The document discusses alveolar and arterial gases and diffusion across the respiratory membrane. It introduces key terms like PACO2, PAO2, PaCO2 and PaO2. It explains that alveolar levels determine arterial levels through diffusion. Factors like ventilation rate, oxygen concentration, and metabolism can affect both alveolar and arterial gas levels. Optimal ventilation-perfusion matching is needed for efficient gas exchange and delivery of oxygen to tissues while removing carbon dioxide.

1. Alveolar Gases and Diffusion
HDT 2:2 – Semester 2

2. Introduction to Terms
• PACO2 is the partial pressure (gas concentration) of CO2 in the alveoli. PAO2 is therefore the
partial pressure (gas concentration) of O2 in the alveoli.
• PaCO2 is the partial pressure (gas concentration) of CO2 in the arteries. PaO2 is therefore the
partial pressure (gas concentration) of O2 in the arteries.
• Hypoventilation (under-breathing) is where the ventilation of the alveoli does not meet the
metabolic demand for removal of CO2, leading to increased PACO2 and PaCO2.
• Hyperventilation (over-breathing) is where the ventilation of the alveoli exceeds the demand for
removal of CO2 from the blood, resulting in decreased PACO2 and PaCO2.
• Hyperpnoea is an increase in respiration rate, in line with an increased metabolic demand both
form removal of carbon dioxide and supply of oxygen.
• Patients presenting with hyperventilation will be dizzy due to vasoconstriction of cerebral blood
vessels, caused by a fall in PaCO2. Patients will potentially present with carpopedal spasm (check
the hands) caused by decreased levels of ionised calcium resulting in increased excitability.
• Dyspnoea is shortness of breath, apnoea is absence of breathing and tachypnoea is fast
breathing.

3. Alveolar and Arterial Oxygen
• The PAO2 is usually 100mmHg and the PACO2 is usually 40mmHg.
• The PaO2 is usually 95mmHg and the PaCO2 is usually 40mmHg.
• The similarity of the blood and alveolar gases indicates that there diffusion is occurring across the
respiratory membrane at a high efficiency. Alveolar levels DETERMINE the arterial levels.
• Quite logically, the PO2 in the alveoli depends on three factors; the concentration of oxygen in the
environment (usually stable, but changes with altitude), the level of replenishment of oxygen in the
alveoli (determined by ventilation rate and depth) and also the rate of removal of oxygen from
capillary blood vessels.
• Decreasing ventilation rate will decrease PAO2 and increasing ventilation rate will increase PAO2.
As these levels directly influence the PaO2, then blood gases can be said to be directly affected by
ventilation rate, assuming that the environmental oxygen concentration doesn’t change. This is
significant in terms of how breathing can affect the carbonic acid buffer system and lead to
disorders of blood pH.
• If metabolism and therefore the rate of removal of oxygen from capillaries were to increase, then
PAO2 would also decrease, assuming that ventilation rate does not change. In reality, respiratory
compensation kicks in and ventilation rate increases to account for the increased consumption of
oxygen by respiring tissues.

4. Alveolar and Arterial CO2
• The PAO2 is usually 100mmHg and the PACO2 is usually 40mmHg.
• The PaO2 is usually 95mmHg and the PaCO2 is usually 40mmHg.
• Levels of carbon dioxide in the alveoli are determined by two factors; the rate of elimination
through ventilation (affected by the ventilation rate – VA) and the rate of delivery of carbon dioxide
to the alveoli from capillaries (affected by the rate of metabolism and blood flow – VCO2).
• Increasing the rate of alveolar ventilation will decrease the concentration or carbon dioxide in the
alveoli and will lead to a decrease in the arterial carbon dioxide concentration, assuming that
metabolic demand does not change. PACO2 is proportional to 1/VA.
• Increasing the supply of carbon dioxide to the alveoli (i.e. an increase in metabolism) will increase
alveolar concentrations if ventilation rate is unchanged. PACO2 is proportional to VCO2.
• The above quoted values for partial pressures of oxygen and carbon dioxide are normal resting
values where metabolic rate is constant and the alveolar ventilation is 4L/min.

5. Gases
• The alveolar gas equation is PAO2 = PIO2 – (PaCO2/R).
• This equation demonstrates that the level of oxygen in the alveoli (and therefore the blood)
depends on the oxygen concentration of inspired air and the removal of carbon dioxide from blood
(breathing). R is the respiratory gas quotient and is assumed to be the same in all patients, with a
value of 0.8. The only variable in this equation that changes is the PaCO2.
• The difference in PAO2 and PaO2 should be less than 10mmHg (1kPa). Differences larger than
this indicate that either diffusion is not occurring as efficiently as it should be (damage to or
thickening of the respiratory membrane) or that a shunt system is in effect. A shunt system means
that deoxygenated blood is mixing with oxygenated blood at some point and being pumped into
systemic circulation. This can occur via thebesian veins or changes in bronchial-pulmonary
circulation.
• The difference in arterial and alveolar oxygen can be useful but where both are low, a normal
difference will be seen despite a problem existing. This could be alveolar hypoventilation.

6. Gases
• Diffusion across the respiratory membrane is governed by Fick’s Law, which is dependent on the
thickness of the barrier, the gradient, the diffusion coefficient and the surface area.
• Carbon dioxide diffuses across the barrier 20x more efficiently than oxygen due to MW and
charge, and so changes in O2 will be seen in disease states much quicker than carbon dioxide.
• Alveolar gases are able to set blood gases through equilibration of the gradient across the
respiratory membrane. Thickening of the diffusion barrier as part of a disease state can occur, i.e.
emphysema, which leads to less efficient exchange and inability of the system to equilibrate.
• This means that at rest, a patient may be able to breathe normally and achieve acceptable levels
of arterial oxygen, however during exercise the system is less able to compensate for the
increased demand (due to inefficiency of exchange), which leads to fatigue on exertion and
exercise intolerance.

7. Ventilation – Perfusion Matching
• When alveolar ventilation and lung perfusion (V/Q) are matched, then gas exchange, oxygen
delivery and carbon dioxide removal are optimised.
• Assuming that alveolar ventilation in a healthy individual is 4L/min and that blood flow to the lungs
from cardiac output is 5L/min, then the V/Q ratio is 0.8. In a perfect scenario, this value would be
1.
• Values much less than 1 could be caused by poor alveolar ventilation or excessive perfusion of
the alveoli. This would be problematic, as oxygen would be rapidly stripped from the alveoli,
lowering the concentration of oxygen, whilst simultaneously increasing the concentration of
carbon dioxide. This would eventually lead to PAO2 equating with venous blood gases, causing
the patient to be become hypoxic and hypercapnic.
• Values higher than 1 could be caused by excessive ventilation of the alveoli or poor/no perfusion.
This would mean that the alveolar gases would equilibrate with inspired gases, leaving the patient
with hypocapnia and hyperoxia.
• Adjustments are made in the lung to accommodate changes in V/Q, for example; hypoxic blood
causes localised vasoconstriction which limits the oxygen carried from the lungs back to the heart
and allows alveolar concentrations to increase again so that equilibration occurs at the desired
oxygen levels. Another adjustment made is the local bronchoconstriction that occurs when PCO2
concentrations are low in the lungs, which limits the removal of alveolar CO2 and allows
concentrations to build again so that equilibration occurs at the desired level.