The respiratory system

Timing and associated features: Nocturnal cough disrupting sleep is a feature of asthma. Occupational asthma and exposure to dusts and fumes cause a chronic cough which improves during weekends and holidays. Coughing during and after swallowing liquids suggests neuromuscular disease of the oropharynx.

Cough syncope may result from raised intrathoracic pressure impairing venous return to the heart, reducing cardiac output.

Colour:

Amount: Bronchiectasis causes large volumes of purulent sputum, which varies with posture. Suddenly coughing up large amounts of purulent sputum on a single occasion suggests rupture of a lung abscess or empyema into the bronchial tree. Large volumes of watery sputum with a pink tinge in an acutely breathless patient suggest pulmonary oedema but, if occurring over weeks (bronchorrhoea), suggests alveolar cell cancer.

Taste or smell: Foul-tasting or smelling sputum suggests anaerobic bacterial infection, and occurs in bronchiectasis, lung abscess and empyema. In bronchiectasis a change of sputum taste may indicate an infective exacerbation.

Solid material: In asthma and allergic bronchopulmonary aspergillosis thick secretions can accumulate in airways and be coughed up as ‘worm-like’ structures that are casts of the bronchi (Fig. 7.4). Other solid matter sometimes coughed up includes necrotic tumour and inhaled foreign bodies, e.g. food, teeth and tablets.

Amount and appearance: Blood-streaked clear sputum or clots in sputum for more than a week suggest lung cancer. Haemoptysis with purulent sputum suggests infection. Coughing up large amounts of pure blood is rare but potentially life-threatening; causes include lung cancer, bronchiectasis and tuberculosis and, less commonly, lung abscess, mycetoma, cystic fibrosis, aortobronchial fistula and granulomatosis with polyangiitis (formerly Wegener’s granulomatosis).

Duration and frequency: Bronchiectasis causes intermittent haemoptysis associated with copious purulent sputum over years. Daily haemoptysis for a week or more is a symptom of lung cancer; other causes include tuberculosis and lung abscess.

Single episodes of haemoptysis, if associated with symptoms, e.g. pleuritic chest pain and breathlessness, suggest pulmonary thromboembolism and infarction and need immediate investigation.

Mode of onset, duration and progression: Psychogenic breathlessness may occur suddenly at rest or while talking. Patients often say they cannot get enough air into their chest and need to take deep breaths. The resultant hypocapnia causes lightheadedness, dizziness, tingling in the fingers and round the mouth and chest tightness. These symptoms, in turn, aggravate anxiety and exacerbate the situation (Box 7.6 and Ch. 2).

Variability and aggravating/relieving factors: Breathlessness when lying flat (orthopnoea) is usually associated with left ventricular failure. It can also be a feature of respiratory muscle weakness, large pleural effusion, massive ascites, morbid obesity or any severe lung disease.

Breathlessness on sitting up (platypnoea) with relief on lying down is rare and due to right-to-left shunting through a patent foramen ovale, atrial septal defect or a large intrapulmonary shunt.

Breathlessness when lying on one side (trepopnoea) is due to unilateral lung disease (patient prefers the healthy lung down), dilated cardiomyopathy (patient prefers right side down) or tumours compressing central airways and major blood vessels.

Breathlessness that wakes the patient from sleep is typical of asthma and left ventricular failure (paroxysmal nocturnal dyspnoea). Patients with asthma typically wake between 3 and 5 a.m. and have associated wheezing. Breathlessness worse on waking is more typical of COPD and may improve after coughing up sputum.

Patients with exercise-induced asthma may notice that the breathlessness continues to worsen for 5–10 minutes after stopping activity. If you suspect asthma, ask about exposure to allergens, smoke, perfumes, fumes, cold air or drugs, e.g. aspirin, non-steroidal anti-inflammatory drugs. Common allergens are house dust mite (shaking bedding, hoovering), animals (cats, dogs, horses) and grass pollens (mowing the lawn, the ‘hayfever season’) and tree pollens. Breathlessness improving at weekends or holidays suggests occupational asthma. Ask about symptoms that accompany the breathlessness, e.g. chest pain, cough, wheeze (Box 7.11).

Severity: Breathlessness while walking on the flat, up gentle inclines or stairs indicates a significant condition. Severely breathless patients are dyspnoeic at rest, walking around the house, washing, dressing and even eating (Box 7.7).

COPD is characterised by airflow obstruction that is usually progressive and not fully reversible. It is defined as a reduced post-bronchodilator forced expiratory volume in 1 second (FEV₁)/forced vital capacity (FVC) ratio of <70%.

Asthma is reversible airways obstruction.

Respiratory rate: Tachypnoea is a respiratory rate >25 breaths/min. It is caused by increased ventilatory drive in fever, acute asthma and exacerbation of COPD, or reduced ventilatory capacity in pneumonia, pulmonary oedema and interstitial lung disease (Boxes 7.17 and Box 7.18). A slow respiratory rate of <10 breaths/min (bradypnoea) occurs in opioid toxicity, hypercapnia, hypothyroidism, raised intracranial pressure and hypothalamic lesions.

Breathing patterns: Periodic breathing (Cheyne–Stokes respiration) is cyclical with increasing rate and depth of breathing, followed by diminishing respiratory effort and rate, ending in a period of apnoea or hypopnoea. This relates to altered sensitivity of the respiratory centre to CO₂ and delay in circulation time between the lung and chemoreceptors.

Hyperventilation is a common response to acute anxiety or emotional distress, and is often associated with respiratory alkalosis with hypocapnia. Breathing is deep, irregular and sighing, and patients feel unable to fill their lungs completely. When acute hyperventilation is sustained, tetany and occasionally grand mal seizure can occur. Hyperventilation with deep, sighing respirations (Kussmaul respiration) occurs in metabolic acidosis caused by diabetic ketoacidosis, acute renal failure, lactic acidosis, and salicylate and methanol poisoning. Although patients may not be aware of breathlessness, their respiratory rate increases and they appear to have ‘air hunger’.

Apnoea is the absence of breathing; hypopnoea is a reduction in airflow or respiratory movements by >50% for 10 seconds or more. Obstructive sleep apnoea/hypopnoea syndrome (OSAHS) is the combination of excessive daytime sleepiness and recurrent upper airway obstruction with sleep fragmentation caused by upper airway obstruction from collapse of the retropharynx. A total of 2–4% of middle-aged men and 1–2% of middle-aged women (Box 7.10) have OSAHS with multiple apnoeas during sleep. They usually describe loud snoring, then a pause in breathing followed by a grunting noise and restoration of snoring. Simple (benign) snoring is more common than OSAHS, affecting 40% of middle-aged men and 20% of middle-aged women. Urgently investigate patients with daytime sleepiness and drowsiness while driving, especially if they have a heavy goods or public service vehicle licence.

Cough: Ask about the duration of the cough and when, during the day, it is most severe. Cough on lying down in the evening may be due to gastro-oesophageal reflux; cough disrupting sleep is typical of asthma; cough on rising in the morning can be caused by rhinosinusitis and postnasal drip.

Wheeze: Ask about precipitating factors such as exercise and exposure to allergens (pets, pollens) and relationship to occupation.

Sputum: Ask patients specifically about sputum as they may find it difficult to discuss or may swallow it. Ask about the colour of any sputum produced and how many teaspoonfuls are coughed up daily.

Haemoptysis: Establish the volume and nature of the blood. Clarify whether the blood was coughed up from the respiratory tract, vomited (upper gastrointestinal tract) or suddenly appeared in the mouth without coughing (nasopharyngeal).

Breathlessness: Use the Medical Research Council grading scale to characterise breathlessness (Box 7.7). How far can the patient walk before stopping to rest? Get an estimate of the time taken to walk a given distance and the number of stops involved: say, from home to a local shop. Ask about the effect on work and hobbies such as golf, gardening, dancing, swimming or hill walking, Can the patient walk up hills or keep up with contemporaries? Box 7.9 outlines some combinations of symptoms in acutely breathless patients.

Chest pain: Characterise chest pain using SOCRATES (Box 2.10).

Respiratory pattern: Ask about any change in the rate or pattern of breathing. If the patient has daytime sleepiness, ask the patient’s bed partner about apnoea, loud snoring, nocturnal restlessness, irritability and personality change (Box 7.11).

Smoking: Although cigarette smoking has declined in the UK, the current prevalence of COPD and incidence of lung cancer reflect historical smoking patterns. Establish when patients started and stopped smoking and their average tobacco consumption as cigarettes/day or ounces/grams of ‘roll-up’ tobacco/week. Calculate the ‘pack year’ consumption: smoking 1 pack of 20 cigarettes per day for 1 year equates to 1 pack year (Box 2.20). Patients with COPD usually have smoked >20 pack years. Stopping smoking at any age is crucial to improving health; beyond 40 years people lose, on average, 3 months of life expectancy for every further year they continue smoking.

Pets: Ask about exposure to pets. Hair and fur from dogs, cats, rodents and horses may aggravate asthma. Hypersensitivity pneumonitis and psittacosis are associated with birds.

Stridor:

Cyanosis:

Blood pressure:

Skin appearances: Erythema nodosum over the shins is a feature of acute sarcoidosis and tuberculosis (Fig. 7.6A). Raised, firm, non-tender subcutaneous nodules may occur in patients with disseminated cancer (Fig. 7.6B).

Clubbing: The majority of patients with finger clubbing have thoracic disease (lung cancer, bronchiectasis, interstitial lung disease) but it is also associated with gastrointestinal disorders and can be familial (Box 3.10). Rarely, clubbing develops relatively quickly over several weeks, in empyema.

Hypertrophic pulmonary osteoarthropathy is rare and almost always associated with lung cancer, usually squamous cancer. Pronounced clubbing of fingers and toes occurs, with pain and swelling affecting the wrists and ankles. X-rays of the distal forearm and lower legs show subperiosteal new bone formation separate from the cortex of the long bones (Fig. 7.7).

Discoloration of the fingers and nails: A brownish stain on the fingers and nails in cigarette smokers is caused by tar, not nicotine (Fig. 7.8). The rare ‘yellow nail syndrome’ is associated with lymphoedema and an exudative pleural effusion (Fig. 7.9).

A fine finger tremor is often caused by excessive use of β-agonist or theophylline bronchodilator drugs.

A coarse flapping tremor (asterixis) is seen with severe ventilatory failure and carbon dioxide retention. This is the result of intermittent failure of parietal mechanisms required to maintain posture. Unilateral asterixis is due to structural abnormality in the contralateral cerebral hemisphere.

Jugular venous pressure (JVP):

Neck nodes:

Chest shape:

Skin: Subcutaneous lesions may be visible, including metastatic tumour nodules, neurofibromas and lipomas, as may vascular anomalies, e.g. the dilated venous vascular channels of SVCO (Fig. 7.11B).

Palpation: Determine the position of the mediastinum by examining the trachea and cardiac apex beat (Box 7.20).

Chest expansion:

Percussion: Percussion allows you to hear the pitch and loudness of the percussed note and to feel for postpercussive vibrations. Percuss in sequence over corresponding areas on both sides of the chest (Fig. 7.18).

Auscultation: Most sounds reaching the chest wall are low-frequency and best heard with the stethoscope bell. The diaphragm locates higher-pitched sounds, such as pleural friction rubs. Stretching the skin and hairs under the diaphragm during deep breathing can produce anomalous noises like crackles, and in thin patients it may be difficult to apply the diaphragm fully to the chest wall skin.

Added sounds: Crackles are interrupted non-musical sounds and result from collapse of peripheral airways on expiration. On inspiration, air rapidly enters these distal airways, and the alveoli and small bronchi open abruptly, producing the crackling noise.

Note when crackles occur within the respiratory cycle (Box 7.25). Early inspiratory crackles suggest small airways disease and can occur in bronchiolitis. In pulmonary oedema crackles occur in mid-inspiration. Fine late inspiratory crackles, which sound similar to rubbing hair between your fingers, are characteristic of pulmonary fibrosis. Bronchiectasis can cause crackles throughout inspiration and expiration.

Crackles may be heard when air bubbles through secretions in major bronchi, dilated bronchi in bronchiectasis or in pulmonary cavities. These crackles sound coarse, have a gurgling quality and change if the secretions are dislodged by coughing.

Wheeze is caused by continuous oscillation of opposing airway walls and has a musical quality. Wheezes imply airway narrowing and are timed in relation to the respiratory cycle. They are louder on expiration because airways normally dilate during inspiration and narrow on expiration. Inspiratory wheeze implies severe airway narrowing. High-pitched wheeze arises from smaller airways and has a whistling quality. Low-pitched wheeze originates from larger bronchi. Distinguish wheeze from the harsh rasping sound of stridor (p. 143).

Wheeze is characteristic of asthma and COPD, but is a poor guide to severity of airflow obstruction. In severe airways obstruction wheeze may be absent because of reduced airflow, producing a ‘silent chest’. A fixed bronchial obstruction, most commonly due to lung cancer, may cause localised wheeze with a single musical note that does not clear on coughing.

A pleural friction rub is a creaking sound similar to that produced by bending stiff leather or treading in fresh snow. It is produced when inflamed parietal and visceral pleurae move over one another and is best heard with the stethoscope diaphragm. It may be heard only on deep breathing at the end of inspiration and beginning of expiration. A pleural rub is usually associated with pleuritic pain and may be heard over areas of inflamed pleura in pulmonary infarction due to pulmonary embolism. Pulmonary embolism is obstruction of part of the pulmonary vascular tree by thrombus that has travelled from a distant site, e.g. deep veins in the legs or pelvis (Figs 7.18 and 7.19; Boxes 7.23 and 7.24). Pulmonary embolism is frequently unrecognised and fewer than one-third of patients have symptoms or signs of deep vein thrombosis (Box 7.26). A pleural friction rub may be heard in pneumonia or pulmonary vasculitis. If the pleura adjacent to the pericardium is involved, a pleuropericardial friction rub may also be heard. Pleural friction rubs disappear if an effusion separates the pleural surfaces.

A pneumothorax click is a rhythmical sound, synchronous with cardiac systole, and produced when there is air between the two layers of pleura overlying the heart.

A mid-expiratory ‘squeak’ is characteristic of obliterative bronchiolitis – a rare complication of rheumatoid arthritis – where small airways are narrowed or obliterated by chronic inflammation and fibrosis.

Vocal resonance:

Respiratory acidosis: An acute rise in PaCO₂ caused by alveolar hypoventilation associated with a decrease in pH occurs in severe acute asthma, severe pneumonia, exacerbations of COPD and neuromuscular disorders. Elevation of PaCO₂ for more than 2–3 days may occur in COPD, respiratory muscle weakness due to neuromuscular disorders and thoracic skeletal deformities, and leads to renal retention of HCO₃^– and normalisation of pH, i.e. compensated respiratory acidosis. In some patients with COPD low PaO₂ levels drive respiratory effort. Removal of this stimulus by excessive oxygen therapy may result in alveolar hypoventilation with further increase in PaCO₂, which can lead to deterioration and death.

Respiratory alkalosis: Hyperventilation occurs with respiratory conditions (asthma, pulmonary thromboembolism, pleurisy), high altitude and acute anxiety. Alveolar hyperventilation leads to decrease in PaCO₂ and a consequent increase in pH. If hyperventilation persists, as occurs with stays at high altitude, increased renal excretion of HCO₃^– results in normalisation of pH, i.e. compensated respiratory alkalosis.

Metabolic acidosis: In acute renal failure, diabetic ketoacidosis and lactic acidosis, metabolic acidosis results from loss of HCO₃^– and decrease in pH. The decrease in pH stimulates arterial chemoreceptors, resulting in alveolar hyperventilation with a consequent decrease in PaCO₂.

Metabolic alkalosis: The primary abnormality of metabolic alkalosis is retention of HCO₃^–, often related to renal tubular K⁺ depletion or loss of H⁺, resulting in an increase in pH. The increase in pH induces alveolar hypoventilation via arterial chemoreceptors, with consequent increase in PaCO₂.