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Shortness of breath
upper airway obstruction, and may indicate impending
airway compromise, which requires urgent evaluation
by someone with appropriate expertise. Inspiratory and
expiratory stridor can indicate fixed obstruction.
• Wheeze: a whistling noise, most commonly in
expiration caused by turbulent airflow through
narrowed intrathoracic airways. Present in conditions
such as asthma and COPD.
HINTS AND TIPS
Asthma typically has a nocturnal cough. Chronic
bronchitis-associated cough is particularly bad in
the morning.
Other factors
• Occupational history, including exposure to asbestos
and dusts: changing the working environment may
relieve symptoms.
• Known lung disease: current, such as asthma, or
previous, such as tuberculosis.
• History of atopy: asthma, seasonal allergic rhinitis (hay
fever) or eczema.
• Pets: can exacerbate asthma or cause chronic lung diseases
(extrinsic allergic alveolitis, e.g. ‘pigeon fanciers’ lung’).
• Current medications: noncardioselective β-blockers
may exacerbate wheeze.
• Previous medications: e.g. amiodarone can cause
interstitial lung disease.
• Angina or previous myocardial infarction: symptoms of
cardiac dyspnoea.
• General health: e.g. weight loss, appetite.
• Recent foreign travel.
• Smoking tobacco, marijuana and other inhaled
compounds.
Examination
The examination findings of common respiratory conditions are listed in Table. 5.1, and the approach to examining
a patient with breathlessness is summarized in Fig.5.1. For
more detailed description of examination findings in respiratory disease, see Chapter28.
Inspection
• Observe the patient from the end of the bed – note the
respiratory rate (normal range in an adult at rest is 12–
20 breaths per minute) and assess the work of breathing,
use of accessory muscles and any audible sounds.
• Look at the shape of the chest and chest movements.
A barrel-shaped chest is common in COPD.
Kyphoscoliosis may affect chest expansion and therefore
effectiveness of respiration. Paradoxical abdominal
movement may indicate diaphragmatic weakness.
• Assess the pattern of breathing (clinical note: patterns
of respiration).
• Central cyanosis (bluish discolouration of the buccal
mucosa due to excess deoxygenated haemoglobin.
• Tar staining of the fingers.
• Clubbing: respiratory causes include carcinoma,
suppurative lung disease (e.g. empyema, lung abscess,
bronchiectasis, cystic fibrosis), interstitial lung disease,
tuberculosis and mesothelioma.
HINTS AND TIPS
Central cyanosis is visible when there is more than
5 g of deoxygenated haemoglobin per 100 mL of
blood. Despite this, it is an unreliable guide to the
Table. 5.1 Findings on examination of common respiratory conditions
Condition
Pleural effusion ↓ Central or deviated away
Pneumothorax ↓ Central or deviated away ↑ ↓ ↓
Pneumonia ↓ Central or deviated
Pulmonary fibrosis ↓ Central or deviated
Movement on
side of lesion Position of trachea Percussion
↓ (‘stony dull’) ↓ ↓ with bronchial
from effusion if massive
↓ ↑ Increased vocal
towards the affected
side if associated with
collapse
↓ ↑ Fine crepitations
towards the affected side
if upper lobe involvement
Tactile vocal
fremitus Breath sounds
48
breathing at top of
effusion
resonance
Bronchial breathing
(absent if obstruction
of bronchus)
Coarse crepitations
Sputum
Lips
(flattened diaphragm)
Jugular vein
−
Pressure raised in
right sided heart failure
Heart
−− Murmurs
(e.g. mitral stenosis)
Lungs
−− Percussion
−− Vocal fremitus
−− Crepitations
−− Breath sounds
−− Wheezes
−− Vocal resonance
Liver
−
Enlarged with
right-sided heart failure
General appearance
−− Cachetic
−− Blue bloater
−− Pink puffer
−− Tachypnoea
−− Anaemia
−− Use of accessory
muscles
Extremities
−− Peripheral oedema
Fig.5.1 Examining the patient with breathlessness.
History and examination findings
−
Pursing
(chronic obstructive
pulmonary disease)
−
Cyanosis
Trachea
−
Deviation
−
Tracheal tug
Suprasternal notch
−
Distance to cricoid
reduced with
hyperinflated lungs
Chest
−
Asymmetrical chest
wall movement
−
Chest wall
deformity
Ribs
−
Indrawing of lower
ribs on inspiration
Hands
−
Tar staining
−
Clubbing (e.g.
fibrosing alveolitis,
bronchiectasis,
bronchial carcinoma)
Legs
−
Deep venous
thrombosis
55
severity of hypoxaemia, it is difficult to appreciate
in anaemic patients and it is common in patients
who have polycythaemia associated with chronic
respiratory and cardiac disease. Peripheral cyanosis
can be due to poor peripheral circulation (e.g.
cardiac failure, peripheral vascular disease, cold
environment).
CLINICAL NOTE
Lip pursing is common in patients with COPD and
alveolar air trapping. Pursing the lips allows the
creation of positive end-expiratory pressure, which
eases the work of breathing.
CLINICAL NOTE
PATTERNS OF RESPIRATION
• Cheyne–Stokes respiration: cyclical variation in
the depth of breathing with periods of rapid and
deep inspiration and apnoea. Causes include
neurological disease (brainstem lesions, raised
intracranial pressure), left ventricular failure and
altitude sickness.
• Kussmaul respiration: deep and laboured
breathing. It is most often associated with
metabolic acidosis.
• Biot respiration: periodic breathing characterized
by quick shallow inspirations followed by
apnoea. Causes include pontine damage and
opioid use.
49
Shortness of breath
HINTS AND TIPS
Always look in the sputum pot:
• purulent, moderate quantity – bronchitis or
pneumonia;
• purulent, copious quantity – bronchiectasis or
pneumonia;
• pink and frothy – pulmonary oedema;
• blood stained – causes of haemoptysis;
• rust coloured – pneumococcal lobar pneumonia.
Palpation
• Cervical lymphadenopathy: malignant disease or
infection.
• Trachea: deviation may indicate underlying chest or
cardiac disease.
• Expansion of the rib cage.
• Tactile vocal fremitus.
Percussion
• Percuss both anteriorly and posteriorly in a systematic
manner.
• Increased resonance: indicates increased air beneath –
acutely in pneumothorax or chronically in emphysema.
• Decreased resonance: indicates increased solid matter
beneath – infection or effusion (classically ‘stony dull’).
Auscultation
• Expiration: may be prolonged in COPD.
• Breath sounds: diminished over an effusion, over a
pneumothorax and in the obese person.
• Bronchial breathing: consolidation, cavitation or at the
top of an effusion.
• Rhonchi or wheeze: partially obstructed bronchi; found
in asthma, COPD and occasionally left ventricular failure.
If polyphonic, this usually suggests multiple small-airway
narrowing. If monophonic and fixed, it can indicate a
fixed single obstruction (e.g. a central malignant lesion).
• Crepitations or crackles (sudden opening of small
closed airways): pulmonary congestion (fine
crepitations in early inspiration); fibrosing alveolitis
(fine crepitations in late inspiration); bronchial
secretions (coarse crepitations).
• Friction rub: pleural disease.
• Vocal fremitus: ask the patient to say and then whisper
‘99’. This provides the same information as tactile
fremitus but is often easier to detect.
INVESTIGATIONS
Acute presentation
• Full blood count: anaemia; leucocytosis in pneumonia.
• Urea and electrolytes: renal failure.
• Blood glucose: diabetic ketoacidosis.
• Chest X-ray: hyperexpanded lungs in COPD;
consolidation in pneumonia; lack of lung markings in
pneumothorax; blunting of the costodiaphragmatic
angle(s) in pulmonary effusion or empyema;
cardiomegaly in heart failure; fluid in the horizontal
fissure, upper lobe pulmonary venous diversion, air
space opacifications classically in a batwing distribution
in pulmonary oedema.
Electrocardiogram: look for evidence of acute or chronic
cardiac or respiratory disease.
• Arterial oxygen saturation: easy to perform and may
obviate the need for blood gas analysis.
• Arterial blood gases: pH, P2 and P2, base excess,
bicarbonate concentration and lactate level (see
Chapter28).
• CT scanning: used to assess both acute and chronic
dyspnoea (e.g. to investigate pulmonary embolism and
to diagnose and quantify interstitial lung disease and
bronchiectasis).
HINTS AND TIPS
The upper lobes of the lungs are best heard on the
anterior chest wall, middle lobe in the axilla and
lower lobes on the posterior chest wall.
Chronic presentation
⚬ Spirometry: distinguish between obstructive and
restrictive lung pathology. This is best done for
diagnosis when the patient is not acutely unwell. Lying
and standing vital capacity will screen the patient for
diaphragm weakness.
50
Investigations
55
⚬ Peak expiratory flow rate: useful for assessing acute
decline, especially in asthmatic patients who often
know their best results.
• Full pulmonary function tests: transfer factor, flow–
volume loop and lung volumes.
• Bronchoscopy: if an endobronchial lesion is suspected.
• Echocardiogram: assess cardiac structure and function,
including pulmonary hypertension.
HINTS AND TIPS
Nail varnish, in particular red nail varnish, will
interfere with pulse oximetry measurements and
should be removed.
Chapter Summary
• Shortness of breath can be a manifestation of disease of different systems, including
respiratory, cardiovascular, renal and neurological.
• Careful history taking and examination will guide you toward the cause. Suspected
disease will guide investigations.
51
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Cough and haemoptysis
6
INTRODUCTION
Cough is a reflex reaction to irritation anywhere in the respiratory tract from the pharynx to the alveoli. Cough lasting more than 8weeks is said to be chronic. Cough lasting
more than 3weeks should be investigated (see Chapter28).
CLINICAL NOTES
DIFFERENTIAL DIAGNOSIS OF COUGH AND
HAEMOPTYSIS
Cough
• Postnasal drip: rhinitis, sinusitis.
• Upper respiratory tract infections:
viral or bacterial, causing laryngitis,
tracheobronchitis, etc.
• Pressure on the trachea: e.g. from a goitre; this
may be associated with stridor.
• Lower respiratory tract causes: almost any
lung disease may be associated with cough,
particularly asthma (classically a nocturnal
cough), chronic obstructive pulmonary disease,
pneumonia, bronchiectasis, interstitial lung
disease or carcinoma.
• Left ventricular failure.
• Drugs: especially angiotensin-converting enzyme
inhibitors and irritants (e.g. occupational agents).
• Psychogenic/habitual cough.
• Gastro-oesophageal reflux disease: reflux is a
common cause of chronic cough and may not
be obvious from symptoms.
Haemoptysis
• Acute infections: e.g. pneumonia, exacerbations
of chronic obstructive pulmonary disease.
• Bronchiectasis: can be responsible for massive
haemoptysis.
• Bronchial carcinoma: secondary malignancies
and benign tumours can also lead to
haemoptysis but are less common.
• Pulmonary tuberculosis.
• Other chronic infection: e.g. lung abscess,
pulmonary aspergillosis.
• Pulmonary embolus: due to lung infarction.
• Left ventricular failure: typically, pink, frothy sputum.
• Alveolar haemorrhage: usually due to a systemic
vasculitis (e.g. Goodpasture syndrome and
granulomatosis with polyangiitis [previously
known as Wegener granulomatosis]).
• Trauma: e.g. contusions to the chest, inhalation
of foreign bodies or after intubation.
Rare causes of haemoptysis:
• bleeding diatheses;
• interstitial lung disease;
• mitral stenosis;
• idiopathic pulmonary haemosiderosis;
• arteriovenous malformations: Osler–Weber–Rendu
disease (hereditary haemorrhagic telangiectasia),
a favourite in examinations but rare in practice;
• Eisenmenger syndrome;
• pulmonary hypertension;
• cystic fibrosis.
In up to 15% of cases, no cause for haemoptysis
is found.
HISTORY AND EXAMINATION FINDINGS
History
The nature of the cough may help in diagnosis (Table6.1).
Assess the following in patients with cough or haemoptysis:
• Onset: The longer a cough is present, the less likely it is
to be due to infection.
• Severity.
• Nature: dry or productive cough? Fresh or old blood?
Are there clots?
• Associated factors: is the cough worse at night? Is there
postnasal drip?
• Weight loss or other systemic symptoms? Think of
carcinoma or lung abscess.
• Has the patient been in contact with any person with
infection? Think of tuberculosis, especially in at-risk
patient groups.
• History of recent foreign travel?
• History of chest trauma?
• Gastro-oesophageal reflux disease: the lack of overt
indigestion or waterbrash does not exclude reflux as a
cause of chronic cough.
53
Cough and haemoptysis
Table6.1 Conditions with characteristic cough.
Pressure on trachea ‘Brassy’ cough—hard and
Tracheitis ‘Hot poker’ cough—often
Laryngeal nerve
paralysis (e.g.
secondary to tumour)
Laryngitis (e.g. croup) ‘Seal’ cough—barking, hoarse
Pharyngitis ‘Hacking’ cough—frequent,
Small airways (e.g.
asthma)
metallic
associated with retrosternal pain
‘Bovine’ cough—often
associated with hoarse voice
cough
irritating
‘Wheezy’ cough—often
associated with shortness of
breath
• Drug history, particularly angiotensin-converting
enzyme inhibitors. 10% to 20% of people taking
angiotensin-converting enzyme inhibitors report
having a dry, tickly cough. It is related to increased
levels of bradykinin. Angiotensin receptor antagonists
are better tolerated as they do not interact with the
bradykinin activation pathway.
• Cigarette smoking: cigarette smoke can cause a cough
by acting as an irritant but is also strongly associated
with bronchial malignancy.
• Occupational agents or exposure to dusts that might
account for the cough.
HINTS AND TIPS
Be sure what the patient means by ‘coughing
up blood’. It is confused with epistaxis and
haematemesis more times than you would believe!
Examination
The approach to the examination is summarized in Fig.6.1.
See also Chapters5 and 28.
• If the patient is breathless, assess the severity by
observing the respiratory rate and the work of
breathing.
• Cyanosis: hypoxaemia, acute (e.g. pneumonia) or
chronic (e.g. chronic obstructive pulmonary disease,
interstitial lung disease).
• Auscultation: bronchial breathing in lobar consolidation,
fine crepitations with left ventricular failure or interstitial
lung disease and coarser crepitations in bronchiectasis.
A pleural rub may indicate pulmonary infarction. A
localized monophonic wheeze, not disappearing on
coughing, suggests a blocked major airway (carcinoma,
foreign body).
• Pulmonary hypertension: loud pulmonary component
of the second heart sound, right ventricular heave,
pulmonary systolic murmur and prominent ‘a’ waves in
the jugular venous pressure.
• Lymphadenopathy: infection or malignancy.
• Examine the patient for a goitre. Is there retrosternal
extension?
• Signs of bronchial carcinoma: e.g. Horner syndrome,
paraneoplastic syndromes.
• Examine the legs for deep vein thromboses: this
may have led to a pulmonary embolus, causing
haemoptysis.
• Skin: systemic vasculitides may have skin manifestations.
• Facial pain in sinusitis.
INVESTIGATIONS
Bedside
• Vital signs: heart rate, respiratory rate, oxygen
saturations, temperature.
• Peak expiratory flow rate.
• Sputum: microscopy, culture and cytology, acid-fast
bacillus test for tuberculosis.
Blood tests
• Full blood count: anaemia is associated with
malignancies, a raised white cell count is associated
with infection, and pulmonary eosinophilia is
associated with several intrinsic and extrinsic
conditions (see clinical notes: conditions associated
with eosinophilia).
• Urea and electrolytes: vasculitis can affect renal
function; electrolytes may be deranged in malignancy
(e.g. small cell carcinoma releasing antidiuretic
hormone (ADH)); urea level may be raised if bleeding
is not haemoptysis but is haematemesis.
• Arterial blood gas.
CLINICAL NOTES
CONDITIONS ASSOCIATED WITH EOSINOPHILIA
Intrinsic eosinophilic syndromes are most
commonly autoimmune or idiopathic; these include:
• chronic eosinophilic pneumonia;
• eosinophilic granulomatosis with polyangiitis
(previously known as Churg–Strauss syndrome):
small and medium vessel vasculitis;
• eosinophilic granuloma: the benign form of
Langerhans cell histiocytosis; it is an interstitial
lung disease;
54
pulmonary hypertension
Lungs
—Respiratory
—Respiratory rate
J
ugular vein
Eyes
—Horner syndrome
—Anaemia
Hands
—Nicotine staining
—Clubbing
—Peripheral cyanosis
examination
Investigations
Face
—Facial pain with
sinusitis
Neck
—Goitre
—Lymphadenopathy
Throat
—Upper respiratory tract
infection
Heart
—Loud pulmonary
component to second
heart sound in
—Murmurs
—Pericardial rub
Skin
Vasculitis
66
Fig.6.1 Examining the patient with cough and haemoptysis.
• asthma;
• eosinophilic bronchitis without asthma.
Extrinsic eosinophilic syndromes are caused
by inhaled or ingested extrinsic factors (e.g.
pathogens, medications); these include:
• Loeffler syndrome: eosinophilic pneumonia
in response to infection (most commonly
parasitic);
• drug rash with eosinophilia and systemic
symptoms (DRESS) syndrome, which is a
hypersensitivity reaction to a medication;
• parasitic and fungal infections, schistosomiasis
or infections with other pathogens.
Legs
—Deep vein thrombosis
General
—Sputum examination
—Cachexia
Imaging
• Chest X-ray: may reveal the pulmonary
cause for presentation (e.g. pneumonia,
carcinoma, bronchiectasis, bilateral hilar
lymphadenopathy).
• CT (sometimes high-resolution CT): to assess
malignancy, interstitial lung disease and
bronchiectasis.
• CT pulmonary angiogram: if pulmonary embolism is
suspected.
Further investigations
• Pharyngoscopy: if an upper respiratory tract cause is
suspected.
55
Cough and haemoptysis
• Bronchoscopy with or without washings, brushings or
biopsies.
• Endobronchial ultrasonography with or without fineneedle aspiration.
• Spirometry: if airway disease is suspected.
• Gastroscopy, barium swallow or 24-hour oesophageal
pH recording: to investigate possible gastrooesophageal reflux disease.
Chapter Summary
• Cough can be of acute or chronic nature. Cough lasting more than 3weeks in high-risk
patients warrants further investigations.
• Haemoptysis without a known cause should always be investigated.
• Cough and haemoptysis are mainly caused by the dysfunction of the respiratory, cardiac
or gastrointestinal systems.
56
Palpitations
7
INTRODUCTION
‘Palpitations’ is usually understood to mean that the patient
is especially aware of his or her heartbeat, but always check
with the patient whether this is what the they mean. The
most common cause is an arrhythmia or dysrhythmia; other
causes include conditions causing an increase in stroke volume (e.g. regurgitant valvular disease) or conditions causing
an increase in cardiac output (e.g. exercise, thyrotoxicosis,
anaemia or anxiety). If an arrhythmia is suspected, determine whether there is an underlying cause. The differential
diagnosis of palpitations is illustrated in Fig.7.1.
HISTORY AND EXAMINATION FINDINGS
History
A carefully taken history will often lead to the correct diagnosis, and is especially important as, between episodes, examination and investigation findings may be unremarkable. Are
the palpitations continuous or intermittent? Are they fast, at a
normal rate or slow? Are they regular or irregular? When did
the palpitations start? This can range from a few minutes ago
to decades ago. If the onset dates back years and there have
been no serious complications (e.g. syncope), the palpitations
are usually benign (but you should enquire if there is any reason why your patient has chosen to seek help now).
How often do the palpitations occur and how long do
they last? They may last for days or seconds, with intervals
between episodes of a few hours to years. Has the patient
learned any manoeuvres to terminate the attacks? Enquire
about the patient's concerns as the patient may fear serious
underlying cardiac disease, although there is often a benign
cause. Are there any associated features? These may be related to the underlying cause (e.g. angina, features of hyperthyroidism) or may be a consequence of the palpitations
(e.g. dizziness or syncope).
Causes and contributing factors
Ask about smoking, alcohol, work, stress, caffeine (tea, coffee, cola) intake and illicit drug use. These may contribute
to extrasystolic beats.
A history of ischaemic and valvular heart disease (including rheumatic fever) should be sought. Structural
heart problems are a predisposing factor for pathological
arrhythmias.
A family history of palpitations or sudden cardiac death
may be important (e.g. hypertrophic obstructive cardiomyopathy or long-QT syndromes).
A full drug history of both prescribed and over-thecounter medications should be taken. Many drugs, both
cardiac and noncardiac, can promote palpitations. Most
antiarrhythmic drugs are also potentially proarrhythmic.
Drug causes of palpitations include cardiac stimulants
(dopamine, dobutamine), β-blockers (atenolol), antimuscarinics (atropine), vasodilators (isosorbide mononitrate,
losartan), antiarrhythmics (digoxin, flecainide, quinidine)
and calcium channel blockers (verapamil, diltiazem).
Noncardiac causes of sinus tachycardia and causes of sinus bradycardia are outlined in Clinical notes: Noncardiac
Regular
Fast Slow
Ventricular tachycardia
Supraventricular
tachycardia
Atrial flutter
Sinus tachycardia
Fig.7.1 Differential diagnosis of palpitations.
Palpitations
Sinus bradycardia
Complete heart block
Atrial flutter (with
high degree of block)
Irregular
Persistent Occasional
Atrial fibrillation
Rarely multiple
ectopic beats
Ectopic beats
Paroxysmal
atrial fibrillation
Atrial flutter
(with variable
block)
57