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ANATOMY AND PHYSIOLOGY OF

THE RESPIRATORY TRACT
Lorraine de Grey

Respiration is the utilisation of oxygen by the body in the production of

energy. Much of the metabolism occurs by aerobic means, i.e. it requires the
presence of oxygen.
The respiratory tract has evolved into a complex series of tubes whose
primary function is to allow the exchange of gases across all aerobic cells.
Maintaining an adequate supply of oxygen to cells requires four basic steps:
1. Oxygen is taken up from the air by the blood.
2. Oxygen is carried by blood.
3. Tissues receive adequate perfusion with blood.
4. Oxygen passes from the blood to cells.
Carbon dioxide is a product of metabolism in the cells and transfer of carbon
dioxide from blood to the air together with step one above are the main func-
tions of the respiratory tract.
A good knowledge of the basic anatomy is an essential prerequisite to under-
standing the complex physiology of the respiratory tract. In this chapter,
I shall start with the central control of respiration and proceed to give an
intertwined description of function and anatomy.

RHYTHMIC CONTROL OF BREATHING

Central control of respiration has evolved such that there is an automatic and
subconscious control of inspiration and expiration.
This may however be overridden by voluntary actions or the reflex actions of
swallowing and speech.

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TRACHEOSTOMY: A MULTIPROFESSIONAL HANDBOOK

Table 1: Factors influencing the medullary respiratory

centre

Central factors Peripheral factors

Cortex Peripheral chemoreceptors

Hypothalamus Pharyngeal mechanoceptors
Pons Vagal afferents
Central chemoreceptors Non-respiratory reflexes

Broadly speaking the respiratory cycle may be divided into:

1. Inspiratory phase, during which pharyngeal dilator muscles start to
contract, shortly followed by increasing activity of the inspiratory muscles.
2. Expiratory phase I, during which there is a decreased activity of the
inspiratory muscles.
3. Expiratory phase II, during which inspiratory muscles show no activity and
the expiratory muscles may be recruited if forcible expiration is necessary.
The neurones central to the repetitive and involuntary movements of respir-
ation are concentrated in the medulla oblongata. This is under the influence
of a variety of factors, summarised in Table 1.
The motor neurones are divided into two groups.
1. The dorsal respiratory group, the main function of which is in relation to
the timing of the respiration. It lies in close relation to the tractus solitarius
and is made up mainly of the inspiratory neurones, crossing over to the
anterior horn cells of the other side.
2. The ventral respiratory group, also known as the expiratory group is
controlled by the nucleus retroambigualis. The dilator functions of the lar-
ynx, pharynx and tongue are controlled by the nucleus ambiguous and the
inspiratory muscles are controlled mainly by the nucleus para-ambigualis.
The pons undoubtedly contributes to the fine-tuning and modification of the
respiratory rhythm but is no longer considered to be the dominant pneumo-
taxic centre.

CENTRAL CHEMOCEPTORS
These respond to changes in the pH of cerebral spinal fluid (CSF), which in
turn is dependent upon pCO2. Compensatory changes are seen in respiratory
and metabolic alkalosis or acidosis.
If pCO2 is kept abnormally high the CSF pH gradually returns to normal due
to changes in CSF bicarbonate levels. Whether this is an active or passive

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 ANATOMY AND PHYSIOLOGY OF THE RESPIRATORY TRACT

distribution remains uncertain, but the gradual resetting results in a pro-

longed period of hyperventilation.

PERIPHERAL CHEMOCEPTORS
The carotid bodies
These are placed close to the bifurcation of the common carotid artery
whence they have a very rich blood supply. Carotid bodies respond to
1. Falls in partial pressure of oxygen (but not content).
2. Decrease of hydrogen ion concentration.
3. Oscillations of partial pressures of carbon dioxide (in response to the rate
of rise as well as to its concentration).
4. Hypotension (!60 mmHg).
5. Hyperthermia.
6. Drug: Sympathomimetics (acetylcholine, nicotine) and cytochrome chain
inhibitors (cyanide, carbon monoxide).
Baroceptor reflexes – These are found in the carotid sinus and the aortic arch.
They are sensitive to changes in the circulation; a decrease in pressure causes
hyperventilation, while a rise causes respiratory depression.
Pulmonary stretch reflexes – These are involved in the classic inflation and defla-
tion reflexes (Hering–Breuer reflexes). There are three main types of receptors.
! Stretch receptors are mainly in the airways.
! Slowly adapting receptors are in the tracheobronchial smooth muscle.
! Rapidly adapting receptors are in the superficial mucosal layer. Afferents are
conducted by the vagus or occasionally the sympathetic nervous system.
! Their role in man is minimal.
J receptors – These are C-fibre endings in close relationship to the capillaries
of the bronchial and the pulmonary microcirculation. They are activated by
tissue damage and produce bradycardia, hypotension, apnoea, bronchocon-
striction and increased mucus secretion.

Upper respiratory tract reflexes

The upper respiratory tract has developed a number of reflexes to protect
itself from ‘foreign material’.
In the nose – Water can trigger apnoea; irritants cause sneezing; cold recep-
tors trigger bronchoconstriction.
In the pharynx – Mechanoceptors cause activation of pharyngeal dilator
muscles, whilst irritants can cause bronchodilatation.
In the larynx – Mechanical stimulation via the superior laryngeal nerve causes
cough, laryngeal closure and bronchospasm.

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In addition the cough reflex has evolved. This involves the inspiration of a
volume of air into the lungs followed by contraction of the lungs against
a closed glottis. This results in forced expiration through narrowed airways
allowing a forceful jet of air to expel irritant materials out into the pharynx.
The pressure generated may be as high as 300 mmHg.

THE ROLE OF THE SPINAL CORD IN CONTROL OF

RESPIRATION
Messages from the upper control centres are transmitted to the lower motor
neurones via three groups of fibres in the spinal tracts.
1. In the ventrolateral cord – nerve fibres originating from the dorsal and
ventral respiratory groups of the medulla.
2. In the dorsolateral and ventrolateral quadrants of the cord – transmitting
nerve fibres relating to the voluntary control of breathing especially speech.
3. A disparate group of fibres innervating the diaphragm, controlling its
rhythmic contraction.
All of these fibres converge onto the anterior horn cells in the spinal cord
from which emerge the lower motor neurones.
There are two efferent fibres
! The alpha fibres passing directly to the neuromuscular junction of the
spinal cord.
! The gamma fibre that ends directly on the intrafusal part of the muscle
spindle.
Contraction of the intrafusal fibres causes stimulation of the annulospiral
endings. These will send off an impulse via the dorsal root that will then cause
an excitatory effect on the alpha fibres, thus closing a reflex loop.

Spindle afferent fibre

Gamma fibre

Alpha fibre

Fig. 1: Diagrammatic representation of lower motor

neurone fibres reflexes.

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The muscles of respiration

The chest wall is a moderately flexible anatomical entity that contains all the
structures surrounding the lungs and pleura. The chest wall behaves as an
elastic container when relaxed. In the absence of any pressure difference
across the chest wall, it comes to its unstressed volume, which is roughly 75%
of total lung capacity.
If the chest wall muscles were to be relaxed (as in quiet expiration), when the
pleural pressure is below atmospheric, the chest wall is pulled inwards. When
the pleural pressure rises above atmospheric pressure (Pw is positive), the
chest wall bows out. In certain disease states the chest wall may stiffen, caus-
ing a restrictive ventilatory defect.

100 TLC

80

60

45 FRC

20 RV

!40 Recoil pressure "40

Fig. 2: Compliance curve of relaxed chest wall.

FRC # Functional residue capacity, RV # Residual volume,
TLC # Total lung capacity.

The only active phase of the respiratory cycle is the phase of inspiration under
resting conditions.
The inspiratory muscles include:
1. The diaphragm: The normal expiratory excursion is about 1.5 cm and
occurs as the insertion and origin of the diaphragm pull against each other.
2. The intercostals: External intercostals are primarily inspiratory; Internal
intercostals are primarily expiratory.
3. The scalenes: These are active in inspiration by lifting up the rib cage to
counteract the diaphragmatic pull.

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4. Sternocleidomastoid: They are potent accessory muscles during forced

inspiration.
These muscles work to overcome two main sources of resistance:
! The work against elastic recoil.
! The work against resistance to gas flow.
The optimal rate and depth of respiration is in proportion to the resistance
offered by either during the respiratory cycle. The work of breathing is meas-
ured in Joules.
The expiratory muscles include:
1. Rectus abdominis
2. External obliques
3. Internal obliques
4. Transversalis
The elastic recoil of the expanded chest cavity drives the phase of expiration.
Expiratory muscles are normally silent in quiet breathing and usually chip in
when the minute volume is in excess of 40 l/min.
The pressure difference across the chest wall will have no relationship to its
size if the respiratory muscles are being used either to move the chest or to
keep it at a particular volume.

The pleura
The lungs are paired organs lying within the thoracic cavity. The left lung has
two lobes, and the right has three. The left lung is smaller than the right
because of space occupied by the heart.
The lungs are encased with the chest wall. Within this, it lies in the pleura –
a thin membrane which lines the walls of the thoracic cavity – the parietal
pleura and the lung surfaces – visceral pleura.
These two sides are continuous, meeting at the lung hilum; they are directly
opposed to one another, and the entire potential space within the pleura con-
tains only a few millilitres of serous pleural fluid.
Anatomically, the parietal pleura starts at the dome of the pleura overlying
the apex of the lung reaching as high as the lower edge of the neck of the first
rib, then moving medially to form the costal pleura.
This can be traced down to the inner margin of the first rib. It then proceeds
down just behind the sternoclavicular joint to the median plane behind the
sternum where the left and right sides are in contact with each other down to
the fourth costal cartilage.

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It sweeps laterally on the right side down to the posterior surface of the
xiphisternum while on the left side; it sweeps up to 25 mm away from the
midline to the sixth costal cartilage.
On each side it sweeps laterally so as to cross the tenth rib in the mid-axillary
line and is just below the twelfth rib at the costo-vertebral junction. The vis-
ceral pleura adhere tightly to the surface of the lung being reflected off the
structures in the hilum.
The surrounding forces exert an Intrapleural pressure (Ppl) within the pleural
space. During quiet breathing, the pleural pressure is negative; that is to say,
below atmospheric pressure.
The pressure gradient in the erect person drops exponentially down the lung
decreasing 1 cm H2O for every 3 cm drop. This has a profound effect on many
features of pulmonary function including airways closure, ventilation/perfu-
sion ratios and gaseous exchange.
The lungs are totally separated from the abdomen by a sheet of skeletal
muscle – the diaphragm, which is dome shaped before lung expansion but
flattens during breathing in.
During active expiration, the abdominal muscles are contracted to force up
the diaphragm and the resulting pleural pressure can become positive.
Positive pleural pressure may temporarily collapse the bronchi and cause limi-
tation of airflow.

Anatomy of the upper airway

This describes the portion of the airway that lies above the vocal cords and
includes:
1. The nasal passages (septum, turbinate, and adenoids)
2. The oral cavity (teeth and tongue)
3. The pharynx (tonsils, uvula, and epiglottis)
4. The glottis
Breathing normally occurs through the nose or mouth and the direction it takes
is under voluntary control utilising the soft palate, tongue and lips.
Normally the mouth is closed and the tongue is applied to the hard palate to
allow nasal breathing. This is the physiological way to breathe, as the nose is
specially adapted for this function. The nose provides:
1. Hairs to filter off particulate matter.
2. Humidification and warming of the air over the increased surface area
provided by the turbinates.

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The mouth is brought into play when the respiratory minute volume is
greater than 35 l/min. Forced mouth breathing is affected by a functional
anatomical change that arches the soft palate upwards and backwards against
the band of the superior constrictor of the pharynx, effectively closing off the
nasopharynx.
The pharynx has two components: The oropharynx, i.e. the throat area and
the nasopharynx is an extension of the throat upwards towards the nasal
passages. The opening into the airways from the oropharynx is called the
glottis, which is closed off during swallowing by a small flap called the
epiglottis.

Hyoid bone

Thyrohyoid
membrane

Thyroid
cartilage

Cricoid
cartilage

Fig. 3: Laryngeal anatomy.

After the glottis, the air enters the larynx, a structure of cartilage and liga-
ments that forms the Adam’s apple. The entire structure is supported by
muscles that suspend the larynx from a small bone in the neck called the hyoid.
Within the larynx are folds of cartilage that form the vocal cords. Air flowing
over these cords causes them to vibrate and so produce sound. Their tension

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determines the tone or pitch of the sound; small muscles that pass from the
cords to the cartilage of the larynx capsule can alter this.

Innervation of the upper airway

The upper airway is innervated by three main cranial nerves:
Trigeminal nerve (Cranial nerve V): Branches of the trigeminal nerve inner-
vate the nose and the anterior two thirds of the tongue.
Glossopharyngeal (Cranial nerve IX): Branches of the glossopharyngeal nerve
innervate the posterior third of the tongue, roof of pharynx and tonsils.
Vagus (Cranial nerve X): The two major divisions of the vagus nerve in airway
innervation are the superior laryngeal and the recurrent laryngeal nerves.

Sensory innervation
1. Trigeminal nerve – the sensory innervation of the nasal mucosa arises from
two divisions:
– The anterior ethmoidal nerve supplies the anterior septum and lateral
wall;
– The nasopalatine nerves from the sphenopalatine ganglion innervate
the posterior areas.
2. Glossopharyngeal nerve – supplies the posterior third of the tongue, soft
palate, epiglottis, fauces and the pharyngo-oesophageal junction.
3. Superior laryngeal nerve – the internal branch of the vagus nerve inner-
vates mucosa from the epiglottis to and including the vocal cords.
4. Recurrent laryngeal nerve – a branch of the vagus nerve innervates mucosa
below the vocal chords to the trachea.

Motor innervation
1. The external branch of the superior laryngeal nerve is responsible for inner-
vation of the cricothyroid muscle.
2. The recurrent laryngeal nerve provides a motor supply to all the muscles of
the larynx (posterior and lateral cricoarythenoid muscles) except the
cricothyroid muscle.
– The lateral cricoarythenoid adducts the cords
– The posterior cricoarythenoid abducts the cords
Unilateral damage to the recurrent laryngeal nerve causes hoarseness.
Bilateral damage causes respiratory distress and stridor whilst chronic dam-
age can cause aphonia.

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Anatomy of the lower airway

This describes the portion of the airway below the vocal cords. In an adult,
the vocal cords are the narrowest portion of the airway.
The lower airway can be divided into:
The larynx is found at the level of the fourth to the sixth of the cervical ver-
tebrae. Protection of the airway remains its most important function.
However it has developed further as the organ of speech. The larynx is made
up of nine cartilages:
1. Unpaired (thyroid, cricoid, and epiglottis). The cricoid cartilage is the only
complete cartilaginous ring the respiratory system. It lies below the thy-
roid cartilage.
2. Paired cartilages (arytenoids, corniculate, and cuneiform).

Fig. 4: Diagrammatic representation of the closure of the vocal cords.

Thyroarytenoid
muscle

Interarytenoid Arytenoids
muscle

Fig. 5: Superior aspect of the larynx.

The larynx also has two groups of muscles:

1. Muscles that open and close the glottis (lateral cricoarytenoid, post
cricoarytenoid, and transverse arytenoid).

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2. Muscles that control the tension of the vocal ligaments (cricothyroid,

vocalis, and thyroarytenoid).
The cricothyroid membrane is another important structure found in the
lower respiratory tract. This membrane connects the thyroid cartilage and the
cricoid ring. It is a thin membrane without major vessels and may be used for
obtaining emergency airway access in emergency cricothyroid puncture.

THE TRACHEOBRONCHIAL TREE

Classically, the tracheobronchial tree has been described as extending from
the trachea (generation 0), doubling with each generation to the alveolar sacs
(generation 23).
The trachea is essentially a fibromuscular tube that is supported by 20
U-shaped cartilages and enters the chest cavity at the superior mediastinum.
It bifurcates at the carina at the level of T4.
The mucosa lining the trachea is columnar ciliated epithelium. Co-ordinated
beating of cilia causes an upward stream of mucus and foreign bodies.
The trachea divides into two main bronchi, which are asymmetrical, the right
being one-third wider and a little shorter than the left. The right bronchus
slopes more steeply (25 degrees off the vertical) than the left (45 degrees off
the vertical), so that foreign bodies of whatever shape, are statistically more
likely to enter the right bronchus. The same rule naturally applies to the
endotracheal tube that is inserted down too far into the trachea.
Each main bronchus divides into three lobar bronchi, which in turn divide
into lobar bronchi that give off segmental bronchi. Each of these supplies
a segment of the lung.
Cartilage supports the main, lobar and segmental bronchi. It is U-shaped in
the main bronchi and helical lower down, with helical bands of muscle com-
pleting the geodesic plates.
Bronchi down to the fourth generation are regular enough to be named
separately:

UPPER LOBE – RIGHT UPPER LOBE – LEFT

1 Apical bronchus Apical bronchus

2 Posterior bronchus Posterior bronchus
3 Anterior bronchus Anterior bronchus

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MIDDLE LOBE – RIGHT LINGULA – LEFT

4 Lateral bronchus Superior bronchus

5 Medial bronchus Inferior bronchus

LOWER LOBE – RIGHT LOWER LOBE – LEFT

6 Apical bronchus Apical bronchus

7 Medial basal –
8 Anterior basal bronchus Anterior basal bronchus
9 Lateral basal bronchus Lateral basal bronchus
10 Posterior basal bronchus Posterior basal bronchus

Small bronchi span generations 5–11. The true bronchi are typified by the close
proximity of the pulmonary artery and pulmonary lymphatics in a sheath.
They rely on the cartilage in their walls for patency combined with a positive
transmural pressure gradient at this level and a negative intrathoracic pressure.
Between generations 12–16 bronchioles form; they are characterised by a lack
of cartilage maintaining their patency by the elastic recoil of the lung
parenchyma in which they are embedded. In the terminal bronchioles due to
the rapid and multiple branching of the bronchioles, the surface is at least 100
times more than at the level of the large bronchi. Nutrition down to this level
is from the bronchial circulation.

AD
TB

A
A
R
AD
R

V A

Fig. 6: Cross-section of respiratory bronchioles.

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Generations 17–19 make up the respiratory bronchioles. It is beyond this point

that gaseous exchange occurs.
– The lining epithelium starts off as cuboidal and ends up as flat alveolar.
– There is a well-demarcated muscle layer that bands over the opening of the
alveolar ducts and mural alveoli.
– The calibre of the advancing generations remains unchanged at about
0.4 mm to provide a total cross-sectional area of several hundred cm2.
Generations 20–22 make up the alveolar ducts. They arise from the terminal
respiratory bronchioles. They have no walls than the mouths of the mural
alveoli; about half the alveoli arise from the ducts.
Generation 23 are the alveolar sacs. They are blind ending sacs, about 17
alveoli arising from each alveolar sac. Around half of the alveoli arise from the
alveolar sacs.

THE ALVEOLI
The primary function of the respiratory system is gaseous exchange. This
occurs at the level of the alveoli.
1. There are 200–600 million in total, with a mean diameter of 0.2 mm.
2. Their size is proportional to the lung volume except at maximal inflation
when vertical gradient in size disappears. This vertical gradient is depend-
ent on gravity. The reduction in size of alveoli and the corresponding
reduction in calibre of the smaller airways in the dependent parts of the
lung have important implications in gas exchange.

Fig. 7: Electron microscopic picture

of alveoli.

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3. Alveoli are polyhedral in shape, this shape being determined by elastic

fibres in the alveolar septum. The septa are perforated by the pores of
Kohn, which allow collateral ventilation.
4. The alveolar septum has a network of fibre forming a mesh from the
peripheral fibres to the bronchioles, supporting capillaries that thread in
and out of the meshwork.
5. The cells rest on a basement membrane. This is made of collagen IV
(which provides great strength), as well as heparin sulphate, laminin, and
entactin (these promote cell attachment and protein permeability).
There are a number of special cells in the alveoli:
1. Capillary endothelial cell: These are continuous with the general circula-
tion. They have a featureless cytoplasm apart from plasmalemmal vesicles
(caveolae) and may be involved in pinocytosis. They serve to further
increase the surface area and have enzymes on their surface. Fairly loose
junctions connect the cells.
2. Alveolar epithelial cells – Type I: These cells form continuous sheets and
meet at tight junctions. These junctions help to prevent the escape of large
molecules. This maintains the oncotic pressure gradient that protects
against pulmonary oedema, while allowing the passage of macrophages
and polymorphs in response to chemotactic stimuli.
3. Alveolar epithelial cells – Type II: These are the stem cells from which the
type I cells arise. They have large nuclei and microvilli, are round in shape
and are situated at the junction of the septa.
4. Alveolar brush cells – Type III: They are uncommon and their function is
uncertain.
5. Alveolar macrophages: These may lie freely on the surface of the alveolar
epithelial cells where they scavenge dust particles. They combat infection
by phagocytosis, use of oxygen-free radicals and enzymes. Neutropils may
also appear especially in the lungs of smokers.
6. Clara cells: This is a type of non-ciliated bronchiolar epithelium that secrete
at least three proteins including antiproteases and a surfactant apoprotein.
7. APUD cells: These are known to produce a range of hormones elsewhere
but their role in the respiratory system is uncertain.
8. Mast cells: There are numerous mast cells that lie in the alveolar septa and
also freely in the luminal airways – they play a role in bronchoconstriction.
Surfactant
There is a potential danger that on breathing out, the walls of alveoli may touch
and adhere to each other. Contact between moist surfaces produces powerful
adhesion because of surface tension. Respiratory movements are unable to
overcome these forces and it is Surfactant, a product of specialised cells lining
the alveoli that prevents alveoli from deflating totally following expiration.

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The main function of surfactant is to reduce the surface tension throughout

the lung. It also indirectly prevents lung oedema and also influences the rate
of alveolar collapse thereby contributing to its general compliance.
Surfactant is a complex substance produced by the Type II alveolar cells. It
lines the alveoli and smallest bronchioles.
Surfactant consists of:
! ~90% phospholipids (mainly dipalmitoyl phosphatidyl choline and phos-
phatidyl glycerol).
! ~10% protein.
The fatty acids are saturated and straight. These tend to pack better in expir-
ation therefore making the actual surface tension vary in different parts of
the respiratory cycle. Cholesterol, phosphatidyl inositol, phosphatidyl serine
and phosphatidyl ethanolamine are also present.
The protein component increases the speed with which the surface film is
reconstituted. Most of the proteins are 26–38 kDa although a group of
hydrophobic 11 kDa proteins also play a role.

Gas
Fatty acids (2)

Interface
Glycerol

Phosphate

Water
Nitrogenous base

Fig. 8: Schematic diagram of surfactant.

The pressure inside a bubble is subject to the law of Laplace’s law viz;
P ! 4T/r (for a sphere with two liquid-gas interfaces, like a soap bubble)
P ! 2T/r (for a sphere with one liquid-gas interface, like an alveolus)
(P ! pressure, T ! surface tension and r ! radius).
That is, at a constant surface tension, small alveoli will generate bigger pres-
sures within them than will large alveoli.
One would therefore expect the smaller alveoli to empty into larger alveoli as
lung volume decreases. However, surfactant differentially reduces surface

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tension (more so at lower volumes) and this leads to alveolar stability avoid-
ing alveolar collapse.
Surfactant is formed relatively late in foetal life; thus premature infants born
without adequate amounts experience respiratory distress and may die.

Elastic forces in the lung

The lungs exhibit a phenomenon of compliance that is the ability to change
volume with pressure as demonstrated by all elastic organs.
This can be explained by hysteresis – a phenomenon whereby the inflation
pressure falls exponentially from its initial value to a lower value attained after
inflation. Rather more than expected pressure is required in inflation while
less recoil pressure is available during deflation.
The lungs exhibit two forms of compliance:
! Dynamic compliance
! Static compliance
Change in volume gradient
Dynamic compliance =
Change in initiaal transmural pressure
Change in volume gradient
Static compliance =
Change in ultimate transmural pressure

There are a variety of factors affecting the lung compliance:

1. Changes in surfactant activity – the surface tension is greater at larger lung
volumes and during inspiration. It is the single most important factor
determining hysteresis. It is also important in maintaining alveolar
patency thus reducing alveolar recruitment during normal respiration.
2. Recent ventilatory history – compliance is maintained by continuous
rhythmic cycling and the effect is dependant on tidal volume as well as the
total lung volume.
3. Restriction of chest expansion – artificial reduction with strapping reduces
lung volume; the compliance remains reduced until a single deep breath
reinflates the lung – the ‘physiological sigh’.
4. Bronchial smooth muscle tone – has a role in dynamic compliance but not
in static compliance.
5. Age – this has no effect on compliance, confirming that the lung ‘elasticity’
is largely determined by surface forces.
6. Stress relaxation – this explains the principle that on pulling an elastic
body to a fixed increase in length, this will result in an initial maximal ten-
sion that declines exponentially to a constant value.

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7. Emphysema – causes increased static lung compliance, but the dynamic

compliance is reduced.
8. Other lung diseases such as pulmonary fibrosis, consolidation, and fibrous
pleurisy, adult respiratory distress syndrome – decrease both static and
dynamic compliance.

AIRFLOW IN THE RESPIRATORY TRACTS

Air will flow from a region of high pressure to one of low pressure – the vel-
ocity of flow is in direct relation to the pressure difference.
Air therefore flows in during inspiration because the alveolar pressure is less
than the pressure at the mouth; conversely the air flows out during expiration
because alveolar pressure exceeds the pressure at the mouth.
Different parts of the airways anatomy have a variety of mechanisms to coun-
teract and maintain patency throughout the respiratory cycle. This allows
easy, continuous and repetitive gaseous exchange to occur efficiently with
minimal energy expenditure.
The pharynx in inspiration is subject to a negative pressure of a few kilo-
pascals that would normally tend to pull the tongue backwards and cause the
pharynx to collapse.
This is countered in an active manner using musculature – mainly the
genioglossus to effectively prevent changes in pharyngeal anatomy in all
the phases of respiration.
The nasopharynx is also kept patent by the tensor palati, palatopharyngeus
and palatoglossus.
Passage of air in the relatively larger airways creates eddies and is described as:

Fig. 9: Turbulent flow.

Driving pressure is proportional to the square of the flow rate and is

described in this formula:
!P " KV2
where P is the driving pressure, K is a constant and V is the air flow.

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TRACHEOSTOMY: A MULTIPROFESSIONAL HANDBOOK

This means that to double the airflow one needs to quadruple the driving
pressure.

Turbulent flow

Transitional flow

Laminar flow

Fig. 10: Locations of flow patterns.

Turbulent flow is found mainly in the largest airways, like the trachea.
When flow is low velocity and through narrow tubes, it tends to be more
orderly and streamlined and flows in a straight line. This type of flow is called
laminar flow.
Unlike turbulent flow, laminar flow is directly proportional to the driving
pressure, such that to double the flow rate, one needs only double the driving
pressure.

Fig. 11: Laminar flow.

Poiseuille’s Law can describe laminar flow:

!P = v(8"l/#r4)

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 ANATOMY AND PHYSIOLOGY OF THE RESPIRATORY TRACT

During quiet breathing, laminar flow exists from the medium-sized bronchi
down to the level of the bronchioles. During exercise, when the airflow is
more rapid, laminar flow may be confined to the smallest airways.

0.08
Resistance (cmH2O/l/sec)

0.06

0.04

0.02

Trachea Bronchus Bronchiole

Terminal
bronchiole

Fig. 12: Resistance/Generation.

Transitional flow, which has some of the characteristics of both laminar and
turbulent flow, is found between the two along the rest of the bronchial tree.

LUNG VOLUMES
At rest, an adult breathes in about 500 ml of air (7–8 ml/kg body weight) with
each breath. This is referred to as the tidal volume.
Hence 5–6 l of air are breathed in and out each minute. This is enough to
meet the needs of the cells of the body at rest, which require around 250 ml
per minute. During exercise, oxygen requirements may reach as much as 4 l
per minute. To keep up with demand, the volume of air inspired per minute
may reach as high as 80 l per minute.
However even at rest, we can consciously increase the volume breathed in, or
further deflate the lung. Thus there are inspiratory and expiratory reserve volumes.
In addition, the lung contains a volume of gas even after maximal expiration
has occurred, as deflation of the alveoli is incomplete and some gas fills the
dead space, i.e. there is a residual volume of gas within the lungs – around 1.5 l
in adults.

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Consequently, the gases within the lung into which inspired air will pass when
we breathe in will be the volume represented by the expiratory reserve plus
the residual volume; this is the functional residual capacity (FRC) – around
2.5 l in an adult. This is equal approximately to half the maximum capacity of
the lungs called the total lung capacity.
If we inflate the lungs maximally and then breathe out maximally, the volume
of gas expired from the lungs represents the maximum volume of gas that can
possibly be expelled from the lung in a single breath; this is called the vital
capacity – around 4 l in an adult.
If we add the vital capacity to the residual volume, then this gives the total
lung capacity – around 5–6 l in an adult.
Lung volumes and capacities are measured using a machine called a spiro-
meter. Such measurements may be of particular importance in patients
undergoing partial or complete lung resections, and in patients with chronic
obstructive or restrictive ventilatory defects.

Inspiratory
reserve Inspiratory
volume capacity
Vital
Tidal volume capacity
Total
lung
Expiratory
Functional capacity
reserve
residual volume
capacity

Residual
volume

Fig. 13: Lung volumes and capacities.

Factors affecting the functional residual capacity:

1. Body size – linearly relates to height although obesity reduces FRC.
2. FRC is greater in females than males by 10%.
3. Diaphragmatic muscle tone – residual end-expiratory tone is a major factor
while in the supine position keeping the FRC around 400 ml above the
volume in the anaesthetised position. The diaphragm also protects the lungs
from the abdominal contents and limits the FRC change from 500 to
1000 ml between the supine and the upright positions.
4. FRC is increased in asthma and emphysema.

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 ANATOMY AND PHYSIOLOGY OF THE RESPIRATORY TRACT

Pleural pressure
Pleural pressure can be estimated in human subjects using an oesophageal
balloon.
The size of the lung is determined by the difference between the alveolar pres-
sure and the pleural pressure, or the transpulmonary pressure – the larger the
difference, the bigger the lung.
As a result of gravity, in an upright individual, the pleural pressure at the base
of the lung base is greater (less negative) than at its apex.
When the individual lies on his back, the pleural pressure becomes greatest
along his back. Since alveolar pressure is uniform throughout the lung, the
top of the lung generally experiences a greater transpulmonary pressure and
is therefore more expanded and less compliant than the bottom of the lung.

4
Resistance (cmH2O/l/sec)

0 2 4 6 8
Lung volume (l)

Fig. 14: Resistance/Volume.

DEAD SPACE
This is the fraction of the tidal volume that serves no function in gaseous
exchange. This is determined by the equation:

VA ! f(VT " VD)

VA ! alveolar ventilation VT ! tidal volume
f ! respiratory frequency VD ! dead space

Dead space consists of:

1. Apparatus dead space – only occurs when an external breathing apparatus is
used. This is further complicated by the fact that the inhaled gas composition

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TRACHEOSTOMY: A MULTIPROFESSIONAL HANDBOOK

may be variable: end-expiratory gas, mixed expired gas or even expired dead
space gas. This makes the actual gas interchange at the functioning alveolar
surface difficult to assess. This may be of importance when using various
breathing circuits during anaesthesia.
2. Anatomical dead space – made up of the conducting air passages. It is not
constant and is subject to a number of variables including:
– Age – usually sees an increase in the anatomical dead space.
– End-inspiratory lung volume – the volume in the air passages varies in
relation to the lung volume.
– Size – volume of air in passageways (ml) ~2.2 ! wt in kg.
– Posture – sitting " supine
Neck extended " normal position " neck flexed.
– Tracheostomy – bypasses all extra thoracic dead space (65–70 ml).
– Hypoventilation (tidal volumes of #250 ml) – reduced dead space by
laminar flow of the gases allows easier passage into the alveoli.
3. Alveolar dead space – this is the inspired gas that passes through the
anatomical dead space to the alveolar surface but does not take part in
gaseous exchange, due to a lack of perfusion. It is of little significance
normally, but may increase appreciably in some situations:
– Pulmonary embolism/pulmonary artery obstruction during surgery –
the alveolar dead space rises in relation to the degree of occlusion of the
pulmonary circulation.
– Ventilation of non-vascular air space in chronic lung diseases.
– Pulmonary hypoventilation – whether due to low output circulatory
failure or during anaesthesia results in less perfusion for the non-
dependant parts with a subsequent increase in the alveolar dead space?
Posture in itself does not affect the dead space to any significant degree
except when under anaesthesia. In the patient lying on one side, the upper
lung will be preferentially ventilated resulting in an increase in the dead
space.
4. Physiological dead space – this is the sum of the alveolar and the anatom-
ical dead spaces and is shown by the Bohr equation:

VD/VT $ (PaCO2 % PECO2)/PaCO2

Factors influencing the physiological dead space include:

– Age – VD/VT increases with age.
– Sex and body size – VD/VT ratios slightly greater in males and VD raises
17 ml for every 10 cm of height.
– Posture – drop from 34% to 30% from the erect to the supine positions.

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 ANATOMY AND PHYSIOLOGY OF THE RESPIRATORY TRACT

– Smoking – can increase the ratio by ~30%.

– Pulmonary disease – as above.
– Anaesthesia – VD/VT is 30–35% below the carina; prolonged use of
PEEP increases dead space.

Pulmonary circulation and ventilation

The total pulmonary circulation at rest is measured as 0.5–1.0 l (10–20%) of
the total blood volume, but will equal the systemic circulation and can rise to
as much as 25 l/min without a significant rise in pressure.
The ability to control pressure by tone is significantly less in the pulmonary
circulation than in the systemic circulation, as a result of which gravity dic-
tates the distribution of blood flow with a mismatch of circulation in the
more dependant areas of the lung.
Factors affecting pulmonary blood volume include:
1. Systole – when inflow exceeds outflow.
2. Valsalva manoeuvre (decreases pulmonary blood flow).
3. Posture – change from supine to erect decreases blood flow by 27%.
4. Vasoconstrictor drugs or catecholamines push blood from the systemic into
the pulmonary circulation.
While the systemic circulation shows a drop of pressures from 90 mmHg to
2 mmHg as it courses through from the arteries, until it gets to the right
atrium, the drop in pulmonary pressure is much smaller and falls from
17 mmHg in the pulmonary arteries to 6 mmHg in the left atrium.

Right Pulmonary Capillary bed Left atrium

ventricle artery

0.8

3.2 2.2 2.2 0.8

3.5

Fig. 15: Pulmonary circulation pressures (kPa).

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TRACHEOSTOMY: A MULTIPROFESSIONAL HANDBOOK

FACTORS AFFECTING PULMONARY VASCULAR

PRESSURES
Several factors have an influence on the pressure in the pulmonary circula-
tion. They include:
1. Cardiac output – there is normally an increase in volume without a rise in
pressures by recruitment of vessels and by passive dilatation. There is a
limit to this and in cases where left to right shunting occurs as in ventral
and atrial septal defects as well as in patent ductus arteriosus, pulmonary
hypertension occurs.
2. Changes in intra-thoracic pressure – intra vascular pressures rise reflect-
ing rises in intra-thoracic pressures. This is seen in the Valsalva manoeuvre
(forced expiration against a closed glottis). There are also rhythmic
changes with the normal respiratory cycle. The upright position is also
associated with a decreased intrathoracic pressure).
3. Chronic hypoxia.
4. Pulmonary thromboembolism.
5. Mitral stenosis and incompetence.
6. Pulmonary vascular resistance.
7. Autonomic control.
8. Changes in oxygen and carbon dioxide tension.

Gas exchange across the alveolus

4
3
2 5
6
1 7

O2

Fig. 16: Passage of O2 molecule

across its diffusing membrane.

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 ANATOMY AND PHYSIOLOGY OF THE RESPIRATORY TRACT

1 ! Alveolus.
The average diameter of an alveolus is 200 "m. Mixing is probably complete
within 10 min. The process is slower for heavier gases but as oxygen, nitrogen
and carbon dioxide are roughly similar, it is unlikely to affect the process
significantly.
2 = Alveolar epithelium – There are 4 separate lipid bilayers measuring a total
of 0.5 "m.
3 = Basement membrane.
4 = Capillary endothelium.
5 = Pulmonary capillary. These are usually about 7 "m, so there is not much
fluid plasma as the RBC squeezes through.
6 = RBC membrane – the erythrocyte diameter is 14 times the thickness of
the alveolar/capillary membrane.
7 = Cytoplasm.
The uptake of oxygen by haemoglobin is the rate-determining step in the
uptake of oxygen from alveolar gas by the erythrocyte.
Mathematically the rate of oxygen diffusion can be defined as:

Oxygen uptake
O2 diffusing capacity =
Alveolar O2 − mean pulm. cap. PO2

Ventilation and perfusion

In the ideal situation, the ventilation and perfusion of all parts of the lung
would be equally and perfectly matched. There are however variations in both
parameters in different parts of the lung.
The pulmonary circulation is a low-pressure system. As a result it is subject to
a variety of pressures, namely the alveolar pressure, flow rate and the vascular
resistance, that determine the relative amount to which each part of the lung
is perfused. The interplay of pressures is mainly dependant on gravity.
In Zone 1, the alveolar pressure is greater than the arterial pressure therefore
keeping the vessel closed, preventing flow.
In Zone 2, the arterial pressure rises thanks to the effect of gravity and there-
fore, it exceeds the alveolar pressure and flow occurs in relation to this pressure
difference. The distal venous pressure in normal subjects has no role to play in
determining the flow in this zone.

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TRACHEOSTOMY: A MULTIPROFESSIONAL HANDBOOK

Zone 1 PA ! Pa! Pv

Zone 2 Pa !PA !Pv

Zone 3 Pa ! Pv !PA

Zone 4 Pa~Pip !Pv

Fig. 17: Ventilation and perfusion.

In Zone 3, the venous pressure is greater than the alveolar pressure and the
flow rate is determined solely as a result of the difference between the arterial
and venous side of the circulation.
In Zone 4, (seen only at reduced lung volumes) the interstitial pressure
increases to reduce blood flow by the occlusion of the larger blood vessels.
A number of factors can affect the perfusion of the lung:
1. Central factors – cardiac failure.
2. Position – in the supine position, the difference between the top and bot-
tom of the lung is only 30 cm so that the uppermost part of the lung
equates to Zone 2 and the bottom of the lung to Zone 3.
3. Effect of inflation of the lung: The larger blood vessels are opened up due
to traction of the surrounding lung tissue but the smaller vessels are col-
lapsed as the lung expands in ventilation. In the collapsed lung, the driving
force is the PO2; the alveolar PO2 is controlled by the pulmonary arterial
PO2 and as a result in the short term will not lead to a decreased blood flow
although in the longer term the blood flow will inevitably decrease.

Distribution of ventilation
In the normal subject the main influence on ventilation is position and the
manner of ventilation.
! The right lung is slightly better ventilated than the left in both the erect
and supine positions.
! The lower lung is better ventilated than the upper lung in the lateral pos-
ition except in the ventilated patient with an open chest who will have
a better ventilation of the upper lung.

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 ANATOMY AND PHYSIOLOGY OF THE RESPIRATORY TRACT

! The rate of ventilation is also important. With ventilatory rates of !1.5 l/s,
the ratio of ventilation of the lower to the upper parts of the lung is 1.5:1.
! The rate of alveolar filling is expressed as a time constant that is the time
required to inflate the lungs if the initial rate of gas flow were maintained
through inflation. The time constant varies for different alveoli, dependant
on their compliance and resistance.
! If the time constants were equal for all alveoli then there would be no
distribution of gases as its distribution would be independent of rate dur-
ation or frequency of respiration.
! However if the time constants were different then gaseous distribution
occurs, dependant on the rate, duration and frequency resulting from a
decreased dynamic compliance with increased frequency of respiration.

Ventilation/perfusion ratios
If ventilation occurs to areas of lung that are not perfused, then it can have no
role to play in gas exchange.
Taking the lung as a whole, the rate of ventilation is ~4 l/min and the pulmonary
blood flow is ~5 l/min making a V/Q ratio of 0.8. If all parts of the lung were
equally ventilated and perfused this would be the case all over the lung.
There is a differential perfusion and ventilation from the unventilated to the
unperfused alveoli in the lung.
The below diagram gives an indication of the V/Q ratios from the completely
unperfused (dead space) on the left to the unventilated (shunt) at the far
right, going through various degrees of relative perfusion to ventilation (with
the ideal as shown on the graph marked at 1.

PO2 (mmHg)
10 50 100 150

60
V/Q
0 0.2 0.5 1
40
3
5
7
20

0 10 15 20
PO2 (kPa)
PCO2 (kPa) PCO2 (mmHg)

Fig. 18: V/Q ratios in different areas of the lung.

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TRACHEOSTOMY: A MULTIPROFESSIONAL HANDBOOK

In practical terms in the young the V/Q ratio varies from 0.5–2.0, increasing
in its range to 0.3–5.0 in the elderly.

Summary of learning objectives

1. The carriage of oxygen and carbon dioxide to and from tissues, and the
exchange of these gases with air, is vital for life.
2. At rest, a person breathes in and out 5 l of air per minute. During exercise
this may increase to up to 100 l per minute. This done by increasing both
frequency and depth of ventilation.
3. Low airway resistance and a high elasticity allow for a very efficient system.
4. Spirometry can be used to measure lung volumes and capacities.
5. Gas exchange occurs across lung alveoli; the rest of the airway comprises
a ‘dead space’.
6. Breathing is mainly involuntary but can be changed consciously, and is
controlled by the rhythmical discharge of nerve impulses from the respir-
atory centres.
7. Blood gas composition is monitored continuously by chemoreceptors
that respond to changes in either oxygen or carbon dioxide/pH content.
8. The upper airway has evolved to produce humidification and warming of
inspired air. It also has the important property of phonation.
9. The lower airway can be divided into 23 generations.
10. Surfactant is a phospholipid that acts to lower the surface tension, and
prevents alveoli from deflating totally following expiration.
11. Dead space is the volume of inspired air that does not take part in gas
exchange. It can be divided into physiological and anatomical dead space.
12. The significance of ventilation/perfusion matching is that areas of the
lung may pathologically exhibit diminished ventilation or perfusion,
leading to abnormal oxygenation of blood.

REFERENCES
1. Lumb AB, Nunn JF. Nunn’s Applied Respiratory Physiology 4th Edition. London:
Butterworth-Heinemann, 1993.
2. McMinn RMH. Last’s Anatomy Regional and Applied, 9th edn. London: Churchill
Livingstone, 1994.
3. Clancy J, McVicar AJ. Physiology and Anatomy: A Homeostatic Approach. London:
Arnold, 2002.
4. John Hopkins School of Medicine. Interactive Respiratory Physiology.
www.airflow.htm.
5. Mallory GB. The Influence of the Physiology of the Upper Airway on the Lower
Airway. www.CIPA.htm.
6. Johnson DR. Introductory Anatomy: Respiratory System.
www.IntroductoryAnatomyRespiratorySystem.htm.

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