Pulmonary gas exchange: the basics

Published on 09/04/2015 by admin

Filed under Surgery

Last modified 22/04/2025

Print this page

rate 1 star rate 2 star rate 3 star rate 4 star rate 5 star
Your rating: none, Average: 0 (0 votes)

This article have been viewed 1341 times

1.2 Pulmonary gas exchange

The basics

Our cells use oxygen (O2) to generate energy and produce carbon dioxide (CO2) as waste. Blood supplies cells with the O2 they need and clears the unwanted CO2. This process depends on the ability of our lungs to enrich blood with O2 and rid it of CO2.

Pulmonary gas exchange refers to the transfer of O2 from the atmosphere to the bloodstream (oxygenation) and CO2 from the bloodstream to the atmosphere (CO2 elimination).

The exchange takes place between tiny air sacs called alveoli and blood vessels called capillaries. Because they each have extremely thin walls and come into very close contact (the alveolar–capillary membrane), CO2 and O2 are able to move (diffuse) between them (Figure 1).

image

Figure 1 Respiratory anatomy.

Pulmonary gas exchange: partial pressures

ABGs help us to assess the effectiveness of gas exchange by providing measurements of the partial pressures of O2 and CO2 in arterial blood – the PaO2 and PaCO2.

Partial pressure describes the contribution of one individual gas within a gas mixture (such as air) to the total pressure. When a gas dissolves in liquid (e.g. blood), the amount dissolved depends on the partial pressure.

Note

PO2 = partial pressure of O2

PaO2 = partial pressure of O2in arterial blood

Gases move from areas of higher partial pressure to lower partial pressure. At the alveolar–capillary membrane, air in alveoli has a higher PO2 and lower PCO2 than capillary blood. Thus, O2 molecules move from alveoli to blood and CO2 molecules move from blood to alveoli until the partial pressures are equal.

A note on … gas pressures

At sea level, atmospheric pressure (total pressure of gases in the atmosphere) = 101 kPa or 760 mmHg

O2 comprises 21% of air, so the partial pressure of O2 in air

= 21% of atmospheric pressure

= 21 kPa or 160 mmHg

CO2 makes up just a tiny fraction of air, so the partial pressure of CO2 in inspired air is negligible

Carbon dioxide elimination

Diffusion of CO2 from the bloodstream to alveoli is so efficient that CO2 elimination is actually limited by how quickly we can “blow-off” the CO2 in our alveoli. Thus, the PaCO2 (which reflects the overall amount of CO2 in arterial blood) is determined by alveolar ventilation – the total volume of air transported between alveoli and the outside world every minute.

Ventilation is regulated by an area in the brainstem called the respiratory centre. This area contains specialised receptors that sense the PaCO2 and connect with the muscles involved in breathing. If it is abnormal, the respiratory centre adjusts the rate and depth of breathing accordingly (Figure 2).

image

Figure 2 Control of ventilation.

Normally, lungs can maintain a normal PaCO2, even in conditions where CO2 production is unusually high (e.g. sepsis). Consequently an increased PaCO2 (hypercapnia) always implies reduced alveolar ventilation.

Key point

PaCO2is controlled by ventilation and the level of ventilation is adjusted to maintain PaCO2within tight limits.

A note on … hypoxic drive

In patients with chronically high PaCO2 levels (chronic hypercapnia), the specialised receptors that detect CO2 levels can become desensitised. The body then relies on receptors that detect the Pao2 to gauge the adequacy of ventilation and low Pao2 becomes the principal ventilatory stimulus. This is referred to as hypoxic drive.

In patients who rely on hypoxic drive, overzealous correction of hypoxaemia, with supplemental O2, may depress ventilation, leading to a catastrophic rise in PaCO2. Patients with chronic hypercapnia must therefore be given supplemental O2 in a controlled fashion with careful ABG monitoring. The same does not apply to patients with acute hypercapnia.

Haemoglobin oxygen saturation (SO2)

Oxygenation is more complicated than CO2 elimination. The first thing to realise is that the PO2 does not actually tell us how much O2 is in blood. It only measures free, unbound O2 molecules – a tiny proportion of the total.

In fact, almost all O2 molecules in blood are bound to a protein called haemoglobin Hb (Figure 3). Because of this, the amount of O2 in blood depends on two factors:

1. Hb concentration: this determines how much O2 blood has the capacity to carry.
2. Saturation of Hb with O2(So2): this is the percentage of available binding sites on Hb that contain an O2 molecule – i.e. how much of the carrying capacity is being used (Figure 4).
image

Figure 3 Relative proportions of free O2 molecules and O2 molecules bound to haemoglobin in blood.

image

Figure 4 Haemoglobin oxygen saturation.

Note

SO2 = O2saturation in (any) blood

SaO2 = O2saturation in arterial blood

A note on … pulse oximetry

SaO2 can be measured using a probe (pulse oximeter) applied to the finger or earlobe. In most cases it provides adequate information to gauge oxygenation, but it is less accurate with saturations below 75% and unreliable when peripheral perfusion is poor. Oximetry does not provide information on PaCO2 so should not be used as a substitute for ABG analysis in ventilatory impairment.

Key point

PO2 is not a measure of the amount of O2 in blood – ultimately the SaO2and Hb concentration determine the O2 content of arterial blood.

Oxyhaemoglobin dissociation curve

We now know that the amount of O2 in blood depends on the Hb concentration and the SO2. So what is the significance of the PO2?

PO2 can be thought of as the driving force for O2 molecules to bind to Hb: as such it regulates the SO2. The oxyhaemoglobin dissociation curve (Figure 5) shows the SO2 that will result from any given PO2.

image

Figure 5 Oxyhaemoglobin dissociation curve. The curve defines the relationship between PO2 and the percentage saturation of haemoglobin with oxygen (SO2). Note the sigmoid shape: it is relatively flat when PO2 is >80 mmHg (10.6 kPa) but steep when PO2 falls below 60 mmHg (8 kPa).

In general, the higher the PO2, the higher the SO2, but the curve is not linear. The green line is known as the ‘flat part of the curve’: changes in PO2 over this range have relatively little effect on the SO2. In contrast, the red line is known as the ‘steep part of the curve’: even small changes in PO2 over this range may have a major impact on SO2.

Note that, with a ‘normal’ PaO2 of around 13 kPa (100 mmHg), Hb is, more or less, maximally saturated (SaO2 > 95%). This means blood has used up its O2-carrying capacity and any further rise in PaO2 will not significantly increase arterial O2 content.

Key point

PO2 is not the amount of O2 in blood but is the driving force for saturating Hb with O2.

Key point

When Hb approaches maximal O2 saturation, further increases in PO2 do not significantly increase blood O2content.

Alveolar ventilation and PaO2

We have now seen how PaO2 regulates the SaO2. But what determines PaO2?

There are three major factors that dictate the PaO2:

1. Alveolar ventilation
2. Matching of ventilation with perfusion (V/Q)
3. Concentration of O2 in inspired air (FiO2)

Alveolar ventilation

O2 moves rapidly from alveoli to the bloodstream – so the higher the alveolar PO2, the higher the PaO2.

Unlike air in the atmosphere, alveolar air contains significant amounts of CO2 (Figure 6). More CO2 means a lower PO2 (remember the partial pressure of a gas reflects its share of the total volume).

image

Figure 6 Composition of inhaled and exhaled gases at various stages of respiration.

An increase in alveolar ventilation allows more CO2 to be ‘blown off’, resulting in a higher alveolar PO2. If, on the other hand, ventilation declines, CO2 accumulates at the expense of O2 and alveolar PO2 falls.

Whereas hyperventiation can increase alveolar PO2 only slightly (bringing it closer to the PO2 of inspired air), there is no limit to how far alveolar PO2 (and hence PaO2) can fall with inadequate ventilation.

Key point

Both oxygenation and CO2 elimination depend on alveolar ventilation: impaired ventilation causes PaO2to fall and PaCO2to rise.

Ventilation/perfusion mismatch and shunting

Not all blood flowing through the lung meets well-ventilated alveoli and not all ventilated alveoli are perfused with blood – especially in the presence of lung disease. This problem is known as ventilation/perfusion (V/Q) mismatch.

Imagine if alveoli in one area of lung are poorly ventilated (e.g. due to collapse or consolidation). Blood passing these alveoli returns to the arterial circulation with less O2 and more CO2 than normal. This is known as shunting1.

Now, by hyperventilating, we can shift more air in and out of our remaining ‘good alveoli’. This allows them to blow-off extra CO2 so that the blood passing them can offload more CO2. The lower CO2 in non-shunted blood compensates for the higher CO2 in shunted blood, maintaining the PaCO2.

The same does NOT apply to oxygenation. Blood passing ‘good alveoli’ is not able to carry more O2 because its haemoglobin is already maximally saturated with O2 (remember: flat part of curve, page 11). The non-shunted blood therefore cannot compensate for the low O2 levels in shunted blood and the PaO2 falls.

Key point

V/Q mismatch allows poorly oxygenated blood to re-enter the arterial circulation, thus lowering PaO2 and SaO2.

Provided overall alveolar ventilation is maintained, V/Q mismatch does not lead to an increase in PaCO2.

image

Figure 7 Effect of shunt on oxygen and carbon dioxide.

FiO2 and oxygenation

The fraction of inspired oxygen (FiO2) refers to the percentage of O2 in the air we breathe in. The FiO2 in room air is 21%, but can be increased with supplemental O2.

A low PaO2 may result from either V/Q mismatch or inadequate ventilation and, in both cases, increasing the FiO2 will improve the PaO2. The exact FiO2 requirement varies depending on how severely oxygenation is impaired and will help to determine the choice of delivery device (Figure 8). When the cause is inadequate ventilation it must be remembered that increasing FiO2 will not reverse the rise in PaCO2.

image

Figure 8 Oxygen delivery devices.

Supplemental O2 makes ABG analysis more complex as it can be difficult to judge whether the PaO2 is appropriately high for the FiO2 and, hence, whether oxygenation is impaired. A useful rule of thumb is that the difference between FiO2 and PaO2 (in kPa) should not normally be greater than 10. However there is often a degree of uncertainty as to the precise FiO2 and, if subtle impairment is suspected, the ABG should be repeated on room air.

Oxygen delivery devices

Nasal prongs: FiO2 < 40%. Comfortable and convenient. FiO2 non-specific: depends on flow rate (1–6 L/min) and ventilation

Standard face mask: FiO2 30–50% at flow rates 6–10 L/min but imprecise. May cause CO2 retention at flows <5 L/min (‘rebreathing’), so not useful for providing lower FiO2.

Fixed performance (high-flow) face mask: FiO2 24–60%. Delivers fixed, predictable FiO2. Ideal for providing controlled, accurate O2 therapy at low concentrations.

Face mask with reservoir: FiO2 60–80%. Can achieve even higher FiO2 with tight-fitting mask. Useful for short-term use in respiratory emergencies.

Endotracheal intubation: FiO2 21–100%. Used in severely unwell patients with very high O2 requirements, especially with ventilatory failure. Patient is sedated and mechanically ventilated.

1 The term also applies to blood that bypasses alveoli altogether (anatomical shunting)

Related posts:

Default ThumbnailWhen and why is an ABG required? Default ThumbnailCommon ABG values Disorders of gas exchange Default ThumbnailAnswers ABG sampling technique 1–25