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SYNDROMES

Contents of the training materials

COUGH

  
Cough is the most frequent symptom of respiratory disease. It is caused by stimulation of sensory nerves in the mucosa of the pharynx, larynx, trachea and bronchi.  
The explosive quality of a normal cough is lost in patients with respiratory muscle paralysis or vocal cord palsy. Paralysis of a single vocal cord gives rise to a prolonged, low-pitched, inefficient 'bovine' cough accompanied by hoarseness. Coexistence of an inspiratory noise (stridor) indicates partial obstruction of a major airway (e.g. laryngeal oedema, tracheal tumour, scarring or compression or an inhaled foreign body) and requires urgent investigation and treatment. Sputum production is common in patients with acute or chronic cough, and its nature and appearance can provide valuable clues as to the aetiology.    
Causes of cough    
  Origin Common causes Clinical features
  Pharynx Post-nasal drip History of chronic rhinitis
  Larynx Laryngitis, tumour, croup Voice or swallowing altered, harsh or painful cough Paroxysms of cough, often associated with stridor
  Trachea Tracheitis retrosternal pain with cough
  Bronchi Bronchitis (acute) and COPD Dry or productive, worse in mornings
  Asthma Usually dry, worse at night
  Bronchial carcinoma Persistent (often with haemoptysis)
  Lung parenchyma Tuberculosis Productive, often with haemoptysis
  Pneumonia Dry initially, productive later
  Bronchiectasis Productive, changes in posture induce sputum production
  Pulmonary oedema Often at night
  Interstitial fibrosis Dry, irritant
  Patients with chronic cough present more of a diagnostic challenge, especially those individuals with a normal examination, chest X-ray and lung function studies. In this context, cough can be explained by post-nasal drip secondary to nasal or sinus disease; cough-variant asthma (where cough may be the principal or exclusive clinical manifestation) or gastro-oesophageal reflux with aspiration. Ten to fifteen per cent of patients (particularly women) taking angiotensin-converting enzyme (ACE) inhibitors develop drug-induced chronic cough.  
DYSPNOEA  
Breathlessness or dyspnoea can be defined as the feeling of an uncomfortable need to breathe.  
  CAUSES OF DYSPNOEA  
  System Acute dyspnoea at rest Chronic exertional dyspnoea
  Cardio-vascular Acute pulmonary oedema Chronic heart failure Myocardial ischaemia  
  Respi-ratory Acute severe asthma Acute exacerbation of COPD Pneumothorax Pneumonia * Pulmonary embolus Acute respiratory distress syndrome Inhaled foreign body Lobar collapse Laryngeal oedema (e.g. anaphylaxis) COPD Chronic asthma Bronchial carcinoma Interstitial lung disease (sarcoidosis, fibrosing alveolitis, pneumoconiosis) Chronic pulmonary thromboembolism Lymphatic carcinomatosis Large pleural effusion(s)  
  Others Metabolic acidosis (e.g. diabetic ketoacidosis, lactic acidosis, uraemia, overdose of salicylates, Psychogenic hyperventilation Severe anaemia Obesity  
  CHRONIC EXERTIONAL DYSPNOEA  
  Chronic obstructive pulmonary disease (COPD)  
  The exertional dyspnoea in COPD typically varies little day to day, but exercise capacity falls over months or years. Patients usually report relief of dyspnoea at rest and overnight, a useful distinction from asthma. If bronchitis is present, chronic cough and sputum is usual, particularly in the mornings, but sputum may be absent when emphysema predominates. There is often a history of recurrent acute exacerbations of breathlessness, usually in winter. Most of the patients have a smoking history. In advanced disease may develop cor pulmonale  
  Asthma  
  Dyspnoea in asthma is associated with episodes of wheeze or chest tightness, usually worse in the morning. There may be a history of childhood wheeze, or of wheeze or rhinitis provoked by allergens. In exercise-induced asthma, wheeze and chest tightness typically come on immediately after exercise.  
  Heart disease  
  Left ventricular function can cause exertional dyspnoea. Orthopnoea, cough and wheeze may also be present, as in lung disease. A history of angina or hypertension may be useful in implicating a cardiac cause. On examination, an increase in heart size. The chest X-ray may show cardiomegaly and an ECG may provide evidence of left ventricular disease.  
  Pulmonary thromboembolism  
  Pulmonary thromboembolism often presents with acute breathlessness with or without chest pain. However, chronic pulmonary thromboembolic disease should be suspected in patients who present with more gradual onset of breathlessness.  
  Psychogenic breathlessness and hyperventilation syndromes  
  Breathlessness which is not caused by organic disease of the heart or lungs is relatively common. It is difficult to diagnose in patients with coexisting disease, such as asthma or heart disease.    
  DIFFERENTIAL DIAGNOSIS OF ACUTE SEVERE DYSPNOEA  
  Condition History Signs Chest radiography Arterial blood gases ECG Other tests
  Pulmonary oedema Chest pain Orthopnoea Palpitations A previous cardiac history* Central cyanosis JVP (→ or ↑) Sweating* Cool extremities Dullness and crepitations at bases* Cardiomegaly Upper zone vessel enlargement* Overt oedema/pleural effusions* ↓ Pa O2 ↓ Pa CO2 Sinus tachycardia Signs of myocardial infarction/ ischaemia* Arrhythmia ECG* (↓ left ventricular function)  
  Massive pulmonary embolus Recent surgery or other risk factors Chest pain Previous pleurisy Syncope* Dizziness* Severe central cyanosis Elevated JVP* Absence of signs in the lung (unless previous pulmonary infarction)* Shock (tachycardia, reduced blood pressure) May be subtle changes only Prominent hilar vessels Oligaemic lung fields* ⇓ Pa O2 ↓ Pa CO2 Sinus tachycardia S1Q3T3 pattern ↓ T (V1-V4) Right bundle-branch block ECG* V/Q scan* CT pulmonary angiography*  
  Acute severe asthma History of previous episodes, asthma medications, wheeze* Tachycardia and pulsus paradoxus yanosis (late) JVP →* ⇓ peak flow, rhonchi* Hyperinflation only (unless complicated by pneumothorax)* ↓ Pa O2 ↓ Pa CO2 (Pa CO2 rises in extremis) Sinus tachycardia (bradycardia with severe hypoxaemia-late)    
  Acute exacerbation of COPD Previous episodes (admissions)* If in type II respiratory failure may not be distressed Cyanosis Signs of COPD* Signs of CO2 retention (warm periphery, flapping tremor, bounding pulses)* Hyperinflation* Signs of emphysema Signs of events precipitating exacerbation ↓ or ⇓ Pa O2 Pa CO2 ↑ in type II failure, with ↑ [H+] and ↑ bicarbonate Nil, or signs of right ventricular strain    
  Pneumonia Prodromal illness* Fever* Rigors* Pleurisy* Fever, confusion Pleural rub* Consolidation* Cyanosis (only if severe) Pneumonic consolidation* ↓ Pa CO2 ↓ Pa O2 Tachycardia ↑ CRP ↑ White cell count Sputum and blood culture  
  Metabolic acidosis Evidence of diabetes/renal disease* Overdose of aspirin or ethylene glycol* Fetor (ketones) Hyperventilation without physical signs in heart or lungs* Dehydration* Air hunger (Kussmaul's respiration) Normal Pa O2 normal* ⇓ Pa CO2 ⇓ pH (↑ H+)      
  Psychogenic (a diagnosis of exclusion) Previous episodes Not cyanosed* No heart signs* No lung signs* Carpopedal spasm Normal Pa O2 normal* ⇓ Pa CO2 pH normal or ↑ (H+ ↓)*   End-tidal P CO2 low at rest and during exercise
  CHEST PAIN  
Central Cardiac · Myocardial ischaemia (angina) · Myocardial infarction · Myocarditis · Pericarditis · Mitral valve prolapse syndrome Aortic · Aortic dissection · Aortic aneurysm Oesophageal · Oesophagitis · Oesophageal spasm · Mallory-Weiss syndrome · Massive pulmonary embolus Mediastinal · Tracheitis Malignancy Peripheral Lungs/pleura · Pulmonary infarct · Pneumonia · Pneumothorax · Malignancy · Tuberculosis · Connective tissue disorders Musculoskeletal · Osteoarthritis · Costochondritis (Tietze's · Rib fracture/injury syndrome) · Intercostal muscle injury · Epidemic myalgia (Bornholm disease) Neurological · Prolapsed intervertebral disc · Herpes zoster · Thoracic outlet syndrome  

 

  
 
HAEMOPTYSIS
Coughing up blood, irrespective of the amount, is an alarming symptom and nearly always brings the patient to the doctor.
CAUSES OF HAEMOPTYSIS  
Bronchial disease · Carcinoma · Bronchiectasis · Acute bronchitis · Bronchial adenoma · Foreign body Parenchymal disease · Tuberculosis · Suppurative pneumonia · Lung abscess · Parasites (e.g. hydatid disease, flukes) · Trauma · Actinomycosis · Mycetoma Lung vascular disease · Pulmonary infarction · Polyarteritis nodosa · Goodpasture's syndrome · Idiopathic pulmonary haemosiderosis  

 

  
 
THE SOLITARY RADIOGRAPHIC PULMONARY LESION  
The incidental finding of a solitary pulmonary nodule (SPN) on a plain chest X-ray in an adult patient is a common dilemma and the differential diagnosis is broad. Between 20% and 30% of all cancers present in this way; the incidence increases with age and accounts for over 50% of nodules in patients aged over 50.    
THE SOLITARY PULMONARY NODULE  
Common causes · Bronchial carcinoma · Single metastasis · Localised pneumonia · Lung abscess · Tuberculoma · Pulmonary infarct Uncommon causes · Benign tumours · Lymphoma · Arteriovenous malformation · Hydatid cyst · Bronchogenic cyst · Rheumatoid nodule · Pulmonary sequestration · Pulmonary haematoma · Wegener's granuloma · 'Pseudotumour'-fluid collection in a fissure · Aspergilloma (usually surrounded by air 'halo')
     

 

  
 
PLEURAL EFFUSION
The accumulation of serous fluid within the pleural space is termed pleural effusion. Accumulations of frank pus (empyema) or blood (haemothorax) represent separate conditions. In general, pleural fluid accumulates as a result of either increased hydrostatic pressure or decreased osmotic pressure ('transudative effusion' as seen in cardiac, liver or renal failure), or from increased microvascular pressure due to disease of the pleural surface itself, or injury in the adjacent lung ('exudative effusion').
PLEURAL EFFUSION: MAIN CAUSES AND FEATURES  
Cause Appearance of fluid Type of fluid Predominant cells in fluid Other diagnostic features
Tuberculosis Serous, usually amber-coloured Exudate Lymphocytes (occasionally polymorphs) Positive tuberculin test Isolation of M. tuberculosis from pleural fluid (20%) Positive pleural biopsy (80%)
Malignant disease Serous, often blood-stained Exudate Serosal cells and lymphocytes Often clumps of malignant cells Positive pleural biopsy (40%) Evidence of malignant disease elsewhere
Cardiac failure* Serous, straw-coloured Transudate Few serosal cells Other evidence of left ventricular failure Response to diuretics
Pulmonary infarction* Serous or blood-stained Exudate (rarely transudate) Red blood cells Eosinophils Evidence of pulmonary infarction Source of embolism Factors predisposing to venous thrombosis
Rheumatoid disease* Serous Turbid if chronic Exudate Lymphocytes (occasionally polymorphs) Rheumatoid arthritis; rheumatoid factor in serum Cholesterol in chronic effusion; very low glucose in pleural fluid
Systemic lupus erythematosus (SLE)* Serous Exudate Lymphocytes and serosal cells Other manifestations of SLE Antinuclear factor or anti-DNA in serum
Acute pancreatitis Serous or blood-stained Exudate No cells predominate High amylase in pleural fluid (greater than in serum)
Obstruction of thoracic duct   Milky Chyle None Chylomicrons
LIGHT'S CRITERIA FOR DISTINGUISHING PLEURAL TRANSUDATE FROM EXUDATE  
Pleural fluid is an exudate if one or more of the following criteria are met: · Pleural fluid protein:serum protein ratio > 0.5 · Pleural fluid lactic dehydrogenase: serum lactic dehydrogenase ratio > 0.6 · Pleural fluid LDH > two-thirds of the upper limit of normal serum LDH
             

 

  
 
RESPIRATORY FAILURE
The term respiratory failure is used when pulmonary gas exchange fails to maintain normal arterial oxygen and carbon dioxide levels. Its classification into type I and type II relates to the absence or presence of hypercapnia Prompt diagnosis and management of the underlying cause is crucial to the management of patients with respiratory failure. Occasionally, rapid reversal of the precipitating event-e.g. tracheostomy for laryngeal obstruction, fixation of ribs in a flail chest injury, reversal of narcotic poisons, nebulised bronchodilators in acute severe asthma or tube drainage of a tension pneumothorax-will restore good gas exchange. In acute left ventricular failure, in massive pulmonary embolism and when pulmonary infarction or pneumonia is the cause of pleural pain, treatment with opiates is entirely appropriate, but these drugs depress respiratory drive and should never be used in asthma or COPD, except immediately prior to and during assisted mechanical ventilation.  
RESPIRATORY FAILURE: UNDERLYING CAUSES AND BLOOD GAS ABNORMALITIES  
  Type I Type II
  Hypoxia (Pa O2 < 8.0 kPa (60 mmHg)) Normal or low Pa CO2 (<6.6kPa(50mmHg)) Hypoxia (Pa O2 < 8.0 kPa (60 mmHg)) Raised Pa CO2 (> 6.6 kPa (50 mmHg))
  Acute Chronic Acute Chronic
H+ → or ↑ → ↑ → or ↑
Bicarbonate → → → ↑
Causes Acute asthma Emphysema Acute severe asthma COPD
  Pulmonary oedema Lung fibrosis Acute exacerbation COPD Sleep apnoea
  Pneumonia Lymphangitis carcinomatosa Upper airway obstruction Kyphoscoliosis
  Lobar collapse Right-to-left shunts Acute neuropathies/paralysis Myopathies/muscular dystrophy
  Pneumothorax Brain-stem lesion Narcotic drugs Ankylosing spondylitis
  Pulmonary embolus   Primary alveolar hypoventilation  
  ARDS   Flail chest injury  
Common to all cases is the need to restore adequate arterial oxygen levels, for which oxygen therapy with or without mechanically assisted ventilation is important. The consequences of untreated severe hypoxaemia include systemic hypotension, pulmonary hypertension, polycythaemia, tachycardia, and cerebral dysfunction ranging from confusion to coma.  
           

 

  
                                     

SYNDROMES

1. Syndrome of the pulmonary tissue consolidation.

2. Syndrome of increased airiness of the pulmonary tissue.

3. Syndrome of bronchium obstruction (bronchospastic syndrome).

4. Syndrome of fluid accumulation in pleural cavity (hydrothorax).

5. Syndrome of air accumulation in pleural cavity (pneumothorax).

6. Syndrome of the cavity in the lung.

 

 
INVESTIGATION OF RESPIRATORY DISEASE
The 'plain' chest X-ray
Chest radiography is performed on the majority of patients suspected of having chest disease. A postero-anterior (PA) film provides information on the lung fields, heart, mediastinum, vascular structures and the thoracic cage. Additional information may be obtained from a lateral film, particularly if pathology is suspected behind the heart shadow or deep in the diaphragmatic sulci.
Increased shadowing may represent accumulation of fluid, lobar collapse or consolidation. Uncomplicated consolidation should not change the position of the mediastinum and the presence of an air bronchogram provides reassurance that proximal bronchi are patent. Collapse (implying obstruction of the proximal bronchus) is accompanied by loss of volume and displacement of the mediastinum towards the affected side.
The presence of ring shadows (diseased bronchi seen end-on), tramline shadows (diseased bronchi side-on) or tubular shadows (bronchi filled with secretions) suggests bronchiectasis. Nodular, reticular or honeycomb patterns are characteristic of diffuse parenchymal lung diseases. The presence of pleural fluid is suggested by a dense basal shadow which, in the erect patient, ascends towards the axilla. The assessment of a solitary pulmonary nodule is discussed below.  
COMMON CHEST X-RAY APPEARANCES
Increased lucency
· Consolidation: infection, infarction, inflammation, and rarely bronchoalveolar cell carcinoma · Lobar collapse: mucus plugging, tumour, compression by lymph nodes · Solitary nodule: see text · Multiple nodules: miliary TB, dust inhalation, metastatic malignancy, healed varicella pneumonia, rheumatoid disease · Ring shadows, tramlines and tubular shadows: bronchiectasis · Cavitating lesions: tumour, abscess, infarct, pneumonia (Staphylococcus/Klebsiella), Wegener's granulomatosis · Reticular, nodular and reticulonodular shadows: diffuse parenchymal lung disease, infection · Pleural abnormalities: fluid, plaques, tumour Increased translucency · Bullae · Pneumothorax · Oligaemia Hilar abnormalities · Unilateral hilar enlargement: TB, bronchial carcinoma, lymphoma · Bilateral hilar enlargement: sarcoid, lymphoma, TB, silicosis Other abnormalities · Hiatus hernia · Surgical emphysema  

 

  
Computed tomography (CT)
  CT scanning provides detailed images of the pulmonary parenchyma, mediastinum, pleura and bony structures. The contrast can be altered to highlight different structures such as the lung parenchyma, the mediastinal vascular structures or bone. Sophisticated software facilitates 3D reconstruction of the thorax and virtual bronchoscopy.
  CT scanning is superior to chest radiography in determining the position and size of a pulmonary lesion and whether calcification or cavitation is present. It is now routinely used in the assessment of patients with suspected lung cancer and facilitates guided percutaneous needle biopsy. Information on tumour stage may be gained by examining the mediastinum, liver and adrenal glands.
  High-resolution CT (HRCT) scanning uses thin sections to provide a detailed assessment of the pulmonary parenchyma and is particularly useful in assessing diffuse parenchymal lung disease, identifying bronchiectasis, and assessing the type and extent of emphysema.
  CT pulmonary angiography (CTPA) is increasingly used in the diagnosis of pulmonary thromboembolism, where it may either confirm the suspected embolism or highlight an alternative diagnosis.
  Ultrasound
  Ultrasound is sensitive at detecting pleural fluid and may also be used to direct and improve the diagnostic yield from pleural biopsy. Information may also be provided on the anatomy of an empyema cavity and facilitate directed drainage.
  Ventilation-perfusion imaging
  The main value of this technique is in the detection of pulmonary thromboemboli. Ventilation is assessed by inhalation of 133Xe and perfusion by the injection of macroaggregates of 99mTc-albumin. A 'filling defect' in the perfusion scan accompanied by preserved ventilation (V/Q mismatch) is highly suggestive of a recent pulmonary embolism. However, the applicability of this technique is limited in patients with underlying lung disease in whom as many as 70% of scans may be non-contributory. Ventilation-perfusion scanning is also useful in pre-operative assessment of the functional effects of lung cancer and bullae.
  Positron emission tomography (PET)
  PET scanners exploit the avid ability of malignant tissue to absorb and metabolise glucose. The radiotracer 18F-fluorodeoxyglucose (FDG) is administered and rapidly taken up by malignant tissue. It is then phosphorylated but cannot be metabolised further, becoming 'trapped' in the cell. PET scanning is useful in the investigation of pulmonary nodules, and in staging mediastinal lymph nodes and distal metastatic disease in patients with lung cancer. The negative predictive value is high; however, the positive predictive value is poor. Co-registration of PET and CT (PET-CT) enhances localisation and characterisation of the metabolic abnormalities.
  Pulmonary angiography
  Conventional pulmonary angiography is performed by passing contrast medium down a catheter inserted via the femoral vein into the main pulmonary artery. The technique represents the gold standard for the diagnosis of pulmonary embolism but is rarely used, particularly now that CTPA is widely available. It is essential in the investigation of patients with pulmonary hypertension, providing information on pulmonary and right heart pressures.  
  ENDOSCOPIC EXAMINATION
  Laryngoscopy
  The larynx may be inspected indirectly with a mirror or directly with a laryngoscope. Fibreoptic instruments allow a magnified view to be obtained.
  Bronchoscopy
  The trachea and larger bronchi may be inspected by either a flexible or a rigid bronchoscope. Flexible bronchoscopy may be performed under local anaesthesia with sedation as an outpatient. Structural changes, such as distortion or obstruction, can be seen. Abnormal tissue in the bronchial lumen or wall can be biopsied, and bronchial brushings, washings or aspirates can be taken for cytological or bacteriological examination. Small biopsy specimens of lung tissue taken by forceps passed through the bronchial wall (transbronchial biopsies) may reveal sarcoid granulomas or malignant diseases and may be helpful in diagnosing certain bronchocentric disorders (e.g. hypersensitivity pneumonitis, cryptogenic organising pneumonia), but are generally too small to be of diagnostic value in other diffuse parenchymal pulmonary disease. Transbronchial needle aspiration (TBNA) may sample mediastinal lymph nodes and assist with staging of lung cancer. Endobronchial ultrasound is currently undergoing assessment as a method of directing and enhancing the diagnostic yield of TBNA.
  Rigid bronchoscopy requires general anaesthesia but is more advantageous in certain situations e.g. evaluating massive haemoptysis or removing foreign bodies. In addition, endobronchial laser therapy and endobronchial stenting may be more easily performed with rigid bronchoscopy.
  Assessment of the mediastinum
  Lymph nodes down to the main carina can be sampled using a mediastinoscope passed through a small incision at the suprasternal notch under general anaesthetic. This procedure is particularly useful in lung cancer as a means of determining whether nodal disease is present. Lymph nodes in the lower mediastinum may be biopsied using an alternative and less invasive method, endoscopic ultrasound (EUS). In this technique an oesophageal endoscope equipped with an ultrasound transducer and biopsy needle is used to aspirate a sample for cytology.
  Pleural aspiration and biopsy
  Pleural aspiration and biopsy using an Abram's needle is a 'blind' procedure but often provides histological evidence of the cause of a pleural effusion. In difficult cases, video-assisted thoracoscopy may be used to obtain pleural or lung biopsies.
  SKIN TESTS
  The tuberculin test may be of value in the diagnosis of tuberculosis. Skin hypersensitivity tests are useful in the investigation of allergic diseases.
  IMMUNOLOGICAL AND SEROLOGICAL TESTS
  The presence of pneumococcal antigen (revealed by counterimmunoelectrophoresis) in sputum, blood or urine may be of diagnostic importance. Exfoliated cells colonised by influenza A virus can be detected by fluorescent antibody techniques. In blood, high or rising antibody titres to specific organisms (such as Legionella, Mycoplasma, Chlamydia or viruses) may eventually clinch a diagnosis suspected on clinical grounds. Precipitating antibodies may be found as a reaction to fungi such as Aspergillus or to antigens involved in hypersensitivity pneumonitis.
  MICROBIOLOGICAL INVESTIGATIONS
  Sputum, pleural fluid, throat swabs, blood and bronchial washings and aspirates can be examined for bacteria, fungi and viruses. In some cases, as when Mycobacterium tuberculosis is isolated, the information is diagnostically conclusive but in other circumstances the findings must be interpreted in conjunction with the results of clinical and radiological examination.
  HISTOPATHOLOGICAL AND CYTOLOGICAL EXAMINATION
  Histopathological examination of biopsy material (obtained from pleura, lymph node or lung) often allows a 'tissue diagnosis' to be made. This is of particular importance in suspected malignancy or in elucidating the pathological changes in interstitial lung disease). Important causative organisms, such as M. tuberculosis, Pneumocystis carinii (now jirovecii) or fungi, may be identified in bronchial washings, brushings or transbronchial biopsies.
  Cytological examination of exfoliated cells in sputum, pleural fluid or bronchial brushings and washings or of fine-needle aspirates from lymph nodes or pulmonary lesions can support a diagnosis of malignancy but if this is indeterminate a tissue biopsy is necessary to confirm the diagnosis. Cellular patterns in bronchial lavage fluid may help to distinguish pulmonary changes due to sarcoidosis from those caused by idiopathic pulmonary fibrosis or hypersensitivity pneumonitis.
  RESPIRATORY FUNCTION TESTING
ABBREVIATIONS USED IN RESPIRATORY FUNCTION TESTING  
       

 

Abbreviation Stands for  
FEV1 Forced expiratory volume in 1 second  
FVC Forced vital capacity  
VC Vital capacity (relaxed)  
PEF Peak (maximum) expiratory flow  
TLC Total lung capacity  
FRC Functional residual capacity  
RV Residual volume  
TLCO Gas transfer factor for carbon monoxide  
KCO Gas transfer per unit lung volume  
In diseases characterised by airway narrowing (e.g. asthma, bronchitis and emphysema) maximum expiratory flow is limited by dynamic compression of small intrathoracic airways, some of which close completely during expiration, limiting the volume which can be expired. Hyperinflation of the chest results, and can become extreme if elastic recoil is also lost due to parenchymal destruction, as in emphysema. In contrast, diseases which cause lung inflammation and/or scarring and fibrosis are characterised by progressive loss of lung volume with normal expiratory flow rates. Gas exchange is impaired by both parenchymal destruction (emphysema) and by interstitial disease, which disrupts the local matching of ventilation and perfusion.
  In respiratory function testing, airway narrowing, lung volume and gas exchange capacity are quantified and compared with normal values adjusted for age, gender, height and ethnic origin.
  Airway narrowing is assessed by forced expiration into a peak flow meter or a spirometer. Peak flow meters are cheap and convenient for home monitoring (e.g. detection and monitoring of asthma) but values are effort-dependent. The forced expiratory volume in 1 second (FEV1) and vital capacity (VC) are obtained from maximal forced and relaxed expirations into a spirometer. FEV1 is disproportionately reduced in airflow obstruction resulting in FEV1/VC ratios of less than 70%. When airflow obstruction is seen, spirometry should be repeated following inhaled short-acting β2-adrenoceptor agonists (e.g. salbutamol); reversibility to normal is suggestive of asthma. To distinguish large airway narrowing (e.g. tracheal stenosis or compression) from small airway narrowing, flow-volume loops are recorded during maximum expiratory and inspiratory efforts.
  Lung volume can be measured by dilution of an inhaled inert gas (usually helium) or by determining the pressure/volume relationship of the thorax by body plethysmography. The former method measures the volume of intrathoracic gas which mixes quickly with tidal breaths, while the latter measures total intrathoracic gas volume, including poorly ventilated areas such as bullae.  
       

 

PATTERNS OF RESPIRATORY FUNCTION ABNORMALITIES IN DISEASE

 

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