Origin	Character	Causes
Naso-pharynx/larynx	Throat clearing, chronic	Postnasal drip, acid reflux
Larynx	Barking, painful, acute or persistent	Laryngitis, pertussis (whooping cough), croup
Trachea	Acute, painful	Tracheitis
Bronchi	Intermittent, sometimes productive, worse at night	Asthma
	Worse in morning	Chronic obstructive pulmonary disease (COPD)
	With blood	Bronchial malignancy
Lung parenchyma	Dry then productive	Pneumonia
	Chronic, very productive	Bronchiectasis
	Productive, with blood	Tuberculosis
	Irritating and dry, persistent	Interstitial lung disease
	Worse on lying down, sometimes with frothy sputum	Pulmonary oedema
ACE inhibitors	Dry, scratchy, persistent	Medication-induced

TABLE 5.3 Differential diagnosis of cough based on its duration

ACE = angiotensin-converting enzyme.

COPD = chronic obstructive pulmonary disease.

PND = paroxysmal nocturnal dyspnoea.

A cough associated with a postnasal drip or sinus congestion or headaches may be due to the upper airway cough syndrome, which is the single most common cause of chronic cough. Although patients with this problem often complain of a cough, when asked to demonstrate their cough they do not cough but clear the throat. An irritating, chronic dry cough can result from oesophageal reflux and acid irritation of the lungs. There is some controversy about these as causes of true cough. A similar dry cough may be a feature of late interstitial lung disease or associated with the use of the angiotensin-converting enzyme (ACE) inhibitors—drugs used in the treatment of hypertension and cardiac failure. Cough that wakes a patient from sleep may be a symptom of cardiac failure or of the reflux of acid from the oesophagus into the lungs that can occur when a person lies down. A chronic cough that is productive of large volumes of purulent sputum may be due to bronchiectasis.

Patients’ descriptions of their cough may be helpful. In children, a cough associated with inflammation of the epiglottis may have a muffled quality and cough related to viral croup is often described as ‘barking’. Cough caused by tracheal compression by a tumour may be loud and brassy. Cough associated with recurrent laryngeal nerve palsy has a hollow sound because the vocal cords are unable to close completely; this has been described as a bovine cough. A cough that is worse at night is suggestive of asthma or heart failure, while coughing that comes on immediately after eating or drinking may be due to incoordinate swallowing or oesophageal reflux or, rarely, a tracheo-oesophageal fistula.

It is an important (though perhaps a somewhat unpleasant task) to inquire about the type of sputum produced and then to look at it, if it is available. Be warned that some patients have more interest in their sputum than others and may go into more detail than you really want. A large volume of purulent (yellow or green) sputum suggests the diagnosis of bronchiectasis or lobar pneumonia. Foul-smelling dark-coloured sputum may indicate the presence of a lung abscess with anaerobic organisms. Pink frothy secretions from the trachea, which occur in pulmonary oedema, should not be confused with sputum. It is best to rely on the patient’s assessment of the taste of the sputum, which, not unexpectedly, is foul in conditions like bronchiectasis or lung abscess.

Haemoptysis

Haemoptysis (coughing up of blood) can be a sinister sign of lung disease (Table 5.4) and must always be investigated. It must be distinguished from haematemesis (vomiting of blood) and from nasopharyngeal bleeding (Table 5.5).

TABLE 5.4 Causes (differential diagnosis) of haemoptysis and typical histories

Respiratory
Bronchitis	Small amounts of blood with sputum
Bronchial carcinoma	Frank blood, history of smoking, hoarseness
Bronchiectasis	Large amounts of sputum with blood
Pneumonia	Fever, recent onset of symptoms, dyspnoea
(The above four account for about 80% of cases)
Pulmonary infarction	Pleuritic chest pain, dyspnoea
Cystic fibrosis	Recurrent infections
Lung abscess	Fever, purulent sputum
Tuberculosis (TB)	Previous TB, contact with TB, HIV-positive status
Foreign body	History of inhalation, cough, stridor
Goodpasture’s^* syndrome	Pulmonary haemorrhage, glomerulonephritis, antibody to basement membrane antigens
Wegener’s granulomatosis	History of sinusitis, saddle-nose deformity
Systemic lupus erythematosus	Pulmonary haemorrhage, multi-system involvement
Rupture of a mucosal blood vessel after vigorous coughing
Cardiovascular
Mitral stenosis (severe)
Acute left ventricular failure
Bleeding diatheses

Note: Exclude spurious causes, such as nasal bleeding or haematemesis.

^* Ernest W Goodpasture (1886–1960), pathologist at Johns Hopkins, Baltimore. He described this syndrome in 1919.

TABLE 5.5 Features distinguishing haemoptysis from haematemesis and nasopharyngeal bleeding

Favours haemoptysis	Favours haematemesis	Favours nasopharyngeal bleeding
Mixed with sputum	Follows nausea	Blood appears in mouth
Occurs immediately after coughing	Mixed with vomitus; follows dry retching

Ask how much blood has been produced. Mild haemoptysis usually means less than 20 mL in 24 hours. It appears as streaks of blood discolouring sputum. Massive haemoptysis is more than 250 mL of blood in 24 hours and represents a medical emergency. Its most common causes are carcinoma, cystic fibrosis, bronchiectasis and tuberculosis.

Breathlessness (dyspnoea) (Table 5.6)

The awareness that an abnormal amount of effort is required for breathing is called dyspnoea. It can be due to respiratory or cardiac disease, or lack of physical fitness. Careful questioning about the timing of onset, severity and pattern of dyspnoea is helpful in making the diagnosis (Questions box 5.2 and Table 5.7).¹ The patient may be aware of this

TABLE 5.6 Causes of dyspnoea

Respiratory

1 Airways disease

Chronic bronchitis and emphysema (chronic obstructive pulmonary disease, COPD)

Asthma

Bronchiectasis

Cystic fibrosis

Laryngeal or pharyngeal tumour

Bilateral cord palsy

Tracheal obstruction or stenosis

Tracheomalacia

Cricoarytenoid rheumatoid arthritis

2 Parenchymal disease

Interstitial lung diseases (diffuse parenchymal lung diseases), e.g. idiopathic pulmonary fibrosis, sarcoidosis, connective tissue disease, inorganic or organic dusts

Diffuse infections

Acute respiratory distress syndrome (ARDS)

Infiltrative and metastatic tumour

Pneumothorax

Pneumoconiosis

3 Pulmonary circulation

Pulmonary embolism

Chronic thromboembolic pulmonary hypertension

Pulmonary arteriovenous malformation

Pulmonary arteritis

4 Chest wall and pleura

Effusion or massive ascites

Pleural tumour

Fractured ribs

Ankylosing spondylitis

Kyphoscoliosis

Neuromuscular diseases

Bilateral diaphragmatic paralysis

Cardiac

Left ventricular failure

Mitral valve disease

Cardiomyopathy

Pericardial effusion or constrictive pericarditis

Intracardiac shunt

Anaemia

Non-cardiorespiratory

Psychogenic

Acidosis (compensatory respiratory alkalosis)

Hypothalamic lesions

Questions box 5.2

Questions to ask the breathless patient

! denotes symptoms for the possible diagnosis of an urgent or dangerous problem.

1. How long have you been short of breath? Has it come on quickly?

2. How much exercise can you do before your shortness of breath stops you or slows you down? Can you walk up a flight of stairs?

3. Have you been woken at night by breathlessness or had to sleep sitting up?—Paroxysmal nocturnal dyspnoea (PND), orthopnoea

4. Have you had heart or lung problems in the past?

5. Have you had a temperature? !

6. Do you smoke?

7. Is there a feeling of tightness in the chest when you feel breathless?—Angina

8. Do you get wheezy in the chest? Cough?

9. Is the feeling really one of difficulty getting a satisfying breath?—Anxiety

10. Is it painful to take a big breath?—Pleurisy or pericarditis

11. Did the shortness of breath come on very quickly or instantaneously?—Pulmonary embolus (very quick onset) or pneumothorax (instantaneous onset)

TABLE 5.7 Differential diagnosis of dyspnoea based on time course of onset

Seconds to minutes—favours:

Foreign body causing airway obstruction

Hours or days—favours:

Exacerbation of chronic obstructive pulmonary disease (COPD)

Cardiac failure

Asthma

Respiratory infection

Pleural effusion

Metabolic acidosis

Weeks or longer—favours:

only on heavy exertion or have much more limited exercise tolerance. Dyspnoea can be graded from I to IV based on the New York Heart Association classification:

Class I—disease present but no dyspnoea or dyspnoea only on heavy exertion

Class II—dyspnoea on moderate exertion

Class III—dyspnoea on minimal exertion

Class IV—dyspnoea at rest.

It is more useful, however, to determine the amount of exertion that actually causes dyspnoea—that is, the distance walked or the number of steps climbed.

The association of dyspnoea with wheeze suggests airways disease, which may be due to asthma or chronic obstructive pulmonary disease (COPD) (Table 5.8). The duration and variability of the dyspnoea are important. Dyspnoea that worsens progressively over a period of weeks, months or years may be due to interstitial lung disease (ILD). Dyspnoea of more rapid onset may be due to an acute respiratory infection (including bronchopneumonia or lobar pneumonia) or to pneumonitis (which may be infective or secondary to a hypersensitivity reaction). Dyspnoea that varies from day to day or even from hour to hour suggests a diagnosis of asthma. Dyspnoea of very rapid onset associated with sharp chest pain suggests a pneumothorax (Table 5.9). Dyspnoea that is described by the patient as inability to take a breath big enough to fill the lungs and associated with sighing suggests anxiety. Dyspnoea that occurs on moderate exertion may be due to the combination of obesity and a lack of physical fitness (a not uncommon occurrence).

TABLE 5.8 Characteristics of chronic obstructive pulmonary disease (COPD)

TABLE 5.9 Differential diagnosis of dyspnoea of sudden onset based on other features

Presence of pleuritic chest pain—favours:

Pneumothorax, pleurisy/pneumonia

Pulmonary embolism

Trauma

Absence of chest pain—favours:

Pulmonary oedema

Metabolic acidosis

Pulmonary embolism

Presence of central chest pain—favours:

Myocardial infarction and cardiac failure

Large pulmonary embolism

Presence of cough and wheeze—favours:

Asthma

Bronchial irritant inhalation

Chronic obstructive pulmonary disease (COPD)

Wheeze

A number of conditions can cause a continuous whistling noise that comes from the chest (rather than the throat) during breathing. These include asthma or COPD, infections such as bronchiolitis and airways obstruction by a foreign body or tumour. Wheeze is usually maximal during expiration and is accompanied by prolonged expiration. This must be differentiated from stridor (see below), which can have a similar sound, but is loudest over the trachea and occurs during inspiration.

Chest pain

Chest pain due to respiratory disease is usually different from that associated with myocardial ischaemia (page 35). The pleura and central airways have pain fibres and may be the source of respiratory pain. Pleural pain is characteristically pleuritic in nature: sharp and made worse by deep inspiration and coughing. It is typically localised to one area of the chest. It may be of sudden onset in patients with lobar pneumonia, pulmonary embolism and infarction or pneumothorax, and is often associated with dyspnoea. The sudden onset of pleuritic chest pain and dyspnoea is an urgent diagnostic problem, as all three of these conditions may be life-threatening if not treated promptly.

Other presenting symptoms

Bacterial pneumonia is an acute illness in which prodromal symptoms (fever, malaise and myalgia) occur for a short period (hours) before pleuritic pain and dyspnoea begin. Viral pneumonia is often preceded by a longer (days) prodromal illness. Patients may occasionally present with episodes of fever at night. Tuberculosis, pneumonia and lymphoma should always be considered in these cases. Occasionally patients with tuberculosis present with episodes of drenching sweating at night.

Hoarseness or dysphonia (an abnormality of the voice) may sometimes be considered a respiratory system symptom. It can be due to transient inflammation of the vocal cords (laryngitis), vocal cord tumour or recurrent laryngeal nerve palsy.

Sleep apnoea is an abnormal increase in the periodic cessation of breathing during sleep. Patients with obstructive sleep apnoea (OSA) (where airflow stops during sleep for periods of at least 10 seconds and sometimes for over 2 minutes, despite persistent respiratory efforts) typically present with daytime somnolence, chronic fatigue, morning headaches and personality disturbances. Very loud snoring may be reported by anyone within earshot. These patients are often obese and hypertensive. The Epworth sleepiness scale is a way of quantifying the severity of sleep apnoea (Table 5.10).

TABLE 5.10 The Epworth sleepiness scale

‘How easily would you fall asleep in the following circumstances?’^*

• Watching television

• At a meeting or at the theatre

• As a passenger in a car on a drive of more than an hour

• Lying down in the afternoon to rest

• Sitting talking to someone

• Sitting quietly after lunch (no alcohol)

• When driving and stopped at traffic lights

^* A normal score is between 0 and 9. Severe sleep apnoea scores from 11 to 20.

Patients with central sleep apnoea (where there is cessation of inspiratory muscle activity) may also present with somnolence but do not snore excessively (Table 5.11).

TABLE 5.11 Abnormal patterns of breathing

Type of breathing	Cause(s)
1 Sleep apnoea—cessation of airflow for more than 10 seconds more than 10 times a night during sleep	Obstructive (e.g. obesity with upper airway narrowing, enlarged tonsils, pharyngeal soft tissue changes in acromegaly or hypothyroidism)
2 Cheyne-Stokes^* breathing—periods of apnoea (associated with reduced level of consciousness) alternate with periods of hyperpnoea (lasts 30 s on average and is associated with agitation). This is due to a delay in the medullary chemoreceptor response to blood gas changes	Left ventricular failure Brain damage (e.g. trauma, cerebral haemorrhage) High altitude
3 Kussmaul’s breathing (air hunger)— deep, rapid respiration due to stimulation of the respiratory centre	Metabolic acidosis (e.g. diabetes mellitus, chronic renal failure)
4 Hyperventilation, which results in alkalosis and tetany	Anxiety
5 Ataxic (Biot^†) breathing—irregular in timing and depth	Brainstem damage
6 Apneustic breathing—a post-inspiratory pause in breathing	Brain (pontine) damage
7 Paradoxical respiration—the abdomen sucks inwards with inspiration (it normally pouches outwards due to diaphragmatic descent)	Diaphragmatic paralysis

^* John Cheyne (1777–1836), Scottish physician who worked in Dublin, described this in 1818. William Stokes (1804–1878), Irish physician, described it in 1854.

^† Camille Biot (b. 1878), French physician.

Some patients respond to anxiety by increasing the rate and depth of their breathing. This is called hyperventilation. The result is an increase in CO₂ excretion and the development of alkalosis—a rise in the pH of the blood. These patients may complain of variable dyspnoea; they have more difficulty breathing in than out. The alkalosis results in paraesthesiae of the fingers and around the mouth, light-headedness, chest pain and a feeling of impending collapse.

Treatment

It is important to find out what drugs the patient is using (Table 5.12), how often they are taken and whether they are inhaled or swallowed. The patient’s previous and current medications may give a clue to the current diagnosis. Bronchodilators and inhaled steroids are prescribed for COPD and asthma. A patient’s increased use of bronchodilators suggests poor control of asthma and the need for review of treatment. Chronic respiratory disease, including sarcoidosis, hypersensitivity pneumonias and asthma, may have been treated with oral steroids. Oral steroid use may predispose to tuberculosis or pneumocystis pneumonia. Patients with chronic lung conditions like cystic fibrosis or bronchiectasis will often be very knowledgeable about their treatment and can describe the various forms of physiotherapy that are essential for keeping their airways clear.

TABLE 5.12 Drugs and the lungs

Cough

ACE inhibitors

Beta-blockers

Wheeze

Beta-blockers

Aspirin (aspirin sensitivity)

Other non-steroidal anti-inflammatory drugs (NSAIDs)

Tamoxifen, dipyridamole (idiosyncratic)

Morphine sulfate

Succinylcholine

Interstitial lung disease (pulmonary fibrosis)

Pulmonary embolism

Oestrogens

Tamoxifen

Raloxifene

Non-cardiogenic pulmonary oedema

Hydrochlorothiazide

Pleural disease/effusion

Nitrofurantoin

Phenytoin, hydralazine (induction of systemic lupus erythematosus)

Methotrexate

Methysergide

Almost every class of drug can produce lung toxicity. Examples include pulmonary embolism from use of the oral contraceptive pill, interstitial lung disease from cytotoxic agents (e.g. methotrexate, cyclophosphamide, bleomycin), bronchospasm from beta-blockers or non-steroidal anti-inflammatory drugs (NSAIDs), and cough from ACE inhibitors. Some medications known to cause lung disease may not be mentioned by the patient because they are illegal (e.g. cocaine), are used sporadically (e.g. hydrochlorothiazide), can be obtained over the counter (e.g. tryptophan) or are not taken orally (e.g. timolol; beta-blocker eye drops for glaucoma). The clinician therefore needs to ask about these types of drug specifically.

Past history

One should always ask about previous respiratory illness, including pneumonia, tuberculosis or chronic bronchitis, or abnormalities of the chest X-ray that have previously been reported to the patient. Many previous respiratory investigations may have been memorable, such as bronchoscopy, lung biopsy and video-assisted thoracoscopy. Spirometry, with or without challenge testing for asthma, may have been performed. Many severe asthmatics perform their own regular peak flow testing (page 128). Ask about the results of any of these investigations. Patients with the acquired immunodeficiency syndrome (AIDS) have a high risk of developing Pneumocystis jiroveci (carinii) pneumonia and indeed other chest infections, including tuberculosis.

Occupational history

In no system are the patient’s present and previous occupations of more importance (Table 5.13).² A detailed occupational history is essential. The occupational lung diseases or pneumoconioses cause interstitial lung disease by damaging the alveoli and small airways. Prolonged exposure to substances whose use is now heavily restricted is usually required. Cigarette smoking has an additive effect for these patients. These occupational conditions are now rare, and the most common occupational lung disease is asthma.

TABLE 5.13 Occupational lung disease (pneumoconioses)

Substance	Disease
Coal	Coal worker’s pneumoconiosis
Silica	Silicosis
Asbestos	Asbestosis
Talc	Talcosis

One must ask about exposure to dusts in mining industries and factories (e.g. asbestos, coal, silica, iron oxide, tin oxide, cotton, beryllium, titanium oxide, silver, nitrogen dioxide, anhydrides). Heavy exposure to asbestos can lead to asbestosis (Table 5.14), but even trivial exposure can result in pleural plaques or mesothelioma (malignant disease of the pleura). The patient may be unaware that his or her occupation involved exposure to dangerous substances; for example, factories making insulating cables and boards very often used asbestos until 25 years ago. Asbestos exposure can result in the development of asbestosis, mesothelioma or carcinoma of the lung up to 30 years later. Relatives of people working with asbestos may be exposed when handling work clothes.

TABLE 5.14 Possible occupational exposure to asbestos

Asbestos mining, including relatives of miners

Naval dockyard workers and sailors—lagging of pipes

Builders—asbestos in fibreboard (particles are released during cutting or drilling)

Factory workers—manufacture of fibro-sheets, brake linings, some textiles

Building maintenance workers—asbestos insulation

Building demolition workers

Home renovation

Work or household exposure to animals, including birds, is also relevant (e.g. Q fever or psittacosis which are infectious diseases caught from animals).

Exposure to organic dusts can cause a local immune response to organic antigens and result in allergic alveolitis. Within a few hours of exposure, patients develop flu-like symptoms. These often include fever, headache, muscle pains, dyspnoea without wheeze and dry cough. The culprit antigens may come from mouldy hay, humidifiers or air conditioners, among others (Table 5.15).

TABLE 5.15 Allergic alveolitis—sources

Bird fancier’s lung	Bird feathers and excreta
Farmer’s lung	Mouldy hay or straw (Aspergillus fumigatus)
Byssinosis	Cotton or hemp dust
Cheese worker’s lung	Mouldy cheese (Aspergillus clavatus)
Malt worker’s lung	Mouldy malt (Aspergillus clavatus)
Humidifier fever	Air-conditioning (thermophilic Actinomycetes)

It is most important to find out what the patient actually does when at work, the duration of any exposure, use of protective devices and whether other workers have become ill. An improvement in symptoms over the weekend is a valuable clue to the presence of occupational lung disease, particularly occupational asthma. This can occur as a result of exposure to spray paints or plastic or soldering fumes.

Social history

A smoking history must be routine, as it is the major cause of COPD and lung cancer (see Table 1.2, page 6). It also increases the risk of spontaneous pneumothorax and of Goodpasture’s syndrome. It is necessary to ask how many packets of cigarettes a day a patient has smoked and how many years the patient has smoked. An estimate should be made of the number of packet-years of smoking. Remember that this is based on 20-cigarette packets and that packets of cigarettes are getting larger; curiously, most manufacturers now make packets of 30 or 35. More recently, giant packets of 50 have appeared. These are too large to fit into pockets and must be carried in the hands as a constant reminder to the patient of his or her addiction. Occupation may further affect cigarette smokers; for example, asbestos workers who smoke are at an especially high risk of lung cancer. Passive smoking is now regarded as a significant risk for lung disease and the patient should be asked about exposure to other people’s cigarette smoke at home and at work.

Many respiratory conditions are chronic, and may interfere with the ability to work and exercise and interfere with normal family life. In some cases involving occupational lung disease there may be compensation matters affecting the patient. Ask about these problems and whether the patient has been involved in a pulmonary rehabilitation programme. Housing conditions may be inappropriate for a person with a limited exercise tolerance or an infectious disease. An inquiry about the patient’s alcohol consumption is important. The drinking of large amounts of alcohol in binges can sometimes result in aspiration pneumonia, and alcoholics are more likely to develop pneumococcal or Klebsiella pneumonia. Intravenous drug users are at risk of lung abscess and drug-related pulmonary oedema. Sexual orientation or history of intravenous drug use may be related to an increased risk of HIV infection and susceptibility to infection. Such information may influence the decision about whether to advise treatment at home or in hospital.

Family history

A family history of asthma or other atopic diseases, cystic fibrosis, lung cancer or emphysema should be sought. Alpha₁-antitrypsin deficiency, for example, is an inherited disease, and those affected are extremely susceptible to the development of emphysema. A family history of infection with tuberculosis is also important. A number of pulmonary diseases may have a familial or genetic association. These include carcinoma of the lung and pulmonary hypertension.

The respiratory examination

Examination anatomy

The lungs are paired asymmetrical organs protected by the cylinder composed of the ribs, vertebrae and diaphragm. The surface of the lungs is covered by the visceral pleura, a thin membrane, and a similar outer layer (the parietal pleura) lines the rib cage. These membranes are separated by a thin layer of fluid and enable the lungs to move freely during breathing. Various diseases of the lungs and of the pleura themselves, including infection and malignancy, can cause accumulation of fluid within the pleural cavity (a pleural effusion).

The heart, trachea, oesophagus and the great blood vessels and nerves sit between the lungs and make up the structure called the mediastinum. The left and right pulmonary arteries supply their respective lung. Gas exchange occurs in the pulmonary capillaries which surround the alveoli, the tiny air sacs which lie beyond the terminal bronchioles. Oxygenated blood is returned via the pulmonary veins to the left atrium. Abnormalities of the pulmonary circulation such as raised pulmonary venous pressure resulting from heart failure or pulmonary hypertension can interfere with gas exchange.

The position of the heart with its apex pointing to the left means that the left lung is smaller than the right and has only two lobes, which are separated by the oblique fissure. The right lung has both horizontal (upper) and oblique (lower) fissures dividing it into three lobes (Figure 5.1).

Figure 5.1 Lobes of the lung

(a) Anterior. (b) Posterior. (c) Lobes of the right lung. (d) Lobes of the left lung. Refer to Figure 5.15, page 137, for a list of the segments in each lobe.

The muscles of respiration are the diaphragm upon which the bases of the lungs rest and the intercostal muscles. During inspiration the diaphragm flattens and the intercostal muscles contract to elevate the ribs. Intrathoracic pressure falls as air is forced under atmospheric pressure into the lungs. Expiration is a passive process resulting from elastic recoil of the muscles. Abnormalities of lung function or structure may change the normal anatomy and physiology of respiration, for example as a result of over-inflation of the lungs (COPD, page 133). Muscle and neurological diseases can also affect muscle function adversely, and abnormalities of the control of breathing in the respiratory centres of the brain in the pons and medulla can interfere with normal breathing patterns.

During the respiratory examination, keep in mind the surface anatomy (Figure 5.1) of the lungs and try to decide which lobes are affected.

Positioning the patient

The patient should be undressed to the waist.³ Women should wear a gown or have a towel or some clothing to cover their breasts when the front of the chest is not being examined. If the patient is not acutely ill, the examination is easiest to perform with him or her sitting over the edge of the bed or on a chair.

General appearance

If the patient is an inpatient in hospital, look around the bed for oxygen masks, metered dose inhalers (puffers) and other medications, and the presence of a sputum mug. Then make a deliberate point of looking for the following signs before beginning the detailed examination.

Dyspnoea

Watch the patient for signs of dyspnoea at rest. Count the respiratory rate; the normal rate at rest should not exceed 25 breaths per minute (range 16–25). The frequently quoted normal value of 14 breaths per minute is probably too low; normal people can have a respiratory rate of up to 25, and the average is 20 breaths per minute. It is traditional to count the respiratory rate surreptitiously while affecting to count the pulse. The respiratory rate is the only vital sign that is under direct voluntary control. Tachypnoea refers to a rapid respiratory rate of greater than 25. Bradypnoea is defined as a rate below 8, a level associated with sedation and adverse prognosis. In normal relaxed breathing, the diaphragm is the only active muscle and is active only in inspiration; expiration is a passive process.

Characteristic signs of chronic obstructive pulmonary disease (COPD)^a

Look to see whether the accessory muscles of respiration are being used. This is a sign of an increase in the work of breathing, and COPD is an important cause. These muscles include the sternomastoids, the platysma and the strap muscles of the neck. Characteristically the accessory muscles cause elevation of the shoulders with inspiration, and aid respiration by increasing chest expansion. Contraction of the abdominal muscles may occur in expiration in patients with obstructed airways. Patients with severe COPD often have indrawing of the intercostal and supraclavicular spaces during inspiration. This is due to a delayed increase in lung volume despite the generation of large negative pleural pressures.

In some cases, the pattern of breathing is diagnostically helpful (Table 5.11). Look for pursed-lips breathing, which is characteristic of patients with severe COPD. This manoeuvre reduces the patient’s breathlessness, possibly by providing continuous positive airways pressure and helping to prevent airways collapse during expiration. Patients with severe COPD may feel more comfortable leaning forward with their arms on their knees. This position compresses the abdomen and pushes the diaphragm upwards. This partly restores its normal domed shape and improves its effectiveness during inspiration. Increased diaphragmatic movements may cause downward displacement of the trachea during inspiration—tracheal tug.