaries causing a negative PTM
 I.E. to diagnose if shunt is present in hypoxic pt: Take ABG, treat w/ 100% O2,
wait 10 minutes; if PO2 is increased hypoxia is not d/t shunt, if PO2 is
unchanged—shunt is present
Shunts do not normally cause an increase in PaCO2
 Chemoreceptors sense the elevated PaCO2 – hyperventilation to drive down
CO2
Shunt
o Hypoxemia responds poorly to added inspired O2 (only w/ shunt according to
Schwarzstein)
o When 100% O2 is inspired, the PaO2 does not rise to the expected level – Dx. Test
o If the shunt is caused by mixed venous blood, its size can be calculated from the shunt
equation --- (umm sure…)
o http://www.medicalexplorer.org/resp_phys1/index.php?ch=5&fig=8B
Ventilation – Perfusion Ratio
Need balanced flow of pulmonary arterial blood to amt of O2 in alveoli to perfuse
If one increases blood flow too much – Hb is not 100% saturated and hypoxia results
Alternatively if pressure in Alveoli is too high and blood flow slows – Hb is highly saturated (i.e. 19.11
ml/dL) – usually not a problem unless alveolar pressure causes collapse of capillary (i.e. PA >> Pa>Pc)
Effect of altering the ventilation – perfusion Ratio of a lung unit
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Mixed venous blood:
o PCO2 = 40 mmHg – higher pressure of CO2 promotes its exchange across alveoli
o PO2 = 100 mmHg
Diseases such as pneumonia, heart failure, asthma, and emphysema can worsen V/Q mismatch
Nonlinear shape of the oxygen dissociation curve creates a different situation for oxygen
content when we mix blood from well ventilated and poorly ventilated alveoli (as occurs w/ V/Q
mismatch)
Low V/Q ratio produces a PO2 value that corresponds to the steep portion of the oxygen
dissociation curve and thus significantly lowers the oxygen content of the outgoing capillary
blood
High V/Q ratio produces a PO2 value that corresponds to the relatively flat portion of the oxygen
dissociation curve and thus does not significantly elevate the oxygen content of outgoing blood
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http://www.medicalexplorer.org/resp_phys1/index.php?ch=5&fig=8C&w=7
Using the link above, vary the V/Q ratios for three alveoli
o Increase the V/Q ratio in one alveolus while decreasing the ratio of another and note
hwo the small elevation in oxygen content caused by the high V/Q ratio alveolus does
not compensate for the significant decrease in oxygen content caused by the low V/Q
ratio alveolus
Regional Gas Exchange in the Lung
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Apex of lung:
o high V/Q ratio (hypodiffusion) – too little air in alveoli
o PO2: 135 mm Hg
o PCO2: 30 mm Hg
o pH: 7.51
o Site of Tuberculosis: anaerobic
Base of lung:
o Low V/Q ratio ( hyperperfusion or wasted perfusion) – lil too much blood in caps
o PO2: 90 mm Hg
o PCO2: 42 mm Hg
o pH: 7.39
Ventilation/Perfusion ratio decreases as one goes from apex to base
See chart 5-10 (west) for more data on differences b/t apex and base
Effect of Ventilation-Perfusion Inequality on overall gas exchange
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Lung w/ V/Q mismatch is not able to transfer as much O2 and CO2 as a lung that is uniformly
ventilated and perfused
Lung w/ V/Q inequality can’t maintain as high PaO2 or as low PaCO2 as regular lung
Majority of blood leaving the lungs comes from base --- where PO2 is low  depression of Pao2
Alveolar ventilation occurs more evenly from apex to base (but still mostly at base)
Note from previous figure: a V/Q mismatch in one alveoli affect the output from the remaining
alveoli near b/c output PaO2 is an avg. of cap’s and alveoli’s together (i.e. bomb the first exam,
and it’s harder to improve avg.)
CO2 has an easier time diffusing b/c it’s saturation curve is essentially linear
Distribution of Ventilation-Perfusion Ratios
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Great – research oriented physiology stuff….
Shoot someone up full of mixed gases
Although much of the gas goes to areas w/ equal V/Q ratios; some portion goes to V/Q
mismatch areas
o Poor V/Q ratios (0.3 to 0.003)
 This areas are poor at eliminating CO2
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Person had arterial hypoxemia but normal PCO2 (i.e. would be hyperventilating
to keep CO2 normal wasted ventilation)
Remember ideal V/Q = 1
Ventilation-Perfusion Inequality as a Cause of CO2 retention
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Note use of term “magical” in text….
With a V/Q mismatch both PO2 and PCO2 are affected
Alveolar dead space: the volume of the alveoli that are not being perfused (about 20-50 ml in
adults)
V/Q ratio determines the gas exchange in any single lung unit
Regional differences of V/Q in the upright human lung cause a pattern of regional gas exchange
V/Q inequality impairs the uptake or elimination of all gases by the lung
Although the elimination of CO is impaired by V/Q inequality, this can be corrected by increasing
the ventilation of the alveoli
By contrast, the hypoxemia resulting from V/Q inequality cannot be eliminated by increases in
ventilation
The different behavior of the 2 gases results from the different shapes of their dissociation
curves
A-aDO2: how you measure V/Q mismatch
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Subtract arterial PO2 from alveolar PO2  PAO2 – PaO2 = A-a DO2
Normal alveolar-arterial oxygen gradient (breathing room air)
Age
A-aDO2
1-30
<,= 10
40
<,= 12
50
<,= 15
70
<,= 25
Physiological Causes of Hypoxemia
A-aDO2
Response to 100% O2
present at rest
Decreased PIO2 (altitude)
Normal
yes
yes
Alveolar Hypoventilation
Normal
yes
yes
V/Q mismatch
Increased
Yes
yes
Shunt
Increased
NO
yes
Diffusion abnormality
increased
yes
not usually, unless severe