Pulmonary 6: Ventilation-Perfusion Relationships Flashcards Preview

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Flashcards in Pulmonary 6: Ventilation-Perfusion Relationships Deck (29)
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Define ventilation. (Work out the equation for adults/children.

V= f x Vt
(15min x 500mL=7.5L/min)

children = 3-5mL/kg


What are typical (volumes) gas:blood ratio? (flows) gas: blood?

Diagram a lung showing typical volumes and flows. (Although there is variation around these values).
Tidal volume, total ventilation, anatomic dead space, frequency, alveolar gas volume, alveolar ventilation, pulmonary capillary blood, pulmonary blood flow

Slide 5

gas: blood

Gas: blood
almost 1:1


What is the functional unit of the lung?

What would happen if all inspired air was diverted to L lung and all the right CO diverted to R lung, what would occur?

The functional unit of the lung is the alveolus including its capillary blood flow.

If all the inspired air was diverted to the L lung and all the right CO was diverted to the R lung, no gas exchange could take place.


What do V/Q ratios dictate? Provide units.

What is the result of collective alveolar units perfusing blood? How do PO2 and PCO2 change?

What is an ideal lung?

Ventilation/perfusion (V/Q) ratios dictate the amount of oxygen added to and CO2 removed from pulmonary capillary blood.

V=mL air/min =mL O2/min
Q=mL blood/min

V/Q= mL O2/mL blood

The collective effort of all alveolar units operating on perfusing blood elevates the PO2 from 40-100mmHg and decrease the PCO2 from 46 to 40mmHg.

Ideal lung (V/Q=1)


What are the PO2 and PCO2 values in:

dry inspired air
humidified tracheal air
alveolar air
mixed venous blood
systemic arterial blood

dry inspired air
PO2: 160
PCO2: 0

humidified tracheal air
PCO2: 0

alveolar air
PAO2: 100
PACO2: 40

mixed venous blood
PvO2: 40
PvCO2: 46

systemic arterial blood
PAO2: 100
PACO2: 40


How do you calculate the PO2 of inspired air?

PO2 falls as the gas moves from the atmosphere
in which we live to the mitochondria where it is utilized. The PO2 of air is 20.93% of the total dry gas pressure (that is, excluding water vapor). At sea
level, the barometric pressure is 760 mm Hg, and at the body temperature of 37°C, the water vapor pressure of moist inspired gas (which is fully saturated with water vapor) is 47 mm Hg. Thus, the PO2 of inspired air is (20.93/100) × (760 − 47), or 149 mm Hg (say 150)


Draw a scheme of O2 partial pressures from air to tissues (atmosphere to mitochondria). Draw ideal/hypoventilation lines. How does PO2 change in air, lung blood, and tissues?

What effect does hypoventilation have on PO2 in alveolar gas?

Why does PO2 fall to about 100mmHg by time reaches alveoli? (What determines PO2 of alveolar gas?)

Slide 6
Scheme of the O2 partial pressures from air to tissues. The solid line shows a hypothetical perfect situation, and the broken line depicts hypoventilation. Hypoventilation depresses the PO2 in the alveolar gas and, therefore, in the tissues.

shows by time O2 has reached alveoli, PO2 has fallen to about 100mmHg (about one-third). This is because the PO2 of alveolar gas is determined by a balance between the removal of O2 by pulmonary capillary blood and its continual replenishment by alveolar ventilation on the other.

When systemic arterial blood reaches tissue capillaries, O2 diffuses to mitochondria where PO2 is much lower.


Describe the V/Q ratio at the level at a single alveolus and at the level of the whole lung.

What is a normal V/Q ratio and what does that mean?

single alvelolus-
alveolar ventilation: capillary flow

whole lung-
total alveolar ventilation: cardiac output

normal is 0.8 (V/Q ratio less than one means perfusion exceeds ventilation)


Draw a graph with PO2 on the horizontal axis and PCO2 on the vertical axis.

How does V/Q ratio change. In what situations does it increase/decrease from normal? What are the values with normal/increased/decreased ratio?


Slide 8 and 9
shunt alveoli are perfused but not ventilated, V/Q ratio =0; alveolar equals mixed venous blood PCO2 and PO2; no gas exchange occurs

as ventilation increases toward a V/Q ratio of 1, normal alveolar and blood gases are achieved.

When perfusion decreases while ventilation is maintained (V/Q ratio increased > 1) alveolar PO2 and PCO2 approach the level of inspired gas.

Alveoli that are ventilated but not perfused (infinite V/Q ratio) contribute to physiological dead space- no gas exchange


What area of the lung receives the largest percentage of ventilation and perfusion?

With distance up the vertical lung will there be a greater drop in blood flow or in ventilation?

The base of the lung receives the largest percentage of ventilation and perfusion. Conversely, the apex receives the lowest percentage of ventilation and perfusion.

With distance up the vertical lung, the drop in blood flow is greater than the drop in ventilation, again due to the fact that gravity exerts a greater effect on the high density blood than on low density air.


From apex to base how does ventilation and perfusion change and which changes faster?

Will apex/base V/Q ratios be greater or less than 1? So how does the ventilation perfusion ratio change as you go up the lung?

Show on a graph rib number on horizontal axis, I/min % of lung volume on L vertical axis and ventilation perfusion ratio on R vertical axis. Draw lines for blood flow, ventilation and V(A)/Q ratio

From apex to base ventilation increases more slowly than perfusion

apex V/Q >1
base V/Q


Analyze the graph on slide 11.

Where are ventilation and blood flow ideally matched? What does this mean in regards to blood flow vs ventilation at the apex/base?

Only in the middle region of the vertical lung are ventilation and blood flow ideally matched.

Base/bottom of lung there is much more blood flow than ventilation, apex/top of lung there is much more ventilation than blood flow.

Ratio is very low at base, ideal in middle, and very high at apex


What is the V/Q ratio like at the apex of the lung? What does this mean in regards to turnover of alveolar gas?

How is PAO2 affected? PACO2?

At the apex of the lung where V/Q is high, the turnover of the alveolar gas with fresh air is more frequent than normal.

This causes alveolar PAO2 to be higher and alveolor PACO2 to be lower than in the middle regions of the lung.


What is the V/Q ratio like at the base of the lung? What does this mean in regards to turnover of alveolar gas?

How is PAO2 affected? PACO2?

At the base of the lung where V/Q is low, the turnover of the alveolar gas with fresh air is less frequent than normal. This causes the alveolar PAO2 to be lower and the alveolar PACO2 to be higher than found in the middle regions of the lung.


On a graph comparing PO2 on horizontal axis and PCO2 on vertical axis, where on the curve would you see low VA/Q or high VA/Q?

Slide 12


Where does the majority of oxygenated blood leaving the lung come from?

majority of oxygenated blood leaving the lung comes from the base

Slide 14.


Describe a normal AaDO2 (alveolar-arterial PO2 difference).

Can you determine the A-a gradient?

What are the reasons this gradient is less?

How do you determine AaDO2?

normal is less than 15mmHg

mean AaDO2 rises about 3-4mmHg per decade of life

A-a gradient is less than [age in years]/4 +4

-V/Q inequality
-Anatomic shunt
-thebesian vessels
-bronchial/pulmonary veins
=2-3% CO

Determination of AaDO2:
PAO2: alveolar gas equation
PAO2/PACO2: arterial blood gas analysis


For Patient A – room air:
PiO2: 150 mmHg

Blood gas analysis:
PaO2 = 95 mmHg
PaCO2 = 40 mmHg


Patient A – room air:
PiO2: 150 mmHg

Blood gas analysis:
PaO2 = 95 mmHg
PaCO2 = 40 mmHg

(150 mmHg – 40 mmHg/0.8) – 95 mmHg

= 100 mmHg – 95 mmHg = 5 mmHg


What is hypoxia and hypoxemia?

What are 4 causes for hypoxemia?

hypoxia- deprivation of the whole body or specific organs and tissues of oxygen, usually due to a mismatch between oxygen supply (too low via vascular routes) and tissues demands (too high in sever exercise).

If there is a complete withdrawal of oxygen supply (as with clot formation), the hypoxia falls out as tissue anoxia (no oxygen).

Hypoxemia is experienced when the oxygen concentration (O2 content) in arterial blood is too low.

Hypoxemia =arterial PO2 (PAO2) less than 80 mmHg under room air at sea level

4 causes: hypoventilation, diffusion limitation, shunt, ventilation-perfusion inequality


Describe how hypoventilation can cause hypoxemia.

(What does alveolar PO2 depend on?)

How are PAO2 and PACO2 and AaDO2 affected?

How can drugs contribute to this problem?

alveolar PO2 depends on rate of removal from the blood (metabolic demand) rate of replenishment of O2 by alveolar ventilation

Alveolar PO2 decreases and CO2 increases. AaDO2 is normal.

drugs that depress central drive to breathe (morphine, heroin, barbiturates) paralyzing drugs
...additional O2 will increase PaO2.

(Slide 18, graph)


Patient B - room air:
PiO2 = 150mmHg

Blood gas analysis:
PaO2 =73 mmHg
PaCO2= 60 mmHg

Calculate PAO2 and AaDO2
What is this a case of?

PAO2 = 150- (60/0.8) = 75 mmHg

AaDO2 = 75-73 = 2mmHg



Describe how diffusion limitation can lead to hypoxemia.

What can lead to diffusion limitation clinically?

Vgas proportional to A/T x D x (P1-P2)
AaDO2 is increased

lung edema, fibrosis, alveolar capillary block

Additional O2 will increase PaO2


Describe how shunt can lead to hypoxemia.

How is AaDO2 affected?
How will additional O2 affect the situation?

AaDO2 is increased

anatomic shunt
physiological shunt (atelectasis)

additional O2 will not increase PaO2 to expected level.


Describe an anatomical shunt.

Two alveoli are ventilated, each of which is supplied by blood from the heart. When ventilation is uniform, half the inspired gas goes to each alveolus, and when perfusion is uniform, half the cardiac output goes to each alveolus. In this normal unit, the ventilation- perfusion ratio in each of the alveoli is the same
and is equal to 1. The alveoli are perfused by mixed venous blood that is deoxygenated and contains increased arterial PCO2. Alveolar O2 is higher than mixed venous O2, and this provides a gradient for
movement of O2 into blood. In contrast, mixed venous
CO2 is greater than alveolar CO2, and this provides a
gradient for movement of CO2 into the alveolus. Note
that in this ideal model, alveolar-arterial O2 values do
not differ.
An anatomic shunt occurs when mixed venous blood bypasses the gas exchange unit and goes directly into arterial blood (Fig. 22-12). Alveolar ventilation,
the distribution of alveolar gas, and the composition of alveolar gas are normal, but the distribution of cardiac output is changed.

The blood that bypasses the gas exchange unit is “shunted,” and because the blood is deoxygenated, the model is called a right-to-left shunt.
Most anatomic shunts occur within the heart, and they occur when deoxygenated blood from the right atrium or ventricle crosses the septum and mixes with blood from the left atrium or ventricle. The effect of
this right-to-left shunt is to mix deoxygenated blood with oxygenated blood, and it results in varying degrees of arterial hypoxemia.


What is a physiological shunt?

A physiological shunt (also known as venous admixture)
can develop when ventilation to lung units is absent in the presence of continuing perfusion. In the two–lung unit model, all of the ventilation
now goes to the other lung unit, whereas perfusion is
equally distributed between both lung units. The lung
unit without ventilation but with perfusion has a V/Q ratio of 0. The blood perfusing this unit is mixed venous blood; because there is no ventilation, no gas
is exchanged in the unit, and the blood leaving this
unit continues to be mixed venous blood. The effect
of a physiological shunt on oxygenation is similar to
the effect of an anatomic shunt; that is, deoxygenated
blood bypasses a gas-exchanging unit and admixes with arterial blood. Clinically, atelectasis (which is
obstruction to ventilation of a gas-exchanging unit
with subsequent loss of volume) is an example of a
lung region with a V/Q of 0. Causes of atelectasis include mucous plugs, airway edema, foreign bodies, and tumors in the airway.


How does ventilation-perfusion inequality lead to hypoxemia?

How is AaDO affected?
How will additional O2 affect PaO2?

ventilation-perfusion mismatch with low V/Q ratio

AaDO2 is increased

Additional O2 will increase PaO2

(slide 26)


What is the most frequent reason for hypoxemia in patients with respiratory disorders?

ventilation-perfusion inequality

slide 26



arterial hypoxemia

Arterial hypoxemia is defined as an arterial PO2 less
than 80 mm Hg in an adult who is breathing room air
at sea level.

Hypoxia occurs when there is insufficient O2 to carry out normal metabolic functions; hypoxia
often occurs when arterial PO2 is less than 60 mm Hg.

Hypercapnia is defined as an increase in arterial PCO2
above the normal range (40 ± 2 mm Hg), and

is an abnormally low arterial PCO2 (usually less
than 35 mm Hg).


Where and why does hypoxic vasoconstriction occur?

How is PVR affected locally? Globally?

Hypoxic vasoconstriction occurs in small arterial
vessels in response to decreased alveolar PO2. The
response is local, and it may be a protective response
by shifting blood flow from hypoxic areas to well-perfused
areas in an effort to enhance gas exchange.

Isolated, local hypoxia does not alter PVR; approximately
20% of the vessels need to be hypoxic before a change
in PVR can be measured. Low inspired O2 levels as a
result of exposure to high altitude will have a greater
effect on PVR because all vessels are affected. High
levels of inspired O2 can dilate pulmonary vessels and
decrease PVR.