The respiratory history

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

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:

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

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

^* 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

^* 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

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)

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

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

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.

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.

Figure 5.2 Basic anatomy of the lungs

Cyanosis

Central cyanosis is best detected by inspecting the tongue. Examination of the tongue differentiates central from peripheral cyanosis. Lung disease severe enough to result in significant ventilation–perfusion imbalance, such as pneumonia, COPD and pulmonary embolism, may cause reduced arterial oxygen saturation and central cyanosis. Cyanosis becomes evident when the absolute concentration of deoxygenated haemoglobin is 50 g/L of capillary blood. Cyanosis is usually obvious when the arterial oxygen saturation falls below 90% in a person with a normal haemoglobin level. Central cyanosis is therefore a sign of severe hypoxaemia. In patients with anaemia, cyanosis does not occur until even greater levels of arterial desaturation are reached. The absence of obvious cyanosis does not exclude hypoxia. The detection of cyanosis is much easier in good (especially fluorescent) lighting conditions and is said to be more difficult if the patient’s bed is surrounded by cheerful pink curtains.

Character of the cough

Coughing is a protective response to irritation of sensory receptors in the submucosa of the upper airways or bronchi. Ask the patient to cough several times. Lack of the usual explosive beginning may indicate vocal cord paralysis (the ‘bovine’ cough). A muffled, wheezy, ineffective cough suggests obstructive pulmonary disease. A very loose productive cough suggests excessive bronchial secretions due to chronic bronchitis, pneumonia or bronchiectasis. A dry, irritating cough may occur with chest infection, asthma or carcinoma of the bronchus and sometimes with left ventricular failure or interstitial lung disease. It is also typical of the cough produced by ACE inhibitor drugs. A barking or croupy cough may suggest a problem with the upper airway—the pharynx and larynx, or pertussis infection.

Sputum

Sputum should be inspected. Careful study of the sputum is an essential part of the physical examination. The colour, volume and type (purulent, mucoid or mucopurulent), and the presence or absence of blood, should be recorded.

Stridor

Obstruction of the larynx or trachea (the extra-thoracic airways) may cause stridor, a rasping or croaking noise loudest on inspiration. This can be due to a foreign body, a tumour, infection (e.g. epiglottitis) or inflammation (Table 5.16). It is a sign that requires urgent attention.

TABLE 5.16 Some causes of stridor in adults

Sudden onset (minutes) Anaphylaxis Toxic gas inhalation Acute epiglottitis Inhaled foreign body

Gradual onset (days, weeks)

Laryngeal or pharyngeal tumours

Cricoarytenoid rheumatoid arthritis

Bilateral vocal cord palsy

Tracheal carcinoma

Paratracheal compression by lymph nodes

Post-tracheostomy or intubation granulomata

The hands

As usual, examination in detail begins with the hands.

Clubbing

Look for clubbing, which is due to respiratory disease in up to 80% of cases (Figure 5.3, Table 4.9 on page 51). An uncommon but important association with clubbing is hypertrophic pulmonary osteoarthropathy (HPO). HPO is characterised by the presence of periosteal inflammation at the distal ends of long bones, the wrists, the ankles, the metacarpal and the metatarsal bones. There is swelling and tenderness over the wrists and other involved areas. Rarely HPO may occur without clubbing. The causes of HPO include primary lung carcinoma and pleural fibromas. Remember, chronic bronchitis and emphysema do not cause clubbing. It is important to note that clubbing does not occur as a result of COPD.

Figure 5.3 Finger clubbing

The face

The nose is sited conveniently in the centre of the face. In this position it may readily be inspected inside and out. Get the patient to tilt the head back. It may be necessary to use a nasal speculum to open the nostrils, and a torch. Look for polyps (associated with asthma), engorged turbinates (various allergic conditions) and a deviated septum (nasal obstruction).

As already discussed, look at the tongue for central cyanosis. Look in the mouth for evidence of an upper respiratory tract infection (a reddened pharynx and tonsillar enlargement, with or without a coating of pus). A broken tooth or a rotten tooth stump may predispose to lung abscess or pneumonia. Patients with sleep apnoea may have ‘crowding’ of the pharynx. This means a reduction in the size of the velopharyngeal lumen, which is the space between the soft palate, tonsils and the back of the tongue. Those who use a sleep apnoea mask at night often have marks from the mask on the face and puffiness around the eyes. They tend to be obese and have a short thick neck and a small pharynx; sometimes the maxilla and mandible appear retracted (receding chin).

Sinusitis is suggested by tenderness over the sinuses on palpation. If acute sinusitis is suspected, a torch can be used to transilluminate the frontal and maxillary sinuses.⁵ A torch is placed in the patient’s mouth and the sinuses examined in a dark room. Normal transillumination generally excludes sinusitis. Complete opacification suggests sinusitis but partial opacification is less helpful. The torch should then be used to look for purulent discharge in the pharynx.

Look at the patient’s face for the red, leathery, wrinkled skin of the smoker.⁶ There may be facial plethora or cyanosis if superior vena caval obstruction is present. Look for the characteristics of obstructive sleep apnoea (see above).

Inspect the eyes for evidence of the rare Horner’s^c syndrome (a constricted pupil, partial ptosis and loss of sweating), which can be due to an apical lung carcinoma (Pancoast^d tumour) compressing the sympathetic nerves in the neck. There may be skin changes on the face that suggest scleroderma or connective tissue disease.

The trachea

The position of the trachea is most important, and time should be spent establishing it accurately. From in front of the patient the forefinger of the right hand is pushed up and backwards from the suprasternal notch until the trachea is felt (Figure 5.4). If the trachea is displaced to one side, its edge rather than its middle will be felt and a larger space will be present on one side than the other. Slight displacement to the right is fairly common in normal people. This examination is uncomfortable for the patient, so you must be gentle.

Figure 5.4 Feeling for the position of the trachea—a similar gap should be palpable on each side

Significant displacement of the trachea suggests, but is not specific for, disease of the upper lobes of the lung (Table 5.17).

TABLE 5.17 Causes of tracheal displacement

A tracheal tug is demonstrated when the finger resting on the trachea feels it move inferiorly with each inspiration. This is a sign of gross overexpansion of the chest because of airflow obstruction. This movement of the trachea may be visible, and it is worth spending time inspecting the trachea when COPD is suspected.

If the patient appears dyspnoeic and use of the accessory muscles of respiration is suspected, the examiner’s fingers should be placed in the supraclavicular fossae. When the scalene muscles are recruited, they can be felt to contract under the fingers. Even more severe dyspnoea will result in use of the sternomastoid muscles. Their contraction is also easily felt with inspiration. Use of these muscles for long periods is exhausting and a sign of impending respiratory failure.

The chest

The chest should be examined anteriorly and posteriorly by inspection, palpation, percussion and auscultation.³ Compare the right and left sides during each part of the examination.

Inspection

Shape and symmetry of chest

When the anteroposterior (AP) diameter is increased compared with the lateral diameter, the chest is described as barrel-shaped (Figure 5.5). An increase in the AP diameter compared with the lateral diameter (the thoracic ratio) beyond 0.9 is abnormal and is seen often in patients with severe asthma or emphysema. It is not always a reliable guide to the severity of the underlying lung disease and may be present in normal elderly people. Severe kyphoscoliosis is a cause of asymmetrical chest deformity.

Figure 5.5 Barrel chest

From McDonald FS, ed., Mayo Clinic images in internal medicine, with permission. © Mayo Clinic Scientific Press and CRC Press.

A pigeon chest (pectus carinatum) is a localised prominence (an outward bowing of the sternum and costal cartilages)(Figure 5.6). It may be a manifestation of chronic childhood respiratory illness, in which case it is thought to result from repeated strong contractions of the diaphragm while the thorax is still pliable. It also occurs in rickets.

Figure 5.6 (a) Funnel chest (pectus excavatum); (b) Pigeon chest (pectus carinatum)

From Mir MA, Atlas of Clinical Diagnosis, 2nd edn. Edinburgh: Saunders, 2003, with permission.

A funnel chest (pectus excavatum) is a developmental defect involving a localised depression of the lower end of the sternum (Figure 5.6). The problem is usually an aesthetic one, but in severe cases lung capacity may be restricted.

Harrison’s sulcus^e is a linear depression of the lower ribs just above the costal margins at the site of attachment of the diaphragm. It can result from severe asthma in childhood, or rickets.

Kyphosis refers to an exaggerated forward curvature of the spine, while scoliosis is lateral bowing. Kyphoscoliosis may be idiopathic (80%), secondary to poliomyelitis, or associated with Marfan’s syndrome. Severe thoracic kyphoscoliosis may reduce the lung capacity and increase the work of breathing.

Lesions of the chest wall may be obvious. Look for scars from previous thoracic operations, or from chest drains for a previous pneumothorax or pleural effusion. Surgical removal of a lung (pneumonectomy) or of the lobe of a lung (lobectomy) leaves a long diagonal posterior scar on the thorax. The presence of three 2–3 cm scars suggests previous video-assisted thoracoscopic surgery, which can be performed to biopsy lymph nodes or carry out lung reduction surgery or pleurodesis. Thoracoplasty causes severe chest deformity; this operation was performed for tuberculosis and involved removal of a large number of ribs on one side of the chest to achieve permanent collapse of the affected lung. It is no longer performed because of the availability of effective antituberculous chemotherapy.^f Radiotherapy may cause erythema and thickening of the skin over the irradiated area. There is sharp demarcation between abnormal and normal skin. There may be small tattoo marks indicating the limits of the irradiated area. Signs of radiotherapy usually indicate that the patient has been treated for carcinoma of the lung, breast or, less often, for lymphoma.

Subcutaneous emphysema is a crackling sensation felt on palpating the skin of the chest or neck. On inspection, there is often diffuse swelling of the chest wall and neck. It is caused by air tracking from the lungs and is usually due to a pneumothorax; less commonly it can follow rupture of the oesophagus or a pneumomediastinum (air in the mediastinal space).

Prominent veins may be seen in patients with superior vena caval obstruction. It is important to determine the direction of blood flow (page 166).

Movement of the chest wall should be noted. Look for asymmetry of chest wall movement anteriorly and posteriorly. Assessment of expansion of the upper lobes is best achieved by inspection from behind the patient, looking down at the clavicles during moderate respiration (Figure 5.7). Diminished movement indicates underlying lung disease. The affected side will show delayed or decreased movement. For assessment of lower lobe expansion, the chest should be inspected posteriorly.

Figure 5.7 Inspecting upper lobe expansion: (a) expiration; (b) inspiration—note symmetrical elevation of the clavicles

Reduced chest wall movement on one side may be due to localised lung fibrosis, consolidation, collapse, pleural effusion or pneumothorax. Bilateral reduction of chest wall movement indicates a diffuse abnormality such as COPD or diffuse interstitial lung disease. Unilateral reduced chest excursion or splinting may be present when patients have pleuritic chest pain or injuries such as rib fractures.

Look for paradoxical inward motion of the abdomen during inspiration when the patient is supine (indicating diaphragmatic paralysis).

Palpation

Chest expansion

Place the hands firmly on the chest wall with the fingers extending around the sides of the chest. The thumbs should almost meet in the middle line and should be lifted slightly off the chest so that they are free to move with respiration (Figure 5.8). As the patient takes a big breath in, the thumbs should move symmetrically apart at least 5 cm. Reduced expansion on one side indicates a lesion on that side. The causes have been discussed above.

Figure 5.8 Palpation for lower lobe expansion: (a) expiration; (b) inspiration

If COPD is suspected, Hoover’s sign^g may be sought (Figure 5.9). The examiner places the hands along the costal margins with the thumbs close to the xiphisternum. Normally inspiration causes them to separate, but the overinflated chest of the COPD patient cannot expand in this way and the diaphragm pulls the ribs and the examiner’s thumbs closer together⁷ (positive LR 4.2).⁸

Figure 5.9 Hoover’s sign

(a) Expiration; (b) inspiration. (c) Normal expiration; (d) normal inspiration.

Lower lobe expansion is assessed from the back in this way. Some idea of upper and middle lobe expansion is possible when the manoeuvre is repeated on the front of the chest, but this is better gauged by inspection.

Apex beat

When the patient is lying down, establishing the position of the apex beat may be helpful (page 60), as displacement towards the side of the lesion can be caused by collapse of the lower lobe or by localised interstitial lung disease (ILD). Movement of the apex beat away from the side of the lung lesion can be caused by pleural effusion or tension pneumothorax. The apex beat is often impalpable in a chest which is hyperexpanded secondary to chronic obstructive pulmonary disease.

Vocal (tactile) fremitus

Palpate the chest wall with the palm of the hand while the patient repeats ‘ninety-nine’. The front and back of the chest are each palpated in two comparable positions, with the palm of one hand on each side of the chest. In this way differences in vibration on the chest wall can be detected. This can be a difficult sign to interpret, with considerable inter-observer variability, and it is no longer a routine part of the examination. It depends on the recognition of changes in vibration conducted to the examiner’s hands while the patient speaks. Practice is needed to appreciate the difference between normal and abnormal. Vocal fremitus is more obvious in men because of their lower-pitched voices. It may be absent in normal people (high-pitched voice or thick chest wall). It is only abnormal if different on one side from the other. The causes of change in vocal fremitus are the same as those for vocal resonance (page 127).

Ribs

Gently compress the chest wall anteroposteriorly and laterally. Localised pain suggests a rib fracture, which may be secondary to trauma or may be spontaneous as a result of tumour deposition, bone disease or sometimes the result of severe and prolonged coughing. Tenderness over the costochondral junctions suggests the diagnosis of costochondritis as the cause of chest pain.

Regional lymph nodes

The axillary and cervical and supraclavicular nodes must be examined (pages 227, 228); they may be enlarged in lung malignancies and some infections.

Percussion

With the left hand on the chest wall and the fingers slightly separated and aligned with the ribs, the middle finger is pressed firmly against the chest. Then the pad of the right middle finger (the plexor) is used to strike firmly the middle phalanx of the middle finger of the left hand (the pleximeter); this was often a piece of wood, ivory or a coin in the 19th century but is now always the examiner’s finger. The percussing finger (plexor) is quickly removed so that the note generated is not dampened (this may be less important if the pleximeter finger is held firmly on the chest wall, as it should be). The percussing finger must be held partly flexed and a loose swinging movement should come from the wrist and not from the forearm. Medical students will soon learn to keep the right middle fingernail short.

Percussion of symmetrical areas of the anterior, posterior and axillary regions is necessary (Figure 5.10). Percussion in the supraclavicular fossa over the apex of the lung and direct percussion of the clavicle with the percussing finger are a traditional part of the examination. For percussion posteriorly, the scapulae should be moved out of the way by asking the patient to move the elbows forward across the front of the chest; this rotates the scapulae anteriorly.

Figure 5.10 Percussion of the chest

(a) Percussing (plexor) finger poised. Inset: plexor finger strikes pleximeter finger. (b) Direct percussion of the clavicle for upper lobe resonance.

The feel of the percussion note is as important as its sound. The note is affected by the thickness of the chest wall, as well as by underlying structures. Percussion over a solid structure, such as the liver or a consolidated or collapsed area of lung, produces a dull note. Percussion over a fluid-filled area, such as a pleural effusion, produces an extremely dull (stony dull) note. Percussion over the normal lung produces a resonant note and percussion over hollow structures, such as the bowel or a pneumothorax, produces a hyperresonant note (Good signs guide 5.1).

GOOD SIGNS GUIDE 5.1 Comparative percussion of the chest

Sign	Positive LR	Negative LR
Dullness—pneumonia	3.0	NS
Hyperresonance—COPD	5.1	NS

NS = not significant.

COPD = chronic obstructive pulmonary disease.

From McGee S, Evidence-based physical diagnosis, 2nd edn. St Louis: Saunders, 2007.

Considerable practice is required before expert percussion can be performed, particularly in front of an audience. The ability to percuss well is usually obvious in clinical examinations and counts in a student’s favour, as it indicates a reasonable amount of experience in the wards.

Liver dullness

The upper level of liver dullness is determined by percussing down the anterior chest in the midclavicular line. Normally, the upper level of the liver dullness is the fifth rib in the right midclavicular line. If the chest is resonant below this level, it is a sign of hyperinflation, usually due to emphysema or asthma. This is a sign with considerable inter-observer variability.

Cardiac dullness

The area of cardiac dullness usually present on the left side of the chest may be decreased in emphysema or asthma.

Auscultation

Breath sounds

Using the diaphragm of the stethoscope, one should listen to the breath sounds in the areas shown in Figure 5.11.^9–11 It is important to compare each side with the other. Remember to listen high up into the axillae and, using the bell of the stethoscope applied above the clavicles, to listen to the lung apices. A number of observations must be made while auscultating and, as with auscultation of the heart, different parts of the cycle must be considered. Listen for the quality of the breath sounds, the intensity of the breath sounds, and the presence of additional (adventitious) sounds.

Figure 5.11 Normal and bronchial breath sounds

Auscultate in each area shown (the numbers represent a suggested order). Distinguish normal breath sounds from bronchial breathing.

Quality of breath sounds

Normal breath sounds are heard with the stethoscope over nearly all parts of the chest. The patient should be asked to breathe through the mouth so that added sounds from the nasopharynx do not interfere. These sounds are produced in the airways rather than the alveoli. They had once been thought to arise in the alveoli (vesicles) of the lungs and are therefore called vesicular sounds. They have rather fancifully been compared by Laënnec to the sound of wind rustling in leaves. Their intensity is related to total airflow at the mouth and to regional airflow. Normal (vesicular) breath sounds are louder and longer on inspiration than on expiration and there is no gap between the inspiratory and expiratory sounds. They are due to the transmission of air turbulence in the large airways filtered through the normal lung to the chest wall.

Bronchial breath sounds are present when turbulence in the large airways is heard without being filtered by the alveoli, producing a different quality. Bronchial breath sounds have a hollow, blowing quality. They are audible throughout expiration and there is often a gap between inspiration and expiration. The expiratory sound has a higher intensity and pitch than the inspiratory sound. Bronchial breath sounds are more easily remembered than described. They are audible in normal people, posteriorly over the right upper chest where the trachea is contiguous with the right upper bronchus. They are heard over areas of consolidation, as solid lung conducts the sound of turbulence in main airways to peripheral areas without filtering. Causes of bronchial breath sounds are shown in Table 5.18.

TABLE 5.18 Causes of bronchial breath sounds

Common Lung consolidation (lobar pneumonia)

Uncommon

Localised pulmonary fibrosis

Pleural effusion (above the fluid)

Collapsed lung (e.g. adjacent to a pleural effusion)

Note: The large airways must be patent.

Occasionally breath sounds over a large cavity have an exaggerated bronchial quality. This very hollow or amphoric sound has been likened to that heard when air passes over the top of a hollow jar (Greek amphoreus).

The heart

Cardiac examination is an essential part of the respiratory assessment and vice versa. These two systems are intimately related.

Lay the patient down at 45 degrees and measure the jugular venous pressure for evidence of right heart failure (page 58). Next examine the praecordium. It is important to pay close attention to the pulmonary component of the second heart sound (P2). This is best heard at the second intercostal space on the left. It should not be louder than the aortic component, best heard at the right second inter-costal space. If the P2 is louder (and especially if it is palpable), pulmonary hypertension should be strongly suspected. There may be signs of right ventricular failure or hypertension. Pulmonary hypertensive heart disease (cor pulmonale) may be due to COPD, ILD, pulmonary thromboembolism, marked obesity, sleep apnoea or severe kyphoscoliosis.

The abdomen

Palpate the liver for ptosis,ⁱ due to emphysema, or for enlargement from secondary deposits of tumour in cases of lung carcinoma.

Other

Bedside assessment of lung function

Spirometry (Figure 5.12)

The spirometer records graphically or numerically the forced expiratory volume and the forced vital capacity. The forced expiratory volume (FEV) is the volume of air expelled from the lungs after maximum inspiration using maximum forced effort, and is measured in a given time. Usually this is 1 second (FEV₁). The forced vital capacity (FVC) is the total volume of air expelled from the lungs after maximum inspiratory effort followed by maximum forced expiration. The FVC is often nearly the same as the vital capacity, but in airways obstruction it may be less because of premature airways closure. It is usual to record the best of three attempts and calculate the FEV₁/FVC ratio as a percentage. In healthy youth, the normal value is 80%, but this may decline to as little as 60% in old age. Normal values also vary with sex, age, height and race.

Figure 5.12 Spirometry tracings

Reversibility of a reduced FEV₁/FVC after the use of bronchodilators is an important test for distinguishing asthma from COPD.

Obstructive ventilatory defect

When the FEV₁/FVC ratio is reduced (<0.7) this is referred to as an obstructive defect. Both values tend to be reduced, but the FEV₁ is disproportionately low. The causes are loss of elastic recoil or airways narrowing, as in asthma or COPD.

Restrictive ventilatory defect

When the FEV₁/FVC ratio is normal or higher than normal, but both values are reduced, the pattern is described as a restrictive defect. This occurs in parenchymal lung disease, such as ILD, sarcoidosis, or when lung expansion is reduced by pneumonia or chest wall abnormalities.

Flow volume curve

As a part of spirometric assessment, the flow volume curve may be measured using a portable electronic device. This measures expiratory and inspiratory flow as a function of exhaled volume rather than against time. It is a simple and reproducible test easily performed in the respiratory laboratory or at the bedside. The FVC, FEV₁ and various flow measurements (e.g. peak flow) can be calculated from the curve (Figure 5.13).

Figure 5.13 Flow volume curves

Look at the shape of the loop in each case. A normal flow volume curve is convex and symmetrical. In chronic obstructive lung disease (COPD), all flow routes are reduced and there is prolonged expiration (creating a ‘scooped out’ shape). In restrictive lung disease (e.g. pulmonary fibrosis), the loop is narrow but the shape normal (like a ‘witch’s hat’). In fixed airway obstruction (e.g. tracheal stenosis), the loops look flattened as both expiration and inspiration are limited.

PEF = peak expiratory flow

TLC = total lung capacity

RV = residual volume

Correlation of physical signs and respiratory disease (Table 5.19)

Pleural effusion

This is a collection of fluid in the pleural space. Note that pleural collections consisting of blood (haemothorax), chyle (chylothorax) or pus (empyema) have specific names, and are not called pleural effusions although the physical signs are similar.

Signs

• Trachea and apex beat: displaced away from a massive effusion.

• Expansion: reduced on the affected side.

• Percussion: stony dullness over the fluid.

• Breath sounds: reduced or absent. There may be an area of bronchial breathing audible above the effusion due to compression of overlying lung.

• Vocal resonance: reduced.

Causes

• Transudate (Light’s criteria): (i) cardiac failure; (ii) hypoalbuminaemia from the nephrotic syndrome or chronic liver disease; (iii) hypothyroidism; (iv) Meigs syndrome^k (ovarian fibroma causing pleural effusion and ascites).

• Exudate (Light’s criteria^l): (i) pneumonia; (ii) neoplasm—bronchial carcinoma, metastatic carcinoma, mesothelioma; (iii) tuberculosis; (iv) pulmonary infarction; (v) subphrenic abscess; (vi) acute pancreatitis; (vii) connective tissue disease such as rheumatoid arthritis, systemic lupus erythematosus; (viii) drugs such as methysergide, cytotoxics; (ix) irradiation; (x) trauma.

• Haemothorax (blood in the pleural space): (i) severe trauma to the chest; (ii) rupture of a pleural adhesion containing a blood vessel.

• Chylothorax (milky-appearing pleural fluid due to leakage of lymph): (i) trauma or surgery to the thoracic duct; (ii) carcinoma or lymphoma involving the thoracic duct.

• Empyema (pus in the pleural space): (i) pneumonia; (ii) lung abscess; (iii) bronchiectasis; (iv) tuberculosis; (v) penetrating chest wound.

Yellow nail syndrome

This is a rare condition which is caused by hypoplasia of the lymphatic system. The nails are thickened and yellow (Figure 5.14) and there is separation of the distal nail plate from the nail bed (onycholysis). It may be associated with a pleural effusion and bronchiectasis, and usually with lymphoedema of the legs.

Figure 5.14 Yellow nail syndrome: (a) hands; (b) feet

From McDonald FS, ed., Mayo Clinic images in internal medicine, with permission. © Mayo Clinic Scientific Press and CRC Press.

SLE = systemic lupus erythematosus.

Remember the three Cs:

Tuberculosis

Mediastinal compression

Mediastinal structures may be compressed by a variety of pathological masses, including carcinoma of the lung (90%), other tumours (lymphoma, thymoma, dermoid cyst), a large retrosternal goitre or rarely an aortic aneurysm.

Carcinoma of the lung

Many patients have no signs.

Sarcoidosis

This is a systemic disease, characterised by the presence of non-caseating granulomas which commonly affect the lungs, skin, eyes, lymph nodes, liver and spleen, and the nervous system. The aetiology is unknown. There may be no pulmonary signs.

Pulmonary embolism (PE)

Embolism to the lungs often occurs without symptoms or signs. One should always entertain this diagnosis if there has been sudden and unexplained dyspnoea when a patient has risk factors for embolism (Table 5.21). Pleuritic chest pain and haemoptysis occur only when there is infarction. Syncope or the sudden onset of severe substernal pain can occur with massive embolism.

TABLE 5.21 Risk factors for pulmonary embolism (PE)

Note: A firm diagnosis cannot be made on the symptoms and signs alone.

The chest X-ray

The radiological appearance of a normal lung, with the lung segments labelled, is shown in Figure 5.15.

Figure 5.15 Lung segments

(a) Posteroanterior view. (b) CT scan through lung bases. (c) Left lateral view. (d) Right lateral view.

Right upper lobe: ä = apical segment; a = anterior segment, p = posterior segment.

Left upper lobe: ä-p = apico-posterior segment, s = anterior segment, sl = superior lingular segment, il = inferior lingular segment.

Right middle lobe (rml): m = medial segment, l = lateral segment.

Right lower lobe: äl = apical segment, mb = medial basal segment, lb = lateral basal segment, ab = anterior basal segment, pb = posterior basal segment.

Left lower lobe: äl = apical segment, lb = lateral basal segment, ab = anterior basal segment, pb = posterior basal segment.

The radiological changes of consolidation, pleural effusion, pneumothorax and hydropneumothorax are shown in Figures 5.16 to 5.19.

Figure 5.16 Right upper lobe consolidation

The right upper lobe is opacified and is limited inferiorly by the horizontal fissure (arrows). There must be some collapse as well, as the fissure shows some elevation. These changes could be due to a bacterial lobar pneumonia per se, but a central bronchostenotic lesion should be considered. If the pneumonia persists, a bronchoscopy is indicated to search for a central carcinoma.

Figure 5.17 Pleural effusion

The upper margin of the effusion is curved (‘meniscus sign’). The left hemidiaphragm is not seen because there is no adjacent aerated lung for contrast. The heart shows some deviation to the right. It is unlikely that this is caused by an effusion of this size. It is probably related to the lower thoracic scoliosis.

Figure 5.18 Pneumothorax

(a) There is a massive right pneumothorax with collapsed lung seen against the hilum (arrow). There is increased translucency because of the absence of vascular shadows. (b) Different patient with a smaller pneumothorax. Small pneumothoraces are easier to see on an expiratory film as the pneumothorax volume remains constant, surrounding the partly deflated lung. The visceral pleural surface is marked (arrow).

Figure 5.19 Hydropneumothorax

An air–fluid level is seen in the upper portion of the right hemithorax. When air and fluid are present in the pleural space, the fluid no longer forms a meniscus at its upper margin. Some aerated lung is seen deep to the fluid.

A pulmonary mass is obvious in Figure 5.20, while multiple metastases are seen in Figure 5.21. Primary tuberculosis is shown in Figure 5.22, and Figure 5.23 illustrates the features of emphysema.

Figure 5.20 A pulmonary mass

There is a large solitary mass lesion in the left lower zone. The differential diagnosis is primary or secondary neoplasm, hydatid cyst or large abscess. No air–fluid level is seen within it to indicate cavitation.

Figure 5.21 Pulmonary metastases

Multiple rounded opacities are seen in both lung fields, mainly at the left base and around the right hilum. The most likely cause is multiple pulmonary metastases. Other rare possibilities are hydatid cysts, large sarcoid nodules or large rheumatoid nodules. Multiple abscesses are extremely unlikely in the absence of cavitation.

Figure 5.22 Primary tuberculosis

Two small rounded areas of shadowing are seen in the right upper zone (solid arrow). The right hilum is enlarged by the enlarged draining lymph nodes (open arrow). This combination of focal shadowing and enlarged lymph nodes is the primary (Ghon) complex of tuberculosis. With healing, calcification may occur in the parenchymal and nodal lesions. In contrast, in tuberculosis reactivation or reinfection, cavitation may occur and there is no lymphadenopathy.

Figure 5.23 Emphysema

The lungs are overinflated with low, flat hemidiaphragms. The level of the hemidiaphragms is well below the anterior aspects of the sixth ribs. The diaphragm normally projects over the sixth rib anteriorly and the tenth intercostal space posteriorly. Count the ribs anteriorly (1–6). There is increased translucency of both upper zones with loss of the vascular markings due to bulla formation (arrow). This increased translucency is not due to overexposure. The hila are prominent because of the enlarged central pulmonary arteries. In contrast, the smaller peripheral pulmonary arteries (the lung markings) are decreased in size and number. This is due to actual destruction, displacement around bullae, and decreased perfusion through emphysematous areas.

Summary

The respiratory examination: a suggested method (Figure 5.24)

Ask the patient to undress to the waist (provide women with a gown), and to sit over the side of the bed. In the clinic or surgery the examination can often be performed with the patient sitting on a chair. While standing back to make your usual inspection (does the patient appear breathless while walking into the room or undressing?), ask if sputum is available for inspection. Purulent sputum always indicates respiratory infection, and a large volume of purulent sputum is an important clue to bronchiectasis. Haemoptysis is also an important sign. Look for dyspnoea at rest and count the respiratory rate. Note any paradoxical inward motion of the abdomen during inspiration (diaphragmatic paralysis). Look for use of the accessory muscles of respiration, and any intercostal indrawing of the lower ribs anteriorly (a sign of emphysema). General cachexia should also be noted.

Figure 5.24 Respiratory system

SVC = superior vena cava.

Sitting up (if not acutely ill)

1. General inspection

Sputum mug contents (blood, pus etc)

Type of cough

Rate and depth of respiration, and breathing pattern at rest

Accessory muscles of respiration

2. Hands

Clubbing

Cyanosis (peripheral)

Nicotine staining

Wasting, weakness—finger abduction and adduction (lung cancer involving the brachial plexus)

Wrist tenderness (hypertrophic pulmonary osteoarthropathy)

Pulse (tachycardia, pulsus paradoxus)

Flapping tremor (CO₂ narcosis)

3. Face

Eyes—Horner’s syndrome (apical lung cancer), anaemia

Mouth—central cyanosis

Voice—hoarseness (recurrent laryngeal nerve palsy)

Facial plethora—smoker, SVC obstruction

4. Trachea

5. Chest posteriorly

Inspect

• Shape of chest and spine

• Scars

• Prominent veins (determine direction of flow)

Palpate

• Cervical lymph nodes

• Expansion

• Vocal fremitus

Percuss

• Supraclavicular region

• Back

• Axillae

• Tidal percussion (diaphragm paralysis)

Auscultate

• Breath sounds

• Adventitious sounds

• Vocal resonance

6. Chest anteriorly

Inspect

• Radiotherapy marks, other signs as noted above

Palpate

• Supraclavicular nodes

• Expansion

• Vocal fremitus

• Apex beat

Percuss

Auscultate

Pemberton’s sign (SVC obstruction)

7. Cardiovascular system (lying at 45°)

Jugular venous pressure (SVC obstruction etc)

Cor pulmonale

8. Forced expiratory time

9. Other

Lower limbs—oedema, cyanosis

Breasts

Temperature chart (infection)

Evidence of malignancy or pleural effusion: examine the breasts, abdomen, rectum, lymph nodes etc

Respiratory rate after exercise

Pick up the hands. Look for clubbing, peripheral cyanosis, tar staining and anaemia. Note any wasting of the small muscles of the hands and weakness of finger abduction (lung cancer involving the brachial plexus). Palpate the wrists for tenderness (hypertrophic pulmonary osteoarthropathy). While holding the hand, palpate the radial pulse for obvious pulsus paradoxus. Take the blood pressure if indicated.

Go on to the face. Look closely at the eyes for constriction of one of the pupils and for ptosis (Horner’s syndrome from an apical lung cancer). Inspect the tongue for central cyanosis.

Palpate the position of the trachea. This is an important sign, so spend time on it. If the trachea is displaced, you must concentrate on the upper lobes for physical signs. Also look and feel for a tracheal tug, which indicates severe airflow obstruction, and feel for the use of the accessory muscles. Now ask the patient to speak (hoarseness) and then cough, and note whether this is a loose cough, a dry cough or a bovine cough. Next measure the forced expiratory time (FET). Tell the patient to take a maximal inspiration and blow out as rapidly and forcefully as possible while you listen. Note audible wheeze and prolongation of the time beyond 3 seconds as evidence of chronic obstructive pulmonary disease.

The next step is to examine the chest. You may wish to examine the front first, or go to the back to start. The advantage of the latter is that there are often more signs there, unless the trachea is obviously displaced.

Inspect the back. Look for kyphoscoliosis. Do not miss ankylosing spondylitis, which causes decreased chest expansion and upper lobe fibrosis. Look for thoracotomy scars and prominent veins. Also note any skin changes from radiotherapy.

Palpate first from behind for the cervical nodes. Then examine for expansion—first upper lobe expansion, which is best seen by looking over the patient’s shoulders at clavicular movement during moderate respiration. The affected side will show a delay or decreased movement. Then examine lower lobe expansion by palpation. Note asymmetry and reduction of movement.

Now ask the patient to bring his or her elbows together in the front to move the scapulae out of the way. Examine for vocal fremitus, then percuss the back of the chest.

Auscultate the chest. Note breath sounds (whether normal or bronchial) and their intensity (normal or reduced). Listen for adventitious sounds (crackles and wheezes). Finally examine for vocal resonance. If a localised abnormality is found, try to determine the abnormal lobe and segment.

Return to the front of the chest. Inspect again for chest deformity, distended veins, radiotherapy changes and scars. Palpate the supraclavicular nodes carefully. Then proceed with percussion and auscultation as before. Listen high up in the axillae too. Before leaving the chest feel the axillary nodes and examine the breasts (Chapter 14).

Lay the patient down at 45 degrees and measure the jugular venous pressure. Then examine the praecordium and lower limbs for signs of cor pulmonale. Finally examine the liver and take the temperature.

Remember that most respiratory examinations are ‘targeted’. Not every part of the examination is necessary for every patient.