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SPL

Session name & Code: Factors influencing gas exchange C&B [018]
Session length: 90 minutes in a 120 minutes session shared with [015]
Session format: LGW

Required resources: Flip chart, pen


Aims
To explain how changing ventilation and pulmonary perfusion affect the exchange
of gases in the lungs.

Objectives
By the end of this lecture and associated reading and SPL, you should be able to:

• Describe with the aid of a diagram, the normal regional variations in


ventilation and perfusion in an upright lung
• Describe and explain the effects of gravity on ventilation and perfusion in the
upright lung at rest
• Discuss the effects of changing posture on ventilation and perfusion
• Describe what is meant by a shunt in respect to pulmonary blood flow
• Describe what is meant by a ventilation-perfusion mismatch and what might
cause this
• Explain the intrinsic pulmonary mechanisms which act to minimise ventilation-
perfusion mismatch
• Define the terms hypoxia and hypoxemia
• Describe and explain possible causes of hypoxia.

Core conditions
• Asthma
• Chronic obstructive pulmonary disease including Bronchiectasis
• Respiratory failure: type 1 and 2

Task one: 30 minutes
Allow students to read the following introduction then proceed with the
rest of the tasks.

Regional variation in alveolar ventilation - Due to the effects of gravity,


intrapleural pressure and transpulmonary pressures vary from apex to base of
lung, therefore there is a regional variation in alveolar ventilation. Alveolar
ventilation is greater at the base of the lung than at the apex. This is due to effects
of unequal size of alveoli and their position on compliance curve.

Pulmonary blood flow. Due to the effects of gravity, perfusion pressure, and
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hence blood flow, at the base of the lung is greater than that at the apex in an
upright (standing) individual. Pulmonary blood flow (cardiac output) can be
measured by the indirect Fick method.

Ventilation-perfusion ratio - Although both ventilation and perfusion increase


on moving from the apex to base of lungs, the ratio of V/Q is higher at the apex
than at the base. The consequences of this variation in V/Q on gas exchange in
different parts of the lung, and subsequently on pulmonary venous blood gases, is
that this blood has a lower than expected PO 2 but a relatively normal PCO2. This
ventilation perfusion mismatch is only one cause of hypoxia. Because of the shape
of the oxygen dissociation curve, blood from overventilated alveoli cannot
compensate the hypoxic blood from underventilated alveoli. Physiological
responses to V/Q inequalities include hypoxic vasoconstriction of pulmonary
vessels and hypocapnic bronchoconstriction.

Pulmonary blood flow


Blood flow through the pulmonary artery is usually taken to be equal to cardiac
output but about 1–2% of blood pumped out of the right ventricle bypasses the
lungs via shunts.
The normal pulmonary blood flow or cardiac output in the average person
at rest is 5 L/min or, when expressed as the cardiac index, 3.0 L/min/m 2 body
surface area. Output from the right ventricle is not distributed equally to the two
lungs: about 45% of deoxygenated blood passes through the left lung and 55%
through the right. The time taken by blood to pass through the lungs from
pulmonary artery to left atrium is about 5 seconds but the time blood spends in
the alveolar–capillary complex during which gasesous exchange can take place is

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about 0.75 seconds. This may fall to 0.3 seconds during strenuous exercise, but
the blood is still fully saturated
in that time because haemoglobin has such a high affinity for oxygen.
Volume of blood in lungs
There is an estimated 100 mL of blood in the pulmonary capillaries. The
pulmonary blood volume can vary under different conditions and therefore acts a
reservoir. This reservoir of blood is important in ensuring that the left side of the
heart is filled during diastole and buffer minor irregularities in the output of the
two ventricles.
Pulmonary arterial and venous pressure
Pulmonary arterial pressures ares much lower than systemic arterial pressures, at
about 25/8 mmHg (mean 11–15 mmHg) compared with 120/80 mmHg in the
aorta. The pulmonary arterial walls are about half as thick as corresponding
vessels in the systemic circulation.
There are no valves between the left atrium and the pulmonary vein, so
pressures in the left atrium are equivalent to those in the pulmonary vein and left
atrial pressure may be taken as a measure of pulmonary venous pressure. The
mean left atrial pressure, equivalent to the pulmonary venous pressure, varies
from 0 mmHg to 5 mmHg. The pressure drop across the lungs is about 12 mmHg.
Pulmonary blood vessels
Sympathetic vasoconstrictor fibres supply the pulmonary blood vessels. Little is
known about regulation of pulmonary vessel diameter, but there must be a certain
level of resting tone since, during exercise, pulmonary resistances must decrease
to accommodate a six-fold increase in cardiac output. Pulmonary blood vessels,
unlike vessels in the systemic circulation, are constricted by hypoxia or acidosis.
The response to hypoxia is non-linear and partly dependent on the carbon dioxide
levels. Hypoxic vasoconstriction is very important as a means of diverting blood
flow away from lung regions where the oxygen tension is low, to regions where
oxygen is available to be taken up by haemoglobin. Chronic hypoxia, as seen in
COPD, will lead to pulmonary hypertension and the development of right heart
failure (cor pulmonale).
Variations in pulmonary blood flow
Pulmonary blood flow varies during normal breathing. Intrathoracic pressure falls
during inspiration, so that blood flows more readily through the veins. There is
increased filling of the right ventricle and so increased right ventricular output.
Pulmonary arterial pressure rises and pulmonary blood vessels engorge. However,
pulmonary venous outflow falls, possibly because of the expansion in capillary
volume, and there is a reduction in left ventricular filling and a slight fall in left
systemic pressure.
During expiration the increased volume of blood in the lungs is expelled
through the pulmonary veins with the result that the left ventricular output
increases, causing a rise in systemic blood pressure. Simultaneously the higher
intrathoracic pressure reduces the return of blood to the right ventricle and the
mean pulmonary artery pressure falls.
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Hypoxia - inadequate oxygenation of the tissues. Not the same as hypoxemia,


which refers to the reduced carriage of O2 in arterial blood. Hypoxia may be
classified based on how it is produced:

Hypoxic hypoxia reduced PO2 in arterial blood supply to


the tissue Anaemic hypoxia reduced O2 carrying capacity
of the arterial blood Stagnant hypoxia inadequate
blood flow to the tissues. PaO2 may be normal
Histotoxic hypoxia poisoning at the tissue level, which prevents oxidative
metabolism.

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Task two: 30 minutes
Allow students to work in groups and share their knowledge together then
the tutor will have an open discussion to explain and clarify their answers.

Regional Variations in VA and Q

The following diagram shows the effect of gravity on intrapleural pressure (Ppl)
in the upright lung at FRC (left) and after inspiring 0.5 litres of air (right). In both
cases, there is no airflow and alveolar pressure is equivalent to atmospheric
pressure (i.e. 0 cmH2O)

1. What effect will this gradient of intrapleural pressure have on alveolar size at
FRC?

2. Will the alveoli at the apex, middle and base of the lung show an equivalent
increase in volume with inspiration of 0.5 litres of air? (Hint: consider the
pressure/volume curve for the lung)

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3. How does gravity exert its effect?

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Now consider the following diagram of the upright lung:

4. On which does gravity exert the greatest effect, pulmonary blood flow or
alveolar ventilation?

5. Is the apex of the lung hypoperfused or hyperperfused in relation to its alveolar


ventilation?

6. Is the base of the lung hypoperfused or hyperperfused with respect to its


alveolar ventilation?

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Task three: 30 minutes
Effect of ventilation-perfusion mismatch on arterial blood gas
composition

Divide the students into 4 groups and let them consider the following
hypothetical situations and calculate the systemic arterial PO2, PCO2 and
SO2.

Example 1: Half the alveoli are poorly ventilated and half normally ventilated.
Both halves are equally perfused. Pulmonary capillary blood leaving these two
groups of alveoli has the following composition:

POORLY VENTILATED NORMALLY VENTILATED


PCO2 = 50 mmHg PCO2 = 40 mmHg
PO = 40 mmHg PO = 95 mmHg
2 2
SO = 75% SO = 98%
2 2

What would be the PO2, PCO2 and SO2 of the resultant systemic arterial blood?

Example 2: Half of the alveoli are hypoventilated, half are hyperventilated to


compensate. The blood coming from the two regions has the following
composition:

HYPOVENTILATED HYPERVENTILATED
PCO2 = 50 mmHg PCO2 = 30 mmHg
PO = 40 mmHg PO = 105 mmHg
2 2
SO = 75% SO = 98/99%
2 2

Assuming both regions to be equally perfused, what would be the resultant PO 2,


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PCO2 and SO2 of the resultant
systemic arterial blood?

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