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2015v1.0
HOUGH’S
Cardiorespiratory Care
For Elsevier
Senior Content Strategist: Rita Demetriou-Swanwick

Content Development Specialists: Joanna Collett and Katie Golsby
Project Manager: Joanna Souch
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Illustrator: MPS North America, LLC
Fifth Edition
HOUGH’S
Cardiorespiratory Care
an evidence-based, problem-solving approach
Alexandra Hough MSc, MCSP, DipTP

Respiratory physiotherapist and freelance lecturer
Edinburgh London New York Oxford Philadelphia St Louis Sydney Toronto 2018
© 2018 Elsevier Ltd. All rights reserved.
No part of this publication may be reproduced or transmitted in any form or by any means, electronic or
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This book and the individual contributions contained in it are protected under copyright by the Publisher
(other than as may be noted herein).
First edition © Chapman and Hall 1991

Second edition © Nelson Thornes 1996
Third edition © Cengage Learning 2001
Fourth edition © Cengage Learning 2014
Fifth edition © Elsevier Limited 2018
ISBN 978-0-7020-7184-3
eBook ISBN 978-0-7020-7527-8
Notices
Practitioners and researchers must always rely on their own experience and knowledge in evaluating and using
any information, methods, compounds or experiments described herein. Because of rapid advances in the
medical sciences, in particular, independent verification of diagnoses and drug dosages should be made. To the
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Printed in Italy
CONTENTS
Dedication, vi PART IV Physiotherapy for specific groups

Preface, vii of people
Acknowledgements, viii
Contributors list, ix 15 Infants, 337
About the author, x 16 Children, 365
17 Hyperventilation syndrome, 391
18 Elderly people with cardiorespiratory
PART I Physiology and pathology disease, 409
19 Palliative respiratory physiotherapy, 417
1 Physiological basis of clinical practice, 1
2 Assessment, 29
3 Respiratory disorders, 69 PART V Critical care
4 Cardiovascular disorders, 133
5 General management, 149 20 Critical care, support and monitoring, 431
21 Physiotherapy for critically ill patients, 477
22 Modifications for different disorders, 519
PART II Physiotherapy techniques
6 Physiotherapy to increase lung volume, 179 PART VI Does it work?
7 Physiotherapy to clear secretions, 199
8 Physiotherapy to decrease the work of 23 Evaluation of cardiorespiratory
breathing, 227 physiotherapy, 555
9 Pulmonary rehabilitation, 247
10 Physiotherapy for people with cardiovascular Glossary of abbreviations, definitions, symbols and
disorders, 269 values, 569
11 Cardiac rehabilitation, 277 Index, 579
PART III Surgery

12 Complications, 287
13 Physiotherapy for surgical patients, 295
14 Modifications for different types of surgery, 307
v
The book is dedicated to Veronica Bastow,
who has contributed much to humane and thoughtful respiratory care.
P R E FAC E
Good facts make good ethics. Each problem and disease also has a comprehensive list
Ashwal, 2013 of validated outcome measures. Clarity is assisted by
glossary terms highlighted throughout.
Cardiorespiratory care is an immensely satisfying The accompanying website contains full references, a
branch of physiotherapy. It challenges our intellect, bibliography, and appendices which include links and
exploits our handling skills and employs our humanity guidelines for professionals, handouts for patients and
to the full. The specialty is both art and science, but not extra case studies.
an exact science. Effectiveness depends on problem- Problem-solving requires thinking rather than expe-
solving, which requires evidence-based information, rience, hence the book is suited to physiotherapists from
provided here in the form of 5000 online references. student level to accomplished practitioner, whether they
Clinicians, students and educationists also expect work in acute or chronic settings, as well as specialist
integration of theory and practice, explanations that are respiratory nurses. The clinician will find here the
physiologically sound, and exact detail of technique. opportunity to achieve clarity of thought and develop
This book is written for such readers and for those who mastery in respiratory care.
question traditional assumptions. Clinical reasoning The fifth edition includes invaluable contributions
boxes in the text facilitate critical thinking, and case from specialists Alison Draper, Jo Sharp, Kath Ronchetti
studies at the end of each chapter aid problem-solving. and David McWilliams.
vii
AC K N OW L E D G E M E N T S
Profound thanks to the patients who have taught me much over the years. I am also indebted to
Paula Agostini and Anne Canby for their clinical expertise, Jodee Tame for her expert eye and
my editor Katie Golsby for her patience and acumen.
viii
CONTRIBUTORS LIST
Alison Draper, MCSP, MSc, Cert HE David McWilliams, BSc, MSc Kath Ronchetti, BSc (Hons) MCSP
Lecturer in Physiotherapy, Consultant Physiotherapist, Highly Specialist Paediatric
School of Health Sciences, Critical Care, Respiratory Physiotherapist,
University of Liverpool, Queen Elizabeth Hospital, Noah’s Ark Children’s Hospital for
Liverpool, UK Birmingham, UK Wales,
Cardiff, UK
Tammy Lea, BSc Paul Ritson, MSc, MCSP
Senior Physiotherapist, Clinical Specialist Physiotherapist in Jo Sharp, MCSP, MSc, MEd, Cert
Queen Elizabeth Hospital, Paediatric Critical Care, HE
Birmingham, UK Alder Hey Children’s NHS Foundation Senior Lecturer in Physiotherapy,
Trust, School of Health Sciences,
Liverpool, UK University of Liverpool,
Liverpool, UK
ix
A B O U T T H E AU T H O R
Alexandra Hough is a physiotherapy lecturer. She has taught in the Bahamas, Canada, Chile,
Denmark, Gibraltar, Greece, Ireland, Israel, Malta, Oman, Portugal, Singapore, South Africa and
around the UK. When not teaching, she works clinically in Eastbourne. She has also worked with
torture survivors who have developed hyperventilation syndrome. Her website www.alexhough.
com provides updated lists of references by topic.
The author’s royalties go to www.reprieve.org.uk.
x
PART I Physiology and Pathology
1
Physiological Basis of Clinical Practice
LEARNING OBJECTIVES
On completion of this chapter the reader should be able to: • use clinical reasoning to relate ventilation and
• understand how the cardiorespiratory system perfusion to clinical practice;
defends the body; • interpret arterial blood gases and apply them to a
• recognize how the control of breathing adapts to problem-based approach to treatment;
different situations; • recognize the adaptability of the cardiorespiratory
• understand the control of breathing and its relation system to different circumstances.
to the work of breathing;
OUTLINE
Defence, 1 Ventilation/perfusion ratio, 13
Control, 4 Arterial blood gases, 14
Mechanics, 5 The oxygen cascade, 19
Ventilation, 10 Variations, 21
Diffusion, 12 Case study: Ms LL, 26
Perfusion, 12 Clinical reasoning, 27
DEFENCE a swimming pool (Hanley & Tyler 1987). It is only by

means of a sophisticated biological barrier that the body
Imagine wearing your insides on the outside.
does not succumb to this onslaught.
British Lung Foundation
Defence against the outside world is based on a
The lung is an ‘outdoor’ organ that has to interact with network of reflexes, filters, secretions and specialized
the environment while facilitating ventilation. It is the cells. Physiotherapists treat patients whose defences
body’s primary route of infection (Waterer 2012). Every are breached when the nose is bypassed by mouth-
day, 500 million alveoli in the adult lungs (West 2016, breathing or an artificial airway, cilia are damaged by
p. 2) allow a surface area the size of a tennis court to be smoking or disease, and cough inhibited by pain or
exposed to a volume of air and pollutants that could fill weakness.
1
2 PART I Physiology and Pathology
Cortical, subcortical and brainstem neural control

Nose centres help coordinate breathing and swallowing
The nasal passages are the gatekeeper of the res- and ensure that swallowing is followed by exhala-
piratory tract, providing the first line of defence by tion, which further helps to prevent aspiration. This
means of: tight respiratory–swallowing coupling is compro-
• sensing suspicious smells mised by neurological impairment or hypercapnia
• sneezing in response to irritating substances (Nishino 2012).
• filtering large particles
• insulating against swings in temperature and Airways
humidity Inhaled irritant particles increase bronchoconstrictor
tone to narrow the airways. This is normally protective,
Oral Cavity but becomes exaggerated and counterproductive in
Between the lips and the junction of the hard and soft asthma, when it is called bronchospasm.
palates, there are over 700 species of microbe, whose Other particles are trapped on a layer of sticky mucus
purpose is to support the immune system (Gupta 2011). lining the airways from the nasopharynx to the terminal
They are harmful only if they reach sites to which they bronchi. This mucous blanket is gripped from under-
do not normally have access, with most hospital- neath by tiny hooks on the tips of hairlike cilia attached
acquired pneumonias being caused by endotracheal to the epithelium. These move ~100 mL mucus per day
tubes or nebulizers (Guggenbichler et al. 2011). up to the throat, from where it is swallowed or expecto-
rated (Dickson et al. 2016). This ‘mucociliary escalator’
Pharynx can cleanse the lungs in 20 min, moving particles at an
The pathways for air and food converge in the pharynx. average 1–2 cm/min, most rapidly in the trachea and
When a person chews, breathing continues through the decreasing with each airway generation as the total cross
nose, but during swallowing the pharynx can only deal section widens (Morris & Afifi 2010, p. 163).
with food and the airway is closed off. The cilia beat in a ‘sol’ layer of watery fluid, reaching
The nasopharynx exposes inspired and expired gas up to penetrate the ‘gel’ layer of mucus, hooking onto it
to a large surface area of highly vascular, moist mucous with the onward stroke and diving beneath it into the
membrane, delivering warmth and humidity to the sol layer on the recovery stroke at 20 beats/s (Fig. 1.1).
inspiratory breath and recovering a third of it on the Balanced systemic hydration keeps the fluid in the sol
expiratory breath (Richards et al. 1996). Its lymphoid layer the same height as the cilia. If the sol layer is too
tissue protects against inhaled antigens (Sepahi & deep or the cilia length shortened by smoking (Leopold
Salinas 2016). 2013), the hooks cannot reach the mucus. If the sol
The oropharynx extends from the mouth to the layer is too shallow, as in cystic fibrosis, mucus clogs up
tonsils. The tonsils are lymphoid tissue that defend the delicate cilia. Systemic hydration is relevant to
against foreign pathogens. Surgical removal of tonsils the gel layer because water constitutes 95% of respira-
and adenoids renders children more vulnerable to tory mucus and helps maintain mucociliary clearance
passive smoking (Chen et al. 1998). (Nakagawa et al. 2004).
The hypopharynx is responsible for the tricky Other protective functions of the mucus are insulat-
process of swallowing, for which 56 muscles are required ing, antibacterial action, and preventing the patient
to ensure airway protection while giving food the right from drying out (Button & Boucher 2008). Moisture in
of way (Higashijima 2010). inspired air helps maintain optimum ciliary beat fre-
The epiglottis is a leaflike lid which snaps shut over quency and acts as a buffer against extremes of tempera-
the larynx during swallowing to prevent aspiration ture because water requires four times more energy to
into the trachea. The functions of the larynx are primar- change temperature than air (Williams et al. 1996).
ily to elevate during swallowing to protect the airway, This finely coordinated mechanism is compromised
secondarily to stabilize the transition between inhala- by smoking, disease, age (Fig. 1.2), immobility, hypoxia,
tion and exhalation (p. 6), and only as an afterthought inflammation, dehydration and prolonged coughing,
to provide speech. which narrow the airways (Wanner et al. 1996).
CHAPTER 1 Physiological Basis of Clinical Practice 3
Airway lining Airway Airway lining Airway
Expired air
Onward stroke
Moisture Moisture
Recovery stroke
Heat
Heat
Moisture
Moisture
Inspired air
Sol layer Cilia Gel layer

FIGURE 1.1 The humidifying effects of nose breathing on inspiration (left) and expiration. (Modi-
fied from Why Humidification is Vital, Fisher & Paykel.)
ing the cilia (Kinnamon 2011). Traffic pollution evades

Tracheal mucociliary transport
12
10
many of these defences and has been linked to cardiores-
velocity (mm/min)
piratory disease as well as impaired brain development

8 in the young and cognitive decline in elders (Clifford
6 et al. 2016).
4 Inflammatory responses in the airway defend against
injury, infection and irritation by cells such as neutro-
2
phils and eosinophils. Failure to remove an inflamma-
0 tory stimulus can lead to chronic inflammation, resulting
s
in tissue injury caused by high numbers of these cells,

er
er
er
er
iti
ch
ok
ok
ok
ok
on
which is the basis of several chronic inflammatory

m
sm
ns
ns
-s
br
g
ex
no
no
cardiorespiratory diseases (Robb et al. 2016).

c
un
i
on
g
g
rly
Yo
un
un
hr
de
Yo
C
Yo
El
FIGURE 1.2 Mucous velocity with different ages and

KEY POINT
conditions. (From Wanner et al. 1996.)
Optimizing systemic hydration should be the first inter-
vention for people with sputum retention.
An extra function of the sol layer is its antimicrobial

property, without which inhaled bacteria could double Cough
in number every 20 min. Failure to clear excess mucus
A cough is only as effective as the deep breath pre-
may disable this chemical shield. An extra function of
ceding it.
the gel layer is to engulf particles as well as carry them
Sobush 2008
along on its surface (Knowles & Boucher 2002).
Airway epithelial cells contain pattern recognition The cough is a forced expulsive manoeuvre against a
receptors, which warn downstream immune cells of closed glottis and is the body’s strongest physiological
approaching bacteria. Further protection is afforded by reflex. It has been known to fracture brittle ribs, cause a
some interesting taste bud cells that have relocated to pneumothorax in an elderly male (O’Beirne et al. 2016)
the airway and respond to noxious particles by stimulat- and in extremis rupture the diaphragm (Reper et al.
2012). More usually, it can cause stress incontinence disease or if the glottis is bypassed by intubation or
(Luginbuehl et al. 2016), bronchospasm and sometimes tracheostomy.
exhaustion.
The protective function of coughing is to expel secre- Other Defences
tions and debris when mucociliary clearance is damaged, Pollutants that manage to reach the alveoli are met
as in bronchiectasis, or overwhelmed, as with some with scavenger macrophages and proteolytic enzymes
chest infections. Like swallowing and belching, it is that would be powerful enough to destroy the alveoli
subject to higher cortical control, either as cough inhibi- themselves if it were not for the presence of an inhibi-
tion or a voluntary cough. tor from the liver called α1-antitrypsin, lack of which
A reflex cough occurs if irritants stimulate inflamma- causes α1-antitrypsin deficiency (p. 73) and predis-
tory, chemical, mechanical or thermal receptors. These poses to HIV (human immunodeficiency virus) (Fer-
are located in the pleura, upper airways and, unexpect- reira et al. 2014). Pathogens that survive this still have
edly, the external auditory canal (Polverino 2012), as to overcome a barrage of inflammation, the main cul-
those who have Arnold’s nerve cough reflex (Ryan et al. prits being traffic pollution and tobacco (Jang et al.
2014) know when they clean their ears. In the airways, 2016). Asbestos particles circumvent all these defences
the receptors are most sensitive at the glottis and carina. because of their peculiar shape. The surface area of the
Vagal afferents then transmit the messages to the brain- lungs is decreased by up to 90% in advanced destruc-
stem, and the phrenic and spinal motor nerves transmit tive diseases such as emphysema and pulmonary fibro-
impulses to the respiratory musculature. Stimulation of sis, and the resulting concentration of microbes may
the pharynx causes a gag rather than a cough. explain the increased bacterial burden in these patients
A cough comprises: (Dickson et al. 2016).
• a deep inspiration to near total lung capacity; The function of the wafer-thin alveolar–capillary
• snapping shut of the glottis (which requires intact membrane is to allow efficient gas exchange, but this
bulbar function); also allows carbon monoxide and chemical warfare to
• a short pause to allow distribution of air past cause their mischief.
secretions; The entire blood volume passes through the lungs,
• sharp contraction of the expiratory muscles to create which help detoxify foreign substances that have made
intrathoracic pressures of at least 100 mmHg; it into the circulation. The pulmonary circulation also
• sudden opening of the epiglottis, exploding the performs a range of metabolic functions and acts as a
trapped gas outwards at up to 800 km/h (Polverino filter to help protect the systemic arterial system, par-
2012). ticularly the coronary and cerebral circulations, from
The resulting shear force overcomes viscous, frictional blood clots, fat cells, detached cancer cells, gas bubbles
and gravitational resistance so that secretions are cleared and other debris. Extracorporeal support systems such
from the upper airway, while deeper secretions are as cardiopulmonary bypass (p. 464) include a filter to
squeezed from the lower airway (Pitts et al. 2013). perform some of these functions.
Coughing is accompanied by violent swings in
pleural pressure, which cause dynamic airway com
pression (p. 7). This is initiated in the trachea during
CONTROL
the cough and extends peripherally as lung volume Breathing is the basic rhythm of life.
decreases, ensuring that the full length of the tracheo- Hippocrates
bronchial tree is involved. The airways normally reopen
with a subsequent deep breath, but for people unable to Breathing is under triple control: metabolic, emotional
take a deep breath, they stay closed for lengthy periods. and voluntary (Guyenet 2014). Metabolic control is
Coughing may be inhibited by pain, and the mechanism exquisitely sensitive and pH in the blood is maintained
is less efficient in some people with obstructive airways within precise limits despite unpredictable demands.
disease if they have poor expiratory flow or airways that Carbon dioxide (CO2) and oxygen are also controlled,
collapse on expiration. It is weakened with neurological but less tightly.
The respiratory centres comprise clusters of neurons MECHANICS

in the pons and medulla, which receive and integrate
stimuli from the rib cage, lungs, chemoreceptors and ‘The mechanics of respiration play a significant role
cortex. They then discharge impulses to the respiratory in posture and stabilization of the spine’.
muscles, triggering contraction. They also perceive and Dimitriadis 2016
respond to posture, coughing, hiccupping, defaecating,
stepping into a cold shower and the lactic acid produced The Respiratory Muscles
by intense exercise (de Souza 2010). Respiratory control The lungs are attached to each other medially by their
occurs at a subconscious level but can be overridden by roots, but do not directly touch any muscle. The chest
breathing exercises and modified by positive emotions wall comprises the rib cage and diaphragm, which
such as pleasure, love and relief, or negative emotions are expandable. The diaphragm contracts downwards
such as panic, pain and anxiety (Ramirez 2014). These against the abdominal contents, which are themselves
emotional and voluntary aspects of control facilitate the incompressible but can push out the abdominal wall,
modulation of breathing as an intervention for anxiety and the pelvic bowl, which is rigid. Other respiratory
(Paulus 2013). muscles extend from the mastoid process, tongue and
The control of breathing is also affected by some nose to the pubic symphysis.
pathological states: The diaphragm is the only skeletal muscle vital to life
• Several neurodegenerative diseases demonstrate and provides the power for the respiratory pump. It also
impaired ventilation as the first sign (Urfy & combines with the abdominal muscles to assist the heart
Suarez 2014). by providing a ‘circulatory pump’ (Uva et al. 2016).
• Chronic obstructive pulmonary disease (COPD)
shows less precise control over breathing during Inspiration
sleep and exercise (Dempsey 2002), and some patients The diaphragm, the seat of the soul according to the
have an altered chemoreceptor response, becoming ancient Greeks, is a dome-shaped sheet of muscle on
dependent on low oxygen levels (hypoxic respiratory which the upright lungs rest, separated by the pleura. It
drive) rather than the more usual high CO2 levels is innervated from C3–C5 via the phrenic nerves and
(hypercapnic respiratory drive) as a stimulus to generates 70% of tidal volume. Attached to the bottom
breathe (Craig 2017). of the rib cage, it separates two compartments of mark-
Respiratory plasticity enables adjustments to normal edly different densities, the thorax and abdomen.
physiological changes such as sleep, altitude, aging and At rest, or if paralysed or ruptured, the diaphragm
pregnancy (Terada & Mitchell 2011). Respiratory and extends upwards almost to nipple level (Fig. 1.3). Con-
cardiovascular control systems are coupled reciprocally traction flattens it, pressing down against the fulcrum
(Dick et al. 2014), e.g. ‘fear bradycardia’ can be a response of the abdominal contents, displacing the abdominal
to threatened respiratory dysfunction (Paulus 2013). viscera by 5–7 cm, protruding the abdominal wall
Sighing is a homeostatic resetting mechanism that (unless prevented by tight clothing or will power) and
reduces cortical excitation and mitigates stress, while levering the lower rib cage outwards in a bucket handle
maintaining lung compliance and gas exchange (Vaschillo action, causing expansion of the lower chest. Displace-
et al. 2015). It is shared with most mammals and ment of the diaphragm creates negative intrathoracic
linked to emotions via the amygdala and hypothalamus pressure, which sucks air into the lungs.
(Ramirez 2014). Muscles assisting this process are:
Yawning is controlled by the hypothalamus and is • the external intercostals, which stabilize the chest
thought to relate to thermoregulation of the brain. wall so that diaphragmatic contraction can create
Boredom and the evening are associated with higher these pressure changes;
brain temperature. Contagious yawning appears to have • the scalenes which stabilize the upper rib cage to
evolved in order to coordinate vigilance in budgerigars prevent it being pulled downwards;
(Gallup et al. 2015), and has even been considered a • pharyngeal muscles, which prevent collapse of the
prerequisite for a belief in God (Walusinski 2015). upper airway from the negative pressure.
expiration (Mondal et al. 2016). When the larynx is

bypassed by intubation, positive end-expiratory pres-
sure (PEEP) is applied to the airway to support this
function, thus avoiding fatigue of the diaphragm during
exhalation. This function of the larynx is called ‘physio-
logical PEEP’.
Normal exhalation is largely passive, lung elastic
recoil providing the driving force. This recoil is created
firstly by surface tension acting throughout the vast gas/
liquid interface lining the alveoli, and secondly by elas-
ticity of the lung tissue, which has been stretched during
inspiration. Elastic recoil is reduced at low lung volumes,
like a slack elastic band, and in emphysema because of
damaged alveolar septa.
Active expiration becomes stronger with speech,
FIGURE 1.3 Paralysed right hemidiaphragm due to exercise, coughing, giving birth and obstructive airways
phrenic nerve palsy. (From Casado-Arroyo et al. 2013.) disease. Abdominal, internal intercostal and pelvic floor
muscles may then be recruited to augment passive
recoil. Latissimus dorsi is enlisted during singing, and
These and other accessory muscles become major inspir- in COPD during forced exhalation, which may explain
atory muscles when there is increased work of breathing the benefit found by some patients from joining a choir
(WOB) such as with airflow obstruction or exercise. (Watson et al. 2012).
During unsupported upper limb activity, intercostal Speech is created when the expiratory column
and accessory muscles are obliged to stabilize the torso, of air is interrupted by vibrating vocal cords, which
forcing the diaphragm to take a greater load. People break it into sound waves. The sound is then modi-
with COPD may find daily activities daunting because fied by the oropharynx, nasopharynx and oral cavity.
of the sustained arm movements required, especially in A person with COPD may have a weak voice because
standing when the diaphragm also contributes to pos- of inability to generate sufficient expiratory pressure,
tural stability. The benefits of Tai Chi may stem from and a person with neurological disease may have poor
optimizing the interaction between breathing and pos- articulation because of weakness of the oropharyngeal
tural control (Holmes et al. 2016). musculature.
The diaphragm’s role in core stability is by control- Respiratory muscle dysfunction can occur with
ling intraabdominal pressure and reducing stress on the COPD, thoracic deformity, critical illness or neurologi-
spine through cooperative action with the abdominal cal disease (Gea 2012).
and pelvic floor muscles (Noh et al. 2014). The postural
functions of the respiratory muscles have led to links PRACTICE TIP
between increased WOB and impaired balance (David Drop your pen, then pick it up. Did you hold your breath?
et al. 2012), between diaphragm fatigue and recurrent This illustrates the postural work of the diaphragm.
back pain (Janssens et al. 2013) and between limited
chest excursion and chronic low back pain, the latter Pressures
responding to thoracic mobilizations and breathing
exercises (Babina et al. 2016). Alveolar pressure: pressure inside the lung.
Pleural (intrapleural/intrathoracic) pressure: pres-
Expiration sure in the pleural space.
The transition between inhalation and exhalation is Pressure equivalents:
• 1 mmHg = 1.36 cmH2O
smoothed by a brake on expiratory flow caused by
• 1 kPa = 7.5 mmHg
airflow resistance, especially at the larynx, and by con-
• 1 torr = 1 mmHg
tinued low-grade diaphragmatic activity during early
Alveolar pressure is negative on inspiration and slightly Pharynx

Rapid
positive on expiration. Pleural pressure is negative to turbulent
keep the lungs open, achieved by inward pull from Bronchi flow
lung elastic recoil and outward pull from rib cage Bronchioles Slow
recoil. Outward recoil is assisted by the pumping out laminar
Alveoli flow
of pleural fluid via the lymphatics, leading to a
total negative pleural pressure of about –6 cmH2O,
Gas exchange surface
modulated by the breathing pattern (Negrini 2013).
FIGURE 1.4 Increase in total cross section of the
Inward and outward forces are in equilibrium at the
airways as they divide, creating less frictional resistance
end of a quiet exhalation, this resting lung volume
as airflow becomes more laminar and streamline.
being termed the functional residual capacity (FRC).
Outward recoil assists inspiration, especially from low
lung volumes.
These pressures are disturbed by:
• a large pneumothorax, which neutralizes pleural
pressure so that the lung’s inward pull is unopposed
and it shrivels inwards;
• emphysema, which reduces lung elastic recoil so that A B A B
the outward pull of the chest wall is less opposed and
the lung hyperinflates;
• lung resection, leading to reduced compliance due to
disturbed pleuro-pulmonary fluid balance (Salito FIGURE 1.5 Left – both alveoli are normal, but the
et al. 2015). airway supplying alveolus B shows airflow obstruction,
which is causing frictional resistance to airflow. Right
Increasing expiratory pressure by coughing or force-
– both airways are normal, but alveolus B shows reduced
ful expiration can only generate extra flow in compliance caused by a thickened alveolar–capillary
theearly stages because, as airways narrow and fric membrane, increasing elastic resistance.
tional resistance increases, pleural pressure exceeds
airway pressure and compresses the airways. This
‘dynamic airway compression’ occurs at about
40 cmH2O (De Beer 2013), presaging the effort-
independent portion of the flow-volume relationship Peripheral airflow resistance is low because at the
(see Fig. 2.33) and can make forceful coughing coun- level of the terminal bronchioles the large number of
terproductive for people with obstructive airways small airways creates a wide total cross-sectional area of
disease. 180 cm2, causing laminar flow. The total cross section
reduces to 2.5 cm2 in the trachea, where there is higher
Resistance resistance, creating turbulent and disorganized airflow
(Fig. 1.4). Fig. 1.5 shows increased resistance due to
Resistance = force that must be overcome airflow obstruction.
during breathing Frictional resistance must also be overcome in the
pre
essure change chest and abdomen as organs are displaced by the
=
flow change moving lung.
Elastic resistance
Airflow resistance Lung tissue, alveolar surface liquid and the chest wall
Resistance to airflow is caused by friction, which is contribute to elastic resistance, which is increased by
created in the airways when gas slides against the walls conditions such as lung fibrosis (Fig. 1.5), pulmonary
over itself. Airflow resistance therefore depends on the oedema, rib cage deformity, obesity or a slumped
speed of airflow and calibre of the airway. posture.
Compliance to avoid either extreme, especially in patients with

damaged lungs.
volume change The contribution of airways to compliance relates to
Compliance =
pressure change their calibre, resistance being increased and compliance
decreased if airways are narrowed by bronchospasm,
Compliance reflects the willingness of the lungs to oedema, the collapsing airways of emphysema, and
distend, and elastance the willingness to return to their sometimes secretions in the large airways where there is
resting position. Compliance is represented by the rela- greater overall resistance and less collateral ventilation.
tionship between volume and pressure, i.e. how much The surface tension of alveolar fluid is partially coun-
pressure (work of breathing) is required to expand the teracted by surfactant, a constituent in the fluid that acts
lungs. This relationship is curved rather than linear due like detergent, preventing the alveolar walls sticking
to a variation in the WOB at different lung volumes together and preventing small alveoli collapsing and
(Fig. 1.6). emptying their contents into large alveoli.
The lung is least compliant, i.e. stiffest, at either
extreme of lung volume, so that it is difficult to inflate PRACTICE TIP
alveoli that are closed or hyperinflate those that are fully
inflated. Clinical reasoning indicates that prevention of Pour some water into a small plastic bag, empty it and
then pull the bag open. The forces of surface tension
atelectasis would therefore be more sensible than treat-
are what make this difficult. Repeat after adding a few
ing it once it has occurred.
drops of washing-up liquid.
PRACTICE TIP
Blow up a balloon and feel your work of breathing at The contribution of extrapulmonary structures to com-
low, mid and high volumes. pliance relates to the ease with which the chest wall can
be pushed away on inspiration. Kyphoscoliosis or a dis-
Compliance is lower on inspiration, i.e. it is harder to tended abdomen reduce compliance.
breathe in than out, due mostly to alveolar fluid surface
tension. This process is known as hysteresis and is dem-
V
onstrated by the pressure–volume loop (Fig. 1.7).
Alveoli are vulnerable to injury at excessively high
or low volume, and mechanical ventilation (MV) aims
n
tio
ra
V
pi
Ex
on
ati
Apex
pir
Ins
Midzone
Base
P
FIGURE 1.6 Pressure–volume (compliance) curve indi-
cating reduced compliance at either extreme of lung P
volume. The symbols represent alveolar size at different FIGURE 1.7 Pressure–volume loop showing how expi-
volumes. V, lung volume; P, pressure, i.e. work to ration requires less effort, i.e. less pressure (P) for the
expand the lung. same change in volume (V), than inspiration.
Static compliance is measured during a breath-hold Inspiratory muscle fatigue

so that equilibrium is achieved between alveolar pres- Fatigue reduces the capacity to develop force in response
sure and mouth pressure, alveoli being filled to a volume to a load. When acute, it is usually reversible by rest. It
determined by their regional compliance. Dynamic can be due to failure of any of the links in the chain of
compliance is measured during breathing. It normally command from brain to muscle. Failure within the
approximates static compliance, but may be less in dis- central nervous system is called central fatigue and
eased lungs if regional variations in compliance and failure at the neuromuscular junction or in the muscle
resistance mean that alveolar filling is not completed is called peripheral fatigue.
during inspiration. The diaphragm differs from other skeletal muscle in
that it has to provide a lifetime of sustained action
Work of Breathing against elastic and resistive loads rather than irregular
Work is done during inspiration to overcome the resis- action against inertial loads. It is equipped for this by
tive and elastic forces of airways, lungs and chest wall. its relative resistance to fatigue and its large reserve so
This work can be defined in two ways: that only during coughing is it fully activated (Mantilla
• the pressure required to move a volume of gas, i.e. et al. 2014), and by the unusual way in which perfusion
transpulmonary pressure × tidal volume; increases during contraction (Anzueto 1992). Fatigue
• oxygen consumed by the respiratory muscles, i.e. the occurs if energy demand exceeds supply, as when WOB
oxygen cost of breathing. is increased by airflow obstruction, or when the ability
Elastic resistance contributes 80% of the WOB and of the respiratory muscles to contract efficiently is
airflow resistance the remaining 20%. Relative contribu- impaired by hyperinflation, scoliosis or a flail chest.
tions to airflow resistance are: Fatigue serves a protective function to avoid deple-
• nasal passages: 50% tion of enzymes. Procedures that force patients to
• larynx: 25% overuse fatigued muscles can cause muscle damage
• trachea to eighth generation: 20% (Kallet 2011), which is most likely to occur when
• peripheral airways: 5% (Eriksson 1996) weaning patients from MV.
Normally, breathing is surprisingly efficient, helped by
fluid coating the moving surfaces of the pleura, assuring Inspiratory muscle weakness
a tight lung–chest wall coupling and allowing lung Weakness is failure to generate sufficient force in an
volume to faithfully follow changes in chest wall volume otherwise fresh muscle. It is not reversible by rest,
during the respiratory cycle (Negrini 2013). The pleural but is treated by addressing the cause and encouraging
cavity however does not appear to be essential: people activity. Weakness of the respiratory muscles may be
who have had a pleurectomy, and elephants (West 2001), caused by:
have no functioning pleura but are able to breathe • neuromuscular disorder
happily. However, it is handy for thoracic surgeons who • disuse atrophy
would have difficulty if the lung was attached directly to • malnutrition
the chest wall. • hypoxia, hypercapnia or acidosis
A change in alveolar pressure of only 1 cmH2O is • low calcium, potassium or phosphate levels
usually enough for airflow (Negrini 2013) and WOB • steroids
uses just 2%–5% of total oxygen consumption at rest, • inflammation, as occurs with COPD, sepsis or mul-
but this may be increased to 40% in people with obstruc- tisystem failure
tive airways disease (Cairo 2012, p. 194). Weakness predisposes a muscle to fatigue. Fatigue differs
Deep breathing increases the work performed against from weakness in that a normal muscle can become
elastic resistance, while rapid breathing increases the fatigued if faced with excess WOB. Fatigue and weakness
work against airways resistance. Most patients find the often coexist, especially in respiratory failure or during
right balance, but some need breathing re-education weaning from MV. The clinical features of fatigue and
to find the optimal breathing pattern to minimize weakness are similar (pp. 37–38). Both are experienced
their WOB. as breathlessness.
VENTILATION Gas that moves in and out of the lungs is made

up of:
We breathe to ventilate and ventilate to respire. • alveolar ventilation, which is the fresh air that gets
Tobin 1991 into alveoli and participates in gas exchange, defined
above;
• dead space ventilation (VD), which does not contrib-
Respiration: (1) exchange of gases between the envi- ute to gas exchange.
ronment and tissue cells, by external respiration at Most dead space is anatomical (Fig. 1.8), which is air in
alveolar–capillary level and internal respiration at the conducting passages that does not reach the alveoli,
capillary–tissue level; (2) regulation of the acid–base, i.e. that which is last in and first out. It comprises one-
metabolic and defence functions of the respiratory
third of VT in a human, more in a giraffe. Alveolar VD,
system.
Ventilation: gas movement between the outside
representing air that reaches the alveoli but does not get
and the alveoli, i.e. inspiration and expiration (the into the blood, is minimal in normal lungs. The sum of
terms ventilation and respiration are sometimes used anatomical and alveolar VD is called physiological VD.
interchangeably). The presence of VD is one reason why it is more efficient
Breathing: the process by which the respiratory to increase V̇ E by breathing deeper than by breathing
pump creates ventilation. faster, although this varies with lung compliance. Dead
Minute ventilation or minute volume (V̇ E): amount of space is most usefully expressed in relation to tidal
gas breathed per minute, i.e. tidal volume × respira- volume (VD/VT) and is normally 30% of VT (Gott &
tory rate (RR). Dolling 2013).
Tidal volume (VT): volume of air inhaled and exhaled Ventilation is not distributed evenly in the lungs (Fig.
at each breath.
1.9). In healthy lungs, most of the tidal volume is
Alveolar ventilation: (tidal volume – physiologic dead
space) × RR.
directed to dependent lung (Wettstein et al. 2014), with
two exceptions:
1. In the upright position, alveoli in upper regions are
more inflated, but mostly with VD gas. Gas travels
A healthy spontaneously breathing adult maintains an more easily at first to the open spaces of these non-
approximate V̇ E of 5–9 L, moving a VT of 450–600 mL dependent regions, but they are rapidly filled and gas
with a respiratory rate (RR) of 10–15 breaths/min. then travels to the dependent regions below. Alveoli
Volumes Flows
Tidal volume Minute volume
500 mL 7500 mL/min
Anatomical dead Frequency 15/min

space 150 mL
Alveolar ventilation
5250 mL/min
Alveolar gas
3000 mL
Pulmonary capillary Pulmonary blood

blood 70 mL flow 5000 mL/min
FIGURE 1.8 Average volumes and flows of gas and blood in the lungs. Frequency = average
breaths per minute. (From West 2016.)
V
Right Left Apex
Ventilation Perfusion lung lung
gradient gradient
Midzone
Alveoli
Base
P
A
V
Alveoli Apex
Ventilation Perfusion
gradient gradient
Mid-zone
Base
P
B
V
Alveoli
Apex
Ventilation Perfusion
gradient gradient Mid-zone
Maximal inspiration Functional residual Base

capacity
P
C
FIGURE 1.9 Effect of gravity on the distribution of ventilation and perfusion (left), with position
of alveoli on compliance curves (right). (A) Upright lungs in a healthy young nonobese person,
showing slight downward ventilation gradient and strong downward perfusion gradient. (B) In
supine, pressure from the abdominal contents stretches the dependent portion of the diaphragm,
compressing dependent alveoli but facilitating more efficient diaphragm contraction. (C) Side-
lying allows greater volume change in the dependent lung due to pressure from the abdominal
contents stretching this side of the diaphragm. P, Pressure required to expand lung; V, lung
volume.
in dependent regions are partially compressed by the e.g. if the patient is slumped in a chair, they will be
weight of the lungs, heavy with blood, above and lower on the compliance curve (see Fig. 1.6) and less
around them. They therefore have more potential to easy to inflate.
expand, i.e. they are more compliant, allowing greater 2. In side-lying, fresh gas arriving in the lower lung
ventilation with fresh gas. This reasoning carries provides a greater contribution to gas exchange, but
through to whatever position a young adult is in. At the upper lung is more expanded and therefore
the same time, if alveoli are collapsed or compressed, responds earlier to deep breathing exercises for
Functional
residual
VT
capacity (FRC)
Increased CV,
e.g. smoking,
Closing
ageing
volume (CV)
Decreased FRC,
e.g. obesity,
supine posture
FIGURE 1.10 Factors that shift tidal breathing into the closing volume range, leading to airway
closure in the lung bases during quiet breathing. VT, Tidal volume.
increasing lung volume. For patients with atelectasis,

therefore, and indeed for most clinical problems,
DIFFUSION
patients are placed with the affected lung on top The wide total cross section of the peripheral airways
(p. 185). means that airflow here essentially ceases, and gas move-
However, unlike the perfusion gradient, the ventilation ment from the respiratory bronchioles to the alveoli
gradient is only slight and responds to minor fluctua- continues by gaseous diffusion. In the alveoli, oxygen
tions, so that: dissolves in alveolar fluid and is driven across the
• It is reversed in elderly people, who have a higher alveolar–capillary membrane by the partial pressure dif-
closing volume (Fig. 1.10), early airway closure and ference, with CO2 coming the other way. The alveolar–
alveolar collapse in dependent regions during expira- capillary membrane is 50 times thinner than airmail
tion (Wettstein et al. 2014). Most patients are elderly. paper (Weibel 2013) or, for readers too young to remem-
• It is reversed in obese people, young children ber airmail paper, 0.2–0.3 µm, which means that lung
(Wettstein et al. 2014), those on some modes of MV, hyperinflation can compromise the barrier function of
those who spend time in slumped positions without the membrane (West 2016, p. 7). It comprises two sheets
taking deep breaths, and in young children. of endothelium held together by wisps of connective
• Prone facilitates a more evenly distributed tidal tissue support. It is semipermeable, preventing plasma
volume, partly by reversing the ventilation gradient proteins and water leaking into alveoli but allowing gas
(Kallet 2015). exchange. Oxygen tension is equalized in one-third of
the time that the blood takes to pass each alveolus, while
CO2 dissolves 20 times more quickly (Wagner 2015).
PRACTICE TIP Impaired diffusion across the membrane does not
play a major role in gas exchange abnormalities except
Auscultate a colleague’s lungs in standing, sitting,
sometimes during exercise or in people with severe
slumped sitting, supine, side-lying and prone.
interstitial lung diseases (Wagner 2015), or when sepsis
causes high cardiac output and shortened transit times
If airways are obstructed, ventilation can continue (Townsend & Webster 2000).
through collateral channels. These are unimportant in
normal lungs and ventilating through them is less effi-
cient than using the main airways because airflow resist-
PERFUSION
ance is 50 times greater. This difference is eliminated in No other capillaries in the body are shielded from
emphysema, when collateral ventilation promotes more the outside environment by such a minute amount
homogeneous ventilation (Cetti et al. 2006). of tissue.
Normal breathing creates a VT of one-tenth the vital West 2013
capacity, but oscillations in VT and involuntary sighs
every 5–10 min help prevent alveolar collapse. Patients The lungs have a dual circulation. The high-pressure
who are drowsy or sedated lose this mechanism. (100 mmHg) bronchial circulation, from the aorta,
supplies the lung tissue itself but is not essential to same place at the same time for gas exchange to occur.
survival, as shown after lung transplantation when the The matching of these two is expressed as the ratio of
bronchial vessels are tied. However, the lungs are alveolar ventilation to perfusion (V̇ A/Q̇ ).
awash with blood from the dominant low-pressure V̇ A/Q̇ matching is assisted by the mixing of expired
(~15 mmHg) pulmonary circulation, which bathes the and inspired gases through the common dead space
surfaces of the alveoli so that gas exchange can occur (Glenny et al. 2013), but a degree of V̇ A/Q̇ mismatch is
(West 2013). The pulmonary vasculature is equivalent normal because of dissonance between ventilation and
to 7000 km of capillaries (Denison 1996), which can act perfusion gradients, the lung bases receiving 18 times
as a blood reservoir in case of need such as during more blood and 3.5 times more gas than the apices in
haemorrhage. the upright lung (Thomas 1997).
The pulmonary circulation can respond to changes Pathological V̇ A/Q̇ mismatch is due to a high or low
in flow with little change in pressure, reducing resistance ratio. A high ratio occurs when the alveoli are ventilated
by dilating, recruiting closed capillaries or shifting blood but perfusion is impaired so the oxygen cannot reach
to the systemic circulation. the blood, causing increased dead space. For example,
The effect of gravity on the low-pressure pulmonary pulmonary vasculopathy in heart failure increases dead
circulation is to create a perfusion gradient with more space and causes breathlessness during exercise (Kee
blood in dependent regions (see Fig. 1.9). This is steeper et al. 2016). A low V̇ A/Q̇ ratio occurs when lung units
than the ventilation gradient because of the density of are perfused but not adequately ventilated, which is the
blood. The perfusion gradient is represented by zones condition most frequently dealt with by physiothera-
(West 2016, p. 51): pists. This creates a shunt, defined as the fraction of
• Zone I is in the upper nondependent lung, where cardiac output that is not exposed to gas exchange in
alveolar pressure exceeds pulmonary arterial pressure the lung. A shunt over 20% limits the utility of oxygen
so that capillaries are squashed and no blood flows. therapy because added oxygen cannot reach the shunted
• Zone II is in the middle, where pulmonary arterial blood. The shunt is measured by comparing arterial and
pressure exceeds alveolar pressure, which in turn mixed venous blood (p. 471), expressed as a percentage
exceeds venous pressure. of cardiac output. A small shunt is normal because part
• Zone III is in dependent lung, where venous pressure of the bronchial circulation mingles with pulmonary
exceeds alveolar pressure. venous drainage. The mixing of shunted venous blood
Zone I in health is small or nonexistent. However, if with oxygenated blood is known as venous admixture,
hypovolaemic shock reduces arterial pressure, or MV which is normally 5% of cardiac output (Takala 2007).
increases alveolar pressure, Zone I becomes significant. Systemic hypoxia stimulates selective vasodilation
MV also pushes blood downwards (p. 449) and the to assist perfusion of vital tissues. Pulmonary hypoxia
pressure of this blood may lead to airway closure in stimulates the opposite response: if a fall in alveolar
Zone III. oxygen tension is detected, an ingenious mechanism
In addition, perfusion is affected by: called hypoxic vasoconstriction helps maintain gas
• lung volume, e.g. the vessels are stretched in the exchange by constricting capillaries adjacent to these
hyperinflated state; alveoli (Fig. 1.11), thus limiting wasted perfusion
• disease, e.g. alveolar destruction in emphysema and improving V̇ A/Q̇ match (Craig 2017). When the
causes disruption of both perfusion and ventilation; lung bases are affected, e.g. in pulmonary oedema,
• position, e.g. in prone, perfusion is more uniform obesity (Pedoto 2012) or the early stages of COPD,
than supine (Nyren 1999) and better matched with local shutdown of vessels forces blood to the better-
ventilation (Henderson et al. 2013). ventilated upper regions, shown radiologically as
enhanced vascular markings towards the apices, or
‘upper lobe diversion’ (see Fig. 4.3). Hypoxic vaso-
VENTILATION/PERFUSION RATIO constriction becomes counterproductive when alveo-
It is no good having a well-ventilated alveolus if it is not lar hypoxia occurs throughout the lung, as occurs in
supplied with blood, nor a well-perfused alveolus that advanced COPD, leading to generalized vasoconstric-
is not ventilated. Fresh air and blood need to be in the tion and pulmonary hypertension.
Ventilation Ventilation
Hypoxic
pulmonary
vasoconstriction
Pulmonary
arterial
blood flow
Pulmonary
venous blood
flow
FIGURE 1.11 Hypoxic pulmonary vasoconstriction. Left: normal alveolar ventilation and perfu-
sion. Right: ↓ ventilation in alveolus (grey) leading to reduced perfusion. (From Dhillon 2012.)
ARTERIAL BLOOD GASES TABLE 1.1 Relationship between

oxygen saturation and tension in arterial
PO2: partial pressure or tension of oxygen, i.e. its blood under normal conditions
concentration
PaO2: partial pressure of oxygen in arterial blood, i.e. SaO2 (%) PaO2 (kPa) PaO2 (mmHg)
oxygen dissolved in plasma; normal 11–14 kPa or 97 12.7–14.0 95–105
82.5–105 mmHg 94 9.3–10.0 70–75
SaO2: extent to which haemoglobin in arterial blood is 92 8.9–9.7 67–73
saturated with oxygen, i.e. capacity of blood to trans- 90 7.7–8.3 58–62
port oxygen; normal 95%–98% 87 6.9–7.7 52–58
SpO2: as above, but described in terms of measure- 84 6.1–6.9 46–52
ment by pulse oximetry (the distinction is rarely
important and normal values are the same)
Haemoglobin (Hb): molecule in erythrocytes that binds
to and transports oxygen and some CO2 around the
thetic cream (p. 300), gels, ice packs or pain-free jet
body injections (McSwain et al. 2015). Ultrasound guidance
PaCO2: partial pressure of CO2 in arterial blood; basis increases success (Gu et al. 2016).
of respiratory acid–base balance; normal 4.7–6.0 kPa Table 1.1 relates the different measurements of arte-
or 35–45 mmHg rial oxygenation.
FiO2: fraction (concentration) of inspired oxygen PaO2 describes the 2% of oxygen that is dissolved in
plasma, and reflects the pressure needed to push oxygen
from blood into tissue cells. SaO2 describes the 98% of
Arterial blood gas (ABG) analysis identifies if breathing oxygen that is bound to haemoglobin (Hb) for trans-
is effective by giving an indication of gas exchange, ven- port. Neither of these gives a measure of oxygenation at
tilation and acid–base status. Readings should be related tissue level. Also, resting levels do not reflect oxygena-
to the FiO2 and previous values. tion during exercise, nor predict nocturnal oxygenation.
Arterial blood samples are taken either from an Oxygen content describes the total amount of oxygen
indwelling arterial catheter or by intermittent puncture carried in blood, and incorporates PaO2, SaO2 and
of the radial artery. Local anaesthesia for this procedure Hb. In practice, oxygen content is assumed from PaO2
is stipulated in the UK Guidelines (BTS 2008) because or SpO2.
the pain of a needle going through the arterial wall is Gas exchange entails:
greater than puncturing a vein (McKeever et al. 2016), • oxygen dissolving in alveolar lining fluid;
sometimes causing either hyperventilation or apnoea, • diffusion of oxygen through the alveolar–capillary
which can invalidate the results (Lee 2012). This ‘signifi- membrane into plasma;
cant morbidity’ can also be prevented by local anaes- • oxygen binding to Hb for transport around the body;
• at its destination, oxygen from Hb dissolving back this encourages loading of oxygen in the high PO2
into plasma; environment of the lung, and discourages unloading
• diffusion of oxygen across the capillary wall and of oxygen before blood reaches the capillary bed. In
delivery to the tissues. disease, there can be a significant change in PaO2, e.g.
The reverse happens to CO2 but it slips back and forth a reduction to 10.7 kPa (80 mmHg), with little change
with ease. The movement of CO2 traditionally does not in SaO2.
come under the term ‘gas exchange’.
Steep portion of the curve
Oxygen Dissociation Curve The dissociation of Hb becomes proportionately greater
The relationship between SaO2 and PaO2 is not direct as PO2 falls, so that small changes in PaO2 greatly affect
but expressed by the oxygen dissociation curve (Fig. SaO2. In health, this means that Hb can offload quanti-
1.12). Its S shape illustrates the protective mechanisms ties of oxygen at cellular level while maintaining oxygen
that function in both health and disease. tension in the blood. In disease, large amounts of oxygen
can be unloaded when tissues are hypoxic. A PaO2
Upper flat portion of the curve <7.3 kPa (55 mmHg) tips the patient onto a slippery
At the plateau of the curve, the combining of oxygen slope whereby further small drops in PaO2 result in
with Hb is favoured by a high PO2, and its stability is tissue hypoxia.
not unduly disturbed by changes in PaO2. In health,
Shift of the curve
Another singular way in which the body responds to
need is to adjust the affinity of Hb for oxygen, as reflected
Left shift by a shift of the curve. A right shift means that Hb
Body temperature unloads oxygen more easily at a given PO2. In health,
2,3-DPG this occurs during exercise, when active muscle gener-
100 PCO2 ates heat and makes blood hypercapnic and acidic. In
pH
disease, this occurs with fever and when tissues need
extra oxygen. A left shift occurs when Hb holds tightly
Ac rma is
No alos
Right shift onto its oxygen, as with hyperventilation, hypometabo-

ido l
sis
Alk
Body temperature lism or a cold environment. Pink ears and noses on

SO2 (%)
2,3-DPG frosty mornings are due to the reluctance of Hb to

50
PCO2 (Bohr effect)
unload oxygen.
pH
Hypoxaemia and Hypoxia

Hypoxaemia
P50 Hypoxaemia is reduced oxygen in arterial blood, defined
0 as PaO2 <8 kPa (60 mmHg) or SaO2 <90%. Causes are:
0 50 100 • low V̇ A/Q̇ ratio or wasted perfusion (↑ shunt)
PO2 (mmHg) • high V̇ A/Q̇ ratio or wasted ventilation (↑ dead space)
• hypoventilation
0 2 4 6 8 10 12 14 16 18
PO2 (kPa) • diffusion abnormality
• ↓ FiO2
FIGURE 1.12 Oxygen dissociation curve relating oxygen
Low V̇ A/Q̇ occurs when blood is shunted through con-
saturation to oxygen tension. 2,3-DPG is an enzyme in
red blood cells that increases in chronic hypoxaemia and
solidated, collapsed or damaged lung without seeing
allows easier unloading of O2 to hypoxic tissues. P50 is any oxygen, somewhat attenuated by hypoxic vaso-
the PaO2 at which Hb is 50% saturated and is the most constriction. High V̇ A/Q̇ occurs, for example, when a
sensitive indicator of a shift in the curve, a high value pulmonary embolus blocks perfusion, thus increas-
suggesting poor affinity of Hb for O2. The shaded area ing alveolar dead space and causing V̇ A/Q̇ mismatch
represents critical tissue hypoxia. at the other end of the spectrum (Fig. 1.13).
Pulmonary
embolus
Normal Atelectasis Consolidation
VA/Q match Wasted

Shunt or wasted perfusion
ventilation
( VA/Q)
( VA/Q)
FIGURE 1.13 Alveoli and surrounding capillary network, showing how impaired ventilation or
perfusion upsets V̇ A/Q̇ matching.
Hypoventilation can be caused by respiratory depres- Effects of hypoxaemia and hypoxia

sion (e.g. from oversedation), respiratory muscle Acute hypoxaemia induces vasodilation of the periph-
weakness (e.g. with neuromuscular disease), or eral vascular beds, increasing cardiac output in an
sometimes with COPD if patients chronically attempt to improve oxygen delivery. Chronic hypoxae-
hypoventilate in order to rest the diaphragm (p. 76). mia thickens blood and may strain the right heart (see
Diffusion abnormalities occur in disorders such as Fig. 3.5) and even transient hypoxaemia may shorten
pulmonary oedema or fibrosing alveolitis, when life (Criner 2013). Cardiac arrhythmias may occur when
a thickened alveolar–capillary membrane increases SaO2 drops below 80%.
the PAO2–PaO2 gradient. Hypoxia leads acutely to tachycardia (Critchley et al.
↓ FiO2 is due to inadequate oxygen therapy, high alti- 2015) and chronically to muscle atrophy (D’Hulst et al.
tude or fire entrapment. 2016). It progressively causes the following:
• PaO2 <7.3 kPa (55 mmHg): memory defect (due to the
Hypoxia sensitivity of the hippocampus), impaired judgement;
The term hypoxia is sometimes used interchangeably • <5.3 kPa (40 mmHg): tissue damage;
with hypoxaemia but it means oxygen deficit at tissue • <4 kPa (30 mmHg): unconsciousness;
level, when demand exceeds supply, leading to anaerobic • <2.7 kPa (20 mmHg): death, except in migrating
metabolism once PaO2 reaches 4.5 kPa (33.8 mmHg) geese and hibernating turtles (Nikinmaa 2013).
(Townsend & Webster 2000). It is more relevant to The brain is the first organ to be affected, followed by
body function than hypoxaemia but more difficult to the gut lining. The kidney is also sensitive to hypoxia
measure. and manifests its distress more obviously, reducing
Hypoxaemic hypoxia occurs when hypoxia is caused urine output and increasing potassium, creatinine and
by hypoxaemia. Anaemic hypoxia is when Hb levels urea levels.
are reduced or abnormal Hb cannot carry enough Chronic hypoxia leads to increased oxygen utilization
oxygen. Ischaemic hypoxia indicates impaired oxygen and reduced energy-demanding processes (Cummins &
transport, e.g. haemorrhage, myocardial infarct or Keogh 2016).
peripheral arterial disease. Histotoxic hypoxia occurs
when cells cannot extract or utilize oxygen, e.g. follow- Hypercapnia
ing cyanide poisoning or in septic shock (Busl & Despite large variations in the metabolic production of
Greer 2016). CO2, PaCO2 is normally kept constant (Guyenet 2014).
Other Indices of Oxygenation

TABLE 1.2 Clinical features of
Gas exchange is best documented in relation to the
hypoxaemia and hypercapnia
inspired oxygen, described as the PaO2:FiO2 ratio. Less
Hypoxaemia Hypercapnia easy to measure, but useful in identifying the cause
Cyanosis Flapping tremor of hands of hypoxaemia, is the difference between alveolar and
↑ RR arterial oxygen, known as the alveolar–arterial gradient,
↑ HR the ‘A–a gradient’, or PAO2–PaO2. A raised gradient
Peripheral Peripheral vasodilation, leading indicates greater difficulty in getting oxygen across
vasoconstriction to warm hands and headache
the alveolar–capillary membrane, as occurs in diffusion
Respiratory muscle weakness
impairment. Hypoventilation or reduced FiO2 does not
Arrhythmias or Bradycardia
bradycardia affect the PAO2–PaO2.
Restlessness → Drowsiness → hallucinations
confusion → coma → coma Acid–Base Balance
HR, Heart rate; RR, respiratory rate.
Normal pH in the human body: 7.35–7.45
However, hypoventilation causes hypercapnia (↑ The degree of acidity or alkalinity is measured by pH,
PaCO2), leading to respiratory acidosis or compensated which shows the hydrogen ions in solution, but nega-
metabolic alkalosis. An acutely rising PaCO2 is a danger tively, namely:
sign if it presages exhaustion (see Fig. 3.39), and with • low pH means more hydrogen ions and greater acidity
acidosis is an indication for mechanical ventilatory • high pH means fewer hydrogen ions and greater
assistance. But chronic hypercapnia is neither dangerous alkalinity
nor damaging and may accompany advanced stable Neutral is 6.8, but body functions occur on the alkaline
lung disease. side of neutral. Acidosis occurs when arterial pH falls
The clinical signs of hypoxaemia and hypercapnia below 7.35. The term means increased acidity in the
are insensitive and nonspecific, but Table 1.2 indicates body, while acidaemia means increased acidity of blood
some similarities and differences. plasma, but the former is normally used for both. Aci-
dosis can lead to myocardial depression, arrhythmias
Interpretation and hypotension, while hypercapnic acidosis weakens
Examples of ABG abnormalities are: the respiratory muscles and can increase inflammation
• ↓ PaO2 with ↑ PaCO2: hypoxaemia, e.g. exacerbation (Bruno 2012). Alkalosis occurs at pH over 7.45.
of COPD, in a patient who is becoming too exhausted The pH independently predicts intensive care unit
to ventilate adequately; (ICU) admission and 12-month mortality (Stokes et al.
• ↓ PaO2 with ↓ PaCO2: hypoxaemia in a patient who 2016a). It responds to metabolic and respiratory change
is breathless, e.g. pneumonia, fibrosing alveolitis, pul- but it cannot differentiate between them.
monary oedema, pulmonary embolus; The following identify acid–base imbalances:
• normal PaO2 with ↓ PaCO2: emotion causing hyper- • Respiratory acidosis occurs when the drop in pH is
ventilation, e.g. painful arterial puncture or hyper- caused by increased PaCO2 and is due to hypoventila-
ventilation syndrome. tion, leading sometimes to ventilatory failure.
Hypercapnia is likely to be longstanding if pH is >7.35 • Respiratory alkalosis occurs when a patient hyper-
(BTS 2008). ventilates, which washes out CO2. This always accom-
Reduced minute volume raises PaCO2 and lowers panies a raised minute volume and often accompanies
SaO2, but the reverse is not true. Increased minute breathlessness, though the rapid shallow breathing
volume blows off CO2, but SaO2 does not rise above pattern of a breathless person is not necessarily effi-
normal because Hb cannot be supersaturated. However, cient, nor synonymous with hyperventilation.
MV with a high FiO2 can raise PaO2 above normal when • Metabolic acidosis occurs when the body produces
the extra oxygen dissolves in the plasma. too much acid or the kidneys cannot remove enough
acid, leading to haemodynamic instability (Celotto Respiratory Metabolic

et al. 2016). Metabolic acids include all the body
acids except dissolved CO2. They are not respirable Acidosis
and have to be neutralized, metabolized or excreted
by the kidney. Lactic acidosis is a form of metabolic [HCO–3 ] [HCO3– ]
pH PCO2 PCO2
acidosis caused by the build-up of lactic acid if
oxygen supply is inadequate.
• Metabolic alkalosis raises pH out of proportion to
changes in PaCO2, a common occurrence in critically Alkalosis
ill patients due to fluid volume loss, diuretics or low
pH
[HCO–3 ] [HCO3– ]
potassium (Oh 2010).
PCO2 PCO2
Patients can have mixed acid–base disorders, e.g. a
patient with acute hypercapnic COPD may have CO2-
induced respiratory acidosis, but comorbidities such as
diabetes or the side effects of diuretics can induce a FIGURE 1.14 Four examples of acid–base imbalance
showing the process of compensation. Thick arrows
metabolic alkalosis, with the knock-on effects of a
in each box indicate which way a value has gone in
depressed respiratory drive and increased airway resist-
order to create the acidosis or alkalosis. Thin arrows
ance (Terzano et al. 2012). indicate which way the other value is going in order to
compensate.
Buffers
A buffer is a weak acid or base that mitigates an upset
pH by mopping up or squeezing out hydrogen ions like
a chemical sponge. Bicarbonate (HCO3−) is a buffer one may dominate and the other partially compensate
whose value provides an estimate of the metabolic com- (Fig. 1.14). The prime mover is the one on which to
ponent of acid–base balance, although it is affected by focus and it is a mistake to treat a compensation.
both metabolic and respiratory components. Values for
HCO3− are:
• normal: 22–26 mmol/L KEY POINT
• metabolic acidosis: <22 mmol/L
If the primary acid–base disturbance is metabolic, pH
• metabolic alkalosis: >26 mmol/L.
and bicarbonate/BE change in the same direction, while
Standard bicarbonate (SBE) is the bicarbonate if the primary problem is respiratory, pH and PaCO2
concentration under standard conditions, being change in opposite directions (see Fig. 1.14).
adjusted as if PaCO2 were 5.3 kPa, i.e. it is similar to
bicarbonate in a person with normal acid–base status.
Base excess (BE) is a calculated value from SBE, Regulation
being positive with metabolic alkalosis and negative Acid–base balance is disturbed if removal of CO2 from
with metabolic acidosis. It represents the quantity of the lungs is abnormal (respiratory acidosis or alkalosis)
acid required to restore pH to normal if PCO2 were or production of acid from the tissues or elimination
adjusted to normal. Like HCO3−, it measures metabolic elsewhere is abnormal (metabolic acidosis or alkalosis).
acid–base balance, but takes buffering by red blood cells Any deviation of pH from normal is fiercely resisted, at
into account and provides a more complete analysis of whatever cost, by three homeostatic mechanisms:
metabolic buffering than HCO3−. BE is calculated from 1. The buffer system neutralizes acids or bases by giving
pH, PaCO2 and haematocrit. Values are: up or absorbing hydrogen ions, all within seconds.
• normal: minus 2 to plus 2 mmol/L The following equation represents the dissociation of
• metabolic acidosis: < minus 3 mmol/L carbonic acid in solution, acting as a sink for hydro-
• metabolic alkalosis: > plus 3 mmol/L gen ions:
Along with clinical assessment, ABG analysis helps iden-
tify the main causes of acidosis or alkalosis, although H2O + CO2 ↔ H2CO3 ↔ H+ + HCO3 −
TABLE 1.3 Interpretation of arterial blood gas trends

Status Causes Effects Recognition
Acute respiratory Hypoventilation, e.g. PaCO2 ↑, pH ↓, HCO3 N (no
−
Shallow breathing,
acidosis exhaustion, weakness renal compensation yet) drowsiness, severe acute
respiratory disease
Chronic Chronic hypoventilation PaCO2 ↑, pH N, HCO3− ↑ Severe chronic respiratory
(compensated) (retention of HCO3− to disease, e.g. COPD
respiratory acidosis restore pH, i.e. full
compensation)
Respiratory alkalosis Acute hyperventilation, e.g. PaCO2 ↓, HCO−3 ↓ , pH ↑ Breathlessness
anxiety, pain, acute (partial compensation)
cardiorespiratory disease,
fever, CNS injury
Metabolic acidosis Shock, lactic acidosis, diabetic HCO3− ↓, pH ↓, PaCO2 ↓, BE Hyperventilation (respiratory
acidosis, severe diarrhoea or < –2 (partial compensation) compensation to blow off
dehydration, kidney failure PCO2)
Metabolic alkalosis Sepsis, heart failure, diuretics, HCO3− ↑, pH ↑, PaCO2 ↑, BE Delirium
severe vomiting, ↓ albumin > +2 (partial compensation)
BE, Base excess; CNS, central nervous system; COPD, chronic obstructive pulmonary disease; N, normal.
An increase in PaCO2 shifts the equilibrium to the To help decide if a change in pH is respiratory or meta-
right, increasing H+ and causing respiratory aci- bolic (if this is not obvious clinically), any change
dosis. A decrease in PaCO2 shifts it to the left. outside the following is likely to be metabolic in
2. If buffering is not adequate, the lungs then present origin (Williams 1998):
an avenue for regulating CO2. Hyperventilation or • For every increase in PaCO2 of 2.6 kPa (20 mmHg)
hypoventilation can stabilize acid–base balance in above normal, pH falls by 0.1.
1–15 min. • For every decrease in PaCO2 of 1.3 kPa (10 mmHg)
3. If this is still not adequate, the kidneys take over, but below normal, pH rises by 0.1.
they need 3–5 days to do so (Ayers & Warrington When pH is restored to normal, full compensation has
2008). occurred. The stages can be identified as follows:
These mechanisms work to dispose of the acids that are • Abnormal pH + change in PaCO2 or HCO3−/BE =
continually produced by the body’s metabolic processes, noncompensation, i.e. an acute process.
caused mostly by the hydration of CO2 to create car- • Abnormal pH + change in PaCO2 and HCO3−/BE
bonic acid. = partial compensation.
• Normal pH + change in PaCO2 and HCO3−/BE =
Interpretation full compensation.
Step 1. Look at the pH: Table 1.3 clarifies the causes, effects and recognition of
• ↓ pH means acidosis ABG imbalances. Examples are in Appendix A.
• ↑ pH means alkalosis Table 1.4 shows how two respiratory disorders can
Step 2. Look at the PaCO2: does it account for an abnor- affect ABG readings. PaCO2 values reflect breathlessness
mal pH? If breathing is the prime mover: in acute asthma and hypoventilation in COPD. HCO3−
• ↑ PaCO2 means respiratory acidosis and pH values reflect an acute noncompensated condi-
• ↓ PaCO2 means respiratory alkalosis tion in acute asthma, and full compensation in COPD.
Step 3. Look at the HCO3− or BE: does it account for
an abnormal pH? If breathing is not the prime
mover:
THE OXYGEN CASCADE
• ↓ HCO3− or BE means metabolic acidosis The raison d’etre of the cardiorespiratory system is to get
• ↑ HCO3− or BE means metabolic alkalosis oxygen to the tissues by means of oxygen cascading from
the outside to the subcellular environment. Even when needs of the tissues and approximating 250 mL/min
ventilation, diffusion and perfusion are in order, oxygen in a resting person. Oxygen delivery depends on
still has to reach and get into the tissues. cardiac output (CO), haemoglobin and SaO2, supplying
Oxygen transport is the passage of oxygen to the approximately 1000 mL/min, so that about 25% of the
tissues via the arteries and capillaries. The arterial cir- arterial oxygen content is used every minute (Law &
culation also acts as a cushion to soften the pulsations Bukwirwa 1999).
generated by the heart so that capillary blood flow is Oxygen moves down a pressure or concentration
stable. The term ‘oxygen transport’ is often used synony- gradient from a high level in air, through alveolar gas,
mously with, and is virtually the same as, oxygen deliv- arterial blood, capillaries and finally the cell, where
ery, which is the oxygen presented to the tissues. Oxygen energy is produced by the mitochondria (Fig. 1.15).
consumption or uptake by the tissues is usually equiva- Oxygen availability to the tissues depends on:
lent to oxygen demand, determined by the metabolic • SaO2, PaO2 and Hb
• cardiac output
• distribution of CO and tissue perfusion
• oxygen extraction
TABLE 1.4 Examples of arterial blood
• the oxygen dissociation curve
gas values in two disordersa
Tissue oxygenation reflects the balance between supply
Normal Acute asthma COPD (oxygen delivery or DO2) and demand (oxygen con-
PaO2 12.7 (95) 9.3 (70) 7.3 (55) sumption or V̇ O2). The cardiorespiratory system, as
PaCO2 5.3 (40) 3.3 (25) 8 (60) with most other systems, has plenty of reserve capacity,
pH 7.4 7.5 7.4 and DO2 is normally four times greater than V̇ O2, creat-
HCO−3 24 24 29 ing an oxygen extraction ratio (V̇ O2/DO2) of 25%.
a
Numbers in brackets indicate mmHg. V̇ O2 varies with metabolic rate, individual tissue
COPD, Chronic obstructive pulmonary disease. blood flows adjusting according to need (Wolff et al.
O2
Alveoli
Pulmonary
artery
Pulmonary
vein
Venous Arterial
circulation circulation
Tissue cells
FIGURE 1.15 Oxygen journey through cardiovascular system to mitochondria.

2016). An increase is usually met without difficulty by nary artery blood, where it is at the end of its journey
increased DO2 (mostly through increased CO, partly before being reoxygenated in the lungs (p. 471).
through increased minute ventilation) and increased
oxygen extraction by the tissues. Once maximum oxygen VARIATIONS
extraction is reached, consumption no longer drives
delivery but becomes dependent on it, leading to anaer- Effects of Obesity
obic metabolism and lactic acidosis. Worldwide, obesity has more than doubled since 1980,
Some organs are greedier than others, e.g.: driving cardiopulmonary morbidity and mortality
• The brain comprises 2.2% of body weight and (Chung 2016). It is second only to tobacco as the leading
receives 1.5% of CO. preventable cause of death (DeTurk & Cahalin 2011,
• The myocardium comprises 0.5% body weight and p. 477).
receives 5% of CO. Obesity loads the respiratory system, pushing up the
• The kidneys comprise 0.5% body weight and receive diaphragm so that FRC approaches residual volume
20% of CO. (Fig. 1.16), leading to closure of dependent airways and
• Skeletal muscle and skin comprise 50% body weight V̇ A/Q̇ mismatch (Salome et al. 2010). Breathing tends to
and receive 10% of CO (Epstein 1993). be rapid, shallow and apical.
Tolerance to hypoxia also varies: Obesity may also cause:
• The brain suffers irreversible damage within 3 min. • a mixed obstructive/restrictive respiratory defect
• The kidneys and liver can tolerate 15–20 min of (Reynolds 2011) and limited ability to take a deep
hypoxia. breath, thus hindering some forms of physiotherapy
• Skeletal muscle withstands 60–90 min and vascular and affecting some lung function test results (Enright
smooth muscle 24–72 h. 2015);
• Hair and nails continue to grow for some days after • breathlessness, which increases in supine (Perino et al.
death (Leach & Treacher 2002). 2016), ↑ WOB and ↑ VO ̇ 2 (Murphy & Wong 2013);
Septic patients may need 50%–60% extra oxygen deliv- • attenuated response to hypoxic and hypercapnic ven-
ered to their tissues, while patients with multiple trauma, tilatory drives, ↓ exercise capacity (Mesquita et al.
septic shock or burns may require 100% extra (Epstein 2015);
1993). At the same time, critically ill patients may be • tissue hypoxia, causing insulin resistance and sys-
affected by: temic inflammation (Ban et al. 2016), the inflamma-
• impaired DO2 because of cardiorespiratory tion leading to airway inflammation, infection risk
dysfunction;
• cellular oxygen extraction hindered by toxins associ- 7 TLC TLC
ated with sepsis, leading to mitochondrial dysfunc-
6
tion (Van Boxel et al. 2012);
• loss of autoregulation, leading to disordered regional 5 IRV
IC
Volume (L)
distribution of blood flow, both between and within 4 IC

organs; VT
3
• hypoxic kidneys and a liver unable to detoxify by-
products of the shocked state. 2
FRC ERV
Some cells can produce energy for a short time without 1 RV RV FRC
oxygen, using anaerobic metabolism, while sensitive
0
organs such as the brain are dependent on aerobic Normal weight Severely obese
metabolism. If tissues are not able to acquire, trans- FIGURE 1.16 Effect of obesity on lung volumes,
port, extract and utilize sufficient oxygen, lactic acidosis showing how FRC can approach residual volume.
occurs. Compare with Fig. 2.30A. ERV, Expiratory reserve
Compared to gas exchange in the lung, which is easily volume; FRC, functional residual capacity; IC, inspiratory
monitored in arterial blood, tissue oxygenation is usually capacity; IRV, inspiratory reserve volume; RV, residual
estimated indirectly from the leftover oxygen in pulmo- volume; TLC, total lung capacity.
(Almond 2013) and reduced muscle mass (King Stickford 2016), with cycle ergometry and cycling being
et al. 2013); especially effective for testing and training (Bott 2016).
• further loss of muscle mass during the meta-
bolic stress of illness, and lack of micronutrients Effects of Smoking
(Abdelhamid et al. 2016); Tobacco is the single most preventable cause of death
• stress on the heart with exercise (Vella et al. 2012), in the world today … it kills up to half of those who
sudden cardiac death (Adabag 2015), risk of heart use it.
failure (Alpert et al. 2016) and, in children, cardio- World Health Organization 2008
vascular risk (Philip et al. 2015);
• urinary incontinence (Wang et al. 2017), osteoporosis Smoking is the world’s leading cause of preventable
(Zhang et al. 2016a) and some cancers (Blackadar death (Siqueira 2017). It disproportionately affects the
2016); poorest members of societies and is rising rapidly in the
• barotrauma during MV (Pedoto 2012); Third World (Agrawal 2016) as multinational compa-
• obesity hypoventilation syndrome (Piper et al. 2016); nies offload their stocks. Each smoker loses at least a
• bias in the health care system (O’Brien et al. 2012). decade of life (Jha et al. 2013). The 5000 toxic chemicals
On the surgical wards, an obese patient should barely in tobacco smoke (Freire et al. 2016) include cyanide,
have emerged from anaesthesia before the physiothera- carbon monoxide, arsenic and over 50 known carcino-
pist becomes involved in pain control and positioning, gens (BMA 2015). The litany of destruction is outlined
closely followed by incentive spirometry and early in Table 1.5 and below.
mobilization, along with regional analgesia if possible Smoking shortens life by an average 11 min for each
(Bluth et al. 2016). Morbidly obese people show a 30% cigarette (Warren 2001). It increases the risk of post-
likelihood of atelectasis or pneumonia after abdominal operative complications, although it eases postoperative
surgery and a greater propensity for thrombosis and nausea and vomiting in patients who can escape the ward
wound infections (Licker et al. 2007). (Talbot & Palmer 2013). It worsens Crohns disease but
On the medical wards, obesity is associated with improves ulcerative colitis (Siqueira 2017). The effects
asthma (Ulrik 2016) and COPD (Katz et al. 2015). can even jump a generation, the grandchildren of smokers
It can disrupt pharmacokinetics, e.g. steroids can being more likely to develop asthma independent of the
augment obesity (Cooper 2011) while obesity itself mother’s smoking status (Magnus et al. 2015).
causes reduced response to steroids and bronchodilators Smoking is neither virile nor sexy, tobacco being
(Sismanopoulos 2013). toxic to ovaries (Camlin et al. 2016) and testes (Yang
In the ICU, obesity prolongs length of stay (Goh et al. et al. 2016b). Smoking during pregnancy increases the
2016) and increases the complications of immobiliza- risks of stillbirths (Westreich 2017), infant deaths and
tion, the latter being moderated by early rehabilitation harm that lasts into adulthood, e.g. impaired cognition,
(Genc et al. 2012). There is a greater need for MV increased impulsivity, hyperactivity and risk of develop-
(Tafelski et al. 2016) along with a requirement for ele- ing an addiction (Siqueira 2017). It increases the likeli-
vated airway pressures (Kaese et al. 2016). Paradoxically, hood of lower birth weight (Duby 2015), gestational
obesity is also associated with improved ICU survival, diabetes in daughters (Bao et al. 2016) and causes as
possibly by secretion of antiinflammatory adipokines much damage to the foetus as if it was smoking itself
(Yusuke et al. 2015). (Le Souëf 2000).
Multidisciplinary rehabilitation is required for
comorbidities (Capodaglio 2013), including pain KEY POINT
management because of altered physiology and drug It is never too late to quit.
utilization (D’Arcy 2016). Physiotherapy is based on Schroeder 2013
developing a long-term exercise habit, along with joint
protection. Oxygenation may increase during exercise Passive smoking can cause heart disease or lung cancer
because of the effect of deep breathing on expansion of in people who have never smoked, 50% of childhood
collapsed lung units (Sood 2009). Exercise training itself asthma and the majority of infant deaths (BMA 2015).
improves breathlessness as well as fitness (Bernhardt & The effect on infant mortality is ameliorated by cigarette
TABLE 1.5 Effects of smoking related to physiotherapy practice

Cardiorespiratory Carnage to both respiratory and cardiovascular systems (Chapters 3 & 4)
Risk of pneumothorax 13-fold (Light 1993)
Risk of sleep apnoea, asthma exacerbations, tuberculosis (Jayes et al. 2016)
↓ Vitamin C, which would otherwise repair some of the lung damage (Banerjee et al. 2008)
↑ Dosage requirements for corticosteroids, theophylline (Sohn 2015) and opioids (Talbot &
Palmer 2013)
Inflammatory damage and mucus production (Yang et al. 2016a), ↓ mucociliary clearance (Freire
et al. 2016)
Musculoskeletal Damage to diaphragm and quadriceps (Ramirez-Sarmiento 2004)
Lumbar disc herniation (Huang et al. 2016a)
Osteoarthritis (Amin et al. 2007)
Muscle weakness, osteoporosis, rheumatoid arthritis (Pignataro 2012)
Nonunion of fractures (Clement et al. 2016)
Ankylosing spondylitis (Ward et al. 2008)
Neurological Some neurological diseases and neuropathic pain (Pignataro 2012)
Risk of ulnar neuropathy (Richardson 2009)
↑ Postoperative pain in males (Chiang et al. 2016)
Other Cough, dyspnoea, reflux, dry throat, irritable upper airway, taste and smell disorders, bad breath,
toothache, nasal congestion, snoring, nasal discharge (Şanlı et al. 2016)
↓ Immunity (Bauer et al. 2013)
↓ Hearing (Chang et al. 2016)
Rotten teeth (Vettore et al. 2016)
Depression (Berk et al. 2013), ↑ risk of drugs misuse (Reed 2017)
↓ Sleep (Mehari et al. 2014)
Wrinkles (Vierkötter et al. 2015)
Kidney injury, erectile dysfunction (Siqueira 2017)
Doubling of the risk of dementia (Pignataro 2012)
taxes (Patrick et al. 2016). Children may also suffer ear A custom loathsome to the eye, hateful to the nose,
and chest infections, dental caries, hearing loss and harmful to the brain and dangerous to the lungs.
some learning disabilities (Duby 2015). King James I
In adults, passive smoking impairs lung function,
reduces mucociliary clearance (Freire et al. 2016) and Effects of Stress
exercise tolerance (Arjomandi et al. 2012), upsets the All ill people suffer stress at times, often as a result of
circadian rhythm (Sundar et al. 2015) and increases and sometimes as a predisposing factor to illness. The
heart and lung disease (Talbot & Palmer 2013), cancers following effects of stress have been identified:
of the lung, larynx and pharynx (Rafiq et al. 2016) and • ↑ RR, blood pressure (BP) and heart rate (HR)
stroke (Kwon et al. 2016). Third-hand smoke is a risk to (Schwartz et al. 2011), ↑ myocardial oxygen con-
children who ride in cars where others have smoked sumption, myocardial ischaemia and arrhythmias
(Talbot & Palmer 2013). (ICS 2014a);
Nicotine is more addictive than heroin and seven • shift of breathing from the diaphragm to the chest
times as addictive as alcohol (Haas & Haas 2000), reach- (Schleifer et al. 2002);
ing the brain 7 secs after inhalation (Siqueira 2017). • inflammation, with links to asthma, cardiovascular
Exposure to e-cigarettes is more than twice as damaging disease, some cancers and depression (Shields
to children as exposure to cigarettes (Kamboj et al. 2016), et al. 2016);
while vaping itself can cause nicotine addiction in ado- • exacerbation of respiratory infections (Stover 2016);
lescents (Liberman 2017). • neurocognitive deficit (Bharwani et al. 2016);
• immunosuppression (Fawcett et al. 2012), which in (p. 150–151 & 160) as well as nights disturbed by breath-
children can last into adult life (Slopen et al. 2013). lessness or coughing.
Anxiety has now been claimed as perhaps the most A full 90-min cycle is needed to gain the benefits of
important risk factor for cardiovascular disease REM sleep, which comprises a quarter of the sleep
(Allgulander 2016). cycle and is associated with dreaming and perceptual
learning. The brain is highly active during this restora-
Effects of Sleep tive phase and consumes more oxygen than when
Nurses and doctors frequently overestimate how awake at rest. It is the time when memories are con-
much sleep patients are getting, and underestimate solidated (McDevitt et al. 2015) and is particularly
the importance of sleep. important for critically ill patients to prevent memory
Gelling 1999 distortion.
Sleep is regulated by melatonin from the pineal
Sleep is necessary for the regulation of mood, memory gland, which is released at about 2200, peaks by 0300
(Kanda et al. 2016) and metabolism (Borbély et al. and is lowest around 0900. Sleep deprivation, poor
2016). It brings cardiorespiratory changes: sleep quality or obliteration of REM sleep contributes
• bronchoconstriction, which is only of consequence to cardiovascular disease, increased mortality (Rittay-
with asthma (Kamdar et al. 2012); amai et al. 2016), stroke, multiple sclerosis (Palma
• ↓ respiratory drive, hypotonia of respiratory muscles, 2013), dementia, impaired learning (Qiu et al. 2016a)
↑ PaCO2 and ↑ upper airway resistance (Sowho et al. and musculoskeletal pain (Li et al. 2017). Poor sleep
2014) especially during rapid eye movement (REM) quality is frequent in people after a cardiac event and
sleep (Fig. 1.17); may affect prognosis or impede cardiac rehabilitation
• dips in SaO2 to 90% or less (BTS 2008), which may (Le Grande et al. 2016). Rest, both physical and cogni-
drive SaO2 down the steep part of the dissociation tive, may also be limited due to illness or the environ-
curve (see Fig. 1.12); ment, and some cardiorespiratory diseases are subject
• ↓ lung volume due to the horizontal position, which to diurnal rhythms, e.g. COPD symptoms are worse
along with ↓ muscle tone leads to V̇ A/Q̇ mismatch in the morning, those of heart failure escalate during
and a doubling of airway resistance (Xie 2012); the day and are worst at night, thromboembolism
• ↓ metabolic rate, HR, and sympathetic tone, ↑ vagal occurs commonly between 1030 and 1230 h and
activity (Garcia et al. 2013). cardiac arrest occurs most frequently between 0600
Most people accommodate all this quite happily, and 1200 (Smolensky et al. 2015).
but those with little cardiorespiratory reserve can
suffer nocturnal desaturation, sometimes dramatically
EFFECTS OF IMMOBILITY
The pandemic of physical inactivity is associated
with a range of chronic diseases and early deaths.
ke
a
Ding et al. 2016

Aw
Minute ventilation
4
3/
ge Immobility predisposes to:
S ta e 2
S tag • ↓ muscle mass by up to 1%–5% per day, cardio-
vascular deconditioning and thromboembolism
REM (Mah 2013);
• orthostatic intolerance, ↓ V̇ O2max (Fig. 1.18) and
cardiovascular instability during position change
(Vollman 2013);
PaCO2 • ↓ survival and quality of life (BTS 2013);
FIGURE 1.17 Control of ventilation during sleep, showing • constipation (Giorgio et al. 2015), depression
reduced respiratory drive at deeper sleep stages. REM, (Hamer et al. 2013), incontinence (Jerez-Roig et al.
Rapid eye movement. (From Douglas et al. 1982.) 2016) and osteoporosis (Armstrong et al. 2016);
Immobility Moving from supine to standing
Blood volume 500 mL blood migrates to pelvis and legs
Sympathetic activity Cardiac output ↓ Venous return, cardiac output and BP
Vasoconstrictive reserve ↓ BP detected by aortic arch and carotid baroreceptors
Information sent to brainstem

Orthostatic intolerance VO2max
FIGURE 1.18 The effect of immobility on maximum
↑ Sympathetic activity and ↓ parasympathetic activity
oxygen consumption (V̇ O2max).
↑ HR and myocardial Arteriolar Venous

• for critically ill patients: pneumonia, delayed weaning, contractility constriction constriction
pressure sores (Vollman 2013), myopathy and delir-
ium (Pawlik 2012), muscle inflammation (Kang & Ji
2013) and joint contractures (Brower 2010). ↑ Cardiac output ↑ Peripheral ↑ Venous
Contractures begin immediately, especially for joints resistance return
held in extension (Trudel et al. 1999), although this is
unlikely to be significant for a patient who is immobile
for just a few days. ↑ Blood pressure
Loss of gravitational stimulus to the cardiovascular FIGURE 1.19 Typical circulatory response to postural
system causes a negative fluid balance within 24 h, change. BP, Blood pressure; HR, heart rate.
impairing vasoconstrictive ability and augmenting
deconditioning. Deterioration occurs more rapidly in
the cardiorespiratory system than the musculoskeletal Effects of Exercise
system, and deterioration is quicker than recovery
Physical activity can increase life expectancy by
(Dean & Ross 1992).
1.3–3.5 years.
Inactive people are said to be contributing to a mor-
Serón 2015
tality burden as large as tobacco smoking (Wen & Wu
2012), with 60% of the world’s population not being During exercise, tidal volume initially rises then RR
physically active enough for health (Vrdoljak 2014). increases rapidly while tidal volume stabilizes (Tsukada
et al. 2016). Exercise increases oxygen delivery, con-
Turning, Sitting and Standing Up sumption and extraction by several mechanisms:
Regular position change as a preventive measure reduces • The cardiovascular response can increase CO five-
haemodynamic instability on movement (Vollman fold, accomplished by a near doubling of stroke
2013). Moving from supine to standing increases minute volume and an increase in HR to about 220 minus
volume (Bahadur et al. 2008) and redistributes blood the person’s age (MacIntyre 2000).
from the thorax to the lower body, followed by compen- • The respiratory response is represented by increased
satory vasoconstriction in most patients to restore BP diffusion, more uniform lung perfusion, recruit-
(Fig. 1.19). ment of dormant capillaries and, except with asthma,
Orthostatic intolerance occurs with inadequate bronchodilation (Dominelli & Sheel 2012).
haemodynamic compensation, e.g. with hypovolaemia • Intense exercise can increase V̇ O2 20-fold (Owens
or autonomic dysfunction, after prolonged bed rest or 2013).
if the patient is elderly or dehydrated. Slow deep breath- • Cerebral oxygenation rises during mild exercise and
ing improves orthostatic tolerance (Lucas 2013). drops during hard exercise (Peltonen 2012).
• Acid–base balance is usually maintained by increased A physically active life is reported to add 8–10 years
ventilation, but metabolic acidosis may develop if of freedom from chronic illness (Di Raimondo et al.
buffering mechanisms are unable to cope with the 2016), the recommended level being at least 150 min
extra CO2 and lactic acid. a week of moderate intensity aerobic activity or 75
• PaO2 remains steady throughout. min of vigorous activity (Wise 2017a), but there is
Exercise also enhances mucous transport (p. 205), helps no lower threshold for benefits to be seen (Wilson
prevent low back pain (Steffens et al. 2016), reduces et al. 2016).
the risk of postoperative delirium (Abelha et al. 2013) For people with cardiopulmonary disease, regular
and a single session helps stabilize posture (Fukusaki exercise may be inhibited by dyspnoea or lack of social
et al. 2016). Gait is worsened by smoking (Verlinden support, in which case motivation is available via online
et al. 2016). forums video blogs, self-monitoring devices and phone
Regular exercise brings the following benefits: apps (Chaddha et al. 2017).
• ↓ mortality (Khan et al. 2017), cardiovascular The evidence base for prescribing exercise for 26 dif-
disease, diabetes and obesity, ↑ mental health and ferent diseases is described by Pedersen and Saltin
quality of life (Chaddha et al. 2017), protection (2015).
against immune dysfunction, some cancers,
Exercise is ‘a miracle drug’.
musculoskeletal disorders, dementia (Di Raimondo
Wen & Wu 2012
et al. 2016) and some of the damage caused by
smoking (Nesi et al. 2016);
• ↓ inflammation related to COPD (Davidson 2012),
CASE STUDY: MS LL
sepsis (Araújo et al. 2012), heart failure (Vlist & A 62-year-old patient from Cape Town is admitted with
Janssen 2010) and knee osteoarthritis (Gomes et al. an exacerbation of COPD. Answer the questions below.
2014);
• ↑ oxygen delivery and extraction (Hellsten & Nyberg Relevant medical history
2015); • Heart failure
• healthier semen in men (Vaamonde et al. 2012); • Hypertension
• ↑ bone mineral density to a greater degree than the • Increased dyspnoea for 2 weeks
drug alendronate (Macias et al. 2012);
• ↓ falls (Yoo et al. 2013) and depression (Stanton et al. Subjective
2015), ↑ sleep, ↓ stress (Williams 2016); • Cannot stop coughing
• the vascular changes shown in Figs 1.20 and 4.2. • Occasionally bring up phlegm
Control artery Athlete’s artery
FIGURE 1.20 Cross section of the artery of a healthy nonathlete (left) and an endurance athlete
(right) which conveys performance and health benefits. (From Green et al. 2012.)
• Cannot sleep • Uncontrolled cough

• Daren’t lie down • Fatigue
• Exhausted • Anxiety
• Sputum retention
Objective • Stress incontinence
• Apyrexial • ↓ Mobility
• Oxygen via nasal cannulae at 2 L/min 3. Goals
• Rapid shallow breathing with prolonged expiration • Short term: optimize oxygen, control cough, clear
• Fluid chart and clinical assessment indicate chest, balance rest and exercise.
dehydration • Long term: educate patient and liaise with family
• No oxygen prescription or monitoring charts for home management.
• Speaking sets off paroxysms of wheezy coughing, 4. Plan
usually nonproductive • Liaise with the team about the need for a Venturi
• Clutches between legs when coughs mask, oxygen prescription and monitoring
• Sits in chair day and night (Chapter 5).
• Can mobilize slowly • Positioning for comfort, breathlessness and
• Blood gases on air: PaO2 10.2 kPa (76.7 mmHg), sputum clearance.
PaCO2 6.4 kPa (48.1 mmHg), pH 7.4, HCO3− • Identify cause of poor sleep e.g. dyspnoea/cough/
28 mmol/L noise/anxiety, then remedy as possible with the
team.
Questions • Educate on cough suppression for use when
1. Analysis? cough is uncontrolled and nonproductive.
2. Problems? • Educate on mucociliary clearance, including fluid
3. Goals? intake. Patient chose manual techniques at first,
4. Plan? then autogenic drainage.
• Educate on effective cough for when secretions
are accessible.
CLINICAL REASONING
• Explain connection between coughing and stress
Comment on the logic of the following conclusion to a incontinence, teach preliminary pelvic floor exer-
research study. cises and refer to continence service.
‘Our data suggest that the use of postural drainage • Show breathlessness management strategies.
and chest percussion in patients without sputum • Mobilize to toilet.
production is not indicated …’ • Provide written daily programme for self chest
Chest (1980), 78, 559–564 management and mobility.
• Liaise with ward staff re. getting dressed and
mobilizing.
Response to Case Study • Rehabilitate to independence, including family.
1. Analysis
• Breathing pattern suggests ↑ WOB.
• Blood gases indicate hypoxaemia, hypercapnia RESPONSE TO CLINICAL REASONING
and compensated respiratory acidosis. It is not indicated to do an unnecessary treatment.
• Oxygen therapy is uncontrolled.
• Coughing is largely ineffective and contributes to
fatigue.
• Coughing, stress incontinence, immobility and RECOMMENDED READING
fluid restriction are likely to be interrelated. Berryman, N., 2017. Relationships between lower body
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• Dyspnoea (1), 53–59.
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model of breathing. Resp. Physiol. Neurobiol. 237, 51–56.
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session of roller massage prolongs voluntary torque
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shifting? Eur. J. Appl. Physiol. 117 (1), 795–807.
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the study of the mechanics of breathing during exercise. Nakajima, K., Oda, E., Kanda, E., 2016. The association of serum
Respir. Physiol. Neurobiol. 180, 2–3. sodium and chloride levels with blood pressure and
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pulmonary vasoconstriction: from molecular mechanisms to 51–57.
medicine. Chest 151 (1), 181–192. Rae, D.E., Chin, T., Dikgomo, K., 2017. One night of partial
Fähling, M., Persson, P.B., 2012. Oxygen sensing, uptake, sleep deprivation impairs recovery from a single exercise
delivery, consumption and related disorders. Acta. Physiol. training session. Eur. J. Appl. Physiol. 117 (1), 699–712.
(Oxf.) 205 (2), 191–193. Roman, M.A., Rossiter, H.B., Casaburi, R., 2016. Exercise, ageing
Feiner, J.R., Weiskopf, R.B., 2017. Evaluating pulmonary and the lung. Eur. Respir. J. 48 (5), 1471–1486.
function: an assessment of PaO2/FIO2. Crit. Care Med. Ruprecht, A.A., De Marco, C., Pozzi, P., et al., 2016. Outdoor
45 (1), e40–e48. second-hand cigarette smoke significantly affects air quality.
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2
Assessment
LEARNING OBJECTIVES
On completion of this chapter the reader should be able to: • analyse radiology findings;
• interpret medical notes and nursing charts; • interpret respiratory function tests;
• analyse a patient’s subjective report in order to develop, • use clinical reasoning to identify cardiorespiratory
with the patient, problem-based goals and plans; problems.
• develop the skills of observation, palpation and
auscultation;
OUTLINE
Introduction, 29 Auscultation, 44
Background information, 30 Imaging, 47
Subjective assessment, 33 Respiratory function tests, 57
Observation, 37 Case study: Ms DT, 65
Palpation, 42 Clinical reasoning, 66
INTRODUCTION unnecessary treatment. Effectiveness is assisted by

incorporating the domains of the International Classi-
It is more important to know what sort of a patient
fication of Functioning, Disability and Health (ICF),
has a disease than what sort of disease a patient has.
which includes environmental and social factors and
William Osler
provides a standardized language on rehabilitation and
Accurate assessment is the linchpin of physiotherapy what matters to the patient, i.e.:
and forms the basis of clinical reasoning. A problem- • body function and structure
based assessment leads to thinking such as: • activity limitation
• This patient cannot cough up her sputum by herself. • participation (Stucki 2016)
Why? The last two concepts relate in particular to the multi-
• Because it is thick. Why? disciplinary team within which the physiotherapist
• Because she is dehydrated. Why? works. Patient participation is embedded in shared deci-
• Because she feels too ill to drink. sion making, particularly for patients who have diffi-
Illogical assessment leads to reasoning such as: ‘This is culty communicating due to dyspnoea or intubation.
chronic bronchitis therefore I will turn the patient side- Relevant parts of the patient assessment should be
to-side and shake her chest’. repeated after treatment to assess outcome. Specific
A thoughtful assessment encourages both efficiency assessment and outcomes for different conditions are in
and effectiveness. Efficiency saves time by avoiding the pertinent chapters.
29
BACKGROUND INFORMATION Charts

Not everything that counts can be measured. Not The charts record:
everything that can be measured counts. • the vital signs of temperature, blood pressure (BP),
Albert Einstein heart rate (HR), respiratory rate and arterial oxygen
saturation (SpO2);
Handover • prescription and monitoring for oxygen and drugs;
It is the physiotherapist’s job to clarify the indications • fluid balance.
for physiotherapy to other staff, and to explain which Respiratory rate (RR) is normally 10–16 breaths/min.
changes in a patient’s condition should be reported. No It increases with exercise, anxiety and sometimes heart
patient is too ill or too well for physiotherapy. or lung disease.
The ward report or handover also provides the Core temperature is one of the most tightly guarded
opportunity to ask three oft-neglected questions: of physiological parameters and is usually maintained
1. Is the patient drinking? at 37°C, but may vary by up to 1°C in health. For acute
2. Is he eating? patients, the chart should be checked at every visit
3. Is he sleeping? because fever is the main harbinger of infection.
Apart from a daily report from the nurse in charge, any Fever may be accompanied by increased RR and HR
other opportunity to communicate should be taken, because excess heat raises oxygen consumption and
such as ward rounds and meetings. For physiotherapists metabolic rate. Clinical examination helps distinguish
working in the community, much communication will respiratory from other infection. Pyrexia can also have
be on the phone, but visits to other teams usually benefit a noninfectious origin, e.g. atelectasis, dehydration,
all concerned. thromboembolism, blood transfusion or drug reaction
If physiotherapy notes are kept separate from the (Cunha 2013).
medical notes, verbal communication can be reinforced Fever is an adaptive response to infection, some
by writing physiotherapy information in the medical microorganisms being adversely affected and some
notes, e.g. a résumé of physiotherapy treatment or defence mechanisms performing better at higher body
request for a minitracheostomy. temperatures (Richardson et al. 2015), but it may have
adverse effects with noninfectious conditions (Walter
Notes et al. 2016).
Relevant details from the medical notes include:
• applicable medical history, e.g. other disorders KEY POINT
needing physiotherapy, and conditions requiring
A pyrexial patient may be referred for physiotherapy
precautions in relation to certain treatments, e.g. with a ‘chest infection’. Sputum retention can accom-
light-headedness, bleeding disorder, history of falls pany a chest infection but does not itself cause pyrexia.
or swallowing difficulty; The treatment for a bacterial chest infection is antibiot-
• relevant investigations, medical treatment and ics while the treatment for sputum retention is physio-
response; therapy. The physiotherapist works on the problem
• social history and home environment; rather than the diagnosis.
• recent cardiopulmonary resuscitation (requiring
X-ray inspection for aspiration or fracture); Blood pressure indicates the force that the blood exerts
• possibility of bony metastases; on the walls of the vessels. Normal at rest is 120/80. A
• longstanding steroid therapy, leading to a risk of systolic BP <90 mmHg in adults indicates hypotension.
osteoporosis; These patients should be mobilized only with close
• history of radiotherapy over the chest. observation for light-headedness, and with a chair close
The last four findings are a warning to avoid percus- behind. A systolic pressure >140 or a diastolic pressure
sion or vibrations over the ribs until sufficient infor- >90 indicates hypertension. The relevance of BP to exer-
mation is available to ensure that there is no risk of rib cise training, heart surgery and manual hyperinflation
fracture. is discussed in the relevant chapters.
CHAPTER 2 Assessment 31
Normal heart rate at rest is 60–100 beats/min (bpm). TABLE 2.1 Examples of criteria for
More than 100 bpm indicates tachycardia, which increases calling the outreach team
myocardial oxygen demand and may indicate sympa-
thetic activity, hypoxaemia, hypotension, hypoglycaemia, Vital sign Patient at risk
dehydration, anxiety, pain or fever. Less than 60 bpm Airway Threatened airway, excessive
indicates bradycardia, which may reflect profound hypox- secretions or stridor
aemia, arrhythmias, heart block or vagal stimulation due Breathing RR <8 or >25 breaths/min
to suctioning. Moderate bradycardia is normal during Circulation HR <50 or >150 beats/min
Systolic BP <90 mmHg,
sleep and in the physically fit. Both tachycardia and brady-
>200 mmHg, or drop of
cardia can impair cardiac output. Voluntary regulation of
>40 mmHg
HR is achievable by yogi masters, or by others with the BP below patient’s normal values
help of biofeedback (Jones et al. 2015a). Consciousness Sustained fall in Glasgow coma
Oximetry gives instant feedback on SpO2 and is scale of >2 in past hour
accurate even in hypoxic or shock states (Overbeck Oxygen SpO2 <90% on >.50 FiO2
2016). The different absorption of light by saturated and Urine output <30 mL/h for >2 h (unless normal
unsaturated haemoglobin (Hb) is detected by a pulse for the patient)
oximeter, which displays the percentage of Hb saturated General Clinically causing concern
with oxygen. The sensor is attached close to a pulsating Not responding to treatment
arteriolar bed on the ear, finger or toe. Average values BP, Blood pressure; FiO2, fraction of inspired oxygen;
for normal adults breathing air is 97.1% at 18 years old HR, heart rate; RR, respiratory rate.
and 95.4% at 70 years old, the lower limits of normal
being 96%–94%, respectively (Pretto et al. 2013). It The vital signs may be correlated by a ‘track-and-
is interpreted in relation to the fraction of inspired trigger’ Modified Early Warning Score (MEWS) system
oxygen (FiO2). (Table 2.1) or an electronic automated system (Schmidt
The relationship between SpO2 and arterial blood et al. 2015) to identify patients at risk. Vital sign
gases is shown in Fig. 1.12 and Table 1.1. Oximetry streaming with Google Glass holds promise (Liebert
becomes less accurate if Hb desaturates below 83% et al. 2016).
(NGC 2001) or if there is too much motion or ambient Prescribed drugs and oxygen are documented on the
light, or too little signal (cold peripheries, anaemia, prescription chart and their effects documented on the
vasoconstriction, peripheral arterial disease, hypoten- observation chart, e.g. peak flow or SpO2.
sion, hypovolaemia, hypothermia or finger clubbing). The fluid chart documents input and output. It
With nail polish, the probe can be turned sideways so should show a positive daily balance of about
that the light does not pass through the nail. The delay 500–1000 mL due to insensible loss from the skin and
between application and an accurate reading may be respiratory tract. There are many reasons for a wide
30 s for a finger probe, and most probes have a light to variation in fluid balance, including ambient tempera-
indicate maximum pulsation. Gentle rubbing may be ture and major fluid shifts after surgery.
needed to encourage vasodilation. Fluid overload may cause hyponatraemia and sys-
Arterial blood gases may be required in the following temic or pulmonary oedema. Dehydration is accompa-
situations: nied by reduced urine output and can be caused by
• unreliable oximetry readings diuretics, laxatives, lack of thirst in old age, dementia,
• critically ill patients inability of a patient to reach or manage their drink, or
• if there is an unexplained drop in SpO2 conscious fluid restriction due to anxiety about reaching
• clinical signs of hypercapnia (p. 40) the toilet. A urine colour chart can be used to assess
• breathless patients at risk of metabolic conditions patients at home or in residential care (Malisova et al.
such as diabetic ketoacidosis or renal failure 2016), but is only reliable for early morning specimens
In smokers, a fall in SpO2 during a 20-s breath-hold at and so long as the colour has not been affected by medi-
end-exhalation may identify lung damage before symp- cation (Heneghan et al. 2012). Table 2.2 shows the fluid
toms become apparent (Inoue 2009). balance of a healthy adult.
TABLE 2.2 Sources of normal fluid gain and loss over 24 h in a 70 kg male
INTAKE AND CATABOLIC PROCESSING OUTPUT
Water via fluids (mL) 1500 Urine (mL) 1500
Water via food (mL) 500 Evaporation from skin and lungs (mL) 800
Water via metabolism (mL) 400 Faeces (mL) 100
Total (mL) 2400 Total (mL) 2400
Dehydration is common in older patients (McCrow are the commonest electrolyte emergency, requiring
et al. 2016) and predisposes to: insulin and glucose to force potassium back into
• sputum retention the cells.
• pressure sores Urea is formed from protein breakdown and is excreted
• constipation by the kidneys. High levels may be caused by impaired
• confusion, short-term memory loss and impaired kidney perfusion from heart failure or shock. Creati-
cognition (Rush 2013) nine is formed from muscle breakdown and is also
• kidney dysfunction renally excreted. Levels rise with kidney failure and
• headache drop with malnutrition. Both urea and creatinine
• delayed BP response to position change (Yadav et al. rise with dehydration.
2016)
• muscle cramps Albumin
• fatigue This antioxidant is the main protein in plasma and the
• impaired motor control (Holdsworth 2012) interstitium, providing 15% of the buffering capacity
• ↑ HR and orthostatic intolerance after exercise and 80% of the osmotic pressure of blood (Vincent
(Charkoudian et al. 2016) 2001). Reduced levels, due to hypermetabolism, malnu-
Fluid loss from the vascular to the interstitial space is trition, blood loss, liver or kidney problems, burns,
caused by altered hydrostatic or oncotic pressures, or ascites, chronic inflammation or critical illness, cause
increased capillary membrane permeability, leading to metabolic alkalosis and reduce osmotic pull from the
effective hypovolaemia. vascular space so that fluid escapes, causing systemic
and pulmonary oedema.
Biochemistry
Normal values are in Appendix A. Microbiology
Microorganisms are identified by culturing specimens,
Urea and electrolytes e.g. blood, sputum or pleural fluid, on various media
Below are the urea and electrolyte results that are most that promote their growth. Most bacteria grow in
relevant to physiotherapy. 24–48 h, but the tubercle bacillus may require 6 weeks.
Sodium is the commonest electrolyte in the blood and Sensitivity tests identify which antibiotics can then
is regulated by the kidneys. Low levels (hypona- tackle the bacteria.
traemia) are due to fluid retention or inappropriate
antidiuretic hormone secretion, while high levels Haematology
(hypernatraemia) indicate dehydration. A full blood count analyses the components of blood to
Potassium is the principal intracellular electrolyte. High assess blood cells and coagulation.
or low values can weaken muscles, including the dia- Red blood cells (erythrocytes) are the most abundant
phragm. Low levels (hypokalaemia) predispose to cell in blood and contain no nucleus so they can
cardiac arrhythmias, and can be caused by loss from penetrate the smallest capillaries. Relevant abnor-
diarrhoea or vomiting, inappropriate steroids (Blann malities are the following:
2006, p. 62) or too-rapid correction of respiratory • Reduced haemoglobin indicates anaemia, which
acidosis (Hammond et al. 2013). High levels (hyper- causes fatigue and is poorly tolerated in people
kalaemia) suggest acidosis or kidney failure and with lung or heart disease. Mobilizing a patient
with low Hb requires close attention to a patient’s add, ‘And she just might be telling you the best
colour and the same precautions as for hypo- management too’
tension. A high concentration of Hb, known Pitkin 1998
as polycythaemia, is the body’s adaptation to
chronic hypoxaemia due to disease or living at The subjective assessment is what matters to the patient.
high altitude. Problems such as breathlessness are more closely related
• Haematocrit (packed cell volume) is the propor- to quality of life than physiological measurements, and
tion of total blood volume that is composed of subjective wellbeing is associated with longevity (Xu &
red cells. Red blood cell count provides the same Roberts 2010). When possible, patients should be
information. assessed in a well-lit area that is quiet, private, warm and
• Erythrocyte sedimentation rate is raised following well ventilated. Respect for privacy includes awareness
myocardial infarction or if there is inflammation, of those within hearing.
tuberculosis (TB), cancer or anaemia.
White blood cells (leucocytes) are part of the immune KEY POINT
system, working to ingest unwelcome micro-
If a patient’s curtain is drawn, it is equivalent to
organisms by phagocytosis. A raised white cell count
their front door and you need to knock.
(WCC) indicates infection or other condition such
Beaven 2012
as cancer, rheumatoid arthritis or the postoperative
state. Neutrophils are the most common white cells
and their number is raised with bacterial infection or The patient requires an explanation because the public
inflammation. They become overactive in sepsis and perception of physiotherapy is often limited to football
start to destroy healthy tissue as well as pathogens. and backache.
Cytotoxic drugs reduce WCC (leukopenia) e.g. with The inequality of the relationship is minimized by:
cancer or following transplantation, indicating that • positioning ourselves at eye level if possible;
the patient is immunocompromised and extra infect- • addressing adults by their surname (Wilkins et al.
ion control precautions are required. 2010, p. 12) unless they ask otherwise;
Clotting studies (see the Glossary) which indicate that • asking permission before assessment.
a patient might bleed easily include low platelet Permission not only encourages patients’ self-respect, it
count (thrombocytopaenia), prolonged prothrom- is a legal necessity in most countries. It is also good
bin time or raised international normalized ratio. practice to ask before moving a patient’s personal
Patients on heparin are at risk. items or opening their locker. In relation to addressing
patients, for elders it can be seen as disrespectful rather
Cytology and histology than friendly to address them by their first name
Cytology is the study of fluids, e.g. in sputum or blood, unprompted.
to identify abnormal or cancerous cells. Histology does Patients are then asked to define their problems and
the same with tissues such as biopsied lung tissue. how these influence their life. Empathy is then facili-
tated by using the patient’s words and phrases rather
Arterial blood gases than our own. Acknowledging a patient’s experience
Arterial blood is usually taken from the radial artery by and respecting their opinion are also potent motivating
a doctor, as opposed to other blood tests in which blood factors.
is taken from a vein by the phlebotomist. Patients should
be undisturbed and stay in the same position for 20 min Patient History
beforehand. Interpretation is on p. 17. ‘I know what my body is telling me’.
Morgan 2012
SUBJECTIVE ASSESSMENT The history from the notes is supplemented with
Osler supposedly said, ‘Listen to the patient. He questions about how the patient’s condition is affecting
is telling you the diagnosis’, to which I would their lifestyle, from which goals can be developed.
Unreliability of recall may be caused by anxiety, accord- Maximum

ing to Barsky (2002), who also suggests that patients breathlessness
should be asked to describe the most recent events first.
If the patient is unable to give a history, relatives can be
questioned, but there is often disparity between rela-
tives’ and patients’ perception of their quality of life
(Carr 2001).
Cardiorespiratory Symptoms
How long have symptoms been troublesome? What is
their frequency and duration? Are they getting better or
worse? What are aggravating and relieving factors?
Breathlessness
Dyspnoea can be as powerfully aversive as pain …
Documentation of dyspnoea is the first step to
improved symptom management.
Stevens et al. 2016
No breathlessness
Shortness of breath (SOB) is the most common
symptom in advanced cardiopulmonary disease (Booth FIGURE 2.1 Visual analogue scale for shortness of
et al. 2008) but it can also be metabolic, neurogenic or breath.
neuromuscular in origin. Respiratory causes usually
relate to excess WOB, which is abnormal if inappropri- gradually, but they often complain of its functional
ate to the level of physical activity. Significant SOB is effects such as difficulty in getting upstairs, which
indicated by the inability to complete a full sentence. underlines the relevance of the ICF approach. Detailed
Visual analogue scales (Fig. 2.1) and numeric rating measurement of SOB is on p. 251. Table 2.3 indicates
scales have been validated (Johnson et al. 2010), or a key possible causes in relation to onset.
question at each visit can be a comparative measure-
ment, e.g.: Cough
• ‘How much can you do at your best/worst?’ Coughing is abnormal if it is persistent, painful or pro-
• ‘What are you unable to do now because of your ductive of sputum. It may be underestimated by smokers
breathing?’ and people who swallow their sputum. Acute cough is
If SOB increases in supine it is called orthopnoea. In normally benign, self-limiting and associated with
lung disease, this is caused by pressure on the diaphragm upper respiratory tract infection, in which the virus
from the abdominal viscera. In heart failure, a poorly hijacks the cough to propagate itself (Atkinson et al.
functioning left ventricle is unable to tolerate the 2016). Chronic cough is one that lasts more than 8
increased volume of blood returning to the heart in weeks and may be associated with gastro-oesophageal
supine. Paroxysmal nocturnal dyspnoea is caused by reflux disease (GORD), asthma, hyperventilation syn-
orthopnoeic patients sliding off their pillows during drome (Benoist 2015), smoking, lung disease, pleural
sleep, leading them to seek relief by sitting up over the effusion, heart failure, post-nasal drip, habit, Tourette
edge of the bed. syndrome, some drugs, and occupational or environ-
Distinguishing SOB due to lung or heart disorder is mental factors (Song et al. 2016a).
achieved by clinical reasoning using peak flow readings,
auscultation, imaging, exercise testing and history. KEY POINT
The quality of SOB can only be judged by the patient,
A cough should be reported if is chronic and of
typical descriptors being identified by Scano et al.
unknown cause, or if it is accompanied by unexplained
(2005), and, specifically for heart failure, by Parshall haemoptysis.
(2012). Patients may deny SOB if it has developed
TABLE 2.3 Approximate time to the onset of dyspnoea

Immediate Hours Days or weeks Months or years
Pneumothorax Asthma Pleural effusion Chronic obstructive pulmonary disease
Pulmonary embolus Pulmonary oedema Lung cancer Lung fibrosis
Foreign body aspiration Chest infection Heart failure
Myocardial infarct Neuromuscular disorder
TABLE 2.4 Characteristics of cough and habit coughs, such as those following viral infect-
ion, usually disappear over time, but a dry cough can
Type of cough Possible causes perpetuate itself by irritating the airways, in which case
Dry Chronic asthma, ILD, pollutants, it can be controlled by the measures on p. 218.
hyperventilation syndrome, airway The cough reflex may be oversensitized by upper res-
irritation, ACE inhibitor drugs, viral piratory tract infection, mouth-breathing, GORD or irri-
infection
tants such as aerosols and cigarette smoke (Morice 2013).
Productive COPD, bronchiectasis, CF, PCD,
Listening to the cough will help identify weakness or
acute asthma, chest infection
With position Asthma, bronchiectasis, CF, PCD, pick up sounds that may be missed on auscultation but
change pulmonary oedema stimulated by a cough. It is best to ask patients to show
With eating or Aspiration of stomach contents, e.g. how they would cough to clear phlegm rather than to
drinking with neurological disease or in ask them to ‘show me a cough’. Cough questionnaires
elderly people include the Leicester Cough Questionnaire (Ward 2016)
With exertion Asthma, COPD, ILD and Cough-specific Quality of Life Questionnaire
Inadequate Weakness, pain, poor understanding (Spinou & Birring 2014). Severity can be measured with
Paroxysmal Asthma, aspiration, upper airway a visual analogue scale (Morice et al. 2007).
obstruction, croup, whooping
cough Secretions
ACE, Angiotensin-converting enzyme; CF, cystic fibrosis; Can the patient clear their secretions independently?
COPD, chronic obstructive pulmonary disease; ILD, interstitial If not, do they need advice or physical assistance?
lung disease; PCD, primary ciliary dyskinesia.
For acute patients, are secretions interfering with gas
exchange? For people with a chronic condition, are
Serious conditions presenting as an isolated cough secretions impairing their lifestyle or contributing to a
include cancer, TB and foreign body aspiration. A vicious cycle that perpetuates hypersecretory disease
chronic cough is only considered idiopathic after assess- (p. 88)? Has sputum changed in quality or quantity?
ment at a specialist cough clinic (Morice 2006).
Suggested questions relating to a cough are: Wheeze
• What started it (e.g. infection)? Airways narrowed by bronchospasm increase the WOB
• What triggers it (e.g. smoking)? and may cause wheezing. The feeling should be explained
• Is there sputum? to patients as tightness of the chest on breathing out,
• Does the cough occur at night (GORD and/or not just noisy, laboured or rattly breathing. If aggravated
asthma)? by exertion or allergic reaction, asthma is a likely cause.
• Does it cause pain (see ‘pleuritic pain’, p. 36)? Airways which are narrowed by factors other than bron-
Clinical reasoning can then be used, with the help of chospasm may also cause a wheeze, but less consistently.
Table 2.4, to identify possible causes. Objectively, wheeze is confirmed by auscultation.
A cough caused by asthma or GORD should disap-
pear once the condition is controlled. A quarter of Other Symptoms
patients taking angiotensin-converting enzyme inhibi- Pain and SOB activate common areas in the brain
tor drugs develop a dry cough, which usually dissolves (Kohberg et al. 2016). Chest pain may be musculoskel-
in 2–3 months (Li et al. 2012). Other nonproductive etal, cardiac, alimentary or respiratory in origin. Many
patients associate chest pain with heart attacks, and 2008). Visual analogue scales fail to assess the impact
anxiety may modify their perception and description of of fatigue on daily functioning, and valid measure-
it. Lung parenchyma contains no pain fibres, but chest ments are in Appendix A or described by Butt et al.
pains relevant to the physiotherapist are the following: (2013). Fatigue serves a protective function (Boullosa &
1. Pleuritic pain, which denotes the nature of the pain Nakamura, 2013) and can lead to exhaustion, which,
rather than the pathology. The pleura is replete with if accompanied by ventilatory failure, may indicate the
nerve endings, and pleuritic pain is sharp, stabbing need for noninvasive ventilation.
and worse on deep breathing, coughing, hiccupping, Sleep may be impaired by anxiety, SOB, a noisy envi-
talking and being moved. Causes include pleurisy, ronment, loss of day/night rhythm, pain or depression.
lobar pneumonia, pneumothorax, fractured ribs or Appetite may be impaired by depression, feeling ill, hos-
pulmonary embolism. pital food or the side effects of drugs.
2. Angina pectoris, a crushing chest pain due to myo- Dizziness may be associated with postural hypoten-
cardial ischaemia, which should be reported. sion, hyperventilation syndrome or a lesion of the 8th
3. Musculoskeletal pain, e.g. costovertebral tenderness, cranial nerve or brain stem. A history of falls requires
which may be due to hyperinflation, when the investigation of the risks on p. 412. Fainting (syncope)
muscles are obliged to work inefficiently, or chronic or near-fainting may be caused by hyperventilation syn-
coughing, which may cause muscle strain. Musculo- drome, prolonged coughing or cardiovascular disorder.
skeletal pain around the neck or shoulders may inter-
fere with the accessory muscles of respiration. KEY POINT
4. Raw central chest pain, worse on coughing, caused
If a patient spends their day flopped in front of their
by tracheitis and associated with upper respiratory
screen, is this because of preference, exercise limita-
tract infection or excessive coughing.
tion or depression?
5. Bronchiectasis pain, which is a deep ache localized to
areas of inflammation.
Postoperative pain is discussed on p. 297. How does the patient feel about their disease? This ques-
Fatigue is a common and often wretched symptom, tion provides the opportunity for patients to describe
closely associated with SOB and depression (Radbruch their feelings but does not pressurize them. Anxiety
2008). Patients may prefer to say that they are tired affects the neural processing of respiratory sensations,
rather than admit to depression, which carries a stigma. which may underlie the increased perception of respira-
The word ‘fatigue’ is not found in all languages, in which tory sensations in anxious individuals (Leupoldt et al.
case the word ‘weakness’ can be used for the physical 2012), particularly if symptoms are unpredictable.
dimension and ‘tiredness’ for the cognitive dimension. Anxiety may also reinforce frustration, embarrassment
Cognitive fatigue complicates activities such as reading, or restricted social function or loss of control. People in
driving and other activities of daily living. The sensation some cultures may express emotions in terms of bodily
fits all domains of the ICF and is characteristic of sensations.
many chronic conditions which may overlap, including It is useful to adopt the practice of asking patients
chronic obstructive pulmonary disease (COPD), heart what they think is the cause of their symptoms, because
failure, cancer and neurological disease. Causes include their perceptions are often surprisingly accurate.
inflammation, anaemia, infection, stress, dehydration,
cachexia or sedatives (Radbruch 2008). Fatigue is severe Activities of Daily Living
if it cannot be relieved by rest or sleep. Many patients express a desire for quality of life
Fatigue and weakness feel similar but may require equal to or greater than their desire for quantity
opposite management strategies, e.g. exercise for weak- of life.
ness and rest for acute fatigue. However, many patients O’Neil et al. 2013
have both and require energy conservation, pacing and
graded exercise. If a patient is not able to describe the Is it difficult to bathe, dress or shop? How much daily
sensation, it is noteworthy that carers may overesti- exercise does the patient take? Limitation of activity is
mate and staff may underestimate fatigue (Radbruch not an accurate indicator of cardiorespiratory disease
because patients gradually reduce their activities of daily

living as they experience slowly increasing breathless-
ness or fatigue, thus perpetuating a vicious cycle. But
questions can be asked such as ‘what have you stopped
doing because of your breathing?’ Reduced mobility
may lead to constipation, which is exacerbated by dehy-
dration, and to urinary incontinence, which is exacer-
bated by coughing.
How many stairs are there at work or home? Is the
environment well-heated, smoky, dusty? Does the
patient live alone, smoke, eat well? Is nutrition affected
by SOB or dysphagia? What support is available?
Problems with personal care, employment, finance and
housing also loom large for people with cardiorespira-
tory disease. Measures of physical functioning are
more related to quality of life than spirometry (Geijer
et al. 2007).
Questionnaires are described in the relevant chapters.
OBSERVATION
Any part of the body not being observed should be kept
covered throughout, with awareness of the needs of dif-
ferent cultures (Wilson et al. 2012).
FIGURE 2.2 Soft tissues draped over the bones and
Breathing Pattern prominent sternomastoid muscles, indicating malnutri-
The breathing pattern should be observed while tion and muscle hypertrophy.
approaching the patient because it will change once they
are aware of the physiotherapist’s presence. Normal
breathing is rhythmic, with active inspiration, passive
expiration and an inspiratory to expiratory (I:E) ratio
of about 1 : 2. There should be synchrony between chest
and abdominal movement, but a relaxed person may
show only abdominal movement. Individual variations
achieve the same minute volume by different combina-
tions of rate and depth or varied chest and abdominal
movements.
Laboured breathing represents increased WOB, e.g.:
• forced exhalation with active contraction of the
abdominal muscles to propel air out through nar-
rowed airways;
• obvious accessory muscle contraction (Fig. 2.2);
• indrawing/recession/retraction of the soft tissues of
the chest wall on inspiration (Fig. 2.3), caused by
excess negative pressure in the chest which sucks in
supraclavicular, suprasternal and intercostal spaces,
thus destabilizing the chest wall and further increas- FIGURE 2.3 Indrawing of the soft tissues between the
ing the WOB. ribs due to extra work of breathing during inspiration.
FIGURE 2.4 Paradoxical inward movement of the abdomen on inspiration due to weakness or
fatigue of the diaphragm.
Disturbed speech may represent increased WOB, e.g. Periods of apnoea interspersed with waxing and waning
prolonged inspiration (which increases the silences), of the rate and depth of breathing are called Cheyne–
short expiration (which reduces the time available for Stokes breathing when regular or Biot’s breathing when
speech), faster RR, smaller tidal volumes or inability to irregular. These indicate neurological damage, but
speak in complete sentences (Tehrany et al. 2016). Cheyne–Stokes breathing is also associated with heart
Paradoxical breathing may be evident by the following: failure (Olson 2014) or nearing the end of life, or it may
• indrawing of soft tissues (as above); be normal in some elderly people.
• Hoover’s sign, which occurs in a hyperinflated chest Irregular breathing indicates tension or may occur
when the flattened diaphragm (see Fig. 2.6) pulls in during normal rapid eye movement sleep. Sighs above
the lower ribs on inspiration, becoming, in effect, an the normal rate of 0–3 in 15 min may indicate hyper-
expiratory muscle; ventilation syndrome (Barker & Everard 2015).
• flail chest due to rib fractures (p. 534);
• abdominal paradox, in which a weak or fatigued General Appearance
diaphragm is sucked up into the chest by negative Is the patient obese, thus compromising diaphragmatic
pressure generated during inspiration so that the function, or cachectic, indicating poor nutrition and
abdomen is sucked in (Fig. 2.4) instead of swelling weakness? If the patient is unkempt, does this reflect
outwards. Palpation distinguishes this from active difficulty with self care or a measure of how disease has
abdominal muscle contraction. It is associated with affected self esteem? Is the patient restless or incoherent,
poor exercise tolerance (Chien et al. 2013) either possibly due to hypoxia?
because it indicates advanced disease or because Does the posture suggest fatigue, pain, altered con-
energy is wasted on the inefficient breathing pattern sciousness or respiratory distress? Breathless people may
itself. brace their arms so that their shoulder girdle muscles
The following may indicate inspiratory muscle fatigue, can work unhindered as accessory muscles of respira-
weakness and/or overload: tion. For mobile patients, gait gives an indication of
• abdominal paradox, as previous; mood, balance, coordination or dyspnoea.
• ↑ RR, ↓ PaCO2, ↑ pH (alkalosis);
• shallow breathing, which reduces elastic loading; Confusion
• less commonly, alternation between abdominal and Clinical reasoning helps to identify which of the follow-
rib cage movement so that each muscle group can ing could be the cause of confusion:
rest in turn, similar to shifting a heavy bag between • hypoxia
arms. • hypercapnia
Exhaustion, indicating that the patient requires mechan- • infection
ical assistance, is evident by: • pain
• ↓ RR, ↑ PaCO2, ↓ pH (acidosis) • polypharmacy
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"Yes," I said; "but many people will tell you that Christianity is
nothing more than a skilfully-framed fable, cunningly devised to
adapt itself to our human needs."
"Christ was, and Christianity was before humanity or its needs came
into being," she made answer; "and the sacrifice of the Cross was no
afterthought given as a concession to our human requirements. On
the contrary, our human requirements were given us that we,
through them, might come by way of Calvary to the feet of Christ;
and it is because it has been God's purpose from all eternity to save
the sinner by the sacrifice of Himself that you and I feel our need of
a Saviour."
"Yes," I said, "I do indeed feel that whatever help comes to me must
be something outside myself, and that no sorrowing of mine can
atone for the past; but I feel also that I, and I only, am responsible
for what I have done, and that to lay that responsibility upon
another is utterly inadequate to satisfy even my limited sense of
justice—besides which I never can and never will believe in the
possibility of the innocent being allowed to suffer for the guilty."
"But the innocent do suffer for the guilty," she said, "even in the
very earth-world, by the laws of which you wish to judge the
heavenly one. You profess yourself willing to abide by the evidence
of your senses, and if you will only look back upon the earth-life
which you have left, you will see that the sins of the fathers are
visited upon the children, and that the innocent are suffering for the
guilty every day, and that God, for some good reason of His own,
allows it to be so. As for what you say about your sense of justice, I
agree with you that if a man run into your debt—run into your debt
by wilful and wicked courses—he must be held answerable for the
repayment of the money. But supposing one comes forward who
loves him, and who has watched his sinnings with sorrow, and says,
'I will pay for my friend that which he cannot pay for himself,' would
not your sense of justice be satisfied?"
"Even then the moral obligation remains," I objected.
"Yes, but that obligation has been transferred," she said, "although
as a matter of fact, it is against God rather than against man, that
our blackest sins are committed. But, independently of that side of
the question, Christ has taken the consequences of your sin, and of
the wrong you did Dorothy—the consequences to her, as well as to
yourself—upon Himself, and has suffered for you and for her in His
own person, and if He be willing to forgive, then are you forgiven
indeed!
"That reconciliation by the Saviour should at any time have been to
me an intellectual stumbling-block is now beyond my
comprehension," she continued earnestly. "In its very adaptability to
our human needs, Christianity bears the stamp of its divine origin.
Left to himself, the very best of us must feel his inability either to
atone for the evil he has already done, or to withstand the
temptations which yet await him in the future, and though he
struggle right manfully to clamber out of the gulf into which he has
fallen, the dead-weight of his sins, which he carries and must carry
chained log-like about him, is ever the heaviest clog to drag him
back. But Christianity does more for a man than merely forgive him
his debts. It sets the bankrupt upon his legs again, a solvent man
and sane, with a clean bill of health, and with a fresh start in life. It
is the religion of Hope, for none is too sinful for the Saviour to save,
and to the man who brings his sins, as well as his inability to resist
his sins, to the feet of Christ, there is indeed a present Help and
Hope in all his troubles! There is much—very much—in Christianity
that I cannot and do not pretend to understand, but I can
understand enough to make me very loving and very trustful. The
only mystery which still sometimes troubles me is that most terrible
of all mysteries—the mystery of human suffering. But even that I am
content to leave, for is not our God Himself a suffering God? and
who that witnessed the sufferings of Jesus Christ (and what
sufferings were ever like to His?) could have foreseen that the cruel
Cross whereon He hung should hereafter be the finger-post to point
the way to heaven? or that beneath His cry of agony in the garden,
God heard the triumph-song of a ransomed world?"
CHAPTER XIV.
HOPE.
AT last there came a time, even in hell, when the burden of my sin
lay so heavily upon me, that I felt I could bear it no longer, and that
if succour there came none, the very soul of me must wither away
and die. It was not that I wanted to evade the punishment of my
crime, for I was willing and wished to undergo it to the uttermost.
No, that which was so terrible to me was the thought that not all the
sufferings of eternity could avail to wipe away the awful stain upon
my spirit, or to undo the evil which I had brought upon the woman I
had ruined. Of myself and of my future, save for the continual
crying-out of my soul after its lost purity, I scarcely cared now to
think. It was of Dorothy that my heart was full; it was for Dorothy
that I never ceased to sorrow, to lament, and—sinner, though I was
—to pray. I saw then the inevitable consequences of the wrong I
had done her pictured forth in all their horror. I saw her, with the
sense of her sin as yet but fresh upon her, shrinking from every
glance, and fancying that she read the knowledge of her guilt in
every eye. I saw her, "not knowing where to turn for refuge from
swiftly-advancing shame, and understanding no more of this life of
ours than a foolish lost lamb wandering farther and farther in the
nightfall," stealing stealthily forth at dusk to hide herself from her
fellow-creatures.
I saw her, when the secret of her shame could no longer be
concealed, recoiling in mute terror from the glance of coarse
admiration on the faces of sensual men, or shrinking in quivering
agony from the look of curious scorn in the eyes of maids and
mothers, who drew aside their skirts as she passed them, as if
fearful of being contaminated by her touch. And then—driven out
from their midst by the very Christian women who should have been
the first to have held out a hand to save her—I saw her turn away
with a heart hardened into brazen indifference, and plunge headlong
into a bottomless gulf of ignominy and sin.
Nor did the vision pass from me until, out of that seething vortex of
lust and infamy, I saw arise the black phantom of an immortal soul
which was lost for ever, crying out unto God and His Christ for
judgment upon the seducer!
As these hideous spectres of the past arose again before me, I fell to
the ground, and shrieked out under the burden of my sin, as only he
can shriek who is torn by hell-torture and despair. But even as I
shrieked, I felt that burden lifted and borne away from me, and then
I saw, as in a vision, One kneeling in prayer. And I, who had cried
out that I could bear the burden of my sin no longer, saw that upon
Him was laid, not only my sin, but the sins of the whole world, and
that He stooped of His own accord to receive them. And as I looked
upon the Divine dignity of that agonized form—forsaken of His
Father that we might never be forsaken, and bowed down under a
burden, compared to which, all the horrors of hell were but as the
passing phantom of a pain—I saw great beads of blood break out
like sweat upon His brow, and I heard wrung from Him a cry of such
unutterable anguish as never before rose from human lips. And at
that cry the vision passed, and I awoke to find myself in hell once
more, but in my heart there was a stirring as of the wings of hope—
the hope which I had deemed dead to me for ever.
Could it be—O God of mercy! was it possible that even now it might
not be too late?—that there was indeed One who could make my sin
as though it had never been?—who of His great love for Dorothy and
for me, would bear it and its consequences as His own burden? and
who by the cleansing power of the blood which He had shed upon
the cross, could wash her soul and mine whiter than the whiteness
of snow?
But to this hope there succeeded a moment when the agonized
thought: "How if there be no Christ?" leapt out at me, like the
darkness which looms but the blacker for the lightning-flash; a
moment when hell gat hold on me again, and a thousand gibbering
devils arose to shriek in my ear: "And though there be a Christ, is it
not now too late?"
I reeled at that cry, and the darkness seemed once more to close in
around. A horde of hideous thoughts, the very spawn of hell,
swarmed like vermin in my mind; there was the breath as of a host
of contending fiends upon my face; a hundred hungry hands laid
hold on me, and strove to drag me down and down as to a
bottomless pit; but with a great cry to God, I flung the foul things
from me; and battling, beating, like a drowning man for breath, I fell
at the feet of a woman, white-veiled, and clad in robes like the
morning, whose hand it was that had plucked me from the abyss in
which I lay.
CHAPTER XV.
HEAVEN.
IT seemed to me then that I fell into a sleep, deep, and sweet, and
restful, in which I dreamt that I was a child lying upon the bosom of
God. I remember that, as I lay, I stirred in my slumber, and, raising
myself, chanced in opening my eyes to look below, but that with a
cry of terror I turned and clung like a frighted babe to my Father's
breast,—for beneath me and afar, there yet yawned the mouth of
hell, from which, ever and anon, rolled dense clouds of hot and
hissing smoke, that seemed to twist and writhe like souls in agony,
and which in colour were like unto the colour of blood.
And I thought that, seeing my fear, my Father stooped to me as a
mother stoops to comfort her frightened babe, and that as He
stooped I beheld His face, and knew it for the face of the Lord
Jesus, and that He bade me be of good cheer, "for underneath thee
are the everlasting arms."
As He so spake I awoke, and saw that she whose hand had plucked
me out of the abyss of horror into which I had fallen, yet knelt
beside me in tender ministry and prayer, and that she was singing a
hymn softly to herself whereof I heard only a verse:—
"I know not where His islands lift
Their fronded palms in air;
I only know I cannot drift
Beyond His love and care."
She ceased, and I arose, but ere I had time to question her, I was
conscious of a sudden stillness, like the hush which follows
benediction after prayer. "Don't you hear it?" she whispered eagerly,
as with upraised hand enjoining silence, she turned her head as if to
catch some far-off murmur, "Don't you hear it? They are praying for
you at home: kneel down!" And as her words died away, there
seemed to float towards me the sound of air-borne music that
stayed for one moment to fold me round with the sweet consolations
of loving companionship and of peace, and in the next stole swiftly
and softly away as if journeying onward and upward to the throne of
God.
And with a great cry of anguish I fell to my knees and prayed: "O
Lord Christ! I am foul and selfish and sinful! I do not know that I
love Thee! I do not know that I have repented of my sins even! I
only know that I cannot do the things I would do, and that I can
never undo the evil I have done. But I come to Thee, Lord Jesus, I
come to Thee as Thou biddest me. Send me not away, O Saviour of
sinners. Amen."
As I ended, it seemed that my companion turned to leave me, and I
fell to sobbing and sorrowing, until at last for very anguish I could
sob no more. But soon I heard again her returning footsteps, and,
looking up, I saw One who stood beside her, thorn-crowned, and
clad in robes of white. His features were the features of a man, but
His face was the face of God!
And as I looked upon that face, I shrank back dazed and breathless
and blinded;—shrank back with a cry like the cry of one smitten of
the lightning; for beneath the wide white brow there shone out eyes,
before the awful purity of which my sin-stained soul seemed to
scorch and shrivel like a scroll in a furnace. But as I lay, lo! there
came a tender touch upon my head, and a voice in my ear that
whispered, "Son."
And as the word died away into a silence like the hallowed hush of
listening angels, and I stretched forth my arms with a cry of
unutterable longing and love, I saw that He held one by the hand—
even she who had plucked me out of the abyss into which I had
fallen—and I saw that she was no longer veiled. It was Dorothy—
Dorothy whom He had of His infinite love sought out and saved from
the shame to which my sin had consigned her, and whom He had
sent to succour me, that so He might set upon my soul the seal of
His pardon and of His peace. And to Him be the praise. Amen.
THE END.
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Dedication, vi PART IV Physiotherapy for specific groups

PART III Surgery

DEFENCE a swimming pool (Hanley & Tyler 1987). It is only by

Cortical, subcortical and brainstem neural control

Airway lining Airway Airway lining Airway

Sol layer Cilia Gel layer

ing the cilia (Kinnamon 2011). Traffic pollution evades

piratory disease as well as impaired brain development

in tissue injury caused by high numbers of these cells,

which is the basis of several chronic inflammatory

cardiorespiratory diseases (Robb et al. 2016).

FIGURE 1.2 Mucous velocity with different ages and

An extra function of the sol layer is its antimicrobial

The respiratory centres comprise clusters of neurons MECHANICS

expiration (Mondal et al. 2016). When the larynx is

Alveolar pressure is negative on inspiration and slightly Pharynx

Compliance to avoid either extreme, especially in patients with

Static compliance is measured during a breath-hold Inspiratory muscle fatigue

VENTILATION Gas that moves in and out of the lungs is made

Anatomical dead Frequency 15/min

Pulmonary capillary Pulmonary blood

Maximal inspiration Functional residual Base

increasing lung volume. For patients with atelectasis,

ARTERIAL BLOOD GASES TABLE 1.1 Relationship between

Right shift onto its oxygen, as with hyperventilation, hypometabo-

Body temperature lism or a cold environment. Pink ears and noses on

2,3-DPG frosty mornings are due to the reluctance of Hb to

Hypoxaemia and Hypoxia

VA/Q match Wasted

Hypoventilation can be caused by respiratory depres- Effects of hypoxaemia and hypoxia

Other Indices of Oxygenation

acid, leading to haemodynamic instability (Celotto Respiratory Metabolic

TABLE 1.3 Interpretation of arterial blood gas trends

FIGURE 1.15 Oxygen journey through cardiovascular system to mitochondria.

distribution of blood flow, both between and within 4 IC

TABLE 1.5 Effects of smoking related to physiotherapy practice

Ding et al. 2016

Immobility Moving from supine to standing

Blood volume 500 mL blood migrates to pelvis and legs

Sympathetic activity Cardiac output ↓ Venous return, cardiac output and BP

Vasoconstrictive reserve ↓ BP detected by aortic arch and carotid baroreceptors

Information sent to brainstem

↑ HR and myocardial Arteriolar Venous

Control artery Athlete’s artery

Dedication, vi PART IV Physiotherapy for specific groups