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

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