Cardiorespiratory Physiotherapy Adults and Paediat... - (1 Anatomy and Physiology of The Respiratory and Cardiac Systems)

ANATOMY AND PHYSIOLOGY
OF THE RESPIRATORY AND
1 CARDIAC SYSTEMS
MANDY JONES ■ ALEX HARVEY ■ ELEANOR MAIN
C H A P T E R O U T L I N E
INTRODUCTION TO RESPIRATION 2 Altered Lung Compliance 18
UPPER RESPIRATORY TRACT 3 Closing Volume 18
Pulmonary Surfactant 18
THE BRONCHIAL TREE 4
Altered Chest Wall Compliance 19
THE LUNGS AND PLEURAE 5 Consequences of Reduced Total Lung
SURFACE MARKINGS OF THE LUNGS 8 Compliance 19
The Right Lung 8 CONTROL OF BREATHING 19
The Left Lung 8 Origin of Breathing 19
The Pleura 9 Respiratory Control Centres (RCCs) 19
THE THORACIC CAGE 9 The Medullary Control Centres 19
Movements of the Ribs 9 The Pontine Control Centres 20
MUSCLES OF RESPIRATION 11 Higher Brain Centres 20
Diaphragm 11 Clinical Failure of the Respiratory Control
Intercostals 13 Centres 20
Accessory Muscles of Inspiration 13 Ondine’s Curse 20
Muscles of Forced Expiration 13 Respiratory Control Feedback Mechanism 20
Clinical Failure of the Effectors 20
RESPIRATORY MECHANICS 13 Respiratory System Sensors 21
Respiratory Pressures 13 Mechanoreceptors 21
Ventilation 14 Irritant Receptors 21
MUCOCILIARY TRANSPORT SYSTEM 15 Juxta-Capillary Receptors 21
Cilia 15 Proprioceptors 21
Copyright © 2016. Elsevier. All rights reserved.
Aqueous (Sol) Layer 15 Spinal Cord Reflexes 21

Viscous (Gel) Layer 15 Nasopulminary Reflexes 21
COLLATERAL VENTILATION 15 Chemoreceptors 21
Peripheral Chemoreceptors 22
AIRWAYS RESISTANCE 16
Central Chemoreceptors 22
Airway Innervation 16
Stimulation of the Central Chemoreceptors 22
Site of Highest Resistance 16
Central Chemoreceptors and COPD 22
Poiseuille’s Law 16
Clinical Relevance of Hypercapnic COPD 23
Clinical Relevance of Poiseuille’s Law 16
Loss of Hypoxic Drive 23
Consequences of Increased Airway Resistance 17
Increased V /Q Mismatch 23
Clinical Signs of Airflow Limitation 17
Haldane Effect 23
Problems Associated with Airflow Limitation 17
Reversal of Airflow Limitation 17 LUNG VOLUMES & VENTILATION 23
Lung Volumes 23
RESPIRATORY COMPLIANCE 18
Lung Capacities 23
Factors Affecting Lung Compliance 18
1
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2 1 Anatomy and Physiology of the Respiratory and Cardiac Systems
Factors Affecting Lung Volumes 23 Carbon Dioxide Transport 33

Clinical Relevance of Lung Volumes and Carbon Dioxide and Haemoglobin 33
Capacities 24 Carbon Dioxide as Bicarbonate 33
Measuring Lung Volumes and Capacities 25 Carriage From Tissue to Lungs 33
Why Assess Spirometry? 25 THE EFFECT OF GROWTH AND AGEING ON
Ventilation Terminology 25 RESPIRATION 34
Anatomical Dead Space 25 Embryonic Period (Weeks 3–5) 34
Alveolar Dead Space 25 Pseudoglandular Period (Weeks 6–16) 34
Physiological Dead Space 25 Canalicular Period (Weeks 17–24) 34
Alveolar Ventilation 25 Terminal Sac Period (Week 24–Term) 34
Clinical Relevance of Alveolar Ventilation 26
RESPIRATORY SYSTEM: ANATOMICAL AND
Alteration of Alveolar Ventilation 26
PHYSIOLOGICAL DIFFERENCES BETWEEN
GAS EXCHANGE 26 CHILDREN AND ADULTS 35
Fick’s Law and Gas Exchange 27 Anatomical Differences in the Respiratory System
Concentration Gradient and Gas Solubility 27 between Children and Adults 35
Transit Time of Red Blood Cell (RBC) 28 Physiological Differences in the Respiratory System
Thickness of the Alveolar Membrane 28 between Children and Adults 38
Surface Area of Alveolar Membrane 28
28 INTRODUCTION TO CARDIAC ANATOMY AND
Ventilation and Perfusion Matching (V /Q)
PHYSIOLOGY 40
Distribution of Ventilation in Healthy Lung 28
Layers of the Heart Wall 41
Distribution of Perfusion in Healthy Lung 29
Heart Valves 41
V /Q Matching in the Self-Ventilating Adult 29
Coronary Circulation 41
Maintaining V /Q Matching 30
Cardiac Cycle 41
Hypoxic Pulmonary Vasoconstriction (HPV) 30
Heart Sounds 42
Pulmonary Capillary Recruitment 30
Electrical Conductivity of the Heart 42
Diagnosis of V /Q Mismatch 30
Electrical Conductivity and Electrocardiogram
Bronchiole Response 30
(ECG) 43
Transport of Oxygen and Carbon Dioxide 31
Autonomic Regulation of Heart Rate 44
Oxygen Transport 31
Blood Pressure 44
Oxygen and Haemoglobin 31
Stroke Volume 44
Haemoglobin’s Affinity for Oxygen 32
Total Peripheral Resistance 45
The Oxygen Dissociation Curve 32
Renal System 45
Why Does O2 Need to Dissociate? 32
Auto Regulation of Blood Pressure 45
Factors Affecting Hb Affinity for O2 32
Diphosphoglycerate (DPG) 32 REFERENCES AND FURTHER READING 46
prised of four stages: ventilation, external respiration,

INTRODUCTION TO RESPIRATION
gas transport and internal respiration (Marieb and
The supply of oxygen to body tissues is essential to life. Hoehn 2013).
As well as nutrients, cells require oxygen in order to The respiratory system is responsible for two of
release energy as part of tissue metabolism. As the cells these stages: ventilation and external respiration. Ven-
use oxygen, they produce carbon dioxide, which is a tilation is the movement of air in and out of the lungs,
metabolic waste product and is toxic if allowed to and external respiration (pulmonary gas exchange) is
accumulate. the diffusion of oxygen from the lungs to the blood,
The primary function of the respiratory system is and carbon dioxide from the blood to the lungs. To
to supply the body with oxygen taken from atmos- achieve this, air is drawn by conductive flow into the
pheric air, and to dispose of carbon dioxide. This alveoli and presented to the gas-exchanging surface
complex process is known as respiration and is com- where the process of exchange occurs by diffusion. The
1 Anatomy and Physiology of the Respiratory and Cardiac Systems 3
carriage of air through the airways depends on the size The nose has a number of important functions,
and patency of the tubes as well as on the compliance including warming, humidifying (moistening) and fil-
of the lung and power of the respiratory muscles. tering the air. As a result, respiratory physiotherapists
Gas transport is the transportation of oxygen and encourage patients who are not breathless to inhale
carbon dioxide to/from the lungs in the blood, and this through the nose rather than the mouth. The nose also
is dependent on the cardiovascular system. The final provides a resonance chamber for speech and contains
stage is internal respiration, and this is the movement olfactory (smell) receptors.
of oxygen from the blood to the cells and carbon Respiratory mucosa lines the nasal cavity. This is
dioxide from the cells to the blood. ciliated epithelium that contains goblet cells. Goblet
In health, the human cardiorespiratory system has cells secrete mucus and this serves to trap inhaled par-
a substantial reserve capacity to cope with the demands ticles. Cilia are microscopic hair-like projections that
of exercise or illness. Breathlessness or fatigue is not move rhythmically to sweep the mucus and any
normally a feature of resting activity. In patients with trapped particles towards the pharynx.
heart or lung disease, the erosion of physiological Just proximal to the nostrils is the nasal vestibule.
reserve eventually imposes limitations upon the activi- This contains short, thick hairs called ‘nasal vibrissae’.
ties of daily life. These hairs filter large particles, e.g. dust, from the
inspired air. Proximal to the nasal vestibule is the nasal
cavity and this contains three mucosa-covered projec-
UPPER RESPIRATORY TRACT tions that protrude medially from the lateral walls.
The ‘upper respiratory tract’ (Fig. 1-1) is the term These projections are the superior, middle and inferior
for the extra-thoracic components of the respiratory nasal conchae (otherwise known as ‘nasal turbinates’).
system. It broadly consists of the nose, the pharynx, The nasal conchae increase the mucosal surface area
the larynx and the trachea. and increase turbulence through the nasal cavity,
Vestibule
Vibrissae
Sinuses
Nasal conchae
External (superior, middle
nose and inferior)
Nasal cavity
Vestibule Opening of
the auditory
Nostril tube Nasopharynx
Pharynx
Tongue
Glottis Oropharynx
Epiglottis
Laryngopharynx
Vocal cords
Larynx
Trachea
Oesophagus
FIGURE 1-1 ■ The upper respiratory tract.
which serves to slow airflow. This allows time for

THE BRONCHIAL TREE
the air to be warmed, filtered and humidified. The
nasal mucosa is also supplied with a large number of The branching pattern of airways is often referred
sensory nerve endings. When irritated by inhaled par- to as the ‘bronchial tree’. The airways divide and
ticles, these sensory nerve endings will trigger a sneeze subdivide again. In all, there are approximately 23
reflex. generations (divisions) of airway in the human lung
The pharynx is commonly termed the ‘throat’ (Fig. 1-2).
and is divided (from superior to inferior) into the The trachea bifurcates into the right and left main
nasopharynx, the oropharynx and the laryngophar- bronchi, which then supply their respective lungs. This
ynx. Only air moves through the nasopharynx, whereas point of bifurcation is termed the ‘carina’. The right
both food and air pass through the oropharynx and main bronchus branches off from the trachea at an
laryngopharynx. The laryngopharynx is the point of angle of 20–30 degrees, while the left main bronchus
bifurcation which leads to the larynx anteriorly and branches off at an angle of 45–55 degrees. As the right
the oesophagus posteriorly. main bronchus is more vertical than the left, aspirated
The lungs are protected from food substances by food and drink are more likely to end up in the right
the flap-like epiglottis that closes over the larynx lung if the person is in an upright position.
during swallowing. The larynx contains the vocal Each main bronchus then divides into lobar
cords and so is essential for voice production. Vocal bronchi: three on the right and two on the left. Each
cord (glottic) function is also essential for an effective lobar bronchus supplies the lobe of a lung and subdi-
cough mechanism. vides into segmental bronchi and then bronchi and
The trachea, or windpipe, descends from the larynx bronchioles of ever decreasing size. Finally, terminal
into the thorax and is situated anterior to the oesopha- bronchioles divide into respiratory bronchioles. Respi-
gus. It contains numerous cartilaginous C-shaped ratory bronchioles are hybrid structures and are part
rings that support the anterior and lateral aspects of bronchiole, part alveoli. The respiratory bronchioles
the trachea. These rings help to prevent tracheal col- then give rise to the 300 million alveoli that are present
lapse during the pressure changes associated with in a healthy adult.
breathing. They are open posteriorly to allow the The structure of the airways changes towards the
oesophagus to expand anteriorly as food is swallowed. lung peripheries. The bronchioles lack cartilage but
Anterior view
R. L.
Trachea
Carina
Right main
bronchus Left main

bronchus
Apical
Apicoposterior
Posterior
Anterior
Anterior
Superior lingula
Lateral Inferior lingula
Medial Superior Anteromedial
Anterior basal
Superior
basal
basal
Lateral
basal Posterior
Lateral
Posterior Medial basal
basal
basal basal
FIGURE 1-2 ■ The bronchial tree.
still have a relative abundance of smooth muscle. smooth muscle contraction, mucosal oedema and
Hence the cartilage that maintains airway patency intraluminal secretions. In chronic bronchitis, obstruc-
is absent, and constriction of the smooth muscle tion occurs by mucosal thickening and mucus secre-
significantly reduces airway calibre in these small tion, but in emphysema the mechanism is different.
airways. Though seldom occurring in isolation from other
The calibre of the airways reduces through their forms of airway obstruction, the result of parenchymal
generations and the major resistance to gas flow is emphysema is to weaken the elastic structure which
normally in the upper airway. The larger airways are maintains radial traction on the airways and allows
supported by cartilage, while the smaller airways are them to close too early in expiration.
held patent by the radial traction of the surrounding
lung so that their calibre increases with the volume
THE LUNGS AND PLEURAE
of the lung. The diameter of these airways is also
controlled by neural tone, which is predominantly The cone-shaped lungs are located in the thoracic cage
parasympathetic. and are positioned vertically around the heart. The
The conducting zone of the lung includes the upper two lungs contain millions of alveoli within a fibro
respiratory tract and the airway divisions up to and elastic matrix. They do not have a very rigid structure
including the terminal bronchioles. The function of and are held in contact with the rib cage by negative
the conducting zone is to transport gas in and out of pressure between the pleural surfaces. The resting
the lungs. The respiratory zone is where gas exchange volume of the lung is determined by the outward
takes place and includes the respiratory bronchioles spring of the rib cage and the inward elastic recoil of
and alveoli (Fig. 1-3). the lung matrix. Expansion and contraction of the
Disruption of airway function can occur through lung involves the controlled stretching or relaxation of
obstruction to a large airway by, for example, a tracheal the lung by the respiratory muscles. The position of
tumour. It may also occur because of more widespread lung resting volume can be influenced if the lung is
disease in asthma, when the calibre of large numbers stiffer than usual (as in interstitial disease) or if it is
of smaller airways is affected by episodic alteration of more compliant (as when damaged by emphysema).
Hyaline cartilage
Smooth muscle
Elastic fibers
Ciliated cells
Goblet cells
Epithelium
Diameter Cross-sectional Glands

Name Division (mm) How many? area (cm2)
Trachea 0 15-22 1 2.5

Main 1 2
Conducting zone
bronchus
2 4
Segmental 3
bronchi 4 1-10
Lobar
bronchi 5
Terminal 6-11 10 000
bronchioles 12-15 0.5-1 20 000 100
Respiratory 16-23 80 000 000 5000
Respiratory
bronchioles
zone
24 0.3 300 000 000- >1 000 000

Alveolar ducts
600 000 000
Alveolar sacs
FIGURE 1-3 ■ Conducting and respiratory zones.
The lungs are divided into lobes (Fig. 1-4). The (separates the upper and middle lobe) and the oblique
right lung is larger and has three lobes: upper, middle fissure (separates the lower lobe from the upper and
and lower. The left lung has just two lobes: upper and middle lobe). The left lung only has two lobes and
lower. The left lung is smaller because the heart is situ- therefore just has an oblique fissure (between the
ated to the left of midline and therefore some of the upper and lower lobe).
space of the left lung is taken up by the heart (cardiac Each lobe of lung is divided into bronchopulmo-
notch). nary segments. There are 10 bronchopulmonary seg-
The lobes of the lungs are separated by fissures. ments in the right lung, and eight in the left lung.
The right lung is divided by the horizontal fissure A bronchopulmonary segment is a functionally and
Right lung Left lung

Upper lobe
Upper lobe
Apical (S1)
Apico-
Anterior (S3) posterior (S1+2) Superior
Posterior (S2) 1 Anterior (S3) division
Horizontal fissure
2 Superior (S4)
Middle lobe Lingular
Inferior (S5)
Lateral (S4) 3 division
Medial (S5) Oblique fissure
4
Oblique fissure Lower lobe
Lower lobe 5 Anteromedial basal (S7+8)
Anterior basal (S8) 6 Posterior basal (S10)
Lateral basal (S9) Lateral basal (S9)
Medial basal (S7) 7
Posterior basal (S10)
A Anterior view
Left lung Right lung

Upper lobe Upper lobe
Superior Apico- T Apical (S1)

division posterior (S1+2) 1
1 Posterior (S2)
Anterior (S3) 2
Lingular 2 Anterior (S3)
3
division 3
Superior (S4) 4 Middle lobe
5 4 Lateral (S4)
Oblique fissure
6 5 Oblique fissure
Lower lobe
7 6 Lower lobe
Superior (S6)
8 7 Superior (S6)
Lateral basal (S9) Lateral
9 8
basal (S9)
Posterior basal (S10) 10 9
10 Posterior
basal (S10)
B Posterior view
FIGURE 1-4 ■ Lung lobes and fissures. (A) Anterior view. (Superior basal segments not visible in anterior view.) (B) Posterior
view.
Right lung Left lung Upper lobe

Upper lobe
Apico-
Apical (S1) posterior (S1+2) Superior
Posterior (S2) Horizontal Anterior (S3) division
Anterior (S3) fissure
Superior (S4)
Middle lobe Oblique Inferior (S5) Lingular
Lateral (S4) fissure division
Medial (S5)
Lower lobe Lower lobe
Superior (S6) Superior (S6)
Anterior basal (S8) Lateral basal (S9)
Lateral basal (S9) Anteromedial basal (S7+8)
C Lateral view
Upper lobe Right lung Left lung Upper lobe

Apical (S1) Apico-
posterior (S1+2) Superior
Posterior (S2)
Anterior (S3) division
Anterior (S3 )
Oblique Superior (S4)
Middle lobe fissure Lingular
Inferior (S5)
Medial (S5) division
Horizontal fissure
Lower lobe
Superior (S6)
Medial basal (S7) Lower lobe
Superior (S6)
Anterior basal (S8)
Anteromedial basal (S7+8)
Lateral basal (S9)
Lateral basal (S9)
Posterior
basal (S10) Posterior basal (S10)
D Medial view
FIGURE 1-4, cont’d ■ (C) Lateral view. (D) Medial view. S, segment number.
anatomically independent unit of lung which has its secretions. Specific segmental bronchi are positioned
own segmental bronchus, artery and vein. Segments perpendicular to gravity in order to drain the affected
are separated from one another by connective tissue bronchopulmonary segment (see Fig. 1-2).
septa. This means that if an isolated tumour or disease The lungs are covered with a thin double-layered
is present in one bronchopulmonary segment, it serous sac called the ‘pleural membrane’. The outer
can be surgically removed (segmentectomy), causing layer of the membrane is the parietal pleura and the
minimal disruption to adjacent segments of lung. Res- inner layer is the visceral pleura (Fig. 1-5). The pari-
piratory physiotherapists should be familiar with the etal pleura lines the inner surface of the thoracic wall
names of the bronchopulmonary segments and the and the superior surface of the diaphragm. The vis-
anatomical position of each segmental bronchus. This ceral pleura covers the outer surface of the lungs and
anatomical knowledge is required in order to perform also lines the fissures. The potential space between the
gravity-assisted positioning (GAP), which is used parietal and visceral pleurae is the pleural cavity, and
to promote drainage of excess bronchopulmonary this contains a small amount of pleural fluid which is
Apical pleura Parietal pleura
Visceral pleura
Costal pleura
Lung fissures
Diaphragmatic
pleura
Diaphragm
Pleural
Medistinal cavity
pleura
Lung fissure
FIGURE 1-5 ■ Pleural layers.
secreted by the pleurae. Pleural fluid acts as a lubri- sternoclavicular joint and close to midline to the level
cant, allowing the two pleural layers to glide over each of the sixth rib. The inferior border goes from the sixth
other during inspiration and expiration. The pleural rib in the mid-clavicular line, to the eighth rib in the
fluid also acts to increase surface tension and therefore mid-axillary line, to the 10th rib posteriorly. Posteri-
‘locks’ the two pleural layers together. This can be com- orly, the apex of the lung is level with T1 and the
pared to a wet plastic bag – when wet, the two sides medial border of the lung is approximately 2 cm from
of the plastic bag are difficult to separate. This means midline and descends from the level of T1 to T10. The
that the lungs will cling to the chest wall throughout horizontal fissure (separating the upper lobe from the
inspiration and expiration. The visceral pleura is middle lobe) follows the line of the fourth rib anteri-
innervated by the autonomic nervous system (ANS) orly and ends where it meets the oblique fissure in
and so is not sensitive to pain. However, the parietal the mid-axillary line. The oblique fissure (separating
pleura is highly sensitive to pain due to innervation the lower lobe from the upper and middle lobes)
from the phrenic and intercostal nerves. As a result, runs posteriorly from T3 and descends diagonally. It
pleural disease such as pleuritis (inflammation of the roughly follows the line of the medial border of the
pleurae) can cause a severe, sharp stabbing pain. scapula with the arm abducted to 90 degrees. It forms
a junction with the end of the horizontal fissure in the
mid-axillary line and ends anteriorly at the level of the

SURFACE MARKINGS OF THE LUNGS sixth rib in the mid-clavicular line.
Respiratory physiotherapists should be able to surface
mark the outline of the lungs, pleurae and fissures. In The Left Lung
particular, surface marking the lungs may be the best The outline of the left lung is the same as the right
way to visually learn that the lower lobes are posi- lung, except that there is a cardiac notch on the
tioned posteriorly. This knowledge may enable more left. Anteriorly, the medial border of the left lung
accurate auscultation of the lungs. deviates laterally by 3–4 cm at the level of the fourth
rib. It then descends vertically to the level of the
The Right Lung sixth rib in the mid-clavicular line. The remaining
Anteriorly, the apex of the right lung is situated outline of the left lung is exactly the same as the right.
2–3 cm superior to the medial third of the clavicle. There is no horizontal fissure on the left lung, only an
The medial border of the lung descends through the oblique.
The Pleura There are 12 pairs of ribs and they slope inferiorly
The pleura follows the outline of the lung except that as they curve anteriorly. All the ribs attach posteriorly
the inferior border of the pleura is situated two ribs to the thoracic vertebrae. Ribs are termed ‘true’, ‘false’
below the inferior border of the lung. Anteriorly, the or ‘floating’ according to their anterior attachment.
inferior border of the pleura runs from the level of the The true ribs (1–7) attach directly to the sternum by
eighth rib in the mid-clavicular line, to the 10th rib in individual costal cartilages. The false ribs (8–10)
the mid-axillary line and the 12th rib posteriorly. This attach to the sternum indirectly, each joining the costal
two-rib difference between the outline of the lung and cartilage immediately above it. The floating ribs
the pleura is not representative of the pleural space; it (11–12) have no anterior attachment (Fig. 1-6).
simply represents full inspiration. The head of the rib attaches to the thoracic verte-
brae posteriorly. It is wedge shaped and has two articu-
lar facets which articulate with the upper border of the
body of its own vertebra and the lower border of the
THE THORACIC CAGE body of the vertebra above. So the head of rib 8 will
To maintain their shape, the lungs depend on the articulate with the upper part of the body of T8 and
support of the rib cage, negative pressure between the the lower part of the body of T7. These articulations
pleural surfaces and the patency of the airways and are the costovertebral joints. The neck of the rib is the
alveoli. The expansion of the rib cage by the respira- narrowed area just lateral to the head. The tubercle is
tory muscles is responsible for the tidal flow of gas into lateral to the neck and has a small oval articular facet.
and out of the lungs. Over the past few years there has This facet articulates with the transverse process of the
been increasing awareness of the importance of dys- same-numbered thoracic vertebra (rib 8 with trans-
function of the respiratory muscles and the bony rib verse process of T8). This articulation is the cos-
cage in contributing to respiratory failure. Such condi- totransverse joint. The shaft makes up the majority
tions include myopathies and polio, as well as skeletal of the rib. The rib angle is approximately 3 cm lateral
malformations such as scoliosis, which decrease rib to the tubercle and is where the shaft angles sharply
cage compliance and reduce the effectiveness of the forwards (see Fig. 1-6).
musculature.
The respiratory muscles include the diaphragm as Movements of the Ribs
the major muscle of inspiration and the intercostal The dimensions of the thorax must change in order
muscles and scalenes. The latter, together with the for respiration to occur. The vertical, transverse and
sternocleidomastoids, are known as the ‘accessory antero-posterior (AP) diameters of the thorax increase
muscles’, of respiration because they assist, but do not during inspiration and decrease during expiration.
play a primary role, in breathing. Weakness of the res- This rib movement is brought about by the inspiratory
piratory muscles will eventually lead to ventilatory muscles (external intercostals and diaphragm).
failure, which may first become apparent during the Rib 1 is capable of very little movement because it
night as an exaggeration of normal nocturnal hypov- is so short and firmly attached to the manubrium by
entilation (Shneerson 1988). the first costal cartilage. The anterior ends of ribs 2–5
The thoracic cage is cone shaped with its wider end are raised during inspiration, along with the body of
inferiorly. It is made up of the thoracic vertebrae dor- the sternum. This increases the AP diameter of the
sally, the ribs laterally and the sternum and costal car- thorax and is known as ‘pump handle movement’.
tilages anteriorly. Inspiration causes the anterior ends of ribs 8–10 to
One function of the thoracic cage is to protect the move in an upwards and outwards direction. This
heart, lungs and great vessels. It also provides support increases the transverse diameter of the thorax. The
for the pectoral girdle and upper limbs, and provides resultant upward and outward movement of the shaft
a point of attachment for neck, trunk and upper limb of the ribs has been compared to lifting the handle
muscles. Finally, the rib cage allows the movement from the side of a bucket and is termed ‘bucket handle
necessary for breathing. movement’ (Palastanga & Soames, 2012) (Fig. 1-7).
Clavicle
1 Scapula
2
3 Manubrium
True Sternal
ribs 4 angle Sternum
Body
5
Xiphoid
6 process
7 Costal
8 cartilage
11
False 9 Ribs
ribs 10 12
Floating
A ribs
Axis of rib rotation
Costal demifacet
for head of 6th rib
Vertebral body (T6) Superior articular
Intervertebral disc facets
Costo- T6 Articular facet for
vertebral Head of 7th rib tubercle of 6th rib
joint Vertebral body (T7)
Transverse
Neck of 7th rib process
T7 of T7 vertebra
Tubercle of 7th rib
Costo-
Elevation Spinous process
transverse
Transverse process of T6 vertebra
joint
of T7 vertebra
Shaft of rib
7th rib
Depression
B Left posterolateral view
Tubercle
of rib
Angle of rib
Neck of rib
FIGURE 1-6 ■ (A) Rib cage. (B) and (C) Costovertebral and cos-
Head of rib totransverse joints. The head of rib articulates with two adjacent ver-
tebral bodies and the disc between them, and the tubercle of rib
Shaft of rib
Articular facet for articulates with the transverse process of a vertebra. The rib moves up
adjoining vertebra and down around an axis that traverses the head and neck of rib.
For articulation
with costal
C cartilage
from the abdomen. It is a large, dome-shaped muscle

and is lower posteriorly than anteriorly. The right
hemidiaphragm sits 1–2 cm higher than the left hemid-
iaphragm due to the presence of the liver on the right.
The superior surface of the diaphragm is covered with
Bucket handle the parietal pleura. The pericardium which encloses the
movement
heart is attached to the central tendon of the dia-
phragm. The diaphragm has three openings to allow
structures to pass between the thorax and the abdomen
(oesophageal opening, aortic opening and vena caval
opening) (Palastanga & Soames, 2012) (Fig. 1-8).
Elevation of lateral
The diaphragm is innervated by the phrenic nerve
shaft of rib (remember that ‘C3, 4, 5 keep the diaphragm alive!’).
The diaphragm has three sets of fibres: sternal,
costal and lumbar. These fibres are all named accord-
A ing to their origin. All fibres converge into a central
trefoil shaped (clover leaf) tendon. The sternal fibres
of the diaphragm arise from the posterior surface of
the xiphoid process. The fibres run upwards and medi-
ally to insert into the anterior border of the central
Pump handle tendon. The costal fibres make up the majority of
muscle fibres of the diaphragm and arise from the
inner surface of the lower six ribs and their costal
cartilages. The fibres run upwards and medially to
insert into the anterolateral part of the central tendon.
The lumbar fibres arise in part from two crura. The
right crus is larger and originates from the anterola-
teral aspects of the bodies and intervertebral discs
of L1–L3. The left crus arises from the bodies and
discs of L1 and L2. The two sets of crural fibres are
Superior and anterior united opposite the disc between T12 and L1 to form
B movement of sternum an arch which is the aortic opening (median arcuate
FIGURE 1-7 ■ Bucket and pump handle rib movement is ligament). Both sets of crural fibres insert into the
caused by the anterior ends of ribs 8–10 moving upwards central tendon. The remainder of the lumbar fibres
and outwards during inspiration. (A) Increasing transverse arise from the medial and lateral arcuate ligaments
dimension. (B) Increasing antero-posterior (AP) dimension.
which are lateral to the crura (see Fig. 1-8).
When contracting, the diaphragm descends and
Ribs 6 and 7 are capable of both pump and bucket increases the vertical diameter of the thorax. During
handle movement. Ribs 11–12 do not contribute to quiet breathing, the diaphragm descends just 1–2 cm
increasing the diameter of the thorax as they have no (from the level of T8 to T9). However, in deep inspira-
anterior attachment. tion it can descend as much as 10 cm. Further descent
of the diaphragm is prevented by compression of the
MUSCLES OF RESPIRATION abdominal organs. In this situation the central tendon
now becomes the fixed point (reversed origin and
Diaphragm insertion) and further contraction of the diaphragm
The diaphragm is the main muscle of inspiration. It is causes upward and outward movement of the ribs and
a musculotendinous sheet which separates the thorax forwards movement of the sternum.
Muscles of inspiration Muscles of expiration

Accessory Quiet breathing
Sternocleidomastoid Expiration results from
(elevates sternum) passive recoil of lungs
Scalenes
Posterior
Middle Active expiration
Anterior Internal intercostals,
(elevate and fix upper ribs) except interchondral
part
Principal
External intercostals Abdominal muscles
(elevate ribs) (depress lower ribs,
Interchondral part compress abdominal
of internal intercostals contents)
(elevates ribs) Rectus abdominis
Diaphragm External oblique
(domes descend,
Internal oblique
increasing longitudinal
dimension of thoracic Transversus
cavity; also elevates abdominis
lower ribs)
A
Central Sternal
tendon attachment of
Inferior diaphragm
vena cava Costal
attachment of
Oesophageal diaphragm
hiatus
Abdominal
Arcuate aorta
ligaments
Transversus
Posterior abdominis
(lumbar) muscle
L1
attachment of Quadratus
diaphragm L2
lumborum
Crura L3 muscle
Psoas major
B muscle
Central tendon
of diaphragm
Dome of
Opening for diaphragm is
inferior vena lower on the
cava left
Diaphragm Oesophagus
Median Diaphragm
arcuate Aorta
ligament
Right crura Left crura of
C of diaphragm diaphragm
FIGURE 1-8 ■ Muscles of respiration. (A) Intercostal and accessory muscles. (B) and (C) The diaphragm.
Intercostals muscles of inspiration can be a sign of respiratory

The intercostal muscles pass between adjacent ribs. distress.
They span the intercostal space and there are 11 pairs
Muscles of Forced Expiration
between ribs 1 to 12. There are three layers of intercos-
tals: external, internal and innermost (see Fig. 1-8). Expiration is normally a passive process brought about
The intercostals are innervated by the intercostal by relaxation of the diaphragm and external intercos-
nerves (T1–11). tals which then allows elastic recoil of the lungs. Forced
The external intercostals are muscles of inspira- expiration such as when coughing or sneezing is
tion and form the outermost intercostal layer. They brought about by the internal intercostals and the
pass from the inferior border of the rib above to abdominal muscles. Contraction of the abdominal
the superior border of the rib below. The fibres run muscles causes the abdominal contents to push up
diagonally in a downwards and forwards direction. against the diaphragm, which then reduces the vertical
Contraction of the external intercostals results in the diameter of the thorax. During strenuous physical
rib below being pulled up towards the rib above, activity, expiration becomes forced or active in order
causing elevation of the rib cage (pump and bucket to increase respiratory rate to the level required to
handle movement). meet metabolic demand. In the absence of strenuous
The interosseous part of the internal intercostals activity, use of the abdominal muscles during expira-
are muscles of expiration (the interchondral part of tion can be another sign of respiratory distress.
the internal intercostals are inspiratory muscles), and
they form the middle intercostal layer. They pass from RESPIRATORY MECHANICS
the inferior border of the rib above to the superior
Respiratory Pressures
border of the rib below. The fibres run diagonally in a
downwards and backwards direction, which is the Before describing the different respiratory pressures, it
opposite direction to the external intercostals. Con- is important to understand the term ‘atmospheric
traction of the internal intercostals assists with forced pressure’. Atmospheric pressure is the pressure exerted
expiration by drawing the ribs together and depressing by the gases in the air. It is the sum of all the partial
the rib cage. pressures of gases in the air (including nitrogen,
The innermost intercostals form the deepest inter- oxygen and carbon dioxide) and is 760 mmHg at sea
costal layer and run in the same direction as the inter- level. The partial pressure of nitrogen in inspired air is
nal intercostals. Their function is probably to stabilize 593 mmHg (78% of 760 mmHg), while the partial
the chest wall, preventing the intercostal spaces from pressure of oxygen is 159 mmHg (21% of 760 mmHg).
‘being sucked in’ on inspiration and from ‘bulging out’ Respiratory pressures are always described in relation
during expiration. to atmospheric pressure. Hence a negative respiratory
pressure is less than atmospheric pressure, a positive
respiratory pressure is greater than atmospheric pres-

Accessory Muscles of Inspiration sure and a respiratory pressure of zero is equal to
There are a number of muscles that can assist with atmospheric pressure.
deep inspiration or during episodes of respiratory dis- Intrapulmonary pressure (Ppul) or intra-alveolar
tress. These include the scalenes and sternocleidomas- pressure is the pressure within the alveoli. It falls with
toid. The scalenes (anterior, middle and posterior) inspiration and rises with expiration. It is important
attach to ribs 1 and 2 and can therefore elevate the rib to note that intrapulmonary pressure always eventu-
cage. Sternocleidomastoid can also bring about eleva- ally equalizes with atmospheric pressure; i.e. returns to
tion of the rib cage due to the action of the sternal 0 mmHg at the end of inspiration and at the end of
head which attaches to the manubrium, and the cla- expiration (Fig. 1-9).
vicular head which attaches to the clavicle. Other pos- Intrapleural pressure (Pip) is the pressure within
sible accessory muscles of inspiration include pectoralis the pleural cavity and also decreases on inspiration
minor and pectoralis major. Use of the accessory and increases on expiration. However, intrapleural
Intrapulmonary pressure:
atmospheric pressure (mmHg)

Inspiration Expiration
pressure decreases in the
lung during inspiration and +2 Intrapulmonary
Pressure relative to
increases during expiration. pressure
0
Intrapleural pressure: Transpulmonary
-2
pressure in the pleural pressure
space becomes more -4
negative during chest wall Intrapleural
-6
expansion and returns to pressure
baseline values as the -8
chest wall recoils.
Volume of breath
Volume (L)
Tidal volume: 0.5
the transpulmonary
pressure gradients above
move air into and out of the
lung during each breath. 0
5 seconds elapsed
FIGURE 1-9 ■ Volume and pressure changes during inspiration and expiration.
pressure is always negative in relation to intrapulmo- Gas flows into the lungs during inspiration and out of
nary pressure. This negative intrapleural pressure is the lungs during expiration.
created by two opposing forces: the tendency of the How do volume changes lead to pressure changes?
chest wall to expand outwards versus the tendency of If the volume of a container increases, then the gas
the lungs to recoil inwards. The pleural fluid keeps the molecules inside it are spaced further apart and there-
pleurae locked together. fore exert less pressure. If the volume of a container
Transpulmonary pressure (Ppul − Pip) is the differ- decreases then the gas will exert more pressure.
ence between the intrapulmonary and intrapleural How do pressure changes result in gas flow? Gases
pressures. The greater the transpulmonary pressure, always flow down pressure gradients, meaning they
the greater the size of the lungs (transpulmonary pres- flow from high pressure to low pressure until the pres-
sure is greatest at the end of inspiration). sure has been equalized.
A pneumothorax is the presence of air in the pleural During quiet inspiration, the inspiratory muscles
space due to an abnormal communication between contract to increase thoracic cage diameter and lung
either the lung and the pleural space, or the atmos- volume. This increased volume causes a fall in intrapul-
phere and the pleural space. This air in the pleural monary pressure and gas flows into the lungs down the
space will result in the loss of negative intrapleural pressure gradient. Air flow ceases when intrapulmo-
pressure and the transpulmonary pressure will then nary pressure becomes equal to atmospheric pressure.
become zero. As a result, the underlying lung will col- During quiet expiration, the inspiratory muscles
lapse. An intercostal drain restores the negative intra- relax and the lungs recoil passively. This reduces tho-
pleural pressure and the lung should then reinflate. racic cage diameter and lung volume, which then leads
to an increased intrapulmonary pressure. Gas now
Ventilation flows down the pressure gradient, from the lungs
Ventilation is a mechanical process that depends on towards the mouth. Once again, gas flow will cease
volume changes within the thorax. Volume changes once intrapulmonary pressure reaches zero (equal to
leads to pressure changes, which then result in gas flow. atmospheric pressure).
Direction of particle movement

Airway
particles Gel
layer
Mucus
Sol
Cilia layer
FIGURE 1-10 ■ Mucociliary transport (MCT) system. Surface Mucus
goblet cells epithelium
Basement Basal cell
membrane Submucosal
gland
MUCOCILIARY TRANSPORT SYSTEM The ultrastructure of cilia is extremely complex.

Primary ciliary dyskinesia is an inherited condition
Ciliated epithelium is present in the upper respiratory where the cilia are structurally abnormal. As a result,
tract and lines the airways down to the terminal bron- cilia move in an uncontrolled way (dyskinesia) and the
chioles. Cilia are microscopic hair-like processes that MCT system becomes ineffective.
are capable of rhythmic motion and are one of the
three components of the mucociliary transport (MCT) Aqueous (Sol) Layer
system (Fig. 1-10). The MCT system sweeps mucus For efficient ciliary motion, the cilia need to be bathed
containing foreign particles towards the laryngophar- in the serous fluid that makes up the aqueous (sol)
ynx, where the mucus is either swallowed or expecto- layer. It can also be referred to as ‘periciliary fluid’. This
rated by coughing. It is therefore an important defence thin, watery fluid extends most of the way up the shaft
mechanism of the lung, reducing the incidence of res- of the cilia. The fluid offers very little resistance to
piratory infection. ciliary motion and actually seems to facilitate it. Ciliary
The three components of the MCT system are movement will be impaired by both increased levels
■ Cilia of periciliary fluid (e.g. pulmonary oedema), or by
■ Aqueous (sol) layer reduced levels (e.g. in dehydration).
■ Viscous (gel) layer.
Viscous (Gel) Layer
For most of the bronchial tree, goblet cells accompany
Cilia the ciliated epithelium. Goblet cells secrete mucus, and
The tips of the cilia hook into the gel layer to sweep it mucus secretion volume is 10–100 mL per day in
towards the laryngopharynx. The cilia situated below healthy adults. This viscous mucus forms the gel layer
the larynx beat in an upwards direction, while the of the MCT system. It acts like flypaper, and foreign
cilia above the larynx beat in a downwards direction. particles, cellular debris and microbes become trapped
Cilia beat in a co-ordinated fashion at a frequency of in it. Ciliary movement will become impaired in
approximately 20 cycles per second, which can propel hypersecretory conditions such as cystic fibrosis and
mucus at a rate of 2 cm/min. Cilia demonstrate bronchiectasis due to the increased volume of the
bi-directional movement. The power (effective) stroke mucus layer or a depleted sol layer (cystic fibrosis).
moves mucus towards the mouth, while the recovery
stroke enables the cilia to sweeps backwards and to the
COLLATERAL VENTILATION
side (see Fig. 1-10).
Ciliary beat frequency can be reduced by a number Collateral channels of ventilation (Fig. 1-11) provide
of factors, including smoking, general anaesthesia and an alternative route for gas flow when peripheral
the inhalation of cold air. airways are obstructed. These collateral channels may
Airway Innervation
The airways are innervated by the autonomic nervous
system (ANS). The parasympathetic nervous system
(PNS) directly innervates bronchial smooth muscle
Interbronchiolar causing bronchoconstriction, which decreases airway
channels of Martin
calibre and increases airways resistance.
Bronchiole–alveolar
canals of Lambert Sympathetic nervous system (SNS) receptors (β2)
are sited in airway walls and are stimulated by cat-
Interalveolar pores echolamines, which relax bronchial smooth muscle,
of Kohn increase airway calibre and decrease airway resistance.
In health, airways resistance is low due to the
FIGURE 1-11 ■ Collateral ventilation pathways. balance between both branches of the ANS.
Site of Highest Resistance

be 1–2 µm interalveolar (pores of Kohn), 25–30 µm
bronchiole-alveolar (canals of Lambert) and 80– The trachea and main airways are large calibre and
150 µm interbronchial (channels of Martin). therefore have low airways resistance. Although resist-
The average adult alveolus has somewhere between ance to air flow is greatest in individual small airways,
5 and 20 pores of Kohn. These are not present in the total resistance to air flow contributed by the
infants under the age of 1 year. Due to this lack of small airways taken together is very low because
‘alveolar escape route’, infants are at particular risk they represent a huge number of parallel pathways.
of barotrauma when positive pressure ventilation is Therefore under normal circumstances the greatest
applied to their lungs. total airways resistance resides in the upper airways:
The resistance to airflow through collateral chan- oro and nasopharynx, larynx (approximately 40%)
nels is extremely high because they are microscopically and medium-sized bronchi. These contain a high pro-
small. Therefore they are probably of little importance portion of bronchial smooth muscle, and a high level
in the normal, healthy lung. However, collateral chan- of ANS innervation (alters calibre).
nels increase in number and have more of a role in In health, airways resistance decreases as lung
obstructive lung disease, so that gas can find alterna- volume increases because the airways distend as the
tive routes to bypass obstructed airways. lungs inflate; wider airways have increased calibre and,
If an airway is occluded by a sputum plug then therefore, lower airways resistance
the distal alveoli will collapse. A number of treatment
techniques used by respiratory physiotherapists aim to Poiseuille’s Law
recruit the channels of collateral ventilation in order Airways resistance is governed by Poiseuille’s law,
to get air behind sputum plugs. The principle behind which states that the flow of gas through an airway is:
any of these treatment techniques is that by increasing
■ directly proportional to the fourth power of its
lung volume, there will be increased airflow through
internal radius
the collateral channels. It is thought that this airflow
■ inversely proportional to its length
will move the sputum plug more proximally, and will
■ inversely proportional to the viscosity of gas.
also recruit the atelectatic lung.
Clinical Relevance of Poiseuille’s Law
AIRWAYS RESISTANCE As the length of airways does not change except during
‘Airways resistance’ refers to the resistance of the res- growth, and at sea level the viscosity of gas remains
piratory tract to airflow during inspiration and expira- constant, a change in radius (airway calibre) is the
tion. The amount of airways resistance is dependent most important factor affecting airway resistance.
on the calibre of the airway, therefore, in general terms Resistance is in turn inversely proportional to airflow
the smaller the airway the greater the resistance. (and the fourth power of the internal radius), so a
small change in radius leads to a big change in airway ■ fixed upper limbs
resistance. Halving the internal diameter of the radius, ■ soft-tissue recession
for example, will increase airway resistance by 16 and ■ prolonged expiration
reduce airflow to 116 th of normal. ■ speaking in half sentences
Respiratory diseases characterised by increased ■ breathlessness

airways resistance and airflow limitation are called ■ wheeze
‘obstructive diseases’, e.g. asthma, chronic obstructive ■ fatigue
pulmonary disease (COPD). ■ reduced alveolar ventilation (VA)
Any pathology which reduces the calibre of airways ■ reduced partial pressure of oxygen (PaO2)
will lead to increased airways resistance, decrease ■ increased partial pressure of carbon dioxide
airflow and cause airflow limitation. Airway calibre (PaCO2).

may be reduced by pathology inside the lumen of the
Signs of obstruction and airflow limitation are
airway or pathology outside the airway causing exter-
always more apparent in expiration first. This is
nal compression.
because expiration occurs secondary to passive recoil
Intra luminal pathology may include:
of the lung and is therefore already associated with
■ bronchoconstriction
shortening and narrowing of the airways. Any pathol-
■ bronchial secretions
ogy which further decreases airway calibre will be most
■ mucosal oedema
apparent in expiration. Airflow limitation can be
■ airway remodelling
assessed and measured using spirometry or a peak
■ tumour/mass
expiratory flow metre.
■ inhaled foreign body.
Extra-luminal pathology may include: Problems Associated with Airflow Limitation

■ tumour/mass. As airflow limitation is increased on expiration,
patients with obstructive respiratory disease have dif-
Loss of radial traction, bronchomalacia, trauma
ficulty fully breathing out. Consequently, some of their
and stenosis may also affect airway calibre and airways
expiratory volume is not expelled and remains in the
resistance.
lungs increasing residual volume (RV). This is called
‘air trapping’ and causes the patient to become hyper-
Consequences of Increased Airway Resistance inflated, giving rise to the characteristic barrel shaped
Decreased airway calibre chest associated with obstructive respiratory disease.
▼ Hyperinflation alters normal respiratory mechanics,
Increased airways resistance as the diaphragm becomes flattened and unable to
▼ effectively contract, holding the thorax in an inspira-
Decreased airflow (airflow limitation) tory position. This leads to reduced inspiratory flow,
▼ poor tidal volumes (VTs) and ultimately ventilation–
Increased work of breathing perfusion (V /Q ) mismatch. Prolonged inadequate VA
▼ culminates in respiratory failure.
Breathlessness
Reversal of Airflow Limitation
Clinical Signs of Airflow Limitation Intraluminal pathology leading to airflow limitation
Clinically, a patient with airflow limitation secondary may be reversed by:
to obstructive respiratory disease may present with ■ pharmacology
one or more of the following symptoms: ■ bronchodilator therapy
■ increased work of breathing □ inhibition of PNS
■ accessory muscle recruitment □ excitation of SNS
■ active expiration □ xanthine (directly affects bronchial smooth
■ pursed lip breathing muscle)
■ anti-inflammatory agents lung compliance makes the generation of a large pres-

□ corticosteroids sure necessary to change volume.
□ cytokine inhibitors
■ diuretic therapy
■ low lung volumes (FRC)
■ atelectasis
■ antibiotic therapy
■ post surgery
■ physiotherapy (airway clearance techniques)
■ prolonged recumbency in supine
■ bronchoscopy
■ surgery. ■ high lung volumes
■ hyperinflation
■ ageing
RESPIRATORY COMPLIANCE ■ reduced pulmonary surfactant

■ pulmonary oedema
Compliance refers to the distensibility (stretchiness) of ■ consolidation
an elastic structure. Physiologically, it refers to the ■ interstitial fibrosis
change in pulmonary volume per unit of pressure ■ idiopathic pulmonary fibrosis
change. Compliance is represented by the pressure– ■ pleural effusion.
volume curve. In health, the respiratory system is
highly compliant and needs very little pressure to
Closing Volume
change volume on inspiration; a 2 mmHg change
in pleural pressure generates inspiratory flow. The FRC is the amount of air left in the lungs after
lungs are most compliant above functional residual tidal expiration (FRC = expiratory reserve volume
capacity (FRC). (ERV) + RV). Within FRC is a critical level called
The distensibility of the lungs is called ‘lung com- ‘closing volume’, which is the point at which there
pliance’ and the distensibility of the chest wall is called is insufficient air left in the lungs to maintain lung
‘chest wall compliance’. For effective inspiration to inflation; subsequently, dynamic compression (col-
occur, both the lungs and chest wall must be compli- lapse) of small airways and alveoli will occur. When
ant. Collectively, lung compliance plus chest wall com- closing volume is reached, inspiration falls below the
pliance is called ‘total lung compliance’ or ‘respiratory lower inflexion point (LIP) on the pressure/volume
system compliance’. curve, meaning a very large pressure is required to
open airways and alveoli, increasing the work of
Reduced Compliance breathing.
To maintain efficient inspiration, total lung compli- Closing volume increases with age, smoking, lung
ance must be optimal. Therefore any pathology which disease and position (supine > upright). Closing
reduces the compliance of either the chest wall or the volume plus RV is called ‘closing capacity (CC)’.
lung will reduce total lung compliance and make inspi-
ration more difficult. Respiratory disease characterized Pulmonary Surfactant

by reduced total lung compliance is classified as restric- Pulmonary surfactant is a surface-active lipoprotein
tive respiratory disease. Patients with restrictive respi- complex, secreted by type II alveolar cells. The main
ratory disease have difficulty breathing in. This can be lipid component of surfactant (dipalmitoylphosphati-
assessed and measured using spirometry. dylcholine) reduces surface tension and increases pul-
monary compliance. This prevents the lung collapsing
Factors Affecting Lung Compliance at the end of expiration.
Lung compliance can change (reduced or increased) In humans, surfactant production begins in type
in various disease states. II alveolar cells during the terminal sac stage of lung
development. Lamellar bodies appear in the cytoplasm
Altered Lung Compliance at about 20 weeks’ gestation. Babies born prematurely
A change in compliance at either end of the pressure before 28–32 weeks’ gestation may develop infant
volume curve makes inspiration very difficult. Reduced respiratory distress syndrome (IRDS), characterized
by poor lung compliance and increased work of CONTROL OF BREATHING

breathing.
Reduced surfactant production ‘Control of ventilation’ refers to the physiological
▼ mechanisms involved in the control of physiological
Increased surface tension ventilation, whereas gas exchange requirements pri-
▼ marily controls the rate of respiration (respiratory
Decreased lung compliance frequency).
▼ Origin of Breathing
Atelectasis
The respiratory system has no intrinsic driving system
▼
like the heart; therefore it is totally dependent on an
Increased work of breathing/O2 consumption
external neural drive. The origin of breathing occurs
in respiratory control centres (RCCs) in the brainstem
Altered Chest Wall Compliance
and occurs automatically without any conscious effort.
In this situation, the lungs are normal but inflation The purpose of breathing is to provide adequate VA,
and inspiration is reduced secondary to reduced chest i.e. oxygen (O2) delivery and carbon dioxide (CO2)
wall compliance. If the thorax is less compliant, it excretion. VA alters in response to changing environ-
will prevent inflation of the underlying lung by pro- mental or metabolic demands, e.g. exercise. Adequate
viding an external limitation. Imagine trying to blow VA is essential to maintain a neutral acid–base balance
up a balloon inside a small box. The walls of the box (7.35–7.45 kPa), which provides an optimal environ-
limit the amount of inflation and distension of the ment for cellular function.
balloon.
Reduced chest wall compliance may occur in the Respiratory Control Centres (RCCs)
presence of: There are four main centres in the brainstem which
■ thoracic deformity regulate respiration:
■ kyphosis
■ Inspiratory centre (medulla)
■ scoliosis
■ Expiratory centre (medulla)
■ sternal deformity
■ Pneumotaxic centre (pons)
■ circumferential thoracic burn ■ Apneustic centre (pons).
■ raised intra-abdominal pressure
■ abdominal distension In general, the medullary respiratory centres
■ post-surgery provide output to the respiratory muscles (diaphragm,
■ pregnancy external and internal intercostals) and the pontine
■ obesity centres influence output from the medullary respira-
■ supine position tory centres. Interaction of activity from these two

■ ageing. centres establishes and modifies breathing (shortens
inspiratory or expiratory phase or alters frequency) to
Consequences of Reduced Total meet metabolic demand or allow other activities such
Lung Compliance as speech, eating or singing.
Reduced total lung compliance produces an increased The Medullary Control Centres
respiratory load, which leads to an increased work
The medullary control centres contain two groups of
of breathing for the patient. In response, they may
respiratory neurones:
recruit the accessory muscles of respiration, which
in turn increases O2 demand and consumption. ■ Ventral respiratory group (VRG) controls
Over time, the respiratory muscles fatigue and VA ■ voluntary forced exhalation
becomes inadequate, ultimately resulting in respira- ■ increases force of inspiration
tory failure. ■ regulates rhythm of inhalation and exhalation.
■ Dorsal respiratory group (DRG) controls ■ Hyperventilation can occur in the presence of
■ inspiratory movements and timing. ■ breathing dysregulation syndrome
■ anxiety
The Pontine Control Centres ■ metabolic disease.
■ Pneumotaxic centre
■ coordinates speed of inhalation and exhalation Ondine’s Curse
■ sends inhibitory impulses to inspiratory centre Primary alveolar hypoventilation, known as Ondine’s
■ provides fine tuning of respiration frequency. curse is a congenital central hypoventilation syndrome,
■ Apneustic centre but can also develop secondary to severe neurological
■ coordinates speed of inhalation and exhalation brainstem trauma. It is a very rare and serious form
■ sends stimulatory impulses to inspiratory of central nervous system failure due to an inborn
centre failure of the autonomic control of breathing, leading
■ activates and prolongs long deep breaths. to episodes of apnoea or breathing cessation during
sleep. In a few patients with severe disease, apnoea may
Higher Brain Centres also occur while awake. The incidence is 1 in 200,000
Cortical inputs can temporarily override the intrinsic live born children with 200 known cases worldwide.
rhythm of the central control centres and lead to a
voluntary increase or decrease of respiratory fre- Respiratory Control Feedback Mechanism
quency, or alter breathing pattern to allow control of The RCCs are responsible for the generation and
speech, singing or the ability to voluntarily hyperven- control of breathing. Medullary centres control basic
tilate, hypoventilate or breath hold. inspiration and expiration; the frequency, timing and
duration of each respiratory phase are fine-tuned by
■ Cerebral cortex
the pontine centres.
■ cortical input can override intrinsic breathing
In addition, direct input from higher centres at
pattern from RCC
both brain and spinal cord level can override basic
■ voluntary pathways synapse with anterior
rate as required. Output from the RCCs leads to
horn cells (AHCs) in spinal cord
depolarization and contraction of the effectors, i.e.
■ directly stimulate respiratory muscles
respiratory muscles. Several different types of sensors
■ necessary for speech, eating, coughing.
monitor effector activity and provide constant feed-
■ Hypothalamus and limbic systems
back, which allows the RCCs to modify their output
■ pain and emotional state can modulate RCC
(respiratory frequency and depth) to meet metabolic
to produce apnoea or a gasp.
demand (Fig. 1-12).
Clinical Failure of the Respiratory
Clinical Failure of the Effectors
Control Centres
The effectors may fail in the presence of neuromuscu-

■ Hypoventilation or absent ventilation can occur
lar diseases of:
in the presence of
■ brainstem cerebral vascular accident (CVA) or ■ nerves (for example injury to phrenic nerve
tumour leading to diaphragmatic weakness)
■ raised intracranial pressure (ICP) ■ the neuromuscular junction (for example
■ central sleep apnoea myasthenia gravis)
■ Primary alveolar hypoventilation e.g. Ondine ■ muscles (for example muscular dystrophy).
curse
Alteration to respiratory mechanics or chest wall dys-
■ decreased level of consciousness secondary to
function may lead to failure of the effectors, for example:
□ alcohol
□ drugs ■ kyphoscoliosis
□ pharmacology ■ obesity
□ neurological event ■ hyperinflation.
Respiratory control centres Irritant Receptors

Located in the epithelial surface of the nasal cavity,
Higher upper airways, larynx, trachea, and large bronchi, irri-
centres
tant receptors are stimulated by irritants such as
noxious gases, cigarette smoke, dust, allergens, cold air
Pons
or secretions. Feedback from irritant receptors can
Medulla
elicit a change in respiratory frequency or depth,
induce a cough, sneeze or bronchospasm.
Juxta-Capillary Receptors
Sensors Effectors
The alveolar capillaries located in the interstitium are
richly supplied with sensory nerve endings called
‘juxtacapillary receptors’ or ‘j-receptors’. These sensors
are stimulated by the accumulation of fluid in alveoli
or capillary walls secondary to inflammation or pul-
Chemoreceptors monary oedema, leading to an increase in ventilation
Lung and other Respiratory muscles
receptors Diaphragm or an abnormal ventilatory pattern, e.g. Cheyne–Stokes
(pain, stretch, Abdominals respiration.
irritant) Intercostals
FIGURE 1-12 ■ Respiratory control centres (RCCs) and Proprioceptors

sensors.
During early stages of exercise, impulses from proprio-
ceptors and mechanoreceptors in muscle, ligaments
and joint capsules stimulate respiratory neurones to
increase the frequency and depth of respiration.
Respiratory System Sensors
Several different types of sensors monitor respiration,
Spinal Cord Reflexes
providing direct feedback to the RCCs: Reflexes at spinal cord level lead to the activation
and recruitment of respiratory accessory muscles to
■ chemoreceptors increase respiratory frequency and volume as a com-
■ central
pensation mechanism secondary to hypoventilation,
■ peripheral
gasping and respiratory distress.
■ mechanoreceptors
■ irritant receptors
Nasopulminary Reflexes
■ juxta-capillary receptors
■ proprioceptors. Located in the nasal mucosa, triggered by a change in
flow or air pressure in the nose, these reflexes provide
Mechanoreceptors feedback (via trigeminal nerve) to the RCCs to regu-
High-threshold mechanoreceptors are sited in bron- late deep breathing (increasing or decreasing) by alter-
chial smooth muscle, trachea and visceral pleurae. ing excitation to the effectors.
They are stimulated by tension in airways and lung
parenchyma during inflation, providing feedback to Chemoreceptors
the RCCs to ensure an optimal level of inflation to The most important of all the respiratory sensors are
meet activity and metabolic demand. A very large the chemoreceptors, which constantly sample arterial
inflation can lead to a critical stretch of the lung paren- blood, providing feedback to the RCCs to maintain
chyma, eliciting the Hering-Breuer reflex to instruct respiratory gases and pH within their normal range
the RCC to stop inspiration. regardless of activity.
Peripheral Chemoreceptors increase the frequency and depth of ventilation until

Peripheral chemoreceptors are located in the aortic pH (CO2/H+) levels are back in normal range.
arch between the ascending aorta and pulmonary Conversely, when pH rises (CO2/H+ low) the
artery (afferents in vagus nerve) and the carotid body central chemoreceptors feedback to RCCs, which stim-
at the bifurcation of the common carotid (afferents in ulate the effectors to decrease the frequency and depth
glossopharyngeal nerve). Both sets of peripheral of ventilation until pH (CO2/H+) levels are back in
chemoreceptors sample surrounding arterial blood normal range.
and are sensitive to arterial hypoxaemia, i.e. peripheral Additionally, the central chemoreceptors can pro-
chemoreceptors are only stimulated when there is vide central feedback to the RCCs, leading to an altera-
>40% reduction in PaO2 (PaO2 8 kPa or less). They tion in sympathetic and parasympathetic activity to
both also have sensitivity to increased free hydrogen alter blood pressure.
ion (H+) concentration and are weakly sensitive to
Central Chemoreceptors and COPD
PaCO2. Additionally, only the peripheral chemorecep-
tors in the carotid bodies are sensitive to a change in In the presence of respiratory disease such as COPD,
pH. Feedback from the peripheral chemoreceptors CO2 may become chronically raised where the effec-
informs the RCCs to alter the frequency and depth of tors are unable to alter respiratory frequency or depth.
respiration to meet demand. For example:
■ hyperinflation
Central Chemoreceptors
■ alveolar destruction
■ V /Q mismatch
Located bilaterally on the ventral surface of medulla, ■ altered respiratory mechanics
the central chemoreceptors are bathed in cerebrospi- ■ effector failure.
nal fluid (CSF). At the blood–brain barrier (BBB), the
concentration of CO2 in CSF is equal to the concentra- In this situation, arterial blood and consequently
tion of CO2 in arterial blood (PaCO2). Central chem- CSF remain acidotic. The brain cannot function ade-
oreceptors are sensitive to free hydrogen ion (H+) quately with a deranged acid–base balance, so a com-
concentration, derived from CO2 and demonstrate pensatory mechanism is instigated.
heightened sensitivity with mild hypoxia and acidosis.
Central chemoreceptors are unaffected by oxygen con- CO2 + H2O ↔ H2CO3 − ↔ HCO3 − + H +
centration. Feedback from the central chemoreceptors
to the RCCs is responsible for 70% of the drive to Normally, hydrogen carbonate (HCO3−) ions lib-
breathe. Once stimulated, the central chemoreceptors erated from the dissociation of carbonic acid are
initiate a change in breathing pattern within 5 breaths excreted via the kidneys. In the presence of hyper-
(10–20 seconds). capnia, HCO3− ions are transported across the BBB
to combine with and ‘buffer’ free H+ ions in the CSF,

essentially ‘neutralizing’ their stimulation of the central
Stimulation of the Central Chemoreceptors chemoreceptors. This may take up to 3 days before
CO2 diffuses across the BBB and combines with being fully effective and is called ‘metabolic compen-
water (H2O) in CSF to form carbonic acid. Car- sation’. Effective buffering returns CSF pH to normal
bonic acid dissociates to form bicarbonate and free to facilitate effective cellular function; sensitivity of
hydrogen ions. central chemoreceptors is reduced, but arterial blood
CO2 (PaCO2) remains raised, producing a persistent
CO2 + H2O ↔ H2CO3 − ↔ CO3 − + H + acidosis (low pH).
When the central chemoreceptors are no longer
The presence of free hydrogen ions increases acidity sensitive to free H+/CO2 the COPD patient’s drive to
and reduces the pH of CSF, which directly stimulates breathe falls to the peripheral chemoreceptors, which
the central chemoreceptors. The central chemorecep- are sensitive to hypoxaemia; this is called ‘hypoxic
tors feedback to RCCs, which stimulate the effectors to drive’.
Clinical Relevance of Hypercapnic COPD transported back to the lung. This is called the ‘Haldane
Patients with COPD have large areas of low ventilation effect’. Conversely, if the COPD patient is given high
resulting in V /Q mismatch, and are unable to alter dose therapeutic O2, Hb dissociates from CO2 in pref-
ventilation to increase excretion of CO2, leading erence to bind with O2. The dissociated CO2 dissolves
to chronic hypercapnia. These patients with COPD in plasma raising PaCO2.
will also be hypoxaemic and require supplemental
oxygen therapy. However, if O2 is given at high LUNG VOLUMES & VENTILATION
levels of concentration (above 28%) there is a risk
of inducing further hypercapnia secondary to three Although inflation and deflation of the lungs is con-
mechanisms: tinuous, the volume of air in the lungs varies at differ-
ent points in the respiratory cycle and in health, is
■ loss of hypoxic drive dependent on activity level. As a respiratory physio-
■ increased V /Q mismatch due to reversal of therapist, it is important to understand the clinical
hypoxic pulmonary vasoconstriction (HPV) relevance of lung volumes and how they may alter in
■ Haldane effect (oxygenated blood has a reduced the presence of dysfunction or disease. Lung volumes
capacity for carbon dioxide). are measured directly; lung capacities are measured in
multiples of two or more lung volumes (Fig. 1-13).
Loss of Hypoxic Drive
Lung Volumes
COPD patients with chronic hypercapnia have reduced
sensitivity of central chemoreceptors and therefore ■ VT is the volume of air inspired during quiet
rely on peripheral chemoreceptors to sense arterial respiration.
hypoxaemia and provide a drive to breathe. As such, if ■ Inspiratory reserve volume (IRV) is the volume
the patient is given high dose therapeutic O2; arterial air inspired from VT to maximal inspiration.
hypoxaemia will be reversed, removing the remaining ■ ERV is the volume of air expelled with forced
drive to breathe. expiration.
■ RV is the volume of air left in lungs which cannot
Increased V /Q Mismatch be expelled.
In the presence of respiratory disease such as COPD, (Table 1-1)
areas of poor ventilation lead to reduced gas exchange
and hypoxaemia. When PaO2 falls to about 6 kPa (oxy- Lung Capacities
haemoglobin saturation (SaO2) in low 80s), hypoxae- ■ FRC is the volume of air left in the lungs at end
mia is sensed by receptors in arterioles passing through of normal quiet expiration (ERV + RV).
the area of poor ventilation. This causes them to ■ Vital capacity (VC) is the total volume of air
constrict to minimize V /Q mismatch and provide from maximal inspiration to maximal expiration
increased blood flow to areas with better ventilation to (IRV + VT + ERV).
facilitate gas exchange. This is called ‘hypoxic pulmo- ■ Total lung capacity (TLC) is the volume from
nary vasoconstriction (HPV)’. If the COPD patient is maximal inspiration to RV (IRV +VT + ERV
given high-dose therapeutic O2, hypoxia in some areas + RV).
of lung may be reduced due to an increased concentra- (Figure 1-13, Table 1-2)
tion gradient. Improved PaO2 is sensed by arterioles
leading to the reversal of HPV, once again causing Factors Affecting Lung Volumes
perfusion of poorly ventilated lung and producing ■ Body size: Taller people tend to have larger lung
increased V /Q mismatch (shunt). volumes. Obese people have smaller lung volumes
as their chest wall is less compliant.
Haldane Effect ■ Age: As a person gets older lung tissue loses elas-
Haemoglobin (Hb) has a strong affinity for O2, but in ticity and lung volumes increase. However, simul-
the presence of hypoxaemia, CO2 binds to Hb to be taneously, ageing leads to reduced compliance
80
Inspiratory
Reserve
Volume
(IRV)
Vital
Capacity
Volume (mL/kg)
37 (VC) Total
Tidal Lung
Volume Capacity
(VT) (TLC)
30
Expiratory
Reserve
Volume
Functional
(ERV)
Residual
15 Capacity
(FRC)
Residual Residual
Volume Volume
(RV) (RV)
0
FIGURE 1-13 ■ Lung volumes and capacities.
TABLE 1-1 of the thoracic cage which is more pronounced

Average Lung Volumes in Healthy Adults than changes to lung elasticity. Therefore overall
there is a reduction in lung volumes.
VALUE (L)
■ Gender: Men tend to be physically bigger than
Volume Men Women women and therefore have larger lung volumes.
Inspiratory reserve volume 3.0 1.9 ■ Muscle training: Inspiratory muscle training
Tidal volume 0.5 0.5 increases lung volumes.
■ Respiratory disease: Respiratory disease may lead
Expiratory reserve volume 1.1 0.7
to an increase or decrease in lung volumes.
Residual volume 1.2 1.1 ■ Altitude: People living at altitude have larger lung
volumes in order to increase gas exchange where

the partial pressure of oxygen is reduced.
TABLE 1-2
Average Lung Capacities in Healthy Adults Clinical Relevance of Lung Volumes
VALUE (L) and Capacities
Capacity Men Women Components ■ VT: an adequate VT is necessary to maintain oxy-
Vital capacity 4.6 3.1 IRV & VT & ERV
genation and CO2 clearance.
■ IRV: required to produce an effective cough and
Functional residual 2.3 1.8 ERV & RV
necessary to sustain increased level of activity or
capacity
exercise.
Total lung capacity 5.8 4.2 IRV & VT & ERV & RV ■ FRC: essential to maintain distal lung patency
ERV, Expiratory reserve volume; IRV, inspiratory reserve volume; on expiration. Within FRC, there is a critical
RV, residual volume; VT, tidal volume. value called closing volume. When FRC falls
below closing volume, distal lung patency can of the VT that is not involved in gas exchange. There
no longer be maintained leading to atelectasis. are 2 types of dead space:
Atelectasis is associated with reduced oxygena- ■ anatomical dead space
tion, poor CO2 clearance, an increased work of ■ alveolar dead space.
breathing, breathlessness and a reduced exercise
tolerance. Together they are called ‘physiological dead space’.
■ RV: an increase in RV occurs in obstructive lung
disease due to air trapping. This leads to altered Anatomical Dead Space
respiratory mechanics, an increased work of The bronchial tree is divided into two zones (see
breathing, reduced VT, poor gas exchange and a Fig. 1-3):
reduced exercise tolerance. ■ conducting zone
■ VC: a VC of 1 L is the critical value used to iden- ■ respiratory zone.
tify if a patient is able to maintain spontaneous
ventilation. The conducting zone consists of the trachea to the
terminal bronchi. Air moves through the conducting
zone by convection towards the alveolar membrane
Measuring Lung Volumes and Capacities
where gas exchange takes place. Within each tidal
VT, VC, inspiratory capacity and IRV can be meas- breath, 150 mL remains in the conducting zone and is
ured directly with a spirometer. These simple meas- therefore not used in gas exchange. This is called ‘ana-
urements form the basis of pulmonary function tomical dead space’.
testing. As it is not possible to completely breathe out, The respiratory zone extends from the respiratory
measuring RV (and FRC) is more complex. Special- bronchiole to the alveolus. Air moves through the
ized testing is required using radiographic planim- respiratory zone by diffusion, culminating in gas
etry, body plethysmography, closed circuit dilution exchange.
(the helium dilution technique) or nitrogen washout
techniques. Alveolar Dead Space
‘Alveolar dead space’ is the term used to describe
Why Assess Spirometry? inspiratory gas reaching alveoli which is unable to par-
As a physiotherapist, understanding spirometry will ticipate in gas exchange due to an insufficient blood
aid the clinical diagnosis and management of a patient supply. In health, alveolar dead space is almost zero,
with respiratory disease. In gross terms, respiratory but in disease, alveolar dead space may occur in the
disease is either categorized as obstructive (difficulty presence of a pulmonary embolus or ventilation of
breathing out) or restrictive (difficulty breathing in), non-vascular air spaces, e.g. emphysematous bullae or
cardiac shunt.
but in some cases both problems can co-exist. Spirom-

etry is also often used as an objective measure to assess Physiological Dead Space
or monitor disease progression and deterioration
during acute exacerbation, the efficiency of an inhaled Physiological dead space is the sum of all parts of VT
drug or its delivery system. which does not participate in gaseous exchange, i.e.
anatomical dead space plus alveolar dead space. There-
fore anything that affects anatomical or alveolar dead
Ventilation Terminology space will affect physiological dead space, e.g. age,
An average adult has a VT of 500 mL and has a respira- gender, body size and posture and the instigation of
tory frequency of 12 breaths per minute (approxi- mechanical ventilation and pulmonary disease.
mately). Therefore the minute ventilation, the amount
of air entering the lungs, is 12 × 500 = 6.0 L/min. Alveolar Ventilation
However, not all VT which enters the lungs is used VA is the amount of minute ventilation reaching the
in gas exchange. ‘Dead space’ is the term for that part respiratory zone that can be used in gas exchange.
Tidal volume − anatomical dead space Alveolar hyperventilation is defined as excessive

= Alveolar ventilation ventilation leading to reduced levels of carbon dioxide
(hypocapnia).
In an average adult Hyperventilation may occur secondary to
■ anxiety/fear
■ 500 mL − 150 mL = 350 mL/breath ■ metabolic disease (hyperthyroidism)
■ 350 mL × 12 breaths per minute = 4.2 L/min. ■ airway obstruction (asthma)
■ parenchymal lung disease (pneumonia)
Clinical Relevance of Alveolar Ventilation ■ neurological disorders (tumour)
Maintenance of VA is of paramount importance ■ altitude.
because it determines the quantity of O2 and CO2 Hyperventilation leads to excess CO2 excretion:
levels in alveolar gas (PAO2, PACO2) and subsequently ■ ↓ PACO2 (alveolar concentration)
arterial blood (PaO2, PaCO2). In particular, there is an ■ ↓ PaCO2 (plasma concentration)
inverse linear relationship between VA and CO2 levels, ■ ↓ CO2 + H2O ⇌ H2CO3 ⇌ HCO3 + ↓ H+
with PACO2 decreasing as VA increases. An alteration ■ ↑pH
in VA will lead to disruption of normal acid–base ■ respiratory alkalosis.
balance; both hypoxaemia and hypercapnia may occur

with respiratory disease.
Other factors which affect the concentration of O2
GAS EXCHANGE
and CO2 in arterial blood are
The requirements of the average cell for oxygen are
■ the rate of O2 consumption (VO2)
quite modest and a mitochondrion may need a
■ the rate of CO2 production (VCO2)
partial pressure of oxygen (PO2) of as little as 1 kPa
■ Hb content of blood
(7.5 mmHg) to function effectively. At sea level, the
■ Hb affinity for O2
atmospheric PO2 is 20 kPa (150 mmHg) (fraction of
■ atmospheric pressure of O2
inspired oxygen (FiO2) = 0.21) and in the process of
■ specific characteristics of the alveolar membrane.
delivering oxygen to the cell, there is a loss along this
gradient.
Alteration of Alveolar Ventilation The mechanics of breathing produce inspiration
Alveolar hypoventilation is defined as insufficient ven- and airflow into the lungs secondary to a change in
tilation leading to raised levels of carbon dioxide volume and subsequently pressure. During inspiration
(hypercapnia). air initially moves into the lungs via convection and
Hypoventilation may present passes through the conducting zone to the respiratory
■ localized to a particular lung, lobe or segment, zone of the bronchial tree. In the most general terms,
e.g. secondary to infection, consolidation or convection refers to the movement of currents within
atelectasis fluids (i.e. liquids, gases).
■ scattered through both lung fields, e.g. second- The first step is the dilution of inspired air with
ary to COPD or asthma expired air within the alveolus. Each tidal breath (VT)
■ generalized, e.g. secondary to pain, a re- contains a portion of gas which will remain within the
duced respiratory drive or reduced level of airways and not come into contact with the alveoli.
consciousness. This is known as the ‘dead space ventilation’ (VD) and
Hypoventilation leads to poor CO2 excretion must be achieved before any effective VA can take place:
■ ↑ PACO2 (alveolar concentration)
■ ↑ PaCO2 (plasma concentration) VT = VD + VA
■ ↑ CO2 + H2O ⇌ H2CO3 ⇌ HCO3 + ↑ H+
■ ↓ pH Alveolar gas therefore contains a mixture of fresh
■ respiratory acidosis. gas and some expired CO2 and the alveolar PO2 is
reduced to about 13.8 kPa (104 mmHg) before gas In the context of respiration and gas exchange, in
exchange begins. accordance with Fick’s law, diffusion is dependent on
Air moves along the smallest airways into the alveoli ■ surface area of alveolar membrane
sacs by diffusion. The actual exchange of gases occurs ■ concentration/pressure gradient
across the capillaries in the alveoli sacs (alveolar mem- ■ gas solubility
brane). ‘Diffusion’ refers to the process by which mol- ■ thickness of alveolar membrane
ecules intermingle as a result of kinetic energy of ■ ventilation/perfusion coupling.
random motion. Diffusion is an extremely rapid
process but can only occur over very small distances. Concentration Gradient and Gas Solubility
In the context of the respiratory gases, concentration
Fick’s Law and Gas Exchange
is described using the term ‘partial pressure’. Partial
Gas exchange takes place in the alveoli sac across the pressure describes the amount of gas dissolved in the
alveolar membrane, which is the boundary between plasma. For example, PaO2 is the amount of O2 dis-
the external environment and interior of the body solved in the plasma of arterial blood or PvCO2 is the
(Fig. 1-14). Respiratory gases cross the respiratory amount of CO2 dissolved in the plasma of venous
membrane by diffusion, in accordance with Fick’s law. blood.
Partial pressures are equivalent to concentration
Fick’s Law gradients. The steeper the difference in partial pressure
■ The rate of transfer of a gas through a sheet of between gas in alveoli and capillary blood, the steeper
tissue is proportional to the diffusion gradient producing faster and more effi-
■ tissue area cient diffusion. Thus the partial pressure difference
■ difference in gas partial pressure between the of 64 mmHg between deoxygenated venous blood
two sides in the pulmonary capillaries (PvO2 = 40 mmHg)
■ diffusion constant and the oxygen rich alveolus (PAO2 = 104 mmHg),
■ inversely proportional to tissue thickness. leads to rapid diffusion of O2 from the alveolus
Inspired air
P ICO2 - 0 mmHg
P IO2 - 150 mmHg
Air moves in and
Blood flow to
out of alveoli
body tissues
PaCO2 - 40 mmHg
PaO2 - 104 mmHg
Capillary
Blood flow from Alveolus

body tissue PACO2 - 40 mmHg
Red blood
P vCO2 - 46 mmHg PAO2 - 104 mmHg cells
P vO2 - 40 mmHg
Net diffusion
of O2 into blood
Net diffusion of
CO2 out of blood
FIGURE 1-14 ■ Alveolar gas exchange.
across the respiratory membrane into the pulmonary activity, but additional recruitment of the gas exchange
capillary. surface can be utilized to maintain acid–base balance
The difference in partial pressure of CO2 between during increased activity, e.g. during exercise.
the venous capillary (PvCO2 = 46 mmHg) and the In some respiratory diseases there is a marked
alveolus (PACO2 = 40 mmHg) is much smaller at only loss of surface area available for gas exchange. There-
6 mmHg. However, as CO2 is 20 times more soluble fore even though diffusion may not be impaired,
than O2, only a small difference in partial pressure adequate oxygenation and carbon dioxide clearance
is necessary. Diffusion of CO2 from venous capillary cannot be maintained, leading to hypoxaemia and
blood into the alveoli occurs extremely rapidly. Indeed, hypercapnia.
in the time available equal amounts of CO2 and O2 are ■ temporary loss of surface area
exchanged across the respiratory membrane. Clini- ■ bronchial obstruction (tumour, mucus plug)
cally, in respiratory disease where diffusion is impaired, ■ atelectasis
O2 will be primarily affected, as it is less soluble. A ■ consolidation
significant impairment is required to lead to poor CO2 ■ permanent loss of surface area
transfer. ■ emphysematous bullae.
Transit Time of Red Blood Cell (RBC) Ventilation and Perfusion Matching (V /Q )
During gas exchange, the total transit time of a In respiratory physiology, the V /Q ratio is the meas-
RBC within the pulmonary capillaries is about urement used to describe efficiency and adequacy of
0.75 sec. However, in health, it normally only takes matching between ventilation (V ) and perfusion (Q )
about 0.25 sec for O2 equilibration to occur (i.e. gas which are necessary for gas exchange.
exchange). This means that with normal partial pres-
sures of O2, there is a large time reserve; this provides ■ V ventilation
a significant safety margin, which means the velocity ■ the air which reaches the lungs
of blood flow can significantly increase (i.e. during ■ Q perfusion

exercise) and still allow enough transit time for full ■ the blood which reaches the lungs.
RBC saturation with O2 to be achieved. Inadequacy of either V or Q will have a significant

impact on the oxygenation of blood and the removal
Thickness of the Alveolar Membrane of carbon dioxide. This is termed a ‘V /Q mismatch’.
The alveolar membrane is 0.5 to 1 µm thick (2000
times thinner than skin). Diffusion efficiency is highly Distribution of Ventilation in Healthy Lung
dependent on distances involved; therefore an ultra- The distribution of ventilation is affected by the pleural
thin membrane facilitates rapid and efficient gas pressure gradient down the upright lung. Pleural pres-
exchange. sure gradient is generated as a net result of the ribs

Clinically, if the alveolar membrane becomes thick- trying to spring upward and outward and the lungs
ened, there is a greater distance between alveoli and trying to recoil inward and downward (Fig. 1-15).
capillary, leading to slower and or impaired diffusion, Pleural pressure becomes less negative down the
which may lead to hypoxaemia. Thickening of the upright lung. Therefore in the self-ventilating adult,
alveolar membrane may occur due to inflammation, lung parenchyma in the apices (non-dependent region)
infection or fibrosis. has the greatest initial volume (i.e. already expanded)
with little additional capacity for volume change. The
Surface Area of Alveolar Membrane lung parenchyma in the bases (dependent region)
The adult lung contains around 300 million alveoli, is minimally expanded and can exhibit the greatest
which gives a gas exchange surface area in the region volume change as the dependent regions of lung are
of 70–80 m2 (40 times greater than the surface area of more compliant than the non-dependent regions.
skin). Full lung surface area is not required for normal However, optimal ventilation occurs in the lower third
Pulmonary
vein
Alveolus Zone 1
PA PA>Pa>Pv
Pulmonary
artery
Pa Pv
Zone 2
Pulmonary PA Pa>PA>Pv
artery Pa Pv
pressure
Pulmonary
venous
pressure
PA
Pulmonary Pulmonary
Pa Pv
artery vein
Zone 3
Pa>Pv>PA
FIGURE 1-15 ■ Lung ventilation distribution. PA, alveolar pressure; Pa, pulmonary artery pressure; Pv, pulmonary venous pres-
sure. (Reproduced with permission from West, J.B., 2000. Respiratory Physiology: The Essentials, Lippincott. Williams & Wilkins, Philadelphia,
p. 37.)
of the lung, as the lung parenchyma in this region is pulmonary hypotension. Zone 3 largely reflects the
partially expanded but still has increased capacity for lungs in health. There is no external resistance to blood
further expansion and volume change. The distribu- flow and blood flow is continuous throughout the
tion of ventilation is also influenced by differences in cardiac cycle. Zone 4 is an additional theoretical region
regional mechanics and airflow resistance. not shown in Figure 1-15. This zone is characterized
by increased pulmonary vascular resistance caused by
Distribution of Perfusion in Healthy Lung an increase in pulmonary interstitial pressure (Pi), in
The distribution of perfusion increases down the which Pa > Pi > Pv > PA, such as when lung volumes
healthy upright lung. The non-dependent–to– are low or in pulmonary oedema. This decrease in
dependent increase in regional perfusion is influenced regional blood flow may be seen in the lung bases with
and affected by the interaction of alveolar, arterial and conditions like acute respiratory distress syndrome
tissue pressure and the fractional geometry (branch- (ARDS) (see Fig. 1-15).
ing) of the pulmonary artery. Gravity only has a
limited affect (7%, 5%, and 25% of perfusion hetero- V /Q Matching in the Self-Ventilating Adult
geneity is due to gravity in the supine, prone and In the self-ventilating adult, optimal V /Q matching
upright postures, respectively). occurs in the dependent region of the lungs; the lower
To aid the explanation of the distribution of per- third, where perfusion is plentiful and the alveoli are
fusion, the lung can be divided into four zones. Zone maximally compliant and have the potential for expan-
1 is not observed in the normal healthy human lung sion. The principles of V /Q matching are utilized by
and refers to positive pressure ventilated non-perfused respiratory physiotherapists when positioning patients
alveoli. In normal health, pulmonary arterial pressure who are hypoxic.
exceeds alveolar pressure in all parts of the lung. In health, ventilation in the lungs is met by ample
Zone 2 refers to the region just above the level of the blood supply from the pulmonary capillaries (V /Q
heart where blood flow may be intermittent, depend- matching), facilitating effective gas exchange.
ing on PA or Pa, which may be influenced by high When V /Q mismatch occurs due to reduced ven-
levels of positive end-expiratory pressure (PEEP), or tilation (e.g. secondary to a sputum plug disrupting
Alveolus Pulmonary Alveolus Hypoxic Pulmonary Vasoconstriction (HPV)

vein Pulmonary
vein In respiratory disease, lung areas with reduced ventila-
Pulmonary Pulmonary tion lead to poor gas exchange, and subsequent hypox-
artery artery
aemia and hypercapnia. When PaO2 falls to about
6 kPa or SaO2 is in the low 80s, hypoxia is sensed by
receptors in arterioles. These arterioles constrict to
A reduce ‘wasted perfusion’ to areas of low ventilation in
an attempt to minimize V /Q mismatch. Blood flow is
Alveolus Alveolus
redirected to areas of lung with good ventilation to
Pulmonary facilitate effective gas exchange.
Pulmonary vein
Pulmonary vein Pulmonary Clinically, persistent HPV occurs in COPD. In this
artery artery instance, pulmonary arterioles have a reduced diam-
eter due to vasoconstriction and therefore an increased
resistance to blood flow through them. Therefore to
maintain blood flow to the lungs the right ventricle of
the heart must work harder to push blood through
B
these narrowed vessels. As a result, the right ventricle
FIGURE 1-16 ■ Lung mechanisms for maintaining initially hypertrophies and then fails ultimately leading
ventilation–perfusion (V /Q ) matching. (A) In the event of to right ventricular heart failure and cor pulmonale.
good perfusion but poor alveolar ventilation (VA) (collapse),
reduced PO2 and increased PCO2 in the alveolus result in
constriction of the pulmonary arterioles that supply it. Hence Pulmonary Capillary Recruitment
both alveolar ventilation and perfusion are reduced. (B) In Conversely, in areas where ventilation is high, addi-
the event of good alveolar ventilation but poor perfusion, tional vessels in the pulmonary arteriole bed are
increased PO2 and reduced PCO2 in the alveolus result in dila-
tation of the pulmonary arterioles that supply it. Hence both
recruited to optimize V /Q matching and maximize
alveolar ventilation and perfusion are increased. gas exchange.
Diagnosis of V /Q Mismatch

In respiratory disease where a V /Q mismatch is sus-
air flow), perfusion remains viable. An area of lung pected, patients undergo a V /Q scan. This involves
with no ventilation but good perfusion (and thus a imaging of the distribution of air and blood in the
V /Q of 0) is termed a ‘shunt’ (Fig. 1-16). lungs following the administration of radio-opaque
When V /Q mismatch occurs due to reduced per- markers.
fusion (e.g. secondary to a pulmonary embolus dis- Patient X’s V /Q scan reveals both a perfusion and
rupting blood flow), ventilation remains viable. An ventilation deficit (Fig. 1-17). Therefore the underly-
area with reduced perfusion but good ventilation (and ing problem is a primary ventilatory defect with sec-
thus a V /Q of infinity) is termed ‘alveolar dead space’ ondary compensatory HPV.
(see Fig. 1-16). If the primary problem was reduced perfusion, a
normal distribution of ventilation would still be seen.
Maintaining V /Q Matching
It is vital to maintain V /Q matching to achieve ade- Bronchiole Response
quate gas exchange. In the presence of respiratory
Bronchioles are highly sensitive to PACO2. A high
disease, a V /Q mismatch triggers autoregulatory
PACO2 leads to bronchodilatation to increase CO2
homoeostatic mechanisms to minimize the gas
excretion (wider airways means reduced airway resist-
exchange deficit:
ance and greater CO2 clearance), in an attempt to nor-
■ HPV or dilatation malize PACO2 and PaCO2. Conversely, a low PACO2
■ bronchiole response (constriction or dilatation). leads to bronchoconstriction to reduce CO2 excretion
A B
FIGURE 1-17 ■ Ventilation–perfusion ( V /Q ) scan reveals both a perfusion and ventilation deficit in patient X, indicating a
primary ventilation defect with compensatory hypoxic pulmonary vasoconstriction. (A) Perfusion defect. (B) Ventilation defect.
(Reproduced with permission from Hansell, D.M., Lynch, D.A., McAdams, H.P., Bankier, A.A., 2009. Imaging of Diseases of the Chest, fifth ed.
Mosby Elsevier, Philadelphia.)
(narrower airways means increased airway resistance Oxygen and Haemoglobin

and less CO2 clearance) in an attempt to normalize Haemoglobin (Hb) is a complex molecule composed
PACO2 and PaCO2 of four iron-containing haem groups, each attached
Transport of Oxygen and Carbon Dioxide to a polypeptide protein chain. The haem molecules
are the O2 binding sites where each of these four
Oxygen and carbon dioxide are transported to and
iron atoms can reversibly bind one O2 molecule (oxy-
from the lungs in blood via several different methods.
haemoglobin). When all four binding sites are bound
Oxygen is immediately bound to haemoglobin and
to O2, it is called fully saturated. The process of O2
released in the tissues under conditions of low oxygen
binding is both rapid and reversible. After the first
tension or acidosis. Very little oxygen is carried in solu-
O2 molecule binds to Hb, the shape of the haem mol-

tion in the blood under conditions of normal pressure,
ecule changes, which facilitates the faster binding
although this can be increased in a hyperbaric chamber.
of subsequent O2 molecules. It takes <0.01 second
By contrast, carbon dioxide is carried in the blood
to bind the first O2 molecule but even less time to
entirely in solution, mostly as bicarbonate. The differ-
bind the second, third and fourth. This principle
ence between the two forms of carriage of the meta-
remains in the reverse situation of O2 unloading at the
bolic gases is fundamental to the interpretation of the
tissues (deoxyhaemoglobin). In combination with Hb,
measurement of arterial blood gases.
blood can routinely transport 20 mL O2 per 100 mL
Oxygen Transport blood.
98% O2 binds to Hb to produce oxyhaemoglobin
Following diffusion at the alveolar membrane, 98.5%
(HbO2).
of O2 is carried by the RBCs, called ‘erythrocytes’, com-
bined with haemoglobin (SaO2) and 1.5% of O2 dis- 

Lungs
→ HbO2 + H +
HHb + O2 ← 
solves directly into the plasma (PaO2). Tissues
Haemoglobin’s Affinity for Oxygen and14 kPa), producing the characteristic plateau phase
At different points of the RBC’s journey from the lung of the curve. As PaO2 falls to approximately 9 kPa,
to the tissue, Hb changes its affinity for O2, in a non- large amounts of O2 are rapidly dissociated from Hb
linear relationship which is represented by the sigmoid into the plasma, producing the steep portion of the
shaped oxygen dissociation curve. This alteration in curve. Finally, at the tissue, Hb has a decreased affinity
Hb’s affinity for O2 serves to maximize and facilitate for O2, leading to dissociation and off-loading as the
the process of O2 loading at the lung and O2 unloading surrounding plasma level (PaO2) has fallen below a
at the tissue, increasing the efficiency of the O2 trans- critical value. This ensures the adequate delivery of O2
port mechanism. to the tissues where it is required for metabolism and
function. In health at rest, Hb only releases 25% of its
The Oxygen Dissociation Curve O2 cargo, as that is all the body requires. Therefore at
The oxygen dissociation curve (Fig. 1-18) describes the rest, Hb remains 75% saturated; this safety margin
relationship between the partial pressure of O2 either allows increased amounts of O2 to be available during
at the alveoli (PAO2) or tissue level (PaO2) and the exertion, e.g. exercise.
degree to which Hb is saturated with O2, i.e. how much
Why Does O2 Need to Dissociate?
O2 is loaded (combined with Hb; SaO2) and how much
is given up (dissociated). To fully understand the oxygen dissociation curve, the
At the lung where PAO2 is high, Hb has a high affin- principles of gas exchange must be reviewed. Gas
ity for O2 to facilitate maximum binding and loading exchange (at both the lung and tissue) occurs via dif-
in the RBC. As blood flows away from the lungs, ini- fusion, which requires a concentration gradient. The
tially very small amounts of O2 are released from Hb necessary gradient is provided by PaO2, i.e. the amount
as the surrounding PaO2 remains high (between 10 of O2 dissolved in plasma, which must be maintained
to drive gas exchange. Therefore before O2 can move
via diffusion to the tissue for utilization, the O2 mol-
Left shift ecule must dissociate from Hb and dissolve into the
(increased affinity)
Decreased PCO2 plasma before passing through the capillary mem-
Increased pH brane into a cell. Hb can be thought of as a ‘holding
Decreased temperature store’ for O2 until it is required to maintain the con-
Decreased 2–3 DPG
Decreased [H+] centration gradient.
Carbon monoxide LUNGS
100 Factors Affecting Hb Affinity for O2
% Saturation of haemoglobin
The rate at which Hb reversibly binds or releases O2 is

80
primarily regulated by PaO2; however, other factors
Right shift also affect Hb’s affinity for O2 such as temperature, pH,
60 (reduced affinity) PaCO2 and blood concentration of an organic chemi-

Increased PCO2
Decreased pH cal called ‘diphosphoglycerate (DPG)’.
40
Increased temperature These factors interact to ensure there is adequate
Increased 2–3 DPG uptake of O2 at the lung and adequate delivery of O2
20 Increased [H+]
to the tissues.
TISSUES Diphosphoglycerate (DPG)

2 4 6 8 10 12 14
RBCs do not possess mitochondria, so can only
Partial pressure of oxygen (kPa)
metabolize anaerobically. DPG is a by-product of RBC
FIGURE 1-18 ■ Oxygen dissociation curve. When there is a anaerobic metabolism or glycolysis. DPG rises with
high concentration of CO2 (in the tissues), the curve moves
down and towards the right. Carbon monoxide; DPG, diphos- raised body temperature, altitude, exercise and in
phoglycerate; H+, hydrogen ion; PCO2, pressure of carbon patients with chronic hypoxic lung conditions, e.g.
dioxide. COPD
Hb has a reduced affinity for O2 where: This conversion involves a series of chemical reac-
■ PCO2 is high (tissues) tions which take place either in the plasma or in the
■ H+ concentration is high (↓pH) RBC. In the plasma, the conversion rate is very slow;
■ body temperature is increased therefore the majority of CO2 passes directly into the
■ DPG production is high. RBC which contains the enzyme carbonic anhydrase,
which catalyses the reaction by 1000 times.
In this situation, the O2 dissociation curve ‘shifts’
down and towards the right, meaning that O2 unload- Carriage from Tissue to Lungs
ing to supply the tissues and CO2 loading and removal CO2 + H2O ↔ H2CO3 ↔ HCO3 + H +
from the tissues occurs more rapidly, e.g. exercise. This
is called the ‘Bohr effect’. When there is a high concentration of CO2 (in the
Conversely, Hb has an increased affinity for O2 tissues), the equation moves towards the right. When
where: there is a low concentration of CO2 (in the lungs), the
■ PCO2 is low (lungs) equation moves towards the left and CO2 and H2O are
■ H+ concentration is low (↑pH) excreted in the expired air.
■ body temperature is decreased The efficiency with which oxygen is transported
■ DPG production is low. from the atmosphere along the steps of the oxygen
transport pathway to the tissues determines the effi-
In this situation, the O2 dissociation curve ‘shifts’
ciency of oxygen transport overall. The steps in the
up and towards the left, meaning that O2 unloading at
oxygen transport pathway include ventilation of the
the tissues and CO2 loading and removal from the
alveoli, diffusion of oxygen across the alveolar capillary
tissues occurs less rapidly.
membrane, perfusion of the lungs, biochemical reac-
Carbon Dioxide Transport tion of oxygen with the blood, affinity of oxygen with
Following diffusion across the capillary membrane, haemoglobin, cardiac output (CO), integrity of the
20–30% of CO2 is carried by the RBCs; combined peripheral circulation and oxygen extraction at the
with haemoglobin, 7–10% of CO2 dissolves directly tissue level (Wasserman et al 2011). At rest, the demand
into the plasma (PaCO2) and 60–70% is carried as for oxygen reflects basal metabolic requirements.
bicarbonate. Metabolic demand changes normally in response to
gravitational (positional), exercise and psychological
Carbon Dioxide and Haemoglobin stressors. When one or more steps in the oxygen trans-
Approximately 20–30% of CO2 binds to the globin port pathway are impaired secondary to cardiopulmo-
portion of the Hb molecule, forming a carbamino nary dysfunction, oxygen demand at rest and in
compound called ‘carbaminohaemoglobin (HbCO2)’. response to stressors can be increased significantly.
O2 binds with the haem portion of the Hb molecule Impairment of one step in the pathway may be com-
so there is no competition between O2 and CO2 for pensated by other steps, thereby maintaining normal
binding sites). gas exchange and arterial oxygenation. With severe
impairment involving several steps, arterial oxygena-

CO2 + Hb ← 
→ HbCO2
Lungs
tion may be reduced, the work of the heart and lungs
Tissues
increased, tissue oxygenation impaired and, in the
Carbon Dioxide as Bicarbonate most extreme situation, multiorgan system failure may
Sixty to 70% of CO2 is carried in the blood as bicar- ensue.
bonate and transported in this form from the tissues While the oxygen transport pathway ensures that
to the lungs. CO2 combines with water to produce an adequate supply of oxygen meets the demands of
carbonic acid, which is an unstable compound that the working tissues, the carbon dioxide pathway
readily dissociates into bicarbonate and a free hydro- ensures that carbon dioxide, a primary by-product of
gen ion. At the lung, the process is reversed to repro- metabolism, is eliminated. This pathway is basically
duce CO2 gas and water ready for exhalation. the reverse of the oxygen transport pathway in that
carbon dioxide is transported from the tissues, via the pneumocytes) line the air spaces. Type I pneumocytes
circulation, to the lungs for elimination. Carbon flatten and elongate to cover the majority of the surface
dioxide is a highly diffusible gas and is readily elimi- area of the saccular air spaces. Type II cells only occupy
nated from the body. However, carbon dioxide reten- approximately 2% of the surface and are responsible
tion is a hallmark of diseases in which the ventilatory for surfactant synthesis and storage (Greenough 1996).
muscle pump is operating inefficiently or the normal Surfactant is a phospholipid, which stabilizes surface
elastic recoil of the lung parenchyma is lost. tension in the alveolus and prevents alveolar collapse
on expiration. Small quantities of surfactant are
present at weeks 23–24 of gestation and the amount
THE EFFECT OF GROWTH AND
present gradually increases until a surge at about week
AGEING ON RESPIRATION
30. Birth itself and the onset of respiration stimulate
The embryological development of the lung can be further surfactant production.
divided into four stages (Inselman & Mellins 1981): Towards the end of the terminal sac period, the air
spaces have developed into primitive multilocular
■ embryonic period (gestational weeks 3–5)
alveoli. After birth, alveoli increase in size and number.
■ pseudoglandular period (gestational weeks 6–16)
The average number of alveoli in the newborn is 150
■ canalicular period (gestational weeks 17–24)
million. By the age of 3–4 years, the adult number of
■ alveolar sac period (gestational week 24–term).
300–400 million alveoli has been reached, but alveolar
Embryonic Period (Weeks 3–5) growth continues for the first 7 years (Hislop et al
The lung bud starts as an endodermal outgrowth 1986). More recent estimations of mean alveolar
of fetal foregut. The single tube thus formed soon number in adulthood have been 480 million (range
branches into two, forming the major bronchi. By cell 274–790 million), with alveolar number closely related
division, the process of growth continues until, at the to lung volume (Ochs et al 2004).
end of this period, the major lung branches are formed. The most obvious differences between children and
adults lie in the development of airway function. The
Pseudoglandular Period (Weeks 6–16) airways develop faster than the alveoli, which may not
During this period the airways grow by dichotomous reach maturity until about the seventh year. As the
branching so that by week 16 all generations of the lung matrix develops, the airway walls remain strong
airway from trachea to terminal bronchioles (i.e. the and relatively patent. As a result, expiratory flow
preacinus) are formed. During this period the pulmo- rates, although lower than in adulthood, are relatively
nary circulation also develops, cartilage and lymphatic high. In addition to airway patency, there are also
formation occur and cilia appear (week 10 onwards) developments in the behaviour of the chest wall with
(Langman 1977). growth. In childhood, the musculoskeletal structures
are immature and flexible. Rib cage distortion is
Canalicular Period (Weeks 17–24) often seen in childhood during illness, but disappears
The respiratory bronchioles, alveolar ducts and alveoli with growth and muscularization. The combination of
(i.e. the acinus) start to develop during this time, airway patency and plasticity of the chest wall allows
simultaneously with the lung capillaries, thus prepar- an interesting experiment. In childhood the RV is not
ing the lungs for their future role in gas exchange determined by airway closure but by the strength of
(Hislop & Reid 1974). The air–blood barrier first the expiratory muscles. Thus if children or young
appears at week 19 and towards the end of this period, adults are hugged at the end of a forced expiration,
surfactant synthesis begins. more air can be expelled. After the age of 25 years, RV
is determined by premature airway closure and the
Terminal Sac Period (Week 24–Term) lungs cannot be emptied further.
Development of the pulmonary circulation continues The respiratory system reaches its peak in the third
and the respiratory bronchioles subdivide to form decade of life. Development of the lung continues
air spaces. Two different cell types (types I and II from birth until the end of adolescence and starts to
deteriorate after the age of 25 years. In the absence of of the chest. Increased ventilatory requirements have
disease there is sufficient reserve capacity to accom- to be met by increasing the respiratory rate rather than
modate the requirements of old age. depth (Konno & Mead 1967).
After 25 years, the tissues become less elastic and
the lung elastic recoil diminishes. Exercise capacity, as Diaphragm
judged by oxygen consumption, shows a decline with The angle of insertion of the infant diaphragm is hori-
age but it can be retarded by regular activity and accel- zontal compared with older children or adults, placing
erated by smoking or disease. it at a mechanical disadvantage. The infant diaphragm
has a lower relative muscle mass and a lower content
of high-endurance muscle fibres, and thus is much
RESPIRATORY SYSTEM: ANATOMICAL more vulnerable to fatigue.
AND PHYSIOLOGICAL DIFFERENCES Maximal diaphragmatic activity during severe res-
BETWEEN CHILDREN AND ADULTS piratory distress or respiratory obstruction leads to an
inward movement of the lower rib cage instead of a
The respiratory system in children differs significantly
downward movement of the diaphragm, as well as
from adults, both anatomically and physiologically.
intercostal and sternal recession (Muller & Bryan
These differences have important consequences for
1979). Despite these disadvantages, the diaphragm
the physiotherapy care of children in terms of respi-
is the main muscle of inspiration in the infant, since
ratory assessment, treatment and choice of techniques.
the intercostals are poorly developed. Ventilation in
Whereas the main reason for adult hospital emergency
the infant is also more affected by impaired diaphrag-
admissions is cardiac failure, the principal reason for
matic function, for example by abdominal distension,
hospital admissions in children aged 0–4 years is res-
hepatomegaly or phrenic nerve damage.
piratory illness. The principles of adult cardiorespira-
tory physiotherapy management cannot be transposed Preferential Nasal Breathing
directly to an infant with pulmonary pathology.
The shape and orientation of head and neck in babies
(large head, prominent occiput, short neck, large
Anatomical Differences in the Respiratory
tongue, smaller retracted lower jaw, high larynx) mean
System between Children and Adults
that the airway is prone to obstruction in young
Rib Cage and Chest Shape infants. Young infants up to about 6 months of age are
The cross-sectional shape of the infant thorax is cylin- preferential nasal breathers and studies suggest that up
drical and not elliptical as in adolescents or adults. The to half of all neonates are unable to breathe through
ribs of the newborn infant are relatively soft and car- their mouths, except when crying, for the first few
tilaginous compared with the more rigid chest wall of weeks of life (King & Booker 2004). The small nasal
older children and adults. They are also placed hori- passages account for between 30% and 50% of the
zontally in relation to the sternum and vertebral total airway resistance in neonates. The narrowest
column compared with the more oblique rib angle of portion of the nasal airway has a cross-sectional area
adults. The bucket handle rib movement seen in older of about 20 mm2. Therefore even a small amount of
children and adults is therefore not possible. As the swelling or obstruction of the nasal passages of infants
infant grows, and begins to develop an upright posture, compromises breathing considerably and causes a dis-
the ribs develop a more oblique angle and the trans- proportionate and detrimental effect on the work of
verse diameter of the rib cage increases. The adult breathing. Some young infants with upper respiratory
chest shape is achieved by 3 years of age (Openshaw tract infections and partial obstruction of their nasal
et al 1984). passages can develop respiratory distress.
The intercostal muscles are poorly developed in
infancy and contraction of the intercostal muscles is Position of Larynx
inefficient at improving thoracic volumes either by In the newborn infant, the larynx and hyoid cartilage
increasing the anteroposterior or transverse diameters are higher in the neck and closer to the base of the
epiglottis, being at the level of C3 in a premature infant smaller, more distal airways do not increase in diam-
and C4 in a child compared with C5–C6 in the adult. eter until nearer 5 years of age. This higher peripheral
The larynx descends with age, but its high position airways resistance is exacerbated by respiratory
enables the infant to feed and breathe simultaneously infections, which cause inflammation of the airways,
for approximately the first 4 months of age. for example in bronchiolitis, or in the presence of
This high position also provides some protection of secretions.
the airway in infants younger than 4–6 months because
it acts as a valve, which helps keep food in the mouth Bronchial Walls
until the pharyngeal swallow is initiated. The airway The bronchial walls are supported by cartilage,
has less anatomical protection, as the larynx assumes which begins to develop from 12 weeks’ gestation and
its lower position in the neck and is not as directly continues throughout childhood. The cartilaginous
protected by the epiglottis. Then, poor closure of the support of an infant’s airways is much thinner than
airway or partial paralysis of the vocal folds may that of an adult, and predisposes the airways to col-
become more evident and coughing, choking or aspi- lapse. However the bronchial walls contain propor-
ration may occur. tionally more cartilage, connective tissue and mucous
glands than do those of adults, but less smooth muscle;
Airway Diameter this makes the lung tissue less compliant. The lack of
The neonatal trachea is short (4–9 cm) and directed bronchial smooth muscle, particularly in the smaller
downward and posteriorly. The diameter of the trachea bronchioles, may be one reason for the lack of response
in the newborn is 4–5 mm and the diameter of an to bronchodilators under the age of 12 months. The
infant trachea is only about one-third that of an adult. β-receptors in infants are also immature, which further
This makes respiratory resistance higher and the work reduces any response to β-adrenergic bronchodilator
of breathing greater. Since the resistance to airflow therapy (Reid 1984). The high proportion of mucous
through a tube is directly related to the tube length and glands in the major bronchi of infants makes the
inversely related to the fourth power of the radius of airways more susceptible to mucus obstruction.
the tube, halving the radius of the trachea will increase
its resistance (reduce flow) 16 times. Tracheal swelling Cilia
as a result of endotracheal intubation or suction can At birth the cilia are poorly developed, which increases
therefore dramatically increase resistance to breathing. the risk of secretion retention, especially in the prema-
These factors give the lungs less reserve, so that a well- ture infant. The airway obstruction caused by secre-
oxygenated infant with upper airway obstruction can tions in a neonate is much greater than in an adult
become cyanotic in a matter of seconds. whose airways are relatively large.
In contrast to adolescents and adults, the narrowest
part of the infant’s airway is not the vocal cords, but Alveoli and Surfactant
the cricoid ring. Thus an uncuffed endotracheal tube The respiratory system is not fully developed at birth,
provides a larger internal diameter compared with a even in the term neonate, and postnatal maturation
cuffed tube and in children will successfully seal against continues for a significant time. Although by 20–27
in the circular subglottic ring. However, the inflexible weeks’ gestation lung acinar have formed, several types
cricoid ring also leaves children more vulnerable to of epithelial cells can be differentiated, and the air–
mucosal oedema and post-extubation stridor. The blood barrier is thin enough to support gas exchange;
right main bronchus is less angled than the left, making true alveoli develop only after about 36 weeks’ gesta-
right mainstem intubation more likely. tion. A term newborn has an average of 150 million
At birth there is no further increase in the number alveoli. The remainder of the eventual average of 400
of airways formed, but there is growth and develop- million alveoli develop after birth, the vast majority
ment in their size. In the first few years of life, there is within the first 2 years of life. Both the number and
a significant increase in the diameter of the larger, size of alveoli continue to increase postnatally until the
more proximal airways (Hislop & Reid 1974). The chest wall stops growing. By 4 years of age, the adult
number of 300 million may exist, although growth can achieved by a network of interconnecting pathways
continue until 7 years of age. The smaller alveolar size linking different structures. Respiratory bronchioles
of an infant makes the infant more susceptible to alve- are linked by channels of Martin. Canals of Lambert
olar collapse, and the smaller number of alveoli reduces connect respiratory and terminal bronchioles with
the area available for gaseous exchange (Reid 1984). alveoli and their ducts; and adjacent alveoli are joined
Pulmonary surfactant is a mixture of phospholipids by openings in the alveolar wall, called ‘pores of Kohn’
(90%) and apoproteins (10%), which act to reduce (Menkes & Traystman 1977). However, none of these
surface tension at the air–liquid interface in the alveo- pathways exists at birth. The pores of Kohn develop
lus, thereby preventing collapse of lung parenchyma at between years 1 and 2, and the canals of Lambert do
the end of expiration. Type II alveolar cells synthesize not appear until about 6 years of age. The collateral
and secrete surfactant from 23 to 24 weeks’ gestation. ventilatory channels between alveoli, respiratory bron-
In preterm newborns, a deficiency of surfactant is a chioles and terminal bronchioles are poorly developed
major factor in the development of neonatal respira- until 2–3 years of age, predisposing towards alveolar
tory distress syndrome (RDS). Male gender is a risk collapse.
factor for neonatal RDS, bronchopulmonary dysplasia
(BPD) and mortality. Boys with neonatal RDS seem to Internal Organs and Lymphatic Tissue
have more health problems than girls during the neo- The lymphatic tissue (adenoids and tonsils) may be
natal period. enlarged in the infant and the tongue is also relatively
large. These factors may contribute to upper airway
Collateral Ventilation obstruction. The heart and other organs are also rela-
Collateral ventilation is the means by which a distal tively large in infants, leaving less space for lung expan-
lung unit can be ventilated, despite blockage of sion. The heart can occupy up to half the transverse
its main airway. Collateral ventilatory pathways are diameter of the chest in chest radiographs (Fig. 1-19).
FIGURE 1-19 ■ Normal chest radiograph in a newborn.
Height and Exposure to Air Pollution expiration) is known as the CC. In the adult, CC
Because children breathe more rapidly compared with usually occurs within FRC, i.e. the volume of gas left
adults and because they spend more time outdoors in the lungs following tidal expiration, whereas in the
being physically active, they tend to be more exposed infant it is greater than FRC and can occur during tidal
to outdoor air pollution and allergens than do adults breathing. The higher closing volumes apparent in
and have greater deposition of particulate matter. infants are due to greater chest wall compliance and
Their reduced height means they are also more exposed reduced elastic recoil of the lungs than in the adult.
to vehicle exhausts and heavier pollutants that concen- Therefore airway closure may occur before the end of
trate at lower levels in the air. There is substantial expiration, e.g. during expiratory chest vibrations,
evidence linking air pollution with respiratory health putting the infant at a much greater risk of developing
problems and children are more vulnerable (Brauer et widespread atelectasis, especially in the presence of
al 2007, Pénard-Morand et al 2005). lung disease, where lung volume is further reduced. In
the event of respiratory distress, the infant grunts on
expiration, adducting the vocal cords in an attempt to
Physiological Differences in the Respiratory
reduce the amount of gas expired, thus maintaining a
System between Children and Adults
higher FRC and minimizing alveolar collapse (Pang &
Respiratory Compliance Mellins 1975). Re-inflation of alveoli, once collapsed,
Respiratory compliance is a measure of the pressure is more difficult in the infant, who has to work con-
required to increase the volume of air in the lungs and siderably harder to overcome the effects of the compli-
reflects a combination of lung and chest wall compliant chest wall.
ance. The lung compliance of a child is comparable to
that of an adult, being directly proportional to the Ventilation and Perfusion
child’s size. However, compliance is reduced in the In the adult, both ventilation and perfusion are pref-
infant because of the high proportion of cartilage in erentially distributed to the dependent lung. The best
the airways. The premature infant, who lacks sur- gas exchange and V /Q match will therefore be in the
factant, demonstrates a further significant decrease dependent region of the lung (Zack et al 1974). In the
in compliance. The chest wall of an infant is cartilagi- infant, however, ventilation is preferentially distrib-
nous and therefore very soft and compliant in com- uted to the uppermost lung (Davies et al 1985),
parison with the more calcified and rigid adult whereas the perfusion remains best in the dependent
structure. The intercostal muscles are also less well regions. This leads to greater gas exchange in the
equipped to stabilize the rib cage during diaphrag- uppermost lung (Heaf et al 1983), but an imbalance
matic contraction. Neonates therefore have an imbal- between ventilation and perfusion (Bhuyan et al 1989).
ance between a relatively low outward recoil of their In acutely ill children with unilateral lung disease, oxy-
chest wall and normal inward elastic recoil, which genation may be optimized by placing the ‘good’ lung
means that they are prone to airway collapse. An uppermost. However, this is contrary to the goal of
awake, spontaneously breathing neonate will maintain improving ventilation to the diseased lung and facili-
its FRC by active measures including laryngeal braking, tating secretion clearance, in which positioning and
the initiation of inspiration before the end of passive postural drainage would require the diseased lung to
expiration (intrinsic PEEP) and persistent inspiratory be uppermost. The therapist would have to balance
muscle activity throughout the respiratory cycle. These their decision based on the stability, tolerance and
active mechanisms are lost during anaesthesia and current therapeutic priorities.
result in a fall in FRC, airway closure, atelectasis and The difference in ventilation distribution between
V /Q mismatch. infants and adults is most likely due to the more com-
pliant rib cage of the infant, which compresses the
Closing Volume dependent areas of lung. In addition, while in the adult
The closing volume is the lung volume at which closure the weight of the abdominal contents provides a pref-
of the small airways occurs. This volume plus the RV erential load on the dependent diaphragm and there-
(the volume of gas left in the lungs following maximum fore improves its contractility, in the infant this does
not happen. The effect on both hemidiaphragms is Muscle Fatigue

similar, due to the abdomen being so much smaller The respiratory muscles of infants tire more quickly
and narrower (Davies et al 1985). It has been shown than those of adults due to a much smaller proportion
in adults that, when the diaphragm is inactivated, e.g. of fatigue-resistant muscle fibre (Keens & Ianuzzo
when ventilated under anaesthetic, the ventilation dis- 1979). There are two main muscle fibre types, type I
tribution changes to that of an infant (Rehder et al and type II. Type I muscle fibres are slow twitch, high
1972). It is not yet known exactly when the ventilation oxidative and slow to fatigue. Type II fibres are fast
distribution in the infant changes to that of an adult, twitch, slow oxidative and tire quickly. Of the muscle
but it is likely to be variable and dependent on lung fibres in the adult diaphragm, 55% are type I com-
health and musculoskeletal maturity. pared with only 30% in the infant. Premature infants
tire even more easily as, at 24 weeks’ gestation, only
Oxygen Consumption, Cardiac Output and
10% of their muscle fibres are fatigue resistant (Muller
Response to Hypoxia
& Bryan 1979). Excessive muscle fatigue results in
Infants have a higher resting metabolic rate than adults apnoea. By 12 months of age the number of type I
and consequently have a higher oxygen requirement. fibres equals that of an adult.
Children have a higher SV and oxygen consumption
per kilogram than adults; in infants this may exceed Breathing Pattern and Rapid Eye Movement Sleep
6 mL/kg min−1, twice that of adults. They support this
higher output with a higher baseline heart rate (HR) Irregular breathing patterns and episodes of apnoea
but lower blood pressure than adults. are relatively common in neonates, especially if pre-
Neonatal myocardium has a large supply of mito- mature, and are related to immature cardiorespiratory
chondria, nuclei and endoplasmic reticulum to support control. Short spells of apnoea can be considered
cell growth and protein synthesis, but these are non- normal in these circumstances, but need careful moni-
contractile tissues, which render the myocardium stiff toring as they may reflect hypoxic conditions.
and non-compliant. This may impair filling of the left During rapid eye movement (REM) sleep there is a
ventricle and limit the ability to increase the SV by reduction in postural tone and tonic inhibition of the
increasing stroke volume (SV) (Frank Starling mecha- infant’s intercostal muscles such that the rib cage is
nism). SV in infants is therefore relatively fixed and the even less well equipped to counteract the contraction
only way of increasing SV is by increasing HR. of the diaphragm during inspiration (Muller & Bryan
The SNS is not well developed, predisposing the 1979). This reduces the efficiency of respiration, causes
neonatal heart to bradycardia. An infant responds to a drop in FRC and increases the work of breathing,
hypoxia with bradycardia and pulmonary vasocon- predisposing the infant to apnoeic episodes (Muller &
striction, whereas the adult becomes tachycardic with Bryan 1979). The premature infant is most at risk,
systemic vasodilatation. The bradycardic response in spending up to 20 hours a day asleep, 80% of which
infants is probably due to myocardial hypoxia and aci- may be in active REM sleep compared with 20% in
dosis, but leads to an immediate reduction in SV and adult sleep.
the development of further hypoxia.
Although anatomical closure of the foramen ovale Response to Cold
can occur as early as 3 months of age, the channel Paediatric patients have an increased surface area per
remains ‘probe patent’ in 50% of children up to 5 years kilogram of body weight and lose heat to the environ-
of age, and persists in about 30% of adults. Similarly, ment more readily than adults. This is compounded
anatomical closure of the ductus arteriosus usually by cold intravenous fluids, dry anaesthetic gases and
occurs between 4 and 8 weeks of age. Any stimulus, exposure. Non-shivering thermogenesis in brown
such as hypoxia or acidosis, that causes an increase in adipose tissue is the major mechanism of heat produc-
pulmonary vascular resistance during the neonatal tion during the first few months of life. Brown fat is
period may allow these two potential channels to specialized tissue located in the posterior of the neck,
reopen, resulting in right-to-left shunting and increas- along the interscapular and vertebral areas, and sur-
ing hypoxia (King & Booker 2004). rounding the kidneys and adrenal glands. Metabolic
heat production can increase up to two and a half The heart has four chambers: the right and left atria
times during cold stress. Shivering is a less economical superiorly and the right and left ventricles inferiorly.
form of heat production but does occur in severely The atria are the receiving chambers of the heart and
hypothermic neonates. Hypothermia is a serious the larger ventricles are the pumping chambers.
problem that can result in increased oxygen consump- In healthy individuals, blood cannot mix between
tion, cardiac irritability and respiratory depression the right and left sides of the heart. This is due to the
(King & Booker 2004). presence of a dividing wall between the two atria
(interatrial septum) and the two ventricles (interven-
tricular septum).
INTRODUCTION TO CARDIAC
The right atrium receives deoxygenated blood from
ANATOMY AND PHYSIOLOGY
the body via the superior and inferior vena cava. The
The heart is a roughly cone-shaped organ which is blood then passes through the right tricuspid (or atrio
about the size of a fist. It lies diagonally between ventricular (AV)) valve into the right ventricle. It then
the lungs in the mediastinum, so that the wider passes through the pulmonary valve into the pulmo-
upper portion (base) of the heart points towards the nary artery and lungs (pulmonary circulation).
right shoulder and the lower tip of the heart (apex) The left atrium receives oxygenated blood from the
points towards the left hip and rests on the diaphragm. lungs via the pulmonary veins. Blood then passes
The major blood vessels of the body emerge from through the left AV (or mitral) valve into the left ven-
the base. tricle. It then goes through the aortic valve into the
The heart pumps blood around the body in order aorta to be circulated around the body (systemic
to provide cells with the oxygen and nutrients that are circulation).
required for metabolism. The right side of the heart The atria are much smaller and thinner walled then
receives deoxygenated blood from the body and pumps the ventricles. This is because the atria only have to
it through the lungs in order for gas exchange to take squeeze blood into the adjoining ventricle, whereas the
place. The left side of the heart receives oxygenated ventricles have to pump blood through the lungs
blood from the lungs and pumps it around the body. (right ventricle) or around the body (left ventricle).
Blood vessels that take blood away from the heart are The left ventricle is thicker walled than the right ven-
called ‘arteries’ and blood vessels that bring blood back tricle as it has to be more powerful in order to pump
to the heart are called ‘veins’ (Fig. 1-20). blood around the systemic circulation.
Left common
carotid artery Left subclavian
Brachiocephalic artery
trunk Aorta
Superior Left pulmonary

vena cava arteries
Right pulmonary
arteries Left pulmonary
Right pulmonary veins
veins Left atrium
Right atrium Atrioventricular
(mitral-bicuspid)
Coronary sinus valve
Atrioventricular Aortic (semilunar)
(tricuspid) valve valve
Right ventricle Left ventricle
Inferior Pulmonary
vena cava (semilunar) valve
Septum
FIGURE 1-20 ■ Internal view of the heart.
Layers of the Heart Wall The pulmonary and aortic valves sit at the bases of
The heart is surrounded by a double walled sac called the pulmonary artery and aorta, respectively. They are
the pericardium. The outer layer of the pericardium is called ‘semilunar valves (half moon)’, as they each have
made up of tough fibrous connective tissue and is three crescent shaped cusps. They prevent backflow
called the fibrous pericardium. This protects the heart, from the great arteries into the ventricles.
prevents overfilling and anchors it to surrounding
Coronary Circulation
structures including the central tendon of the dia-
phragm. This attachment to the diaphragm explains The blood supply to the heart is provided by the coro-
why hyperinflated lungs and a flattened diaphragm nary arteries. The right and left coronary arteries arise
will result in a thin, elongated heart on chest radio- from the base of the aorta. The left coronary has two
graph. The inner layer of the pericardium is the main branches, which are the left anterior descending
serous pericardium, which consists of two layers: the artery and the circumflex artery. The right coronary
parietal pericardium and the visceral pericardium. artery’s main branches are the right marginal artery
The parietal pericardium lines the internal surface of and the posterior descending artery (Fig. 1-21).
the fibrous pericardium. The visceral pericardium is The coronary arteries are superficial as they are
fused to the external layer of the heart wall, and is also located in the epicardium, before sending branches
known as the epicardium. There is a potential space deeper into the myocardium. This means they are rela-
between the parietal and visceral layers of the serous tively easily isolated for coronary artery bypass graft
pericardium and this is called the ‘pericardial cavity’. surgery. Blood flow to the myocardium occurs when
This cavity contains serous pericardial fluid which the heart is relaxed as the blood vessels within the
lubricates and creates a frictionless environment. It myocardium become compressed when the heart is
allows the parietal and visceral pericardial membranes contracting.
to glide over one another as the heart beats. An increase The coronary veins empty deoxygenated blood into
in pericardial fluid will compress the heart and impair the coronary sinus, which is located in the right atrium.
its ability to pump (cardiac tamponade).
Cardiac Cycle
The heart wall is made up of three layers: the epi-
cardium, the myocardium and the endocardium. The When the heart contracts it is termed ‘systole’ and
epicardium is the outer layer and is the visceral peri- when it relaxes it is termed ‘diastole’. Both atria fill and
cardium. The bulkier myocardium is the middle layer contract together and both ventricles fill and contract
and is mostly composed of cardiac muscle. The endo- together in sequence. The cardiac cycle refers to the
cardium makes up the inner lining of the heart. mechanical events that occur with the flow of blood
through the heart in one heartbeat. These mechanical
Heart Valves events are preceded by electrical activity discussed
Heart valves ensure that blood flows in one direction below.
(from atria to ventricles to arteries). The heart valves Early diastole: The whole heart is relaxed and the
open and close as a result of pressure differences on pulmonary and aortic valves are shut. The AV valves
either side of the valve. When pressure is greater (tricuspid and mitral) are open and blood is flowing
behind the valve, the leaflets open and blood flows passively from the great veins (superior and inferior
through the valve. When pressure is greater in front of vena cavae and the pulmonary vein) through the atria
the valve, the leaflets shut. into the ventricles.
The right AV valve has three leaflets or cusps and is Atrial systole: Following atrial depolarization (P
called the tricuspid valve (remember that the tRIcus- wave), the atria contract forcing blood into the ventri-
pid valve is on the RIght). The left AV valve has two cles. This maximizes the volume of blood in the ven-
cusps and is a bicuspid valve. It is also known as the tricles (end-diastolic volume). The atria now relax.
mitral valve because it resembles the shape of a bish- Isovolumetric contraction: Following ventricular
op’s mitre. When the ventricles contract the valves shut depolarization (QRS complex) the ventricles contract
preventing backflow (regurgitation) into the atria. causing ventricular pressure to rise and the AV valves
Left pulmonary
Aorta artery
Superior Left coronary
vena cava artery
Right Left pulmonary
atrium veins
Right Left atrium
coronary Left circumflex
artery artery
Right Left marginal
marginal artery
artery Left anterior
descending (or
Posterior
interventricular)
descending
artery
artery
Left
Right ventricle
ventricle
Diagonal
branch
FIGURE 1-21 ■ Arterial blood supply to cardiac muscle.
to shut. The aortic and pulmonary valves are still shut Electrical Conductivity of the Heart
at this point, so this contraction does not bring about The heart’s muscle is made of specialized tissue and its
any change in volume. ability to pump is controlled by an electrical conduc-
Ventricular ejection: As the pressure in the ventri- tion system that synchronizes the contraction of the
cles continues to rise, the aortic and pulmonary valves heart chambers (Fig. 1-22). This ensures coordinated
are forced open and blood is rapidly ejected into the blood flow through the cardiac cycle to provide suffi-
great arteries (pulmonary artery and aorta). While the cient SV to maintain blood pressure and oxygen deliv-
ventricles are in systole, the atria are in diastole and ery to the body (Levick 2010).
filling with blood. An electrical stimulus is generated by the sino-atrial
Isovolumetric relaxation: Following ventricular (SA) node or ‘cardiac pacemaker’. This is a collection
repolarization (T wave), the ventricles relax and ven- of specialized tissue located in the right atrium that
tricular pressure drops. Blood in the aorta and pulmo- spontaneously generates an electrical stimulus 60–100
nary artery starts to flow back towards the heart times per minute. The wave of electrical activity gener-
causing the aortic and pulmonary valves to shut. ated by the SA node spreads through the right and
As the atria continue to fill, pressure on the atrial left atria at a rate of 0.5 m/sec, initiating depolariza-
side of the AV valves will become greater than on the tion and contraction of both atria, which pushes
ventricular side and so the AV valves will open allow- blood through the open valves in to the corresponding
ing ventricular filling to begin once more. ventricles
Heart Sounds ■ right atrium via tricuspid valve to right

ventricle
The heart sounds heard on auscultation are commonly
■ left atrium via bicuspid (mitral) valve to left
termed ‘lub dup’. This relates to the sound of the heart
ventricle.
valves closing. The first sound (lub) is the sound of the
AV valves closing. The second sound (dup) is created The electrical impulse travels to the AV node, where
by the closing of the semilunar valves (pulmonary and it is slowed down to 0.05 m/sec (AV delay) to allow
aortic valves). sufficient time for atrial contraction and ventricular
Sino-atrial
(SA) node Interatrial tract
(Bachmann bundle)
Right Left atrium
atrium
Atrioventricular
Anterior, middle bundle (Bundle
and posterior of His)
internodal tracts
Left
Posterior ventricle
internodal Conduction
tract myofibres
(Purkinje fibres)
Atrioventricular
(AV) node
Conduction
Right pathways
ventricle Left and right
bundle branches
FIGURE 1-22 ■ Electrical conductivity of the heart.
filling. The electrical impulse then continues via the R

right and left bundle of His and Purkinje fibres, which
10 mm = 1 mV
cause ventricular depolarization and contraction.

■ Contraction of the right ventricle pushes blood P T
through the pulmonary valve through the lungs
for gas exchange.
Q S
■ Contraction of the left ventricle pushes blood
through the aortic valve into the systemic PR ST
circulation.
QT
Each contraction of the ventricles represents one
heartbeat. The atria contract a fraction of a second 0 0.2 0.4 0.6 0.8
before the ventricles so their blood empties into the Time (sec)
ventricles before the ventricles contract. FIGURE 1-23 ■ Typical electrocardiogram (ECG) trace.
Electrical Conductivity and

Electrocardiogram (ECG) P wave should not exceed 0.08 sec. An abnormally
The electrical conduction system of the heart can be wide P wave may be indicative of left atrial hypertro-
graphically represented on an ECG trace. The charac- phy, as it would take a longer period of time for the
teristic ‘P-QRS-T’ complex represents depolarization, impulse to travel through the larger atrial wall. The last
contraction and repolarization of the atria and ventri- part of the P wave is also flat, as the electrical impulse
cles (Fig. 1-23). is held at the AV node. Following AV delay, the spread
The P wave indicates that the atria are electrically of electrical activity through both ventricles produces
stimulated (depolarized) to pump blood into the ven- depolarization and contraction of the ventricles repre-
tricles. The first part of the P wave is flat and represents sented by the QRS complex.
electrical impulse generation by the SA node. As both ‘PR interval’ refers to the time taken for atrial depo-
atria depolarize and subsequently contract, a peak is larization and AV delay. A normal duration of PR
visible in the P-wave complex. The duration of the interval is 0.12–0.20 seconds. In situations where AV
delay is increased, such as heart block, the PR interval Physical factors such as level of physical activity and
may be lengthened. Conversely, PR interval may be core body temperature will lead to a change in HR,
shortened in situations where an impulse may arise secondary to ANS activation.
from the AV node itself, such as Wolff-Parkinson-
White syndrome. Blood Pressure
The QRS complex indicates that the ventricles are Blood pressure (BP) is defined as the pressure exerted
electrically stimulated (depolarized) to pump blood by blood against the tunica interna (inner wall) of an
out. Note the increased size of the peak in the QRS artery. This pressure ensures that blood flows through
complex, indicating a greater muscle mass and there- the body between heart beats and provides adequate
fore, an increased force of contraction from the ven- perfusion to maintain oxygen delivery.
tricular myocardium compared to the relatively smaller Blood pressure is maintained via several physiologi-
atria. The QRS complex should not exceed 0.12 cal variables.
seconds; a longer duration is indicative of abnormal ■ HR: beats per minute
conductivity in the ventricles. ■ SV: the volume of blood ejected from a ventricle
The ST segment indicates the amount of time from
per contraction
the end of the contraction of the ventricles to the ■ CO: the amount of blood ejected from a ven-
beginning of the T wave. The ST segment is displaced
tricle per minute (SV × HR)
or depressed in the presence of ischaemia and can ■ Total peripheral resistance (TPR): friction
become elevated following a myocardial infarction
encountered by blood as it passes through a
(MI). ECG changes may vary slightly depending on the
peripheral artery.
exact location of the MI.
T wave: As the ventricles relax and repolarization Blood pressure can be represented by the following
takes place the T-wave can be seen. The T wave may equation:
become inverted in the presence of ischaemia.
An electrical impulse initiated at the SA node, BP = SV × HR(CO) × TPR
which passes sequentially through the cardiac con-
Therefore a change in any of the contributing phys-
ducting system is described as ‘sinus rhythm’.
iological variables will lead to a change in BP.
Autonomic Regulation of Heart Rate Stroke Volume

The ANS regulates the electrical conductivity of the In an average human heart, SV is approximately
heart, adjusting HR in response to various stimuli. The 70 mL/beat. When greater SV is required (e.g. during
two branches of the ANS, the SNS (adrenergic system) exercise, stress or with increased core body tempera-
and the PNS (cholinergic system) work reciprocally, ture), SV can be increased by three methods:
meaning that as discharge from one branch increases, ■ Increased venous return (VR) (Frank Starling’s
discharge from the other decreases.
law)
Increased SNS activity will: ■ Frank Starling’s law states that SV increases in
■ increase HR via direct stimulation to the SA node response to an increase in the volume of blood
(chronotropy) or the AV node (dromotropy or filling the heart.
conduction velocity) and the myocardium ■ Increased blood filling produces a stretch
■ release catecholamines, adrenaline and noradren- to the cardiac muscle fibres producing an
aline, and will increase HR. enhanced force of contraction.
■ Increased blood filling occurs with increased
Increased PNS activity will:
VR.
■ decrease HR via direct stimulation (vagus nerve) ■ During exercise, increased activity of the
to the SA and AV nodes and the myocardium. skeletal muscle squeezes blood vessels and
■ release of acetylcholine will decrease HR. increases VR (pre-load).
■ Negative pressure generated by the respiratory of Blood Pressure). When BP is low, the kidneys release
muscles aids VR by ‘drawing’ blood towards an enzyme called ‘renin’ into the blood. The presence
the heart from the lower limbs. of renin leads to a cascade of chemical reactions which
■ VR is also increased via SNS stimulation, convert the inert ‘angiotensin I’ to ‘angiotensin II’.
causing a small degree of vasoconstriction. Angiotensin II is a potent vasoconstrictor, which
■ Increased VR = increased volume of blood when activated leads to an increase in TPR and subse-
filling the heart and increased SV. quently, an increase in BP. Additionally, angiotensin I
■ Reduced after-load also stimulates the adrenal cortex to release a substance
■ After load is the pressure the ventricle must called ‘aldosterone’. Aldosterone is a steroid hormone
overcome to eject blood. released from the adrenal cortex, which increases
■ After-load for the right ventricle is the pres- sodium ion (Na+) reabsorption and potassium (K+)
sure in the pulmonary circulation (pulmonary excretion by the kidneys; the presence of increased
artery pressure) and for the left ventricle is blood Na+ concentration leads to increased movement
pressure in the aorta (systemic BP). of water (via osmosis), increasing blood volume and
■ Additionally, if after-load is reduced (i.e. therefore, VR and pre-load. Increased blood volume
vasodilatation), for any given volume of blood improves contractility via Frank Starling’s law of the
in a ventricle, more SV can be ejected. heart.
■ Increased contractility of the ventricle (inotropy) Other factors which influence TPR are:
■ Cardiac muscle has the ability to increase
■ temperature
the force of its contraction irrespective of ■ When the body’s core temperature is reduced
the volume of blood filling; this is called’
peripheral vasoconstriction may occur. Con-
inotropy’.
versely, an increased core temperature leads to
■ Inotropy occurs secondary to SNS activation
vasodilatation.
and SNS-induced release of catecholamines ■ chemicals
(from adrenal medulla), directly affecting the ■ Substances such as nicotine (vasoconstriction,
muscle fibres of the myocardium.
increased BP) and alcohol (vasodilatation,
■ SNS activation also leads to an increased
decreased BP) have an effect on the calibre of
release of calcium ions (Ca+), in a process
blood vessels and therefore BP.
called ‘calcium-induced calcium release ■ diet
(CICR)’. CICR leads to increased cross-bridge ■ In general, a diet high in salt, saturated
formation and therefore, an enhanced force of
fat and cholesterol adversely affects blood
contraction and increased SV.
vessel calibre (narrows) and blood volume
(increases), leading to increased BP.
Total Peripheral Resistance
In health, TPR is held in a mild state of vasoconstric- Auto Regulation of Blood Pressure
tion; from this baseline, TPR can be increased second-
BP is monitored and regulated by pressure receptors
ary to vasoconstriction or decreased secondary to
called ‘baroreceptors’, which are located in pressure
vasodilatation of blood vessels to ensure BP is ade-
receptor zones.
quate to maintain homoeostasis. TPR alteration pre-
dominantly occurs via SNS activation, controlled by ■ high-pressure zones, e.g. carotid sinuses (bilater-
the vasomotor centre in the medulla oblongata in the ally) and the aortic arch
brainstem. ■ low-pressure areas, e.g. the venae cavae, pulmo-
nary veins and both atria.
Renal System Baroreceptors send signals to the medulla of the
The renal system has an important role in the regula- brain stem, where ANS stimulation leads to the adjust-
tion of TPR and BP as a whole (see Auto Regulation ment of mean arterial pressure by altering both the
force and speed of the heart’s contractions, as well as King, H., Booker, P.D., 2004. General principles of neonatal anaes-
the TPR to maintain homoeostasis. thesia. Curr. Anaesth. Crit. Care 15, 302–308.
Konno, K., Mead, J., 1967. Measurement of the separate volume
The renal system aids the long-term regulation of changes of rib cage and abdomen during breathing. J. Appl.
BP by altering TPR and blood volume. If blood volume Physiol. 22, 407–422.
is low, specialized cells in the hypothalamus are stimu- Langman, J., 1977. Medical Embryology. Williams and Wilkins,
lated and trigger the release of antidiuretic hormone Baltimore.
(ADH) from the pituitary gland. Release of ADH Levick, J.R., 2010. An Introduction to Cardiovascular Physiology,
fifth ed. Hodder Arnold, London.
affects the renal collecting ducts and causes increased Marieb, Elaine N., Hoehn, Katja, 2013. Human Anatomy and Physi-
reabsorption of water (i.e. less urine is produced) to ology, ninth ed. Pearson, Harlow, England.
increase blood volume, VR and pre-load. Conversely, Menkes, H.A., Traystman, R.J., 1977. Collateral ventilation. Am. Rev.
if blood volume is high, the kidneys will excrete more Respir. Dis. 116, 287–309.
water, producing dilute urine to reduce blood volume, Muller, N.L., Bryan, A.C., 1979. Chest wall mechanics and res-
piratory muscles in infants. Pediatr. Clin. North Am. 26 (3),
VR and pre-load. 503–516.
Ochs, M., Nyengaard, J., Jung, A., et al., 2004. Number of alveoli in
the human lung. Am. J. Respir. Crit. Care Med. 169, 120–124.
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posture on the distribution of pulmonary ventilation and per- Palastanga, N., Soames, R.W., 2012. Anatomy and Human Move-
fusion in children and adults. Thorax 44, 480–484. ment: Structure and Function: Structure and Function, sixth ed.
Brauer, M., Hoek, G., Smit, H.A., et al., 2007. Air pollution and Churchill Livingstone, London, UK.
development of asthma, allergy and infections in a birth cohort. Pang, L.M., Mellins, R.B., 1975. Neonatal cardiorespiratory physiol-
Comment in Eur. Respir. J. 29 (5), 825–826. ogy. Anesthesiology 43 (2), 171–196.
Davies, H., Kitchman, R., Gordon, G., Helms, P., 1985. Regional Pénard-Morand, C., Charpin, D., Raherison, C., et al., 2005. Long-
ventilation in infancy: reversal of the adult pattern. NEJM 313, term exposure to background air pollution related to respiratory
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Heaf, D.P., Helms, P., Gordon, I., Turner, H.M., 1983. Postural effects Shneerson, J., 1988. Disorders of Ventilation. Blackwell Science,
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ANATOMY AND PHYSIOLOGY

OF THE RESPIRATORY AND

Aqueous (Sol) Layer 15 Spinal Cord Reflexes 21

Factors Affecting Lung Volumes 23 Carbon Dioxide Transport 33

prised of four stages: ventilation, external respiration,

FIGURE 1-1 ■ The upper respiratory tract.

which serves to slow airflow. This allows time for

bronchus Left main

FIGURE 1-2 ■ The bronchial tree.

Diameter Cross-sectional Glands

Trachea 0 15-22 1 2.5

24 0.3 300 000 000- >1 000 000

FIGURE 1-3 ■ Conducting and respiratory zones.

Right lung Left lung

Medial basal (S7) 7

Posterior basal (S10)

Left lung Right lung

Superior Apico- T Apical (S1)

Right lung Left lung Upper lobe

Upper lobe Right lung Left lung Upper lobe

Apical pleura Parietal pleura

mid-axillary line and ends anteriorly at the level of the

from the abdomen. It is a large, dome-shaped muscle

Muscles of inspiration Muscles of expiration

Intercostals muscles of inspiration can be a sign of respiratory

respiratory pressure is greater than atmospheric pres-

atmospheric pressure (mmHg)

Direction of particle movement

MUCOCILIARY TRANSPORT SYSTEM The ultrastructure of cilia is extremely complex.

Site of Highest Resistance

reduce airflow to 116 th of normal. ■ speaking in half sentences

Respiratory diseases characterised by increased ■ breathlessness

airflow and cause airflow limitation. Airway calibre (PaCO2).

Extra-luminal pathology may include: Problems Associated with Airflow Limitation

■ anti-inflammatory agents lung compliance makes the generation of a large pres-

RESPIRATORY COMPLIANCE ■ reduced pulmonary surfactant

ration more difficult. Respiratory disease characterized Pulmonary Surfactant

by poor lung compliance and increased work of CONTROL OF BREATHING

■ supine position tory centres. Interaction of activity from these two

becomes inadequate, ultimately resulting in respira- ■ increases force of inspiration

tory failure. ■ regulates rhythm of inhalation and exhalation.

The effectors may fail in the presence of neuromuscu-

Respiratory control centres Irritant Receptors

FIGURE 1-12 ■ Respiratory control centres (RCCs) and Proprioceptors

Peripheral Chemoreceptors increase the frequency and depth of ventilation until

to combine with and ‘buffer’ free H+ ions in the CSF,

TABLE 1-1 of the thoracic cage which is more pronounced

volumes in order to increase gas exchange where

but in some cases both problems can co-exist. Spirom-

Tidal volume − anatomical dead space Alveolar hyperventilation is defined as excessive

Maintenance of VA is of paramount importance ■ altitude.

arterial blood (PaO2, PaCO2). In particular, there is an ■ ↓ PaCO2 (plasma concentration)

with PACO2 decreasing as VA increases. An alteration ■ ↑pH

in VA will lead to disruption of normal acid–base ■ respiratory alkalosis.

balance; both hypoxaemia and hypercapnia may occur

Blood flow from Alveolus

of blood flow can significantly increase (i.e. during ■ Q perfusion

RBC saturation with O2 to be achieved. Inadequacy of either V or Q will have a significant

exchange. sure gradient is generated as a net result of the ribs

of blood flow can significantly increase (i.e. during ■ Q perfusion

RBC saturation with O2 to be achieved. Inadequacy of either V or Q will have a significant

Diagnosis of V /Q Mismatch