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BiologyExchange surfaces and gas exchange › Lungs: seventy square metres, folded into a chest

Lungs: seventy square metres, folded into a chest

Your gas exchange surface is roughly the area of a badminton court and it fits under your ribs because it is divided into about three hundred million sacs. Getting air to it takes a branching tree of tubes whose walls change composition all the way down, and a set of muscles that never touch the lungs at all.

Before this Surface area to volume ratio and Fick's law · Squamous and ciliated epithelium as tissues

Before you start

Breathing in works by the lungs expanding and pulling air into themselves. Almost everyone starts here, and it inverts the mechanism. Lung tissue contains no muscle that could pull anything; it is elastic, and left alone it recoils inwards. What expands is the thoracic cavity, moved by the diaphragm and the intercostal muscles in the chest wall, and the lungs follow it outwards because they are pressed against it. Only once the cavity is larger does the pressure inside fall, and only then does air move in. Muscles first, volume second, pressure third, air last. Write that order the wrong way round and a six-mark question collapses to two.

What you should be able to do

From trachea to alveolus, and what changes on the way

Air entering the nose is warmed, moistened and filtered before it goes anywhere, then passes down the trachea, a tube about 10 cm long held permanently open by rings of cartilage. The rings are C-shaped rather than complete, with the gap at the back where the oesophagus lies against the trachea, so a swallowed mouthful can bulge into that space instead of being crushed against a rigid tube.

The trachea divides into two bronchi, one to each lung, and each bronchus divides again and again into bronchioles of decreasing diameter. Around twenty-three rounds of branching separate the trachea from the smallest air spaces. The finest bronchioles open into clusters of alveoli, and it is only there that any gas exchange happens at all.

The interesting thing is what disappears. Cartilage runs out before the bronchioles, cilia and goblet cells run out shortly after, and the wall of an alveolus is a single layer of flattened cells with nothing rigid in it whatsoever.
Cartilage
A firm, flexible supporting tissue. In the trachea it forms incomplete rings, and in the bronchi irregular blocks, holding the airway open against the pressure drop of inspiration.
Ciliated epithelium
An epithelium whose cells carry cilia that beat in a co-ordinated wave, sweeping mucus and trapped particles up towards the throat.
Goblet cell
A cell in the airway epithelium that secretes mucus, which traps dust, pollen and bacteria.
Smooth muscle
Involuntary muscle in the airway wall; its contraction narrows the lumen, and it is the tissue that contracts inappropriately during an asthma attack.
Elastic fibres
Fibres that stretch as the lungs inflate and recoil as the muscles relax, providing most of the force for quiet expiration.
Squamous epithelium
An epithelium of very flattened cells, giving a wall a fraction of a micrometre thick; the lining of an alveolus.

Cambridge candidates should treat the distribution of these tissues as a learned list, because CAIE 9700 asks for them explicitly and expects the structures to be recognised in slides, photomicrographs and electron micrographs. The identification is easier than it looks if you go in with one question: what holds this tube open? Rings of cartilage means trachea. Blocks of cartilage means bronchus. No cartilage but a conspicuous ring of smooth muscle means bronchiole. No wall to speak of, just a thin sheet against a capillary, means alveolus.

Smooth muscle and elastic fibres run the whole length of the tree, and they work against each other. Smooth muscle contracts to narrow an airway; elastic fibres stretch when it does and recoil to widen it again when the muscle relaxes. Elastic fibres are not antagonistic muscles, and a mark scheme will not accept them described as such.

The surface itself

An adult has somewhere around 300 million alveoli with a combined surface area of roughly 70 m². The folding is the whole point: that area sits inside a chest cavity of a few litres, which is the first term of Fick's law bought at almost no cost in volume.

Each alveolus is lined by a single layer of squamous epithelium and wrapped in a dense network of capillaries so narrow that red blood cells pass through in single file, squeezed against the capillary wall. Between the air and the haemoglobin lie only the alveolar epithelium, a basement membrane shared with the capillary, the capillary endothelium and a film of plasma.

Two cells and a shared basement membrane, and the whole path measures less than a micrometre. Compare that with the diffusion times from the first lesson: at this thickness, a molecule of oxygen crosses in well under a millisecond.

The gradient is held up from both sides at once, which is the second term of Fick's law being managed. Ventilation replaces alveolar air several times a minute, so the oxygen partial pressure in the alveolus stays around 13.3 kPa. Blood arriving from the pulmonary artery has an oxygen partial pressure of about 5.3 kPa and is swept away as soon as it is loaded, so the blood side never has time to equilibrate and stop the process. Carbon dioxide crosses the other way down a much smaller gradient, roughly 6.1 kPa in the arriving blood against 5.3 kPa in the alveolus, and that suffices because carbon dioxide diffuses far more readily than oxygen.

Two details are worth carrying. The alveolar lining is kept moist, because a gas has to dissolve before it can diffuse across a membrane. And the fluid contains a surfactant secreted by specialised cells in the alveolar wall, which lowers surface tension and stops the smallest alveoli collapsing shut between breaths. Premature babies are often short of it, which is why respiratory distress syndrome is a risk of early birth.

Elastic fibres in the alveolar walls stretch during inspiration and store energy while they do. Releasing it is what drives quiet expiration. In emphysema those fibres are destroyed and the alveolar walls break down into fewer, larger spaces, so the surface area falls and the recoil weakens at the same time. Both changes reduce gas exchange, and questions on lung disease almost always want both named.

Ventilation: muscles, then volume, then pressure, then air

The lungs are passive. They sit in a sealed cavity, and the muscles that ventilate them are in the wall of that cavity: the diaphragm underneath and the intercostal muscles between the ribs.

Watch the order rather than the picture. Nothing moves through the trachea until after the cavity has changed size and the pressure has changed with it. Under a reduced-motion setting the animation holds on the first stage and the sequence is set out in this caption instead.
InspirationQuiet expiration
DiaphragmContracts, flattens, moves downRelaxes, returns to its domed shape
External intercostalsContract, pulling ribs up and outRelax
Internal intercostalsRelaxedRelaxed in quiet breathing; contract in forced expiration
Volume of thoraxIncreasesDecreases
Pressure in the lungsFalls below atmosphericRises above atmospheric
AirMoves in down the pressure gradientMoves out down the pressure gradient
EnergyAlways active: muscles are contractingLargely passive: elastic recoil does the work

The external and internal intercostals are an antagonistic pair. Externals contract for inspiration, internals for forced expiration, and at any moment one set is relaxed. In quiet breathing the internals do essentially nothing, because recoil of the stretched elastic tissue and the weight of the ribcage are enough. They come into play when you blow out hard, along with the abdominal muscles, which push the abdominal contents up against the diaphragm.

That asymmetry is worth a mark on its own. Inspiration always costs energy, because it always involves muscle contraction. Quiet expiration is largely passive, so an answer describing it as the diaphragm 'pushing up' or 'contracting upwards' is describing something that does not happen: a muscle can only pull, and the diaphragm returns to its dome because it has stopped pulling.

The pressure changes involved are small. Between breaths the pressure in the alveoli equals atmospheric pressure exactly, so no air moves. During quiet inspiration it falls by only a fraction of a kilopascal, which is ample: gases move quickly down even a shallow pressure gradient. Questions sometimes give a trace of alveolar pressure against time and ask you to mark where air is entering. It is entering wherever the trace lies below the atmospheric line, and leaving wherever it lies above it.

Putting numbers on it

AQA names one calculation of its own in this topic, and it is the volume of air moved per minute. OCR A reaches the same quantity through a spirometer trace.

pulmonary ventilation rate = tidal volume × ventilation rateTidal volume in dm³, ventilation rate in breaths per minute, so the answer is in dm³ min⁻¹. AQA names this quantity in its own specification and expects the calculation.

Tidal volume
The volume of air moved in or out in one normal breath at rest, about 0.5 dm³ in an adult.
Ventilation rate
The number of breaths taken per minute, about 12 to 15 at rest. Also called breathing rate.
Vital capacity
The largest volume that can be breathed out after the deepest possible breath in; roughly 4.6 dm³ in a young adult man and 3.1 dm³ in a young adult woman.
Residual volume
The volume left in the lungs after the hardest possible breath out, about 1.2 dm³. It cannot be measured with a spirometer, because it never leaves the lungs.

From a trace to a rate

A spirometer trace shows twelve complete breaths in 48 seconds, each moving 0.45 dm³. Calculate the pulmonary ventilation rate. The same subject then exercises, and the tidal volume rises to 2.1 dm³ while the ventilation rate rises to 28 breaths per minute. Calculate the new rate and the factor by which it has changed.

First convert to a rate per minute. Twelve breaths in 48 s is 12 × (60 ÷ 48) = 15 breaths per minute.

Pulmonary ventilation rate = 0.45 × 15 = 6.75 dm³ min⁻¹.

During exercise: 2.1 × 28 = 58.8 dm³ min⁻¹.

The factor is 58.8 ÷ 6.75 = 8.7. Notice where that came from. The breathing rate not quite doubled; the tidal volume went up more than fourfold. Depth contributes more than frequency, and a question asking you to comment on the change is asking for that.

A spirometer records the volume of air in a closed circuit against time, and OCR A expects lung volumes and oxygen uptake to be read from one. The trick with oxygen uptake is the soda lime in the circuit: it absorbs the carbon dioxide the subject breathes out, so the total volume of gas in the apparatus falls steadily by exactly the volume of oxygen consumed. Draw a line through the midpoints of the oscillations, take its gradient, and that gradient is the rate of oxygen uptake. Without the soda lime the exhaled carbon dioxide would roughly replace the oxygen removed and the trace would stay level.

One refinement that separates a good answer from a correct one. About 150 cm³ of each breath never reaches an alveolus; it stays in the trachea and bronchi, which are conducting tubes with no exchange surface. That volume is the dead space. It means a shallow, rapid breathing pattern moves less useful air than a slow deep one at the same pulmonary ventilation rate, because the dead space is paid for on every breath.

TRY IT — Explaining a histology slide

A student is shown a section of lung tissue containing a tube about 0.4 mm across. The wall contains a thick layer of smooth muscle and some elastic fibres, but no cartilage, and the lining cells carry no cilia. Identify the tube and justify the identification. Suggest why the absence of cartilage matters during an asthma attack.

Check your answer

It is a bronchiole. Cartilage is present in the trachea and bronchi and absent from bronchioles, so its absence rules the larger airways out, and the diameter and the thick smooth muscle layer both fit a bronchiole. The lack of cilia points to one of the smaller bronchioles close to the alveoli.

Without cartilage there is nothing rigid holding the tube open. When the smooth muscle contracts, as it does in an asthma attack, the lumen narrows sharply and the resistance to air flow rises, so less air reaches the alveoli per breath.

The trap is answering 'bronchus' because the tube looks large on the slide. Judge from the wall, not from the apparent size: magnification varies between slides and cartilage does not.

In the exam

Check yourself

Explain how the structure of an alveolus and the blood supply around it together maximise the rate of oxygen uptake. Refer to all three terms of Fick's law in your answer.

Answer

Surface area. There are about 300 million alveoli, giving a combined area of roughly 70 m². Area is on the top of the fraction, so a larger area means a proportionally faster rate.

Thickness. The alveolar wall is a single layer of flattened squamous epithelium and the capillary wall is a single layer of endothelium, sharing one basement membrane, so the whole barrier is under a micrometre. Thickness divides, so a short pathway means a fast rate. The capillaries are narrow enough to force red cells against the wall, which shortens the path further.

Difference in concentration. Ventilation keeps replacing the alveolar air, holding the alveolar oxygen partial pressure near 13.3 kPa, while blood flow keeps removing oxygenated blood and bringing in blood at around 5.3 kPa. Neither side is allowed to equilibrate, so the gradient is maintained rather than used up.

The point that ties them together is that all three are maintained at once. Any one of them failing — scarring that thickens the wall, emphysema that destroys area, a blocked bronchiole that stops ventilation — reduces the rate on its own, which is why lung diseases with quite different causes produce the same breathlessness.

Questions

Written to the command words the boards use. Try them on paper before opening a scheme: the marks go to points made, not to length.

Question 15 marks

A spirometer trace shows 21 complete breaths in 84 seconds, each moving 0.55 dm³ of air. Calculate the pulmonary ventilation rate in dm³ min⁻¹. About 0.15 dm³ of every breath stays in the dead space; calculate the volume of air reaching the alveoli each minute.

Mark scheme
  1. M1 ventilation rate = 21 × (60 ÷ 84), converting the count to a number of breaths per minute
  2. A1 15 breaths per minute
  3. M1 pulmonary ventilation rate = tidal volume × ventilation rate = 0.55 × 15
  4. A1 8.25 dm³ min⁻¹, with the unit given
  5. A1 alveolar volume = (0.55 − 0.15) × 15 = 6.0 dm³ min⁻¹, because the dead space is paid for on every breath

Question 24 marks

Describe how air is drawn into the lungs during inspiration, giving the events in the order in which they happen.

Mark scheme
  1. B1 the external intercostal muscles contract, pulling the ribcage upwards and outwards
  2. B1 the diaphragm contracts, flattens and moves downwards
  3. B1 the volume of the thoracic cavity increases, and the lungs are stretched with it
  4. A1 the pressure inside the lungs falls below atmospheric pressure, so air moves in down the pressure gradient

Question 34 marks

Explain why inspiration always costs the body energy while quiet expiration costs almost none.

Mark scheme
  1. B1 inspiration depends on the diaphragm and external intercostal muscles contracting, and muscle contraction requires ATP
  2. B1 elastic fibres in the alveolar walls and airways are stretched as the lungs inflate, storing energy as they do so
  3. B1 in quiet expiration those muscles simply relax, and the stretched elastic tissue recoils, which needs no contraction of any muscle
  4. A1 the recoil reduces the volume of the thorax, so pressure in the lungs rises above atmospheric and air moves out

Question 43 marks

In emphysema the elastic fibres of the alveolar walls are destroyed and the walls themselves break down, so that many small alveoli are replaced by fewer, larger air spaces. Suggest why a person with emphysema becomes breathless on mild exertion.

Mark scheme
  1. B1 the total surface area available for gas exchange falls, and rate of diffusion is proportional to surface area
  2. B1 loss of elastic fibres weakens the recoil, so expiration is no longer largely passive and less air is expelled per breath
  3. A1 less oxygen therefore reaches the blood each minute, so ventilation has to rise steeply to meet the extra demand of exercise and the person feels breathless

Question 52 marks

A section through an airway shows irregular blocks of cartilage in the wall, together with a ciliated epithelium containing goblet cells. Name this airway, and name the tissue that holds a bronchiole open instead of cartilage.

Mark scheme
  1. A1 the airway is a bronchus, identified from the blocks of cartilage in its wall
  2. A1 a bronchiole has a conspicuous layer of smooth muscle, with elastic fibres, and no cartilage at all

Worth remembering

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