Expert Review Examination of the Respiratory System
Dr Fahd Mahmood1, Prof Robert J O Davies2 and Dr John M Wrightson3
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The Journal of Clinical Examination 2011 (11): 69-89
Abstract
This article describes a comprehensive method for performing an examination of the Respiratory System. The
signs of common and important diseases that affect the respiratory system are discussed. It is based on a
thorough review of the literature and is consistent with The Principles of Clinical Examination. We welcome
responses to this article which provide evidence for improvements to the method described here but in the
meantime we recommend this as a peer-reviewed and evidence-based method for the Examination of the
Respiratory System. Word count: 8,708 (excluding abstract, figures, tables and references).
Key words: physical examination, auscultation, palpation, percussion, respiratory.
Address for correspondence: [email protected]
Author affiliations: 1Foundation House Officer, Glasgow Royal Infirmary, NHS Greater Glasgow & Clyde.
of Respiratory Medicine, University of Oxford and Consultant Physician, Oxford Radcliffe Hospitals
NHS Trust. 3NIHR Oxford BRC Clinical Research Fellow and Specialist Registrar, Oxford Radcliffe Hospitals NHS
Trust.
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2Professor
Introduction
The Principles of Examination of the Respiratory
System
Authors have proposed various methods for
performing an examination of the respiratory system
in medical literature. At best, most of the methods
advocated can be described as ‘expert opinion’
rather than having a stronger evidence base; the
best examination method is controversial. Where
there is no good evidence we have taken a
pragmatic approach guided by The Principles of
Clinical Examination [1]. This article aims to
synthesize evidence from medical literature together
with descriptions advocated by major clinical
medicine textbooks to produce a method suitable
for medical school examinations, post-graduate
examinations and routine clinical practice.
The examination routine described here is designed
to detect the signs of common and important
respiratory diseases, together with multisystem
disorders that also have respiratory sequelae, such
as rheumatoid arthritis. An astute physician will
always be vigilant for such multisystem disorders
and use findings to guide further examination of
non-respiratory systems.
This article describes a comprehensive and
idealised version of the clinical examination of the
respiratory system, which can be modified when a
more focused examination is required in clinical
practice. For acutely unwell patients, an ‘Airway,
Breathing, Circulation, Disability, Exposure –
ABCDE’ approach may be more appropriate.
When the examination of the respiratory system is
performed as part of medical school or postgraduate examinations it will be observed by at
least one official examiner. In these circumstances
it is not only necessary to perform a competent
examination it is also necessary to be seen to be
performing a complete examination. This includes
communicating to the examiner when signs have
been detected and justifying ad hoc decisions to
modify the examination routine. An approach to
dealing with these difficulties is beyond the scope of
this article but where relevant we provide some
suggestions for dealing with specific issues.
Clinical examination is just one part of a
comprehensive assessment of the patient which
usually includes bedside investigations such as
pulse oximetry and measurement of blood pressure.
This account includes all the bedside tests relevant
to the examination of the respiratory system.
Formal investigations such as chest radiographs
and full lung function testing do not form part of the
69
clinical examination and are therefore beyond the
scope of this article.
Anatomy and physiology
Air enters through the oropharanx and nasopharanx
passing through the larynx to the trachea which
commences at the level of the cricoid cartilage in
the neck (C6) and terminates at the carina into the
left and right main bronchi (at the angle of Louis
(T4/5)). The right bronchus is more vertical than the
left; hence inhaled objects and chemical
pneumonitis secondary to aspiration are more likely
to be found on the right side. The main bronchi
divide into lobar bronchi, which further subdivide
into segmental bronchi. These segmental bronchi
each feed into a bronchopulmonary segment of the
lung. Alveoli within these segments allow gas
exchange, the primary function of the lung, to occur.
The lungs are surrounded by continuous
membrane, the pleura, that is folded back on itself
to create two layers: the visceral (inner) and parietal
(outer) pleura. The visceral pleura is attached to the
surface of the lung and the parietal pleura, which is
innervated by the intercostal nerves, to the thoracic
cavity. The space between these layers is referred
to as the pleural cavity and contains a small amount
(~10ml) of pleural fluid. Surface tension of the
pleural fluid allows the lung to expand with
inhalation, however in the case of pneumothorax,
gas in the pleural cavity, this surface tension is lost
and the lung cannot expand. Each lung is divided by
fissures into lobes, the right lung has three lobes
whilst the left has two (Figure 1). During normal
inspiration, contraction of the intercostal muscles
increases the transverse diameter of the thorax
whilst contraction of the diaphragm increases the
vertical length of the thorax. These changes
increase the volume of the lungs, thereby
decreasing intrapulmonary pressure relative to
atmospheric pressure; allowing air into the lungs. In
deep inspiration, the accessory muscles of
respiration further maximise thoracic capacity.
Overlying the lungs, the rib cage protects the lungs.
In mid inspiration, the lungs’ lower borders cross the
6th rib in the mid clavicular line, the 8th in the mid
axillary line and reach the 10th rib posteriorly. An
appreciation of the anatomy and physiology of the
lungs will allow accurate interpretation of any
examination findings.
Figure 1a (top) and 1b (bottom). The surface
anatomy of the lungs showing the right upper
(RU), right middle (RM), right lower (RL), left
upper (LU) and left lower (LL) lobes.
Figure 1c The cervical lymph nodes, including
A) submental, B) submandibular, C) Jugular, D)
pre-auricular, E) post-auricular F), occipital, G)
posterior triangle and H) supraclavicular nodes.
Common diseases
Pulmonary pathology is varied and diverse in
nature. Through your examination, you may
elucidate signs relating to the following common
conditions. Lung disease can be classified in
different ways. See Table 1.
70
Obstructive
Disease
caused by
obstruction
of airways
Restrictive
Disease
caused by
restricted
lung
expansion
Infectious
Due to
infection of
the lung
Disease
related to
inflammator
y response
in the lung
Pathology
related to
pulmonary
vasculature
Inflammatory
Vascular
Pleural cavity
disease
Pathology
affects
pleural
space
Asthma
Chronic
Obstructive
Pulmonary
disease
Interstitial lung
disease
Asbestosis
Pulmonary
fibrosis
Sarcoidosis
Pneumonia
Cystic fibrosis
Acute
respiratory
distress
syndrome
Pulmonary
embolus
Pulmonary
oedema
Haemorrhage
(eg.
Goodpasture’s
syndrome)
Pneumothorax
Pleural
plaques/mesoth
elioma
Table 1 Categories of lung disease
Literature Review
In developing this article, a literature review of
publications related to respiratory examination was
performed.
The ‘diagnosis category’ of the PubMed Clinical
Queries database was searched, using the ‘narrow,
specific search’ filters with the following terms;
(respiratory AND examination)
(pleural AND (percussion OR auscultation))
(pneumonia AND (percussion OR auscultation))
(bronchiectasis AND (percussion OR auscultation))
(fibrosis AND (percussion OR auscultation))
(((lung OR bronchial) AND (cancer OR malignancy))
AND (percussion OR auscultation))
A further PubMed search was performed for clinical
prediction rules, using the following strategy;
(clinical prediction rule) AND (respiratory system)
(clinical prediction rule) AND (pulmonary OR
respiratory)
Retrieved articles from all search strategies were
reviewed for relevance. Articles from the first
strategy were also reviewed for the presence of
clinical prediction rules. Review was limited to
articles published in English, pertinent to humans.
Only articles available through the University of
Oxford or the National Health Service agreement
were examined.
The Journal of the American Medical Association’s
“Rational Clinical Examination” series [2] was
reviewed, with all entries under ‘Pulmonary
Diseases’ examined. The British Medical Journal’s
Clinical Evidence series [3] was also examined. All
reviews under ‘Respiratory disorders (acute)’ and
‘Respiratory disorders (chronic)’ were inspected.
Evidence Based Medicine was also searched, with
articles in Evidence Based Medicine collections
relevant to ‘EBM Diagnosis’ and ‘EBM Clinical
Prediction Guides’ fully reviewed.
The following textbooks of clinical examination were
searched:
Clinical Examination: A Systematic Guide to
Physical Diagnosis[4]
Macleod’s Clinical Examination[5]
Sapira’s Art and Science of Bedside Diagnosis[6]
Evidence Based Physical Diagnosis[7]
Preparation
Clinical examination should ideally take place in a
warm environment which is private and has good
illumination. Make sure you have the necessary
equipment available as listed in Table 2. The
examiner should be appropriately dressed and a
chaperone should be present if appropriate. Wash
your hands, introduce yourself to the patient and
obtain informed consent. Next confirm the patient’s
identity (if this has not been done already), ensure
he/she is positioned appropriately, lying on a bed or
examination couch at an incline of approximately
forty five degrees, and that there is adequate
exposure. Ideal exposure is from the waist upwards
but in practice less complete forms of exposure may
be adequate and examiners should be pragmatic.
Stethoscope
Peak expiratory flow meter
Pulse oximeter
Thermometer
Table 2 Equipment required for the respiratory
examination
71
Finally check the patient is comfortable and does
not have any pain. You must be sensitive and
responsive to signs of pain at this stage and
throughout the examination. If necessary ask the
patient before you proceed with a maneuver if it is
likely to cause any pain.
Recurrent laryngeal nerve palsy can be caused by
invasion of the nerve by lung cancer [4]. The
inability to finish sentences in one breath implies
significant respiratory distress and has prognostic
significance; for example in exacerbations of
asthma.
Beginning the Examination
Start from the end of the bed with an initial global
inspection of the patient and their surroundings.
Next assess the rate, in breaths per minute, and the
pattern of respiration. The rate can be affected if
the patient is aware that it is being measured and
many authors recommend doing it covertly later in
the examination but it is justifiable to do it at this
point. Suitable points for covert measurement are:
whilst palpating the radial pulse, during close
inspection of the chest, during palpation of the
chest, during auscultation of the chest.
Figure 2 Initial global inspection with patient
appropriately exposed
Consider explaining what you are doing beforehand
to avoid embarrassment. Note the environment in
which the examination is taking place and look for
walking aids, medical equipment and any other
relevant items. Next look for signs of disease. Most
signs are best detected during the detailed
examination of individual anatomical areas but
some signs such as cachexia, the use of accessory
muscles of respiration (sternocleidomastoids,
platysma and the strap muscles of the neck:
sternothyroid, sternohyoid, thyrohyoid and
omohyoid[8]) and the tripod position (sitting leaning
forward with hands supported on the knees) which
is frequently seen in patients in respiratory distress
are best detected from the end of the bed. Any sign
is potentially relevant and it is not possible to
provide a full list here but the most important signs
and their significance are described below.
Look for equipment used to deliver oxygen therapy,
inhalers and equipment for drug nebulisation. Look
for a sputum pot and if a sample of sputum is
available you should inspect it. Sputum is produced
by the airways and should contain very little saliva.
Note the colour and volume of the sputum and try to
categorise. See Table 3.
Whilst speaking to the patient note any
abnormalities in the character of their voice, the
ability to finish sentences in one breath and assess
for the presence and character of any cough. See
Table 4. A hoarse voice may be a sign of laryngitis,
laryngeal cancer or recurrent laryngeal nerve palsy.
The most time-efficient and accurate method is to
count the number of breaths in a specific period,
such as twenty seconds, and then calculate the
number of breaths per minute. The time period
should be defined using a watch or another
timepiece. With experience it is possible to estimate
the respiratory rate after listening for a brief
undefined period but this is likely to be less
accurate. The normal respiratory rate for an adult is
8-20 breaths per minute. Less than 8/min is
bradypnoea and greater than 20/min is tachypnoea.
Is the pattern of breathing normal or abnormal?
Normally, inspiration is an active process being 75%
diaphragmatic and 25% thoracic, whilst expiration
occurs passively; the ratio of the length of
inspiration to that of expiration is normally 1:2.
Tachypnoea and bradypneoea can occur in a
variety of situations as detailed in Table 5. CheyneStokes ventilation describes a cyclical pattern of
ventilation in which there is a periodic increasing
rate and depth of ventilation followed by a
decreased respiratory rate and effort, eventually
reaching a state of temporary hypopnoea or
apnoea. Cheyne-Stokes ventilation can be
observed in patients with conditions that affect
blood gas buffering such as congestive heart failure,
carbon monoixide poisoning and toxic metabolic
encephalopathy. It can also be present in conditions
affecting the respiratory centres in the brainstem
such as stroke, traumatic brain injury and brain
tumours. Finally, it is also observed in palliative care
patients and has also been reported as a normal
finding during sleep in the elderly [10]. Kussmaul
respiration describes deep sighing respirations,
although patients may not feel subjectively
dyspnoeic; it is observed in metabolic acidosis[10].
72
Tachypnoea
Airway obstruction
(Asthma, COPD)
Pneumonia
Pulmonary Fibrosis
Pulmonary embolism
Pneumothorax
Pleural Effusion
Cardiac Failure
Bradypnoea
Exhaustion in severe
airway obstruction
Sedation
Raised intracranial
pressure
Opiate overdose
Intoxication
Table 5 Causes of tachypnoea and bradypnoea
seen when apical lung tumours (Pancoast’s tumour)
impinge on the C8/T1 nerve roots, and changes
seen in rheumatoid arthritis which may be
associated with bronchiectasis and pulmonary
fibrosis [7]. Peripheral cyanosis may also be
detected in the hands [5] giving a blue colour to the
tissues caused by the presence of deoxygenated
haemoglobin. Note that, in the absence of central
cyanosis, this is reflective of peripheral
vasoconstriction and stasis of blood in the
peripheries. Central cyanosis is seen in the tongue
and lips due to desaturation of central arterial blood.
Assess if the patient is in respiratory distress; in
which tachypnoea and increased respiratory effort
(indicated by the use of accessory muscles, the
tripod position and nasal flaring may be seen).
Look for pursing of the lips, where the lips are
brought together on expiration, characteristic of
patients with chronic obstructive pulmonary disease
(EB1 and Clinical Prediction Rule 1). Lip pursing is
thought to generate positive end-expiratory
pressure, helping reduce dynamic airway collapse
during expiration[7].
Listen for the presence of stridor, which is a harsh
inspiratory noise, indicating upper airway
obstruction, potentially secondary to a laryngeal
tumour, bilateral vocal cord palsy or, more acutely,
due to anaphylaxis. If you are unsure, ask the
patient to cough, then take deep breaths with their
mouth open[5]. Any stridor should always be
investigated. Also listen for an audible expiratory
wheeze, secondary to reduced lower airways calibre
or for inspiratory ‘white noise’ - irregular, constantly
varying in frequency and amplitude[17]. Both findings
are present in patients with chronic obstructive
pulmonary disease (EB1 and Clinical Prediction
Rule 1) (COPD) or asthma (EB2).
The Hands
Move to the right-hand side of the patient [1] and
examine the hands. Ask the patient to hold-out their
hands and hold them gently with yours. Begin by
looking at the fingers, especially the finger tips, and
the nails.
Examine for finger clubbing. See The JCE Expert
Review: Examination for Finger Clubbing19 for a
review of this examination.
Other signs in the hand may include: nail changes
(Table 6), tar staining indicative of recent smoking
[5], wasting of the small muscles of the hand,
especially at the thenar and hypothenar eminences,
Figure 3 Examination of the hands for clubbing
in A) non clubbed and B) clubbed fingers
Ask the patient to hold their arms out in front of
them, elbows extended, for about ten seconds and
assess if they have a tremor. Then, maintaining this
position, ask them to fully dorsiflex their wrists and
hold that position for about thirty seconds whilst you
closely observe for asterixis (Figure 4). It is best to
give these instructions whilst demonstrating the
position at the same time. Asterixis is manifest by
sudden loss of dorsiflexion causing flexion
movements towards the neutral position at the wrist
and may be a sign of carbon dioxide retention
(‘carbon dioxide flap’) or hepatic encephalopathy
(‘liver flap’).
73
Nail
abnormality
Koilonychia
Onycholysis
Yellow Nail
Definition
Transverse and
longitudinal
concavity –
giving a spoon
shaped nail
Separation of
nail plate from
nail bed, leaving
a white
discolouration.
Slow growing
nail, with
‘heaped up’
appearance.
The lunula
disappears and
the nail shows a
yellow hue.
Associated
condition
Iron deficiency
anaemia
Sarcoidosis,
ankylosing
spondylitis
Pleural
effusion,
bronchiectasis
Table 6 Nail findings in respiratory disease
mouth and elevate their tongue to inspect the
underside for marked blue discolouration indicating
central cyanosis, reflecting inadequate blood
oxygenation in the lungs or increased oxygen
extraction in the tissues.
A malar rash is a characteristic macular, non itchy
rash in the shape of a butterfly over the bridge of
the nose and across the cheeks. It is present in
systemic lupus erythematosus which is associated
with pulmonary fibrosis, pleural effusion and
pulmonary emboli.
Lupus pernio is a rash
characterised by violaceous smooth shiny plaques
on the face which is a sign of sarcoidosis which is
associated with pulmonary fibrosis and
bronchiectasis.
Ptosis, miosis (small pupil), anhydrosis and
apparent endophthalmos are seen in Horners
Syndrome. Horner’s syndrome is caused by
disruption of the sympathetic input to the face and
can be caused by Pancoast’s tumour. This is an
eponym for apical lung tumours which are prone to
invading the cervical or thoracic sympathetic chain
interrupting the supply to the neck, head and face.
The neck
The neck is a sensitive area and examination may
be uncomfortable so it is important to inform the
patient in advance.
Figure 4 Examining for Asterixis.
Radial Pulse
Palpate the radial pulse and assess its rate, rhythm
and character. For a fuller account of the
cardiovascular examination and signs please the
relevant Journal of Clinical Examination Review [20].
Pulsus paradoxus is a sign especially relevant to
the respiratory examination, it is considered in EB3.
Start by examining the trachea for deviation and for
tug. Placing your index and ring finger of the right
hand on the head of each clavicle, use the middle
finger of the same hand to palpate the trachea in
the sternal notch (Figure 5). Roll you finger across
the trachea in the axial (horizontal) plane to assess
for deviation.
The trachea is a midline structure and should lie
equidistant between the clavicular heads. Causes
for tracheal deviation are summarised in Table 7.
The Face
Begin by looking at the eyes. Assess pupil size and
symmetry. Look at the eyelids, the normal upper lid
lies 1.5mm below the superior corneal limbus.
Ptosis refers to drooping of the upper eyelid, this
can be partial or complete. Enophthalmos is a sign
which refers to posterior displacement of the eye, a
difference of 2mm between the eyes is usually
evident on examination.
Look at the facial skin for rashes and anhydrosis
(loss of sweating). Ask the patient to open their
Figure 5 Examining for tracheal deviation
74
Displacement
towards the
lesion
Lobar collapse
Pneumonectomy
Displacement
away from
the lesion
Large pleural
effusion (see
Evidence Box
4)
Tension
pneumothorax
Other
displacem
ent
Mediastinal
masses
Pulmonary
fibrosis
Table 7 Causes of tracheal displacement[9]
Next place your index finger of the right hand on the
trachea against the inferior edge of the cricoid
cartilage. Place subsequent fingers, in the sagittal
(vertical) plane, below this into the sternal notch
until the trachea is no longer palpable and the
sternum is reached, this is referred to as the cricosternal distance and is normally three finger widths
(5cm) or above (Figure 6). Note whether the trachea
moves inferiorly, reducing the crico-sternal distance
on inspiration, referred to as tracheal tug. A
reduction in the crico-sternal distance and tracheal
tug signify marked chest hyperexpansion, usually
secondary to airflow obstruction and are commonly
seen in COPD.
Examine for cervical lymphadenopathy from behind
the patient if possible (Figure 7). Standing directly
behind the patient place both hands under their chin
to assess for cervical lymphadenopathy. Use the
sensitive pulps of your fingers to simultaneously
palpate the left and right; submental,
submandibular, anterior and posterior cervical
chains, supraclavicular, pre-auricular, post-auricular
and occipital lymph nodes, in turn. Comparing with
the contralateral side note the location, size and
characteristics of any masses using the techniques
described in The Journal of Clinical Examination:
Examination of lumps and bumps.
Next examine the JVP. With the patient is lying at a
45 degree angle, ask them to turn their head slightly
away from you whilst relaxing their head against a
pillow. Observe along the surface of the neck rather
than observing in a perpendicular orientation, as the
movement is easier to discern in this plane, for the
double pulsation of the jugular venous pressure
(JVP) which originates between the two heads of
the sternocleidomastoid muscle. If you are unsure,
you can attempt to palpate the pulse, unlike the
carotid pulse, it will be impalpable. Under normal
conditions, the JVP should be less than 4cm above
the sternal angle in the vertical plane (Figure 8).
Figure 6 Measuring crico-sternal distance
Figure
7
Examining
lymphadenopathy
for
cervical
The JVP is an indirect measure of central venous
pressure and can be raised secondary to right heart
failure (cor pulmonale), which can exist secondary
to a variety of chronic lung diseases, including
COPD (EB1 and Clinical Prediction Rule 1), fluid
overload, increased intrathoracic pressure (tension
pneumothorax or severe acute asthma, EB2,
cardiac tamponade or constrictive pericarditis. It
may also occur in superior vena cava obstruction.
Such obstruction can be caused by a bronchial
carcinoma, especially of the right upper lobe. This
leads to venous distension and oedema in the neck,
face, upper chest and arms.
75
of the sternum. Spinal deformity, kyphosis or
lordosis, may impinge on respiration and may be
associate with systemic disease such as ankylosing
spondylitis, which can lead to apical lung fibrosis.
Thoracotomy scars and those from breast surgery
(which could suggest malignant pleural effusion)
may be obvious but it is important to pay close
attention to the skin as more subtle scars for
example from previous chest drain insertion could
give significant clues to underlying pathology yet
may not be seen even on close inspection.
Radiotherapy tattoos, suggesting the presence of
malignancy, may be associated with well
demarcated inflammation of the skin in the acute
stage, or pulmonary fibrosis, potentially detectable
on auscultation in the longer term.
Figure 8 Measuring the JVP
The Chest
Anterior Aspect of the Chest
Inspect
Inspect the chest from the front and the side. You
should have already briefly inspected the chest at
the beginning of the examination but at this stage
take some time to inspect more closely. Do not
neglect the lateral aspect of the chest and axillae
which may only be visible by asking the patient to
move their arms. Any sign is potentially relevant
and it is not possible to provide a full list here but
the most important signs and their significance are
described below. The most important things are to
note the shape of the chest, the respiratory rate the
character of the movement.
An increased anteroposterior diameter describes a
‘barrel shaped’ chest, seen in patients with severe
airflow obstruction (such as chronic obstructive
pulmonary disease or severe asthma). This is often
coupled with a dorsal kyphosis and prominence of
the sternum[23]. In contrast, a pectus carinatum
(‘pigeon-shaped’ chest) results from localised
deformity of the sternum and costal cartilage, which
bulge outwards. This can exist secondary to chronic
respiratory disease in childhood. Pectus excavatum
(‘funnel-shaped’ chest) is a developmental defect
which can arise due to connective tissue disease. It
results in a localised depression of the inferior part
Palpate
Examine expansion of the chest. Place your hands,
palm down either side of the manubrium, with your
thumbs equidistant from the midline and raised
slightly with your fingers on the chest, wrapped
around the thorax. Ask the patient to take deep
breaths in and observe your hands simultaneously
rising with each inspiration (Figure 9). Place your
hands on the lower anterior thorax and using the
same technique. Ask the patient to breathe out and
then take a deep breath in. As the patient inspires,
you should be able to measure the expansion of
both sides of the chest by observing your thumb’s
movements relative to the midline. This should
normally be at least 5cm.
Place you right hand against the thorax over the fifth
intercostal space, mid-clavicular line to palpate for
the cardiac apex beat. In female patients, it may be
appropriate to lift the left breast using the back of
your left hand to lift the breast from underneath
whilst palpating with your right. Place the base of
your right hand firmly against the chest to the left of
the sternum at the level of the heart to palpate for
the heart. If the heart beat is palpable this is
referred to as a parasternal heave (Figure 10).
76
Figure 10 – Palpating for a parasternal heave
Reduced expansion may be secondary to fibrosis,
consolidation, effusion (EB4), collapse or
pneumothorax. The cardiac apex beat may not be
palpable in obesity and severe lung
hyperexpansion. It may be displaced from the fifth
intercostal space, mid-clavicular line in pleural
effusion, lobar collapse, pneumothorax or
pneumonectomy. A parasternal heave is suggestive
of right ventricular hypertrophy which may exist
secondary to pulmonary hypertension in chronic
obstructive pulmonary disease (EB1 and Clinical
Prediction Rule 1), interstitial lung disease or
multiple pulmonary emboli.
Percussion
Percuss the thorax by placing the middle finger of
the left hand firmly against the chest wall. Use the
tip of the distal phalynx of the right middle finger to
strike the middle phalanx of the left middle finger.
The striking motion should be firm and brisk. If you
are left-handed you may prefer to reverse the roles
of the left and right hands but the ergonomics of
examining from the right mean that the method
described above is ideal if possible. The striking
action should generate a ‘percussion note’ which on
a normal chest is said to be resonant. Abnormal
percussion notes are classified as either dull or
hyper-resonant. See Table 8 for a description of the
types of percussion note and their causes.
Figure 9
Measuring chest expansion in
expiration (a and c) and inspiration (b and d)
Whilst palpating the chest, be vigilant for a crackling
sensation under your fingers, which may indicate
subcutaneous emphysema.
Begin by percussing over the apex of the lung. This
can be achieved either by percussing in the
supraclavicular fossa or by percussing the clavicle.
It is not necessary to percuss both. If percussing in
the supraclavicular fossa it may be easier to apply
the thumb to the chest wall rather than the finger.
The clavicle should be percussed directly with the
middle finger of the right hand – there is no need to
apply a finger to the chest wall at this site.
77
Percussion
Note
Dull *
Resonant
Hyperresonant
Common
Causes
Pleural effusion
(EB4), presence
of hepatic tissue,
consolidation,
pleural thickening
Normal lung
Solid organ or
fluid
Aerated lung
tissue
Hyperinflated
lung tissue or
air in the
pleural space
Pneumothorax,
COPD (EB1 and
Clinical
Prediction Rule
1)
* Some authors refer to stony-dull as a separate
percussion note. We have not included this here.
Table 8 Percussion Notes
Figure 11 Suggested sites for percussion and
auscultation of the chest from the anterior (a),
posterior (b) and lateral (c and d) perspective
Begin by percussing over the apex of the lung. This
can be achieved either by percussing in the
supraclavicular fossa or by percussing the clavicle.
It is not necessary to percuss both. If percussing in
the supraclavicular fossa it may be easier to apply
the thumb to the chest wall rather than the finger.
The clavicle should be percussed directly with the
middle finger of the right hand – there is no need to
apply a finger to the chest wall at this site.
Next percuss the anterior aspect chest wall followed
by the lateral aspect of the chest wall. The
percussion sites will depend on the clinical context
but in a routine examination there is no agreement
on the number and distribution of percussion sites
78
that should be chosen. The conventional method is
to choose three points on the anterior chest wall
close to the midclavicular line and two points on the
lateral chest wall close to the midaxillary line (Figure
11) – this allows a thorough assessment of each of
the lobes of each lung. The exact site of percussion
is not crucial but it is important to percuss the same
site in each hemithorax one after the other to allow
comparison.
Auscultation
Using the bell of the stethoscope auscultate the
supraclavicular fossae in turn with the patient taking
normal breaths through an open mouth.
heard was said by Laennec to be ‘quavering and
jerky, like the bleating of a goat.’ Alongside
whispering pectoriloquy, aegophony is a sensitive
physical finding for consolidation[6].
Posterior chest
Ask the patient to lean forwards. The arms should
be crossed to abduct the lower pole of the scapulae
(Figure 13). Inspect, palpate, percuss and
auscultate the posterior chest as described above,
repeat in four to five parallel locations; ensuring that
you are auscultating down to the level of the 10th rib.
Next using the diaphragm auscultate the anterior
and lateral chest in the same distribution as
described for percussion comparing each
hemithorax in turn - figure 11. In thin patients with
prominent ribs the bell may need to be used to
ensure good skin contact. Pay particular attention
when auscultating the right axilla, right middle lobe
pathology may only be demonstrated here.
Repeat auscultation over the same areas,
comparing each hemithorax in turn, whilst asking
the patient to say ‘ninety-nine’ each time the
stethoscope touches their chest to assess for vocal
resonance. If consolidation is suspected, see below,
auscultation can be further repeated with the patient
whispering ninety-nine’ to assess for ‘whispering
pectoriloquy’. Alternately instruct the patient to say
the letter ‘E’ or the word ‘bee’ each time you
auscultate as above to test for aegophony. If it is
present you will hear ‘A’ (as in ate) rather than ‘E’,
again suggesting consolidation. Be sure to remove
your stethoscope for a second to verify the patient is
still saying ‘E’!
Whilst auscultating, listen for the quality of the
breath sounds, the loudness of these sounds (EB5)
and note any added sounds. See Table 9. Vocal
resonance tests the lung’s ability to transmit sound.
In an area of consolidation (EB6 and Clinical
Prediction Rule 2), the patient’s voice becomes
clearer, whilst if there is a pleural effusion (EB4), the
sound will be damped and the patient’s voice
becomes further muffled. If vocal resonance is
increased to the point where a whisper can be
heard clearly this is termed ‘whispering
pectoriloquy.’ Aegophony is another test for areas of
consolidation (EB6 and Clinical Prediction Rule 2).
This phenomenon was originally described by
Laennec[29], the term aegophony is thought to mean
‘goat sound,’ named as such because the sound
Figure 12 The correct position for examination
of the posterior chest.
Expose the lower limbs to the mid thigh. Inspect
specifically looking for oedema and rashes. Palpate
the legs to assess for calf tenderness and for the
presence of pitting oedema by applying pressure
over a bony prominence for ten seconds to see if
pitting is observed (Figure 13). The level to which
pitting oedema extends should be noted, and
sacrum should also be examined for this
phenomenon.
79
Ascultate the left lower sternal edge for a pan
systolic murmur loudest during inspiration as this is
classically of tricuspid regurgitation, which can be
secondary to right ventricle dilatation seen with
pulmonary hypertension.
Aucsultate the left upper sternal edge for a high
pitched early diastolic murmur loudest during
inspiration, a Graham Steell murmur, caused by
high velocity regurgitant flow across the pulmonary
valve typical of pulmonary hypertension.
Figure 13
oedema
Examining for peripheral pitting
Peripheral oedema may represent congestive
cardiac failure or cor pulmonale secondary to
pulmonary disease. A deep venous thrombosis may
present with lower limb swelling or erythema.
Erythema nodosum, a panniculitis which causes
tender nodules; often on the shins may be
observed. Erythema nodosum may be seen in
respiratory disease such as streptococcal infection,
tuberculosis and sarcoidosis.
Auscultating the Heart
A full examination of the cardiovascular examination
is beyond the scope of this article but some
cardiovascular signs are of direct relevance to the
examination of the respiratory system and should
be specifically sought-out. For a full account of how
to perform the cardiovascular examination please
see The Journal of Clinical Examination’s:
Examination of the Cardiovascular System [34].
Note the components of the heart sounds and listen
for a right ventricular S4, giving a gallop rhythm.
Note the cadence of the 3 heart sounds – S1, S2
and S4 which are said to resemble that of the word
‘Tennessee’ which are seen in pulmonary stenosis
or pulmonary hypertension. Finally, note the volume
of the components of the heart sounds for a loud P2
which will be evident in pulmonary hypertension.
Completing the examination
To complete the examination you should perform
pulse oximetry to measure oxygen saturations and
measure the temperature. If obstructive airways
disease is suspected then you should measure
peak expiratory flow using a peak flow meter.
Finally, wash your hands, thank the patient and
allow him/her redress in privacy.
Conflict of interest
None declared
80
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82
Type
Purulent
Mucoid
Serous
Blood
Characteristics
Thick, yellow/green sputum
Clear, grey/white
Clear, frothy, can be pink
Blood
Associated pathology
Infectious – pneumonia, bronchiectasis and abscess
Chronic obstructive pulmonary disease and asthma
Pulmonary oedema
Malignancy, pulmonary embolus, clotting disorders,
infection
Table 3 Categories of sputum
Characteristic
s of cough
Productive
Dry
Bovine
Wheezy
Potential significance
Chronic bronchitis, lower respiratory tract infection, bronchiectasis or cancer.
Infection (upper or lower respiratory tract), asthma (see Evidence Box 2) (particularly
nocturnal), gastro-oesophageal reflux disease, post-nasal drip, pulmonary fibrosis,
drugs (e.g. ACE-inhibitors) or cancer.
Vocal cord paralysis, potentially secondary to invasion of recurrent laryngeal nerve by
lung cancer.
Airflow limitation, e.g. asthma (see Evidence Box 2).
Table 4 The potential significance of cough[9]
83
Quality
Normal breath sounds
(vesicular sounds)
Bronchial breathing
Amphoric breath sounds (less
common)
Intensity
Reduced intensity (decreased
air entry)
Added sounds
Wheeze (polyphonic)
Wheeze (monophonic)
Stridor
Crackles
Pleural rub
Inspiratory phase longer than expiratory phase, without interposed gap.
Due to transmitted air turbulence[6].
Harsher noises; prolonged during expiration. Heard over areas of
consolidation, where sound is not filtered by alveoli[6].
Hollow noises, heard over a large cavity. The sound is said to be like the
noise of air passing over the top of a hollow jar.
Muffled breath sounds as a result of pleural effusion (see Evidence Box
4), pneumonia (see Evidence Box 6 and Clinical Prediction Rule 2),
chronic obstructive pulmonary disease (see Evidence Box 1 and Clinical
Prediction Rule 1) collapse, pneumothorax or a mass.
Continuous sounds with a musical quality. Note when in the respiratory
cycle the wheeze occurs; usually louder in expiration. Due to airway
narrowing in asthma (see Evidence Box 2) or chronic obstructive
respiratory disease (see Evidence Box 1 and Clinical Prediction Rule 1).
Single note, due to fixed obstruction such as a space occupying lesion.
Unlike wheeze, stridor is inspiratory; due to upper airway obstruction
Interrupted, non-musical sounds, often occurring due to opening of small
airways. Early inspiratory crackles suggest chronic obstructive respiratory
disease (see Evidence Box 1 and Clinical Prediction Rule 1); whilst later
or pan-inspiratory crackles suggest that the disease is limited to the
alveoli.
Fine crackles sound like Velcro being pulled apart, they are characteristic
of pulmonary fibrosis; medium crackles are typical of left ventricular
failure whilst coarse crackles indicate pools of retained secretions in
conditions such as bronchiectasis.
A continuous grating sound which occurs with pleurisy as the inflamed
pleura rub against each other (e.g. secondary to a pulmonary infarct or
pneumonia (see Evidence Box 6 and Clinical Prediction Rule 2))
Table 9 Breath sounds
Modified Medical Research Council Dyspnoea Scale
0 “I only get breathless with strenuous exercise”
1
“I get short of breath when hurrying on the level or walking up a slight hill”
2
“I walk slower than people of the same age on the level because of breathlessness or have to stop
for breath when walking at my own pace on the level”
3
“I stop for breath after walking about 100 yards or after a few minutes on the level”
4
“I am too breathless to leave the house” or “I am breathless when dressing”
Appendix 1 MRC Dyspnoea Scale
84
Clinical signs in Chronic Obstructive Pulmonary Disease
COPD is an oft encountered pathology. A number of signs have been associated with COPD, these include:
• Laryngeal height <4cm: The distance between the thyroid cartilage and suprasternal notch is
thought to be reduced as the clavicles and sternum are higher than normal. +LR – 3.6, -LR –
0.7[11].
• Hoover’s sign (costal paradox) – The examiner places one hand on each costal margin. Usually,
the ribs move outwards whilst in a patient with chest hyperexpansion in COPD, the costal margins
are instead pulled closer together. +LR – 4.2, -LR – 0.5[12].
• Hyper resonance of upper right anterior chest - +LR 5.1, -LR not significant[13].
• Absence of cardiac dullness on percussion – +LR 11.8, -LR not significant[13].
• Early inspiratory crackles - +LR 14.6, -LR – not significant[14].
Evidence Box 1 Chronic Obstructive Pulmonary Disease
British Thoracic Society guidelines for assessment of acute asthma
The British Thoracic Society[18] has produced guidelines for the assessment of acute asthma in adults:
Moderate asthma
Severe asthma
Life threatening asthma
Peak expiratory flow > 50-75%
best or predicted
Peak expiratory flow 33 – 50%
best or predicted
Peak expiratory flow <33% best or
predicted
SpO2 ≥92%
Speech normal
SpO2 ≥92%
Can’t complete sentences
SpO2 < 92%
Silent chest, cyanosis or poor
respiratory effort
Respiration < 25 breaths/min
Respiration ≥25 breaths/min
Exhaustion, altered consciousness
Pulse <110 beats/min
Pulse ≥ 110 beats/min
Arrhythmia or hypotension
Guidelines for management are also included, for further information please review the full guidance at the
British Thoracic Society website[18]
Evidence Box 2 Assessment of acute asthma
Pulsus paradoxus results in an exaggeration of the normal variation of the pulse with respiration – the pulse
becomes weaker in inspiration, then stronger in expiration. This sign can be caused by a number of
conditions; those relevant to the respiratory system include asthma (EB2), chronic obstructive pulmonary
disease (EB1 and Clinical Prediction Rule 1) and tension pneumothorax. In these conditions, decreased blood
return to the left heart during inspiration results in a decreased stroke volume, which in turn causes a lower
systolic pressure. The lower pressure renders the pulse impalpable. The paradox lies in the fact that if one
were to auscultate the chest whilst palpating for the radial pulse, beats would be heard but not felt. Pulsus
paradoxus can be quantified by measuring the variation of blood pressure during respiration – a decrease of
>10 mmHg in inspiration will be found if the sign is positive[21]. Carbon dioxide retention may result in a rapid,
bounding pulse[22].
Evidence Box 3 Pulsus paradoxus
85
Diagnosing pleural effusion
Diacon et al[24] performed a study in 67 patients comparing physical examination with pleural ultrasound,
finding that clinical examination had a sensitivity of 76%, sensitivity of 60%, a PPV of 85% and an NPV of
45%. Patterson et al[25] performed a similar study, finding that examination had a lower sensitivity than
ultrasound (50% vs. 80%), but a similar specificity (71%)
Kalantri et al[26] conducted a study of 278 patients in a rural Indian hospital, making a blinded comparison in
two physicians’ assessment of a number of clinical signs in relation to pleural effusions. Effusions were
confirmed by chest x-rays. The likelihood ratios for their findings are given in the table below:
Physical Sign +ve likelihood -ve Likelihood ratio
ratio
Asymmetric
8.14 (5.25 –
0.29 (0.18-0.43)
chest
12.71)
expansion
Dullness to
4.82 (3.610.13 (0.06-0.26)
percussion
6.46)
Decreased
5.24 (3.860.15 (0.07-0.28)
breath
7.17)
sounds
Reduced
6.49 (4.410.7 (0.16-0.41)
vocal
9.59)
resonance
No crackles
1.48 (1.090.71 (0.51-0.94)
1.93)
Pleural rub
3.88 (0910.96 (0.87-1.0)
16.33)
A further meta-analysis[27] of 5 such studies concluded that the presence of dullness to percussion (+ LR 8.7)
and asymmetric chest expansion (-LR 8.1) were the signs most indicative of a pleural effusion. It would
appear that Osler’s observation – “In a pleural effusion the percussion signs are very suggestive” holds
true[28].
Evidence Box 4 Pleural effusion
Breath sound scoring
Pardee et al[30] have developed a scoring system for breath sounds as follows, the clinician auscultates at the
following six locations – bilaterally over the upper anterior portion of the chest, in the mid-axillae and at the
bases posteriorly. Intensity is measured on inspiration, with the patient being asked to take a deep breath in
with their mouth open, the loudest sounds heard were recorded. Grading was as follows:
Breath sounds absent
Barely audible
Faint but definitely heard
0 points
1 point
2 points
Normal
3 points
Louder than normal
4 points
A breath sound score which is ≤9 has +LR of 10.2 in the diagnosis of chronic airflow obstruction, whereas a
score of ≥16 has a +LR of 0.1 against such a diagnosis[31], [32].
Evidence Box 5 Breath Sound Scoring
86
Diagnosing Pneumonia
A study of 1819 patients found cachexia had a +LR of 4.0 for pneumonia, with the –LR insignificant[32].
Percussion dullness was also found to have a +LR of 3.0, -LR insignificant[32].
Heckerling et al studied pneumonia in 464 patients, concluding that bronchial breathing had a +LR of 3.3,
again the –LR was insignificant[33].
Vocal resonance was found to have a +LR of 4.1, with the –LR insignificant[32].
However, crackles have a +LR of only 1.8, with a –LR of 0.8; the evidence for wheezing is even poorer (+LR
0.8, -LR NS) [7].
Evidence Box 6 Pneumonia
The BODE index
The BODE index [15] is a clinical prediction rule which predicts death in COPD. The index is calculated as
detailed below:
Variable
Points on BODE index
0
1
2
3
FEV1 (% of predicted)
≥65
50-64
36-49
≤35
Distance walked in
6min (m)
MMRC dyspnoea scale
(see appendix 1)
Body mass index
≥350
250-349
150-249
≤149
0-1
2
3
4
>21
≤21
The acronym BODE refers to Body mass index, airflow obstruction, dyspnoea and exercise capacity.
Hazard ratios for each 1 point increase in the BODE index were shown to be significant (p <0.001) with the
hazard ratio for death from all causes 1.34 and death from respiratory causes 1.62)
The BODE index has been demonstrated[16] to be a better predictor of both the number and severity of
exacerbations compared to the FEV1 alone. (p <0.01)
Clinical Prediction Rule 1 The BODE index
87
Pneumonia
Heckerling et al[33] devised a clinical prediction rule using the following findings which gave a +LR of 8.2 for a
diagnosis of pneumonia if 4 or 5 of the following findings are present: temperature >37.8°C, HR >100bpm,
crackles, diminished breath sounds, absence of asthma. 0-1 finding gave a likelihood ratio of 0.3, with 2-3
findings giving an insignificant positive likelihood ratio.
The CURB-65 score stratifies patients into mortality risk groups and suggests the most appropriate
management. Devised by Lim et al[35], the rule is scored as follows:
Any of –
Confusion (Abbreviated Mental Test Score ≤8 or new
disorientation in place, person, time)
Urea > 7 mmol/l
Respiratory rate ≥30/min
Blood pressure (systolic BP <90 mm Hg or diastolic BP
≤60 mm Hg)
Age ≥ 65 years
The CURB-65 score is interpreted as below:
CURB-65 score –
0-1 (low mortality): Likely suitable for home treatment
2 (intermediate mortality): Consider hospital supervised
treatment
3+ (high mortality): Manage in hospital as severe
pneumonia
CURB-65 has been demonstrated, in a study of over 700 patients to have a PPV of 9.3% for a score of 1,
rising to over 37.4% for a score of 4+, the NPV is 99.3% for a score of 1 and 93.5% for a score of 4+[35].
The CURB-65 score is recommended by the British Thoracic Society for assessment of patients with
suspected community acquired pneumonia[36].
Clinical Prediction Rule 2 CURB-65 score
88
Pulmonary embolism
There are few physical findings which provide strong evidence for the diagnosis of a pulmonary embolism; hence
it is often a difficult condition to diagnose. The Wells score[37], [38] is a clinical prediction rule for pulmonary
embolism, summarised below:
Characteristic
Points
Clinical findings
Haemoptysis
1
Heart rate >100 bpm
1.5
Clinical signs of deep venous thrombosis
3
Risk factors
Previous pulmonary embolism or DVT
1.5
Immobilisation or surgery in past 4 weeks
1.5
Malignancy
1
Other
Alternative diagnosis less likely than pulmonary
3
embolism
Interpretation:
0-1 points : low probability
2-6 points : moderate probability
7+ points : high probability
The Wells score has been shown to have a PPV of 5.0 for scores of 7+ and a NPV of 0.2 for scores of 0-1[7].
Clinical Prediction Rule 3 Wells score
89