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J Alastair Innes
https://t.me/medicina_free
Peter T Reid
5
The respiratory system
Anatomy and physiology 84
The history 84
Common presenting symptoms 85
Past medical history 90
Drug and allergy history 90
Family history 90
Social history 91
Systematic enquiry 92
The physical examination 92
Inspection 92
Palpation 96
Percussion 97
Auscultation 98
Interpretation of the findings 99
Investigations 99
OSCE example 1: Respiratory history 101
OSCE example 2: Respiratory examination 102
Integrated examination sequence for the respiratory system 103
84 • THE RESPIRATORY SYSTEM
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Anatomy and physiology
Understanding the surface anatomy of the lungs (Fig. 5.1)and
their relation to adjacent structures is essential for the practice
of respiratory medicine. At the end of tidal expiration, the dome
of the diaphragm extends high into the thorax, level with the
anterior end of the fifth rib, slightly lower on the left. The lower
lateral ribs therefore overlie the liver on the right and the
stomach and spleen on the left, with the parietal pleura
extending lo wer than the lungs on the lateral chest wall. Posteriorly, the lungs extend much lower, approaching the 12th rib
on full inspiration.
The lung apex lies immediately beneath the brachial plexus, so
apical lung tumours commonly disrupt T1 root fibres, causing
pain and numbness in the inner aspect of the upper arm and
wasting of the small hand muscles. The upper thoracic sympathetic outflow to the eye may also be compromised, leading to a
constricted pupil and ptosis. In the mid and lower mediastinum,
tumours can invade and compromise the pericardium, atria and
oesophagus.
In health, the lungs optimise gas exchange by close matching
of regional ventilation and perfusion. Airway and parenchymal
lung diseases disrupt this matching, causing hypoxia and
cyanosis, and commonly stimulate breathing through lung
afferent nerves, leading to a history of breathlessness and
tachypnoea upon examination.
The history
The key features of the history are summarised in Box 5.1.
Fig. 5.1 Surfaceanatomy of the thorax. A Anteriorview. B Right lateralview.
C Lobar anatomy of the lung surfaces: anterior view (upper),lateralview(lower).
5.1 Respiratory history-taking/documentation
framework
History of presenting symptoms
Specific respiratory symptoms
• Breathlessness
• Wheeze
• Cough
• Sputum/haemoptysis
• Chest pain
• Fever/rigors/night sweats
• Weight loss
• Sleepiness
Past medical history
• Respiratory disease
• Other illness/hospital encounters
Drug and allergy history
• Drugs causing or relieving respiratory symptoms
• Allergies to pollens/pets/dust; anaphylaxis
Social and family history
• Family history of respiratory disease
• Home circumstances/effect of and on disease
• Smoking
• Occupational history
Systematic review
• Systemic diseases involving the lung
• Risk factors for lung disease
The history • 85
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Common presenting symptom s
Breathlessness
Breathlessness (dyspnoea) denotes the feeling of an ‘uncomfortable need to breathe’ and is the most commonly reported
respiratory symptom. It is also one of the most challenging to
quantify, being inherently subjective. Breathlessness may be
caused by respiratory or cardiac disease and also occurs in
anaemia or as a manifestation of psychological distress.
Respiratory disease can cause breathlessness through a
range of mechanisms:
• stimulation of intrapulmonary afferent nerves by interstitial
inflammation or thromboembolism
• mechanical loading of respiratory muscles by airflow
obstruction or reduced lung compliance in fibrosis
• hypoxia due to ventilation/perfusion mismatch, stimulating
chemoreceptors.
The Medical Research Council (MRC) breathlessness scale
(Box 5.2) is a useful and validated way to document formally the
patient’s level of dyspnoea.
Specific questions may help to distinguish the causes of
breathlessness. Ask in particular:
• How did the breathlessness start? If the onset was instan-
taneous, think of pneumothorax, pulmonary embolus or
anaphylaxis. Paroxysmal nocturnal dyspnoea (p. 47) may
wake a sleeping patient with breathlessness. Onset over
hours is typical in asthma, acute pulmonary oedema, lobar
pneumonia, or acute hypersensitivity pneumonitis, while an
insidious onset is more typical of an evolving pleural effusion,
chronic obstructive pulmonary disease (COPD), interstitial
lung disease and lung tumours.
• How is your breathing at rest and overnight? Asthma
commonly wakes patients, while most patients with COPD are
comfortable at rest and when asleep but struggle with exertion. Breathlessness provoked by lying down (orthopnoea) is a
feature of heart failure (p. 47) but also occurs frequently in
patients with severe airflow obstruction or diaphragmatic
5.2 Medical Research Council breathlessness scale
Grade Degree of breathlessness related to activities
1 Not troubled by breathlessness except on strenuous exercise
2 Short of breath when hurrying on the level or walking up a
slight hill
3 Walks slower than most people on the level, stops after a mile
or so, or stops after 15 min walking at own pace
4 Stops for breath after walking about 100 yards or after a few
minutes on level ground
5 Too breathless to leave the house, or breathless when
undressing
Used with the permission of the Medical Research Council.
weakness because the weight of the abdomen displaces the
diaphragm cranially on lying down, compromising the vital
capacity.
• Does your breathlessness vary from day to day or week to
week? Variable breathlessness is typical of asthma, whereas
patients with COPD or interstitial lung disease usually report
consistent daily limitation.
• Can you tell me something you do that would make you
breathless? and How far can you walk on a good day? These
questions reveal the disability caused by respiratory disease.
Record restrictions on normal activity or work and the corresponding MRC breathlessness score. Enquiring about
hobbies and daily activities reveals the time course of
breathlessness; for example, ‘When was the last time you
could walk to the shops / play a full round of golf?’
• When does the breathlessness start? Asthma induced by
exercise frequently appears only after exercise during early
recovery, because sympathetic drive during exercise defends
airway patency.
Certain phrases in the history strongly suggest a psychological
aetiology of breathlessness, particularly ‘I feel I can’t get enough
air (or oxygen) into my chest.’ In patients with hyperventilation
due to anxiety, this symptom is frequently accompanied by a
normal measured vital capacity. Associated symptoms induced
by hypocapnia in hyperventilation include digital and perioral
paraesthesia, light-headedness and chest tightness.
Fig. 5.2 summarises how to use the history and examination
findings to distinguish some common causes of breathlessness.
Remember that patients do not always report exactly what
textbooks describe.
Wheeze
Wheeze describes the high-pitched musical or ‘whistling’ sounds
produced by turbulent air flow through small airways narrowed
by bronchospasm and/or airway secretions. It is heard mostly
during expiration, which additionally narrows the airways.
Wheeze must be distinguished from the rattling inspiratory and
expiratory sounds caused by loose, mobile secretions in the
upper airways, and from the louder, dramatic croak of stridor
(see below) caused by obstruction in the trachea or large airways. Patients may be unaware of nocturnal wheeze, which may
be noticed only by their bed partner.
Wheeze is most commonly associated with asthma and
COPD but can also occur with acute bronchitis, exacerbations of
bronchiectasis or congestive cardiac failure (‘cardiac wheeze’).
Ask:
• Is the wheeze worse during or after exercise? If it occurs
during exercise and limits it, this suggests COPD; in asthma,
wheeze and tightness usually appear after exercise.
• Do you wake with wheeze during the night? This suggests
asthma.
• Do you have hay fever or other allergies? Atopy is common in
allergic asthma. A family history of wheeze or asthma is
common.
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Acute or
subacute
Diagnostic approach to breathlessness
Time courseDuration
Pleuritic pain
Sudden
Crushing central pain
Examination and other findings DiagnosisOther history
Haemoptysis,
swollen leg
Unilateral absent
breath sounds
Crackles in chest
Normal breath
sounds,
JVP
Pulmonary embolus/
infarct
Pneumothorax
MI with pulmonary
oedema
Large pulmonary
embolus
Breathlessness
Chronic
Hours/days
Insidious
Occurs at
rest/night
Exertional
Fever, cough, green
sputum
Tightness, atopy/pets
Weight loss, cough
Dry cough
Angina, frothy sputum
Tightness, atopy/pets
Paraesthesia, ‘can’t
get enough air’
Smoker
Dry cough
Signs of
consolidation, rigors
Wheeze
Wheeze
Unilateral dullness,
clubbing
Crackles, night
sweats
Fine inspiratory
crackles
Crackles, peripheral
oedema
Wheeze
Carpopedal spasm,
anxiety
Hyperinflation
Fine inspiratory
crackles
Pneumonia
Acute bronchitis
New onset of
asthma
Malignant pleural
effusion
Tuberculosis
New interstitial
disease
Congestive cardiac
failure
Asthma
Hyperventilation
COPD
Interstitial lung
disease
Fig. 5.2 Common causes of breathlessness: distinguishing features on history and examination. COPD, Chronic obstructive pulmonary disease; JVP, jugular
venous pressure; MI, myocardial infarction.
• Is it worse on waking in the morning and relieved by clearing
sputum? This is common in COPD and bronchiectasis.
Cough
The cough reflex has evolved to dislodge foreign material and
secretions from the central airways and may be triggered by
pathology at any level of the bronchial tree. Inspiration is followed
by an expiratory effort against a closed glottis. Subsequent
sudden opening of the glottis with rapid expiratory flow produces
the characteristic sound.
Cough is most commonly a symptom of acute viral bronchitis,
which is usually self-limiting over days to weeks. A cough that
fails to settle within 3 weeks should prompt consideration of
underlying respiratory disease. Causes of chronic cough and
features in the history that may indicate the underlying cause are
summarised in Box 5.3.
Ask about:
• Duration of the cough.
• Whether it is present every day.
• If it is intrusive/irresistible or whether the patient coughs
deliberately to clear a perceived obstruction (throat clearing).
• Whether it produces sputum. If so, how much, and what colour?
• Any haemoptysis?
• Any triggers (such as swallowing, cold air, during or after
exercise, allergens).
The history • 87
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5.3 Causes of chronic cough and accompanying clues
in the history
Suggestive features in history/
Pathophysiology
Airways inflammation
• Asthma –‘cough-variant
asthma’
• Chronic obstructive
pulmonary disease
• Persisting airway reactivity
following acute bronchitis
• Bronchiectasis
Lung cancer Persistent cough, especially in smokers
Rhinitis with postnasal drip Chronic sneezing, nasal blockage/
Oesophageal reflux Heartburn or acid reflux after eating,
Drug effects Angiotensin-converting enzyme inhibitors
Interstitial lung diseases Persistent dry cough
Idiopathic cough Long history with no signs and negative
examination
Affects children and some adults
Often present at night
Associated wheezing, atopy
History of smoking and intermittent
sputum
Cough persisting after recent infection
Daily purulent sputum for long periods
Pneumonia or whooping cough in
childhood
Recurrent haemoptysis
Any haemoptysis
Pneumonia that fails to clear in 4–
6 weeks
discharge
bending or lying
Nocturnal and daytime cough
Fine inspiratory crackles at bases
investigations – diagnosis of exclusion
with upper respiratory tract secretions and saliva and is swallowed. In disease, the accumulation of inflammatory cells, mucus
and proteinaceous secretions in the airways results in cough with
expectoration of sputum. Ask the patient about the colour, volume and consistency of sputum. Direct examination of the
sputum is useful to verify the account (Fig. 5.3).
In acute or chronic airway infection, the characteristics of
sputum help to clarify the pathology. A change in colour or
consistency, or an increase in volume may indicate a new
infection in chronic disease.
Colour
• Clear (mucoid): COPD/bronchiectasis without current
infection.
• Yellow (mucopurulent): acute lower respiratory tract infection/
asthma.
• Green (purulent): current infection – acute disease or exac-
erbation of chronic disease, such as COPD. In bronchiectasis
(and COPD), the colour and volume of sputum may be used
to guide the need for antibiotics (see Fig. 5.3A) whereas in
asthma, mucopurulent sputum may be the result of sputum
eosinophilia.
• Red/brown (rusty): pneumococcal pneumonia (see Fig. 5.3B).
Try to distinguish between rusty and frank red blood (see
below).
• Pink (serous/frothy): acute pulmonary oedema.
Volume
• Establish the volume produced over 24 hours: small amounts
into a tissue or enough to fill a spoon(s), eggcup(s) or cup(s).
• Compare the current volume with the patient’s baseline
volume.
5
• Smoking. This increases the likelihood of chronic bronchitis or
lung cancer.
• Associated clinical features:
• Wheeze: may signal cough-variant asthma.
• Heartburn or reflux: gastro-oesophageal reflux commonly
triggers cough.
• Altered voice or swallowing: consider laryngeal causes.
• Drug history, especially angiotensin-converting enzyme (ACE)
inhibitors.
Cough that produces green or yellow sputum suggests
bronchial infection. Large volumes of sputum over long periods
suggest bronchiectasis.
In patients with malignancy at the left hilum, damage to the left
recurrent laryngeal nerve may paralyse the left vocal cord, making it
impossible for the patient to close the glottis and generate a normal
explosive cough. The resulting hoarse forced expiration without the
initial explosive glottal opening is called a ‘bovine cough.’
Sputum
In health, the airway lining fluid coating the tracheobronchial tree
ascends the mucociliary escalator to the larynx, where it mixes
Consistency
• An increase in stickiness (viscosity) may indicate exacerbation
in bronchiectasis.
• Occasionally, sputum is produced as firm ‘plugs’ by patients
with asthma (see Fig. 5.3C), sometimes indicating underlying
allergic bronchopulmonary aspergillosis.
• Large volumes of frothy secretions over weeks/months are a
feature of the uncommon bronchoalveolar cell carcinoma.
Haemoptysis
Haemoptysis means coughing up blood from the respiratory
tract. Whilst it can complicate any severe forceful cough, never
assume haemoptysis has a benign cause, particularly in a
smoker, until underlying pathology has been excluded.
Enquire about these features:
• Was the blood coughed up from the chest? Blood in the
mouth may be vomited, may have come from the nose in
epistaxis, or may appear on chewing or tooth brushing in
patients with gum disease.
• When did blood appear, how much blood, were there
associated symptoms and over what time period was it
present?
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MUCOID
MUCOPURULENT
PURULENT
B
1 cm
C
Fig. 5.3 Sputum appearance in disease. A Colour chart of sputum purulence used in bronchiectasis. B Rusty red sputum of pneumococcal pneumonia. C
Mucus plug from a patient with asthma. (A, Courtesy Medical Photography, NHS Lothian.)
• Any fever/symptoms of infection? Acute or chronic bronchial
infections, including tuberculosis, often trigger haemoptysis.
• Recurrent blood streaks in clear sputum should prompt a
search for lung cancer.
• Recurrent blood streaks in purulent sputum over years suggests bronchiectasis.
• A sudden episode of haemoptysis with pleuritic pain and
breathlessness suggests pulmonary embolism.
• Large volumes of haemoptysis (> 20 mL) suggest specific
causes:
• lung cancer eroding a pulmonary vessel
• bronchiectasis (such as in cystic fibrosis)
• cavitary disease (e.g., complicating an aspergilloma or
cavitary pulmonary tuberculosis).
• pulmonary vasculitis
• pulmonary arteriovenous malformation.
Stridor
This harsh, grating respiratory sound is caused by vibration of the
tracheal walls or major bronchi when the airway lumen is critically
narrowed by compression, tumour or inhaled foreign material.
Inspiration lowers the pressure inside the extrathoracic trachea,
so critical narrowing here leads to inspiratory stridor. In contrast,
the intrathoracic large airways are compressed during expiration
by positive pressure in the surrounding lung, leading to fixed
expiratory wheeze or stridor. Large airway narrowing at the
thoracic inlet (e.g., tracheal compression by a large goitre) may
cause both inspiratory and expiratory stridor. Rapid investigation
and treatment are vital when this sign is present.
Chest pain
Chest pain can arise from the chest wall, parietal pleura, mediastinal structures, tracheobronchial tree, pericardium, oesophagus and subdiaphragmatic organs (liver and gallbladder). Pain
does not originate in the lung parenchyma or visceral pleura, as
they have only an autonomic nerve supply.
Establish:
• Site and severity.
• Character: sharp suggests pleural pain.
• Onset: gradual or rapid?
The history • 89
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• Exacerbating or relieving factors: worsening with cough or
deep breaths suggests pleural disease.
• Associated symptoms: breathlessness, fever and cough
suggest an infective cause.
A large pulmonary embolus can cause angina-like chest pain
(p. 85), due to increase of right ventricular work together with
reduced coronary oxygen delivery caused by hypotension and
hypoxaemia, resulting in right ventricular ischaemia.
Pleuritic pain is worse on inspiration and coughing, and is
usually described as sharp, stabbing or knife-like. It is usually
sited away from the midline and may be localised or affect a wide
area of chest wall. Disease causes parietal pleural pain in several
ways:
• pneumonia and pulmonary infarcts: either direct pleural
inflammation or adhesions with pleural traction on respiratory
movement
• pneumothorax: mechanical distortion of pleura with lung
collapse
• lung cancer: pleural distortion by infiltration, although con-
stant pain is more typical
Musculoskeletal chest pain is common and may occur with
chest trauma, forceful coughing or connective tissue disease.
The chest is characteristically tender to palpation, and the pain
can be reproduced by respiratory movements and/or movement
of the spine or shoulder muscles. There may be associated soft
tissue injury or rib fractures. A detailed history of events preceding the onset is vital, as injury is easily overlooked.
Two other uncommon conditions can cause acute chest pain.
Bornholm disease is an infection with an enterovirus (Coxsackie
B). This causes acute but self-limiting inflammation of intercostal
muscles, with episodes of severe unilateral intercostal myalgia
lasting a few days. Costochondritis (called Tietze’s syndrome
when costochondral swelling is present) is idiopathic inflammation of the costochondral cartilages adjoining the sternum, with
acute localised pain and tenderness. The pain is eased by simple
analgesia and settles spontaneously in both conditions.
Herpes zoster infection (shingles) may start with superficial itch
or burning pain in a thoracic dermatome, followed by the
appearance of a vesicular rash (a ‘belt of roses from hell’). Pain
and altered sensation may persist long after the rash has
resolved, often with scarring in the affected dermatome.
Burning retrosternal pain may indicate oesophagitis but also
occurs with myocardial ischaemia. Worsening of oesophageal
discomfort after eating or relief after antacids helps to distinguish
it from cardiac pain.
Cardiac pain is described on page 45.
Central, constant, progressive, non-pleuritic chest pain may
represent mediastinal disease, particularly malignancy. Similarly,
chest wall pain (without trauma) that is constant, progressive and
non-pleuritic suggests chest wall invasion by malignancy. Sleep
disturbance is a feature of such malignant pains.
Fevers/rigors/night sweats
These symptoms are not specific but are commonly reported by
patients with respiratory illnesses. Infection (acute or chronic) is
the usual cause, but other aetiologies such as lung cancer,
lymphoma or vasculitis should also be considered.
Patients use many different terms to describe fever (e.g.,
shivers, chills, shakes), so take care to clarify their actual
symptoms.
Rigors are generalised, uncontrollable episodes of vigorous
body shaking lasting a few minutes. Despite high fever, the patient may complain of feeling cold and seek extra clothing. Rigors
usually indicate bacterial sepsis; lobar pneumonia and acute
pyelonephritis are the most common causes.
Night sweats, particularly if persistent, are associated with
chronic infection such as tuberculosis or malignancy, particularly
lymphoma. Occasional episodes are inconclusive, but if patients
report having to change their nightclothes or sheets frequently
due to profuse nocturnal sweating over several weeks, this
suggests underlying disease.
Weight loss
Weight loss is a common feature of respiratory diseases,
including lung cancer, COPD, interstitial lung disease, and
chronic infections such as tuberculosis and bronchiectasis. The
pathophysiology is complex; however, breathlessness is associated with diminished appetite, and the systemic inflammatory
response is also thought to contribute to weight loss.
Weight loss also occurs in acute infection with loss of appetite,
particularly during hospitalisation. Ask the patient to estimate the
extent and duration of weight loss and enquire about appetite
and dietary intake.
Sleepiness
Excessive daytime sleepiness may be a symptom of an underlying sleep-related breathing disorder – obstructive sleep apnoea
(OSA) or OSA/sleep hypopnoea (OSASH). In these conditions,
the upper airway collapses intermittently and repeatedly during
sleep. Partial obstruction results in snoring, but complete
collapse stimulates increased respiratory effort resulting in transient wakening. Repeated episodes of sleep disturbance cause
excessive daytime sleepiness and poor concentration. OSASH is
more common in men; particularly if obese and with a large neck
(collar sizes >17 inches) and can be aggravated by alcohol.
Ask about:
• Normal sleeping habit: does the patient keep hours that allow
reasonable rest?
• Shift or night work: this can disrupt and prevent healthy sleep
patterns.
• Does the person wake refreshed or exhausted? Sleep
apnoea patients are exhausted in the morning.
• Have they struggled to stay awake in the day: for example, at
work or when driving?
It is vital to advise cessation of driving pending investigation if
OSA is suspected.
Ideally, seek a description of any night-time breathing disturbance from a bed partner. In OSA, the partner may observe periodic cessation of breathing, accompanied by increasing respiratory
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efforts, followed by a sudden and loud resumption of breathing,
often with postural repositioning, then repetition of this cycle.
Validated sleepiness scores (such as the Epworth Sleepiness
Scale: http://epworthsleepinessscale.com/) can be used to
quantify daytime somnolence and are helpful if considering
referral to a sleep clinic.
Past medical history
Past illnesses relevant to respiratory disease are summarised in
Box 5.4. These include respiratory disease that may recur or
cause long-term symptoms, and disease in other systems that
may cause, complicate or present with respiratory symptoms,
including thromboembolic, cardiovascular, haematological, malignant and connective tissue diseases.
Note prior respiratory treatments (including need for critical
care) and the degree of chronic symptoms, such as usual
exacerbation frequency, prescription rate and hospitalisation.
5.4 Previous illness relevant to respiratory history
History Current implications
Eczema, hay fever Allergic tendency relevant to asthma
Childhood asthma Many wheezy children do not have
Whooping cough, inhaled
foreign body, measles
Pneumonia, pleurisy Recurrent episodes may be a
Tuberculosis Reactivation if not previously treated
Connective tissue disorders,
e.g., rheumatoid arthritis
Previous malignancy Recurrence, metastatic/pleural disease
Cancer, recent travel, surgery
or immobility
Recent surgery, loss of
consciousness
Neuromuscular disorders Respiratory failure
asthma as adults, yet many adults with
asthma had childhood wheeze
Recognised causes of bronchiectasis,
especially if complicated by pneumonia
manifestation of bronchiectasis. Some
pneumonias may cause bronchiectasis
effectively
Post-tuberculous bronchiectasis –
sputum, haemoptysis.
Aspergilloma in lung cavity may present
with haemoptysis
Many have respiratory manifestations,
e.g., pulmonary fibrosis, effusions,
bronchiectasis
Immunomodulatory treatments for
rheumatological diseases may cause
pulmonary toxicity or make patients
susceptible to respiratory infection
Chemotherapy can cause pulmonary
fibrosis (e.g., bleomycin)
Radiotherapy-induced pulmonary
fibrosis
Pulmonary thromboembolism
Aspiration of foreign body, gastric
contents leading to pneumonia, lung
abscess
Aspiration
Drug and allergy history
Note all drugs that the patient is currently using, including inhalers, nebulised therapy, domiciliary oxygen, non-prescription
remedies and recreational drugs. Cross-check the drug names
and doses with a separate source such as the general practitioner’s records.
Drugs given for other problems commonly cause respiratory
side effects; these are summarised in Box 5.5.
Ask whether the patient has allergies such as hay fever, as
allergic asthma is far more common in those with a history of
atopy.
Family history
Respiratory diseases with a known genetic cause are relatively
rare. Patients with autosomal recessive conditions such as cystic
fibrosis usually have unaffected carrier parents but may have
affected siblings. A family history of venous thromboembolism
should prompt investigation of inherited thrombophilias such as
Factor V Leiden or protein C or protein S deficiency. In rare
cases, idiopathic pulmonary fibrosis and primary pulmonary hypertension may be familial.
5.5 Respiratory problems caused by drugs
Respiratory
condition Drug
Bronchoconstriction Beta-blockers (including eye drops)
Cough Angiotensin-converting enzyme inhibitors
Bronchiolitis
obliterans
Diffuse parenchymal
lung disease
Pulmonary
thromboembolism
Pulmonary
hypertension
Pleural effusion Amiodarone
Respiratory
depression
Tuberculosis Reactivation by glucocorticoids or disease
Opioids
Nonsteroidal anti-inflammatory drugs
Penicillamine
Cytotoxic agents: bleomycin, methotrexate
Anti-inflammatory agents: sulfasalazine,
penicillamine, gold salts, aspirin
Cardiovascular drugs: amiodarone, hydralazine
Antibiotics: nitrofurantoin
Oestrogens
Oestrogens
Dexfenfluramine, fenfluramine
Nitrofurantoin
Phenytoin
Methotrexate
Pergolide
Opioids
Benzodiazepines
modifying antirheumatic drugs (DMARDs)/
biological immunomodulators given for
rheumatic disease
The history • 91
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Social history
Exposures at home may cause or aggravate respiratory disease.
Passive smoking increases the risk of respiratory infection and
burning biomass fuels in confined spaces increases the risk of
bronchitis and COPD. Domestic pets, especially cats and rodents, may be the cause of suboptimal asthma control. A pet
bird, feather duvet or an infestation of mould may cause hypersensitivity pneumonitis or suboptimal asthma control.
The home circumstances may reveal the impact of respiratory
disability, for example if the patient has relocated to ground-floor
accommodations or relies on others for shopping.
Smoking
Obtaining an accurate history of tobacco use is difficult and is
covered on page 16 (Chapter 2). Ask if any cohabitees smoke;
this can be a major obstacle to cessation. Remember also to ask
about cannabis, waterpipes and e-cigarettes. Cannabis may be
smoked without tobacco; for example using a bong; or cut with
tobacco as an unfiltered joint. Waterpipes (‘narghileh’, ‘shisha’ or
‘hookah’) are used to smoke tobacco, cannabis or flavoured
tobacco (maassel). E-cigarettes are used increasingly to assist
with smoking cessation.
Occupational history
Many respiratory diseases are caused by occupational exposure to
inhaled substances; these are summarised in Box 5.6.Askthe
patient about their work history, starting with their first job documenting the employers’ names, the dates and duration of
exposure, and whether any protective masks were offered or used.
Occupational asthma should be considered if symptoms
improve on days away from work.
5.6 Occupational factors in respiratory disease
Respiratory disease Toxic agent(s) Affected occupations
Asthma
Rhino-conjunctivitis
Chronic obstructive
pulmonary disease
Byssinosis Cotton dust Flax workers
Pneumoconiosis Coal (Coal Miners Pneumoconiosis)
Hypersensitivity
pneumonitis
Pneumonia Strep. pneumonia
Tuberculosis Silica (silicotuberculosis) See above
Granulomatous disease Beryllium (Berylliosis) Aerospace industry, nuclear industry, oil/gas drilling, dental technicians
Pleural disease Asbestos: pleural plaques, diffuse pleural
Lung cancer Asbestos
Connective tissue disease Silica increases the risk of scleroderma. See above
Isocyanates
Flour, grain dust, enzymes
Animal dander/urine
Wood dust
Cadmium fumes
Coal dust
Silica
Coke dust
Silica (Silicosis)
Asbestos (Asbestosis)
Iron (Siderosis)
Tin (Stannosis)
Thermophilic bacteria:
• Mouldy hay
• Mouldy grain
• Mushroom compost
• Mouldy sugar cane (Bagassosis)
Avian serum/excreta
Metal working fluids
Q fever (Cox.burnetii)
Psittacosis ( C. psittaci)
Leptospirosis (Leptospira)
thickening, mesothelioma
Silica
Coke dust
Spray painters
Baking industry
Laboratory and veterinary workers
Joiners
Solderers
Underground miners
Stone cutting, masonry, tunnelling, quarrying, pottery, metal ore mining,
siliceous abrasive users, foundry workers
Coke oven workers
Miners
see above
Former laggers, asbestos textile manufacture; asbestos insulation work
including marine engineering, shipbreaking.
Iron ore miners, welders, iron foundry fettlers
Tin smelters
Farmers
Grain workers
Mushroom pickers
Sugar workers
Bird fanciers
Machinists
Welders
Dairy farmers, abattoir workers
Poultry workers
Sewage workers, animal handlers, vets
See above
See above
5
92 • THE RESPIRATORY SYSTEM
https://t.me/medicina_free
Inhalation of organic dusts may trigger hypersensitivity pneumonitis. Whilst the cause is often unknown, contact with birds,
bird droppings or feathers, metal working fluids, hay and mould
remain common causes.
Inhalation of inorganic dusts such as asbestos, coal or silica
cause pneumoconiosis, with gradual onset of cough and breathlessness, often years after exposure. Despite improved controls,
asbestos and silica exposure remain important causes of ill health.
Certain occupations increase the risk of respiratory infection,
for example Q fever in abattoir workers and leptospirosis in
sewage workers and animal handlers.
Systematic enquiry
Systematic enquiry may reveal extrapulmonary symptoms linked
to underlying respiratory disease. For example, morning headaches can indicate an elevated PaCO
dysphagia following stroke can increase the risk of aspiration
pneumonia, and joint pains may indicate connective tissue disease underlying pleural or parenchymal lung disease.
in respiratory failure,
2
The physical examination
Observations made during history taking can be valuable. For
example, how easily did the patient converse? Did they cough
repeatedly?
It is often easiest to examine the patient reclining on the bed or
an examination couch at about 45 degrees, with the thorax
exposed and the head supported by a pillow.
Inspection
Much can be learned about the respiratory system by careful
inspection from the end of the bed. The normal shape and
respiratory movements of the chest wall are significantly altered
by the hyperinflation that accompanies chronic airflow obstruction (Fig. 5.4). Such obstruction also causes prolonged expiration
relative to inspiration, and sometimes ‘pursed-lip’ breathing on
expiration. Forceful inspiration at these very high lung volumes
may cause indrawing of the intercostal spaces during midinspiration and the recruitment of muscles not normally
involved in breathing (‘accessory muscles’). These include the
sternocleidomastoid muscles lifting the sternum, and the trapezius and the scalenes lifting the shoulder girdle. Patients sometime sit forwards and brace their arms on a surface, allowing
them to use the pectoralis major to pull the ribs outwards during
inspiration. In contrast to the hyperinflation of obstructive disease, interstitial disease causes small, stiff lungs, diminishes
thoracic volume and raises resting respiratory rate.
Chest deformity (Fig. 5.5) may be congenital, as in pectus
excavatum, or acquired, as in pectus carinatum. The latter is an
inward displacement of the lower ribs with a prominent sternum,
caused by severe airflow obstruction in early childhood, during
rib cage development. Asymmetry of the chest may be
A Normal
B Hyperinflated
Fig. 5.4 Respiratory movement of the ribs, sternum and diaphragm. A In normal adults. B In chronic hyperinflation due to obstructive lung disease.
Hyperinflation causes upward displacement of the sternum and clavicles, increased anteroposterior thoracic diameter, loss of cardiac dullness at the lower left
sternal edge, and a low flat diaphragm that pulls the lower ribs in during inspiration.
Normal
cricosternal
distance
Heart causes
dullness at
left sternal edge
Expiration Inspiration
Reduced cricosternal
distance (sternum high)
Lingula overlies heart
– loss of cardiac dullness
Low, flat diaphragm
Upward, outward
rib movement
Outward movement
of lower ribs
Reduced outward
movement
Paradoxical inward
movement of lower ribs
due to flat diaphragm
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