Upper and lower airways: structure-function

Exam Target

Quick check: airway structure-function frame

What is the most useful way to learn airway anatomy for anaesthesia?

Reveal answer

Attach each structure to the failure it prevents or causes: obstruction, aspiration, humidification loss, tube resistance, secretion retention, atelectasis, or surfactant failure.

What does the upper airway mainly do before gas reaches the trachea?

Reveal answer

It conducts, warms, humidifies, filters, smells, protects against aspiration, and helps coordinate speech and swallowing.

What is the distal airway goal?

Reveal answer

Deliver gas to a thin, stable, dry alveolar-capillary surface where oxygen and carbon dioxide can diffuse efficiently.

EDAIC trap: airway anatomy is rarely tested as naming alone. First identify the structure, then ask what happens when tone, radius, lining, humidity, reflexes, or surface tension fails under anaesthesia.

Overview of the Respiratory Tract

How to use this figure: trace gas from nose and mouth to trachea, bronchi, lungs, and diaphragm. Then attach one function to each level: conditioning proximally, conduction through branching airways, and gas exchange distally.

Functional division

For EDAIC Part I, the respiratory tract is best divided by what each region does under stress. Proximal structures conduct, protect, warm, humidify, and filter. Distal structures exchange gas and remain open only if diffusion distance, surface tension, and lung volume are favourable.

Anatomical division

How to use this table: first separate anatomical region from function, then attach the anaesthetic problem: obstruction, aspiration, resistance, secretion retention, atelectasis, or diffusion failure.

Some texts place the larynx at the boundary between upper and lower airway. For anaesthetists, it is best treated as the functional gateway between the pharynx and trachea because it is essential for airway protection, phonation, cough, laryngoscopy, intubation, and emergency front-of-neck access.

Functional division

The conducting zone includes the trachea, bronchi, bronchioles, and terminal bronchioles. The respiratory zone includes respiratory bronchioles, alveolar ducts, alveolar sacs, and alveoli.

Major functions of the airway and lung

The airway and lung have both respiratory and non-respiratory functions.

Respiratory functions

• Movement of gas between atmosphere and alveoli.
• Oxygen transfer from alveoli to pulmonary capillary blood.
• Carbon dioxide transfer from pulmonary capillary blood to alveoli.
• Maintenance of alveolar stability through surfactant.

Non-respiratory functions

• Humidification and warming of inspired gas.
• Filtration of particles.
• Mucociliary clearance.
• Cough and sneeze reflexes.
• Immune defence.
• Acid-base regulation through CO₂ excretion.
• Metabolic and endocrine functions, including angiotensin-converting enzyme activity in pulmonary endothelium.
• Blood reservoir and filter for small embolic material.

Quick check: airway map

Where does the conducting zone end?

Reveal answer

At the terminal bronchioles, which are the last purely conducting airways and do not participate in gas exchange.

Where does the respiratory zone begin?

Reveal answer

At the respiratory bronchioles, where alveoli begin to appear in the airway walls and gas exchange starts.

Why is anatomical dead space clinically important?

Reveal answer

Only tidal volume beyond dead space reaches alveoli, so small tidal volumes can move gas visibly while producing poor alveolar ventilation.

EDAIC trap: the upper airway is not just an entry route. It is the conditioning and protection system that anaesthesia commonly disables, especially at the collapsible pharynx.

Upper Airway: Structure and Function

Definition and components

The upper airway consists of air passages above the larynx:

• nose,
• nasal cavity,
• paranasal sinuses,
• mouth,
• pharynx:
  • nasopharynx,
  • oropharynx,
  • laryngopharynx.

Its main function is to conduct air to the lower respiratory tract, but it also filters, warms, humidifies, smells, protects, and participates in speech and swallowing.

Nose and nasal cavity

How to use this figure: focus on the collapsible pharyngeal segment behind the tongue and soft palate. Sedation removes dilator tone; jaw thrust, oral airways, and CPAP work by moving or splinting this segment.

In exam terms, the nose is an airway conditioning organ. It adds resistance, but it also warms, humidifies, filters, and protects the lower airway. Tracheal tubes and mouth breathing remove much of that protection.

Functions of the nose

The nasal turbinates, also called conchae, increase surface area and create turbulent airflow. Turbulence is useful in the nose because it improves contact between inspired gas and warm, moist mucosa. The price is increased resistance.

Anaesthetic relevance

1. Nasal breathing adds resistance. The nose contributes substantially to upper airway resistance.
2. Nasal obstruction increases work of breathing. This matters during sedation and sleep.
3. Nasal mucosa is vascular. Nasal instrumentation can bleed, especially with anticoagulation, trauma, polyps, pregnancy, or inflamed mucosa.
4. Vasoconstrictors reduce bleeding. Phenylephrine, xylometazoline, or cocaine-containing preparations are used in some awake nasal intubation techniques.
5. Bypassing the nose bypasses humidification. Tracheal intubation exposes the lower airway to dry gases unless humidification is provided.

Mouth

The mouth provides an alternative airway route. It has lower resistance than the nose, but less effective warming, humidification, and filtration.

Anaesthetic relevance:

• Mouth opening is essential for direct laryngoscopy.
• The tongue is a major cause of airway obstruction during anaesthesia.
• Oropharyngeal airways displace the tongue away from the posterior pharyngeal wall.
• Dental status matters because teeth may be damaged during airway manipulation.

Pharynx

How to use this figure: separate nasopharynx, oropharynx, and laryngopharynx. Obstruction, aspiration risk, airway adjunct placement, and laryngoscopy all depend on this shared food-air pathway.

The pharynx is a muscular tube shared by the respiratory and gastrointestinal systems.

It is divided into:

The pharynx has several functions:

• conduction of air,
• swallowing,
• speech resonance,
• immune defence through lymphoid tissue,
• protection of the airway during swallowing.

Pharyngeal muscles

Two functional groups are important:

1. Pharyngeal constrictors help propel a food bolus during swallowing.
2. Pharyngeal dilators maintain airway patency during breathing.

The most important pharyngeal dilator for airway patency is the genioglossus, which pulls the tongue forward and away from the posterior pharyngeal wall.

Why the pharynx collapses

The pharynx is a collapsible muscular tube. It has no rigid cartilage. During inspiration, contraction of the diaphragm creates negative intrathoracic and airway pressure. Negative pressure tends to suck the pharyngeal walls inward.

In the awake patient, pharyngeal dilator muscles activate before and during inspiration, stiffening the airway and preventing collapse.

Important muscles include:

• genioglossus,
• palatal muscles,
• geniohyoid and other hyoid-positioning muscles.

During anaesthesia

General anaesthesia, sedation, opioids, and sleep reduce upper airway dilator muscle tone. The tongue, soft palate, and pharyngeal tissues fall backward. Negative inspiratory pressure worsens collapse.

This explains why airway obstruction is common after induction, especially in:

• obesity,
• obstructive sleep apnoea,
• pregnancy,
• children,
• patients with reduced mandibular space,
• patients with large tongue or tonsils,
• excessive sedation,
• supine positioning.

Why simple airway manoeuvres work

Swallowing and aspiration protection

The airway and oesophagus cross at the pharynx. Protection requires coordination of breathing and swallowing.

During swallowing:

• breathing briefly stops,
• soft palate closes nasopharynx,
• larynx elevates,
• vocal cords close,
• epiglottis helps deflect the bolus,
• upper oesophageal sphincter relaxes,
• pharyngeal constrictors propel the bolus.

Anaesthetic relevance

General anaesthesia impairs:

• consciousness,
• airway reflexes,
• cough,
• swallowing coordination,
• lower oesophageal sphincter tone,
• protective laryngeal closure.

This increases aspiration risk. Patients at increased risk include those with full stomach, bowel obstruction, pregnancy, obesity, reflux, diabetes gastroparesis, trauma, and reduced consciousness.

Quick check: upper-airway collapse and aspiration

Why does the pharynx obstruct so easily during sedation or anaesthesia?

Reveal answer

It is a collapsible muscular tube without cartilage; reduced dilator tone lets the tongue, soft palate, and pharyngeal tissues fall backward.

Why do jaw thrust, airway adjuncts, and CPAP work?

Reveal answer

They move soft tissues away from the posterior pharyngeal wall or splint the collapsible segment open with positive pressure.

Why does anaesthesia increase aspiration risk?

Reveal answer

It depresses consciousness, cough, swallowing coordination, laryngeal reflexes, and protective glottic closure.

EDAIC trap: laryngeal nerve questions are usually functional. Above the cords is internal superior laryngeal sensation; cricothyroid is external superior laryngeal motor; almost everything else motor is recurrent laryngeal.

The Larynx: The Airway Gatekeeper

Position and functions

The larynx lies roughly from C3 to C6. The trachea begins at the lower border of the cricoid cartilage, around C6.

Functions:

• airway protection,
• phonation,
• cough generation,
• regulation of airflow resistance,
• contribution to physiological PEEP,
• passage for tracheal intubation,
• landmark for emergency cricothyroidotomy.

Laryngeal cartilages

How to use this figure: identify epiglottis, vocal folds, thyroid cartilage, cricoid cartilage, and the cricothyroid membrane. These landmarks connect airway protection, laryngospasm, intubation, and emergency front-of-neck access.

There are nine cartilages: three unpaired and three paired.

Vallecula

The vallecula is the space between the base of the tongue and the epiglottis. In adult direct laryngoscopy with a Macintosh blade, the tip is placed in the vallecula to lift the epiglottis indirectly.

Cricoid cartilage and cricothyroid membrane

The cricoid cartilage is the only complete ring in the airway. The cricothyroid membrane lies between the thyroid and cricoid cartilages and is the site for emergency front-of-neck access.

Vocal cords and glottis

The true vocal cords are formed by vocal ligaments covered by mucosa. They run from the thyroid cartilage anteriorly to arytenoid cartilages posteriorly.

The opening between the vocal cords is the rima glottidis.

Movement during breathing

• During inspiration, the vocal cords abduct to reduce resistance.
• During expiration, the cords adduct slightly.

Slight expiratory adduction creates a small physiological PEEP, around 3-4 cmH₂O. This helps maintain functional residual capacity, reduce small-airway collapse, assist cough, and support phonation.

Intubation and loss of physiological PEEP

When a patient is intubated, the endotracheal tube holds the glottis open and bypasses normal cord function. Physiological PEEP from glottic adduction is lost. This contributes to atelectasis and ventilation-perfusion mismatch unless external PEEP is applied.

This is why applying about 3-5 cmH₂O of PEEP during controlled ventilation often reproduces a normal physiological effect rather than being a purely artificial intervention.

Laryngeal muscles

Key intrinsic muscles

High-yield facts:

• Posterior cricoarytenoid is the only abductor of the vocal cords.
• Cricothyroid is the only intrinsic laryngeal muscle supplied by the external branch of the superior laryngeal nerve.
• All other intrinsic laryngeal muscles are supplied by the recurrent laryngeal nerve.

Laryngeal innervation

The larynx is supplied by branches of the vagus nerve.

Clinical relevance

• Internal superior laryngeal nerve block anaesthetises the larynx above the cords.
• Transtracheal local anaesthetic through the cricothyroid membrane anaesthetises trachea and below the cords by coughing local anaesthetic upward.
• Recurrent laryngeal nerve injury may cause hoarseness, aspiration, or airway obstruction depending on whether unilateral or bilateral.
• Bilateral recurrent laryngeal nerve palsy can cause severe airway obstruction if cords lie near the midline.
• Left recurrent laryngeal nerve has a longer intrathoracic course and is vulnerable to thoracic pathology.

Laryngeal reflexes

The larynx is highly reflexogenic because it protects the lungs from aspiration.

Important reflexes:

Laryngospasm

Laryngospasm is reflex closure of the vocal cords. It is more likely with:

• light anaesthesia,
• airway secretions,
• blood in pharynx,
• airway instrumentation,
• children,
• recent upper respiratory infection,
• extubation in an irritable airway.

It can cause complete airway obstruction, negative-pressure pulmonary oedema, hypoxaemia, bradycardia, and cardiac arrest if untreated.

Quick check: laryngeal protection and innervation

Which intrinsic laryngeal muscle abducts the vocal cords?

Reveal answer

Posterior cricoarytenoid is the only vocal cord abductor, and it is supplied by the recurrent laryngeal nerve.

Which intrinsic laryngeal muscle is the superior-laryngeal-nerve exception?

Reveal answer

Cricothyroid is supplied by the external branch of the superior laryngeal nerve; most other intrinsic muscles are recurrent laryngeal nerve.

What makes laryngospasm dangerous?

Reveal answer

Reflex vocal cord closure can become complete obstruction, causing hypoxaemia, negative-pressure pulmonary oedema, bradycardia, and arrest.

EDAIC trap: do not treat lower-airway branching as a diagram only. The right main bronchus explains tube malposition and aspiration; bronchioles explain bronchospasm and collapse because they have no cartilage.

Lower Airways and the Tracheobronchial Tree

Trachea

How to use this figure: notice C-shaped cartilage, posterior membranous trachea, and proximity to the oesophagus. Tube cuff pressure, tracheomalacia, and airway injury all become easier to reason through from this structure.

The trachea begins at the cricoid cartilage around C6 and extends to the carina around T4/T5 in adults, where it divides into right and left main bronchi.

Key features:

• C-shaped cartilaginous rings support the anterior and lateral walls.
• Posterior wall contains trachealis muscle.
• Lined by pseudostratified ciliated columnar epithelium with goblet cells.
• Contains mucus glands and immune cells.

Anaesthetic relevance

• Endotracheal tubes can irritate the trachea and provoke cough or bronchospasm.
• Cuff pressure must be controlled to avoid mucosal ischaemia.
• Carina stimulation is very irritating and can cause coughing or sympathetic response.
• Tube position matters: too deep often enters the right main bronchus.

Bronchi

The trachea divides into right and left main bronchi.

Right main bronchus

The right main bronchus is generally:

• wider,
• shorter,
• more vertical.

Clinical relevance:

• Aspirated material more often enters the right bronchial tree.
• A tracheal tube advanced too far commonly enters the right main bronchus.
• Right upper lobe obstruction can still occur depending on tube position.

Bronchial structure

As bronchi divide:

• cartilage becomes less regular,
• smooth muscle becomes more important,
• submucosal glands decrease,
• airway diameter becomes smaller,
• total cross-sectional area increases.

Bronchioles

Bronchioles are small airways without cartilage.

Features:

• no cartilage,
• prominent smooth muscle,
• fewer goblet cells,
• ciliated epithelium becomes simpler,
• terminal bronchioles are the last purely conducting airways.

Anaesthetic relevance

Because bronchioles lack cartilage, their calibre is strongly influenced by:

• smooth muscle tone,
• lung volume,
• surrounding parenchymal traction,
• airway inflammation,
• mucus plugging,
• bronchospasm,
• intrathoracic pressure.

Small-airway collapse is common when lung volume falls, especially under general anaesthesia, obesity, pregnancy, and supine positioning.

Conducting zone

The conducting zone extends from trachea to terminal bronchioles.

Functions:

• conduct gas,
• warm and humidify inspired air,
• filter particles,
• distribute ventilation,
• contribute to airway resistance,
• provide anatomical dead space,
• clear mucus by mucociliary transport.

There is no gas exchange in the conducting zone because the airway walls are too thick and not closely associated with pulmonary capillaries.

Anatomical dead space

Anatomical dead space is the volume of conducting airway that does not participate in gas exchange.

Approximate adult value:

• about 150 mL,
• or 2 mL/kg.

This matters because alveolar ventilation depends on tidal volume minus dead space:

Alveolar ventilation = respiratory rate × (tidal volume - dead space)

A patient taking small tidal volumes may move gas in and out of the mouth but ventilate alveoli poorly.

Respiratory zone

How to use this figure: terminal bronchiole is the end of the conducting zone; respiratory bronchiole begins the respiratory zone. Smooth muscle without cartilage explains small-airway narrowing and collapse.

How to use this figure: connect type I pneumocytes with thin diffusion distance, type II pneumocytes with surfactant and repair, macrophages with defence, and capillaries with rapid gas transfer.

The respiratory zone begins where alveoli appear in airway walls.

It includes:

• respiratory bronchioles,
• alveolar ducts,
• alveolar sacs,
• alveoli.

Functions:

• oxygen diffusion into blood,
• carbon dioxide diffusion into alveoli,
• surfactant production,
• immune surveillance by alveolar macrophages.

The respiratory zone is specialised for diffusion:

• enormous surface area,
• very thin barrier,
• dense pulmonary capillary network,
• short diffusion distance,
• large partial-pressure gradients.

Airway generations

A useful model is Weibel's airway generation model.

Exam point:

• Terminal bronchioles are the last part of the conducting zone.
• Respiratory bronchioles are the first part of the respiratory zone.

Structural changes down the airway

Quick check: lower-airway structure

Why is the right main bronchus a common site for aspiration or tube malposition?

Reveal answer

It is generally wider, shorter, and more vertical, so aspirated material and overly deep tracheal tubes tend to enter it.

Why are bronchioles vulnerable to collapse and bronchospasm?

Reveal answer

They lack cartilage, so calibre depends heavily on smooth muscle tone, lung volume, radial traction, mucus, oedema, and intrathoracic pressure.

What structural change makes alveoli suited for diffusion?

Reveal answer

They have a huge surface area, thin type I pneumocytes, close capillaries, and a very short diffusion distance.

EDAIC trap: resistance is a radius problem before it is a ventilator problem. Small oedema, secretions, bronchospasm, kinking, or a narrow tube can cause a large work-of-breathing penalty.

Airway Resistance and Flow

Why airway radius matters

For laminar flow, Poiseuille's law states:

Resistance proportional to 1 / radius^4

This means a small decrease in radius produces a large increase in resistance.

Example:

If airway radius halves, resistance increases by 16 times.

This is crucial in:

• bronchospasm,
• airway oedema,
• secretions,
• small endotracheal tubes,
• paediatric airway obstruction,
• upper airway collapse.

Laminar, turbulent, and transitional flow

Turbulence increases with:

• high flow,
• large airway diameter,
• high gas density,
• irregular airway shape,
• sharp bends and branching,
• obstruction.

Heliox reduces resistance in turbulent flow because helium has low density. It may improve airflow in upper airway obstruction, severe asthma, or narrowed airways, but it does not treat the underlying cause.

Endotracheal tube resistance

An endotracheal tube is narrower and longer than the normal upper airway route, so it increases resistance. Resistance is especially important with small tubes.

Clinical implications:

• A 6.0 mm tube has much greater resistance than an 8.0 mm tube.
• Work of breathing increases during spontaneous ventilation through small tubes.
• Secretions or kinking further increase resistance.
• In children, 1 mm of oedema causes a major proportional reduction in radius.

Quick check: resistance and tube physiology

Why does a small reduction in radius matter so much?

Reveal answer

For laminar flow, resistance varies inversely with the fourth power of radius, so halving radius increases resistance about sixteen-fold.

When is endotracheal tube resistance especially important?

Reveal answer

During spontaneous breathing or weaning through small, kinked, or secretion-narrowed tubes, because the patient must generate the pressure to overcome that resistance.

Why can heliox reduce work in selected obstructed airways?

Reveal answer

Its lower density reduces turbulent-flow resistance, but it is a bridge and does not treat the cause of obstruction.

EDAIC trap: humidification failures are slow but important. A tube bypasses the nose and pharynx; dry gas thickens secretions, impairs cilia, raises resistance, and can block the tube.

Humidification and Airway Conditioning

Normal humidification

By the time inspired gas reaches the alveoli, it is normally:

• warmed to body temperature,
• fully saturated with water vapour,
• filtered of many particles.

At 37 degrees C, saturated water vapour pressure is approximately 47 mmHg or 6.3 kPa.

The nose and upper airway normally provide most of this conditioning.

What happens when the upper airway is bypassed?

Tracheal intubation bypasses the nose, mouth, and much of the pharynx.

Dry, cold gas delivered to the trachea may cause:

• thick secretions,
• impaired ciliary function,
• mucus plugging,
• atelectasis,
• increased airway resistance,
• epithelial injury,
• heat and water loss,
• tube blockage.

This is why humidification is required during prolonged ventilation.

Humidification devices

Heat and moisture exchangers are simple and common but may increase dead space and resistance. Heated humidifiers are useful when secretions are thick, ventilation is prolonged, or leak/high flow reduces HME effectiveness.

EDAIC trap: suction removes visible secretions but does not replace mucociliary clearance. The exam often links dry gas, hypothermia, smoking, dehydration, and intubation to impaired ciliary function.

Mucociliary Clearance

How to use this figure: relate goblet cells, cilia, and mucus layers to the mucociliary escalator. Dry gas, smoking, infection, intubation, and dehydration impair exactly this mechanism.

Definition

Mucociliary clearance is the movement of mucus and trapped particles from the lower respiratory tract toward the pharynx by coordinated ciliary beating.

It is often called the mucociliary escalator.

Structure

The conducting airways are lined by respiratory epithelium containing:

• ciliated epithelial cells,
• goblet cells,
• submucosal glands,
• mucus layer,
• periciliary sol layer,
• immune cells.

Mucus has two functional layers:

Cilia beat in a coordinated direction toward the pharynx. Mucus is swallowed or expectorated.

Functions

Mucociliary clearance removes:

• dust,
• pathogens,
• cell debris,
• inhaled particles,
• excess secretions.

It protects the distal lung from infection and obstruction.

Factors impairing mucociliary clearance

Anaesthetic relevance

Ventilated patients are vulnerable to secretion retention because:

• the upper airway is bypassed,
• cough is reduced or abolished,
• humidification may be inadequate,
• immobility promotes atelectasis,
• suctioning may injure mucosa,
• infection risk increases.

Good airway care requires humidification, suctioning when needed, hydration, physiotherapy, appropriate PEEP, and early mobilisation where possible.

Quick check: humidification and clearance

What happens when the upper airway is bypassed for a long time?

Reveal answer

Dry cold gas can thicken secretions, slow cilia, injure epithelium, increase resistance, promote mucus plugs, and cause atelectasis.

What does mucociliary clearance require?

Reveal answer

A hydrated mucus layer, functioning cilia, appropriate airway humidity, intact epithelium, and enough cough or suction support to clear larger secretions.

Why are ventilated patients prone to retained secretions?

Reveal answer

The tube bypasses conditioning, reduces cough efficiency, irritates mucosa, increases infection risk, and often combines with immobility and inadequate humidification.

Cough and Airway Defence

Cough reflex

Cough is a protective reflex that clears the airway.

Receptors

Cough receptors are found in:

• larynx,
• trachea,
• carina,
• large bronchi,
• pleura,
• external auditory canal in some individuals.

Afferent pathway is mainly via the vagus nerve to the medulla.

Phases of cough

1. Inspiratory phase - deep inspiration increases lung volume.
2. Compression phase - glottis closes; expiratory muscles contract; intrathoracic pressure rises.
3. Expulsive phase - glottis opens suddenly; high-velocity airflow expels mucus or foreign material.

Anaesthetic relevance

Cough requires:

• consciousness or brainstem reflex integrity,
• intact laryngeal sensation,
• glottic closure and opening,
• adequate respiratory muscle strength,
• adequate lung volume,
• unobstructed airway.

Anaesthesia, opioids, neuromuscular blockade, stroke, high spinal cord injury, critical illness weakness, and tracheostomy can all impair cough.

Other airway defence mechanisms

Alveoli and the Gas Exchange Surface

Alveolar structure

Alveoli are tiny air sacs specialised for gas exchange. There are hundreds of millions of alveoli, producing a very large surface area for diffusion.

Important cells:

Type I pneumocytes cover most of the alveolar surface area. Type II pneumocytes are more cuboidal, produce surfactant, and help repair alveolar injury.

Alveolar-capillary membrane

The diffusion barrier includes:

1. surfactant layer,
2. alveolar epithelial cell,
3. epithelial basement membrane,
4. interstitial space,
5. capillary basement membrane,
6. capillary endothelial cell,
7. plasma,
8. red cell membrane.

Gas exchange is efficient because the barrier is extremely thin and the capillary network is dense.

This becomes more important in later modules on oxygen transport, CO₂ transport, and alveolar diffusion.

Alveolar pores and collateral ventilation

Alveoli communicate through small pores, often called pores of Kohn. Additional collateral channels may exist between bronchioles and alveoli.

Collateral ventilation can help ventilate alveoli distal to partial obstruction, but it can also spread infection or air leak.

EDAIC trap: surfactant is not only a neonatal topic. It is the mechanism that links Laplace law, compliance, atelectasis, shunt, ARDS, aspiration, and anaesthesia-related lung collapse.

Surfactant

How to use this figure: compare high surface tension without surfactant with stabilised alveoli when surfactant is present. This is the visual version of Laplace law and neonatal respiratory distress.

Definition

Pulmonary surfactant is a mixture of phospholipids and proteins produced by type II pneumocytes that reduces surface tension at the air-liquid interface in alveoli.

A good exam definition:

Composition

Surfactant contains:

• phospholipids,
• neutral lipids,
• surfactant proteins.

The most important phospholipid is:

• dipalmitoylphosphatidylcholine, abbreviated DPPC.

Important surfactant proteins:

Production and fetal development

Surfactant is produced by type II pneumocytes.

High-yield developmental points:

• Type II pneumocytes begin producing surfactant from around 24 weeks' gestation.
• Functional maturity increases later in gestation.
• Full lung maturation is usually closer to 35 weeks.
• Antenatal corticosteroids increase fetal surfactant production when preterm delivery is expected.

Stimuli increasing surfactant production include:

• alveolar stretch,
• glucocorticoids,
• catecholamines,
• thyroid hormones.

Surface tension problem

Alveoli are lined by a thin liquid layer. Water molecules attract each other, producing surface tension. Surface tension tends to collapse alveoli and draw fluid into them.

If there were no surfactant, the lungs would be stiff, unstable, and wet.

Laplace's law

For a spherical alveolus:

P = 2T / r

where:

• P = pressure needed to keep the alveolus open,
• T = surface tension,
• r = radius.

If surface tension were constant, small alveoli would need higher pressure to stay open than large alveoli. Therefore, small alveoli would empty into large alveoli and collapse.

Surfactant solves this problem because it reduces surface tension more in small alveoli than in large alveoli. As an alveolus becomes smaller, surfactant molecules become more concentrated at the surface, reducing surface tension further.

Functions of surfactant

Surfactant and compliance

Compliance is the change in volume for a given change in pressure:

Compliance = ΔV / ΔP

By lowering surface tension, surfactant increases lung compliance. A more compliant lung requires less pressure and less work to inflate.

When surfactant is deficient or inactivated:

• compliance falls,
• work of breathing rises,
• alveoli collapse,
• oxygenation worsens,
• pulmonary oedema may develop,
• ventilation becomes uneven.

Surfactant deficiency and dysfunction

Infant respiratory distress syndrome

Premature neonates may have inadequate surfactant. Consequences:

• low compliance,
• atelectasis,
• increased work of breathing,
• hypoxaemia,
• respiratory failure,
• diffuse alveolar collapse.

Prevention/treatment:

• antenatal corticosteroids when preterm delivery is expected,
• CPAP or ventilatory support,
• exogenous surfactant therapy in selected neonates.

ARDS

In acute respiratory distress syndrome, surfactant may be inactivated by inflammation, oedema fluid, plasma proteins, and epithelial injury.

Consequences:

• stiff lungs,
• widespread atelectasis,
• shunt,
• severe hypoxaemia,
• reduced compliance.

Near-drowning and aspiration

Surfactant can be washed out or inactivated, causing atelectasis, low compliance, and pulmonary oedema.

General anaesthesia

General anaesthesia promotes atelectasis through:

• reduced FRC,
• loss of respiratory muscle tone,
• absorption atelectasis with high FiO₂,
• loss of physiological PEEP after intubation,
• supine position,
• diaphragmatic displacement,
• obesity or pregnancy.

Surfactant helps resist collapse, but anaesthesia can overwhelm normal stabilising mechanisms.

Quick check: alveoli and surfactant

Which cells produce surfactant?

Reveal answer

Type II pneumocytes produce surfactant and also help repair injured alveolar epithelium.

How does surfactant stabilise small alveoli?

Reveal answer

As alveoli become smaller, surfactant molecules become more concentrated and reduce surface tension more, preventing small alveoli emptying into larger ones.

Why does general anaesthesia promote atelectasis despite normal surfactant?

Reveal answer

It lowers functional residual capacity, removes physiological PEEP after intubation, encourages dependent collapse, and may cause absorption atelectasis with high inspired oxygen.

EDAIC trap: paediatric airway danger is proportional narrowing. The same millimetre of oedema removes far more radius in a child, so obstruction and desaturation progress quickly.

Paediatric and Special Airway Considerations

Why children obstruct quickly

Children have smaller airways. Because resistance varies with the fourth power of radius, a small amount of oedema or secretions causes a large increase in resistance.

Example:

If airway radius is already small, 1 mm of circumferential oedema produces a much larger proportional narrowing than in an adult.

Clinical relevance:

• croup,
• post-intubation swelling,
• epiglottitis,
• inhalational burns,
• airway infection,
• laryngospasm.

Infant airway features

Important tendencies in infants and young children:

• relatively large tongue,
• more cephalad and anterior larynx,
• floppy, omega-shaped epiglottis,
• small airway diameter,
• high oxygen consumption,
• low oxygen reserve,
• compliant chest wall,
• rapid desaturation during apnoea.

The practical message is that small anatomical differences have major physiological consequences.

Clinical Integration

Why a sedated patient obstructs

Sedation reduces pharyngeal dilator muscle tone. The tongue and soft palate fall posteriorly. Negative inspiratory pressure worsens collapse. Obesity and OSA increase collapsibility.

Treatment:

• reduce sedation if possible,
• head tilt/chin lift/jaw thrust,
• airway adjunct,
• CPAP,
• supraglottic airway or intubation if needed.

Why intubation can cause atelectasis

Intubation bypasses the larynx and prevents expiratory vocal cord adduction. Physiological PEEP is lost. Anaesthesia also reduces FRC and promotes dependent lung collapse. External PEEP helps maintain alveolar recruitment.

Why dry gases are harmful

Dry gases bypassing the upper airway remove heat and water from airway mucosa. Cilia slow, secretions thicken, mucus plugs form, and atelectasis develops. Humidification prevents this.

Why small tubes increase work of breathing

Endotracheal tube resistance rises steeply as radius decreases. A small tube may be acceptable during controlled ventilation but can impose high work during spontaneous breathing or weaning.

Why asthma increases airway resistance

Asthma narrows bronchi and bronchioles through smooth muscle contraction, mucosal oedema, and mucus plugging. Because resistance depends strongly on radius, small narrowing causes large resistance rise. Expiration is especially affected because intrathoracic airway pressure compresses small airways.

Why surfactant deficiency causes respiratory distress

Without surfactant, alveolar surface tension is high. Small alveoli collapse. Lung compliance falls. Work of breathing rises. Fluid is drawn into alveoli. Gas exchange becomes uneven and shunt develops.

Quick check: clinical integration

Why can a small amount of oedema be severe in children?

Reveal answer

Their baseline airway radius is small, so the same absolute swelling causes a much larger proportional narrowing and a steep resistance rise.

What is the common physiology behind sedation obstruction, asthma, and tube narrowing?

Reveal answer

Reduced airway radius increases resistance dramatically; the cause may be soft-tissue collapse, smooth-muscle constriction, oedema, secretions, or the tube itself.

What is the fastest structure-function summary of this module?

Reveal answer

Upper airway protects and conditions; larynx guards the inlet; conducting airways deliver and clear; alveoli exchange gas; surfactant keeps the surface open.

How to use these tables: first separate structure from function, then convert the row into the likely EDAIC consequence: obstruction, aspiration, resistance, dead space, humidity loss, nerve injury, atelectasis, or surfactant failure.

High-Yield Tables

Upper vs lower airway

Conducting vs respiratory zone

Laryngeal nerve supply

Surfactant essentials

Definitions and Values to Memorise

EDAIC Traps

1. The pharynx collapses because it is a muscular tube without cartilage.
2. Genioglossus is the main pharyngeal dilator.
3. Sedation and anaesthesia reduce pharyngeal dilator tone.
4. Posterior cricoarytenoid is the only vocal cord abductor.
5. Cricothyroid is supplied by the external branch of the superior laryngeal nerve.
6. The internal superior laryngeal nerve supplies sensation above the cords.
7. The recurrent laryngeal nerve supplies sensation below the cords and motor to all intrinsic laryngeal muscles except cricothyroid.
8. Terminal bronchioles are conducting airways; respiratory bronchioles are where gas exchange begins.
9. Bronchioles have no cartilage.
10. Anatomical dead space is about 150 mL or 2 mL/kg.
11. Resistance varies inversely with radius to the fourth power during laminar flow.
12. Intubation bypasses humidification and removes physiological laryngeal PEEP.
13. Surfactant reduces surface tension, increases compliance, stabilises alveoli, and reduces fluid transudation.
14. Do not confuse surfactant-related atelectasis with metabolic causes of hyperthermia; they are separate mechanisms.
15. The earliest sign of airway obstruction is often increased work or abnormal airflow, not desaturation.

End-of-Module Summary

The upper airway conducts, warms, humidifies, filters, protects, and participates in speech and swallowing. The nose conditions gas; the pharynx is a collapsible muscular tube; the larynx protects the lower airway and controls airflow through the vocal cords.

The pharynx remains open during wakefulness because dilator muscles such as genioglossus counteract negative inspiratory pressure. Anaesthesia and sedation reduce this tone, making obstruction common. Simple manoeuvres such as jaw thrust, chin lift, airway adjuncts, and CPAP work because they restore structure or pressure to a collapsible airway.

The larynx is anatomically and clinically central. Vocal cords abduct during inspiration and adduct slightly during expiration, creating physiological PEEP. Intubation bypasses this and may promote atelectasis unless external PEEP is used. Laryngeal innervation is high yield: internal superior laryngeal nerve gives sensation above the cords, external superior laryngeal nerve supplies cricothyroid, and recurrent laryngeal nerve supplies sensation below the cords and motor supply to all other intrinsic muscles.

The conducting zone extends from trachea to terminal bronchioles. It conducts, warms, humidifies, filters, and clears gas but does not exchange it. The respiratory zone begins at respiratory bronchioles and is specialised for diffusion. Bronchioles lack cartilage, so smooth muscle tone, lung volume, secretions, and inflammation strongly affect their calibre.

Mucociliary clearance protects the lower airway by moving mucus and trapped particles toward the pharynx. Smoking, dry gases, infection, dehydration, intubation, and anaesthesia impair it.

Surfactant is produced by type II pneumocytes. Its main phospholipid is DPPC. It reduces surface tension, increases compliance, reduces work of breathing, stabilises small alveoli, prevents atelectasis, reduces fluid transudation, and supports innate immunity. Laplace's law explains why surfactant is essential: without it, small alveoli would collapse into larger ones.