Respiratory system .pdf

RESPIRATORY SYSTEM QUES NO : 10 MARKS : 20 COLOUR CODE : YELLOW : ★★ GREEN : ★★★ RED : ★★★★★ SBA/MCQ Marked : EXAM NIGHT TOPIC  IJ Clifton DAB Ellames...

RESPIRATORY SYSTEM QUES NO : 10 MARKS : 20 COLOUR CODE : YELLOW : ★★ GREEN : ★★★ RED : ★★★★★ SBA/MCQ Marked : EXAM NIGHT TOPIC  IJ Clifton DAB Ellames 17 Respiratory medicine Clinical examination of the respiratory system 480 Tumours of the bronchus and lung 528 Functional anatomy and physiology 482 Primary tumours of the lung 528 Secondary tumours of the lung 532 Investigation of respiratory disease 484 Tumours of the mediastinum 532 Imaging 484 Endoscopic examination 486 Interstitial and inltrative pulmonary diseases 533 Microbiological investigations 487 Diffuse parenchymal lung disease 533 Immunological and serological tests 487 Lung diseases due to systemic inammatory disease 538 Cytology and histopathology 487 Pulmonary eosinophilia and vasculitides 539 Respiratory function testing 487 Lung diseases due to irradiation and drugs 540 Rare interstitial lung diseases 541 Presenting problems in respiratory disease 489 Cough 489 Occupational and environmental lung disease 541 Breathlessness 489 Occupational airway disease 541 Chest pain 492 Pneumoconiosis 542 Finger clubbing 492 Lung diseases due to organic dusts 544 Haemoptysis 492 Asbestos-related lung and pleural diseases 545 ‘Incidental’ pulmonary nodule 493 Occupational lung cancer 546 Pleural effusion 494 Pulmonary vascular disease 546 Respiratory failure 496 Pulmonary embolism 546 Obstructive pulmonary diseases 499 Pulmonary hypertension 549 Asthma 499 Diseases of the upper airway 550 Chronic obstructive pulmonary disease 505 Diseases of the nasopharynx 550 Bronchiectasis 509 Sleep-disordered breathing 550 Cystic brosis 510 Laryngeal disorders 552 Infections of the respiratory system 512 Tracheal disorders 553 Upper respiratory tract infection 512 Pleural disease 553 Pneumonia 512 Diseases of the diaphragm and chest wall 555 Tuberculosis 518 Disorders of the diaphragm 555 Respiratory diseases caused by fungi 525 Deformities of the chest wall 555 480  RESPIRATORY MEDICINE Clinical examination of the respiratory system 6 – 9 Thorax 6 Inspection (see opposite) Deformity (e.g. pectus excavatum) Scars 5 Face, mouth and eyes Intercostal indrawing Pursed lips Symmetry of expansion Central cyanosis Hyperinflation Anaemia ~ pancoast tumour of lung Paradoxical rib movement Horner syndrome (low flat diaphragm) (Ch. 28) 6 4 Jugular venous pulse 5 Elevated Idiopathic kyphoscoliosis Pulsatile 4 7 7 Palpation From the front: 3 Blood pressure Trachea central Arterial paradox 8 Cricosternal distance 3 Cardiac apex displaced Expansion 9 From behind: 2 Radial pulse Cervical lymphadenopathy Rate Expansion Rhythm 2 8 Percussion Resonant or dull ‘Stony dull’ (effusion) 1 Hands 1 9 Auscultation Digital clubbing Tar staining Breath sounds: Peripheral cyanosis normal, bronchial, louder or softer Signs of occupation Added sounds: CO2 retention flap wheezes, crackles, rubs Spoken voice (vocal resonance): absent (effusion), increased (consolidation) Whispered voice: 10 whispering pectoriloquy 10 Leg oedema Salt and water retention Cor pulmonale Observation Venous thrombosis Finger clubbing  Respiratory rate  Locale:  Cachexia, fever, rash Oxygen delivery  Sputum (see below) (mask, cannulae)  Fetor Nebulisers ★★★★★ Inhalers Sputum !"#%$& '$%( TB 1st cause Serous/frothy/pink Mucopurulent Purulent Blood-stained Cancer Pulmonary oedema Bronchial or pneumonic Bronchial or pneumonic Cancer, tuberculosis, Broncheictasis infection infection bronchiectasis, pulmonary embolism P. embolism Insets (idiopathic kyphoscoliosis) Courtesy of Dr I. Smith, Papworth Hospital, Cambridge; (serous, mucopurulent and purulent sputum) Courtesy of Dr J. Foweraker, Papworth Hospital, Cambridge. Rusty sputum -> preumococcal pneumonia  ⚫ ⚫ Clinical examination of the respiratory system  481 ★★★★★ Exam night topic Chronic obstructive pulmonary disease Pulmonary fibrosis Pursed lip breathing Central cyanosis Central cyanosis Prolonged expiration Tachypnoea Reduced cricosternal Small lungs Use of accessory distance Reduced muscles expansion Intercostal Auscultation indrawing Fine inspiratory Hyperinflated during crackles at ‘barrel’ chest inspiration bases of lungunaltered with cough Cardiac apex not Auscultation palpable Reduced breath Loss of cardiac sounds – wheeze dullness on percussion See also Fig. 17.55 Heart sounds Inward movement Dull percussion at bases loudest in of lower ribs (high diaphragm) epigastrium on inspiration Collapse and fibrosis SBA + MCQ (low flat diaphragm) Also: finger clubbing common in ) CXR '* Ribs '$+# Vesicular e prlonged idiopathic pulmonary fibrosis; raised JVP expiration : Also: raised jugular venous pressure (JVP), and peripheral oedema if cor pulmonale ,#%-.# peripheral oedema from salt and Asthma water retention and/or cor pulmonale Right middle lobe pneumonia Right upper lobe collapse COPD Inspection Inspection Tachypnoea Volume R upper zone Central cyanosis (if severe) Palpation Palpation Trachea deviated to R 17 Expansion on R Expansion R upper zone Percussion Percussion Dull R mid-zone and axilla Dull R upper zone Auscultation Auscultation Bronchial breath sounds Breath sounds with and vocal resonance over central obstruction consolidation and whispering pectoriloquy X-ray Obscures R heart border Pleural rub if pleurisy Deviated trachea (to R) on X-ray Elevated horizontal fissure Volume R hemithorax Central (hilar) mass may be seen Right pneumothorax Large right pleural effusion Inspection Inspection Pleural Tachypnoea (pain, deflation Tachypnoea reflex) Palpation effusion ) Palpation Expansion on R Expansion R side Trachea and apex may be CXR '* Percussion moved to L Resonant or hyper-resonant Percussion Ribs '$+# on R Stony dull Auscultation R mid- and lower zones ,#%- Absent breath sounds on R Auscultation Absent breath sounds and Tension pneumothorax also vocal resonance R base causes Bronchial breathing or Deviation of trachea to crackles above effusion opposite side Tachycardia and hypotension Cause of central cyanosis : Insets (upper lobe collapse) From http://3.bp.blogspot.com; (pneumothorax) http://chestatlas.com; (pleural effusion) www.ispub.com. ★ Pneumonia ★ Fibrosis Cause of peripheral cyanosis : Bronchial breath sound : ★ COPD REMEMBER CCF ★ Vasoconstriction ★ Asthma * Consolidation ★ Shock * Cavitations ★ P. embolism ★ Cold exposure * Fibrosis ★ HF ★ Congestive heart failure ★ Congenital heart disease ★ Raynaud's disease ★ CO poisoning ★ Peripheral vascular disease 482  RESPIRATORY MEDICINE Respiratory infections such as tuberculosis, pneumonia and virus infec- moisture occurs on expiration. Total airway cross-section is smallest in SBA tions (e.g. inuenza, COVID-19) represent a major burden of morbidity the glottis and trachea, making the central airway particularly vulnerable and mortality globally. The increasing prevalence of allergy, asthma and to obstruction. Normal breath sounds originate mainly from the rapid chronic obstructive pulmonary disease (COPD) contributes to the burden turbulent airow in the larynx, trachea and main bronchi. of chronic disease in the community. By 2025, the number of cigarette The multitude of small airways within the lung parenchyma has smokers worldwide is anticipated to increase to 1.5 billion, ensuring a a very large combined cross-sectional area (over 300 cm 2 in the growing burden of tobacco-related respiratory conditions. third-generation respiratory bronchioles), resulting in very slow ow Respiratory disease covers many pathologies, including infectious, rates. Airow is virtually silent here and gas transport occurs largely inammatory, neoplastic and degenerative processes. The practice of by diffusion in the nal generations. Major bronchial and pulmonary respiratory medicine thus requires collaboration with a range of disci- divisions are shown in Figure 17.1 plines. Recent advances have improved the lives of many patients with The acinus (Fig. 17.2) is the gas exchange unit of the lung and com- SBA obstructive lung disease, cystic brosis, obstructive sleep apnoea and prises branching respiratory bronchioles and clusters of alveoli. Here pulmonary hypertension, but the outlook remains poor for lung and other the air makes close contact with the blood in the pulmonary capillaries respiratory cancers and for some of the interstitial lung diseases. (gas-to-blood distance < 0.4 µm), and oxygen uptake and CO 2 excretion occur. The alveoli are lined with attened epithelial cells (type I pneumo- cytes) and a few, more cuboidal, type II pneumocytes. The latter produce TYPE 1: 95% Functional anatomy and physiology surfactant, which is a phospholipid mixture that reduces surface tension Type 2 : 5% and thereby counteracts the tendency of alveoli to collapse. Type II pneu- of surface area The lungs occupy the upper two-thirds of the bony thorax, bounded mocytes can divide to reconstitute type I pneumocytes after lung injury. medially by the spine, the heart and the mediastinum and inferiorly by the MCQ/SBA diaphragm. During breathing, free movement of the lung surface relative Lung mechanics to the chest wall is facilitated by sliding contact between the parietal and visceral pleura, which cover the inner surface of the chest wall and the Healthy alveolar walls contain a ne network of elastin and collagen bres lung respectively, and are normally closely apposed. Inspiration involves (see Fig. 17.2). The volume of the lungs at the end of a tidal (‘normal’) SBA downward contraction of the diaphragm (innervated by the phrenic breath out is called the functional residual capacity (FRC). At this volume, nerves originating from C3, 4 and 5) and upward, outward movement of the inward elastic recoil of the lungs (resulting from elastin bres and the ribs, caused by contraction of the external intercostal muscles (inner- surface tension in the alveolar lining uid) is balanced by the resistance vated by intercostal nerves originating from the thoracic spinal cord). of the chest wall to inward distortion from its resting shape, causing neg- Expiration is largely passive, driven by elastic recoil of the lungs. ative pressure in the pleural space. Elastin bres allow the lung to be The conducting airways from the nose to the alveoli connect the easily distended at physiological lung volumes, but collagen bres cause external environment with the alveolar surface. As air is inhaled through increasing stiffness as full ination is approached, so that, in health, the the upper airways it is ltered in the nose, heated to body temperature maximum inspiratory volume is limited by the lung (rather than the chest and fully saturated with water vapour; partial recovery of this heat and wall). The weight of lung tissue compresses the dependent regions and At rest , Lung volume is the Functional residual capacity Major bronchial subdivisions 3 2 Upper 3 lobe Upper lobe 2 1 1 1 4 Middle 1 1 lobe 2 4 4 5 Lower RIGHT lobe LEFT Lower lobe 3 2 3 Spine 2 Spine Upper Fig. 17.1 The major bronchial divisions and the ssures, lobe 2 lobes and segments of the lungs. The angle of the oblique 3 Anterior ssure means that the left upper lobe is largely anterior to the Upper 3 lower lobe. On the right, the transverse ssure separates the upper 2 lobe from the anteriorly placed middle lobe, which is matched by the 1 1 1 lingular segment on the left side. The site of a lobe determines Transverse fissure 1 whether physical signs are mainly anterior or posterior. Each 1 Middle lobe is composed of two or more bronchopulmonary segments lobe ure 4 2 that are supplied by the main branches of each lobar bronchus. 4 fiss 4 2 Bronchopulmonary segments: Right Upper lobe: (1) Anterior, Lower ue 3 (2) Posterior, (3) Apical. Middle lobe: (1) Lateral, (2) Medial. Lower 2 liq lobe lobe: (1) Apical, (2) Posterior basal, (3) Lateral basal, (4) Anterior Lower Ob 5 lobe basal, (5) Medial basal. Left Upper lobe: (1) Anterior, (2) Apical, 3 (3) Posterior, (4) Lingular. Lower lobe: (1) Apical, (2) Posterior basal, Lateral aspects of lungs (3) Lateral basal, (4) Anterior basal.  Functional anatomy and physiology  483 1-2 % of cardiac output A B Smooth Terminal C Pulmonary Bronchial Pulmonary muscle bronchiole artery artery vein Cartilage plates Bronchus Respiratory bronchiole Elastin fibres Bronchiole Interlobular Alveolar Terminal septum capillaries bronchiole Respiratory bronchiole Alveoli Pores of Kohn Alveoli Fig. 17.2 Functional anatomy of the lung. and elastin bres. The latter also run through the alveolar walls. Gas exchange occurs in the alveoli, which are connected to each other by the pores of Kohn. 17 SBA anatomy of an acinus. Both the pulmonary artery (carrying desaturated blood) and the bronchial artery (systemic supply to airway tissue) run along the bronchus. The venous drainage to the left atrium follows the interlobular septa. From www.Netter.com: Illustrations 155 (bronchus, acinus) and 191 (circulation), Elsevier. Hypoxia dilates systemic vessels but constricts Pulmonary arterioles. distends the uppermost parts, so a greater portion of an inhaled breath Ventilation/perfusion matching and the pulmonary SBA passes to the basal regions, which also receive the greatest blood ow circulation as a result of gravity. Elastin bres in alveolar walls maintain small airway SBA patency by radial traction on the airway walls. Even in health, however, The regional distribution of ventilation and perfusion must be matched for these small airways narrow during expiration because they are sur- optimal gas exchange within the lungs. At segmental and subsegmen- rounded by alveoli at higher pressure, but are prevented from collapsing tal level, hypoxia constricts pulmonary arterioles and airway CO 2 dilates by radial elastic traction. The volume that can be exhaled is thus limited bronchi, helping to maintain good regional matching of ventilation and purely by the capacity of the expiratory muscles to distort the chest wall perfusion. Lung disease may create regions of relative under-ventilation inwards. In emphysema, loss of alveolar walls leaves the small airways or under-perfusion, which disturb this regional matching, causing res- SBA unsupported, and their collapse on expiration causes air trapping and piratory failure. In addition to causing ventilation–perfusion mismatch, limits expiration at a high end-expiratory volume. diseases that destroy capillaries or thicken the alveolar capillary mem- brane (e.g. emphysema or brosis) can impair gas diffusion directly. The pulmonary circulation in health operates at low pressure (approx- Control of breathing MCQ/SBA imately 24/9 mmHg) and can accommodate large increases in ow with The respiratory motor neurons in the posterior medulla oblongata are minimal rise in pressure, e.g. during exercise. Pulmonary hypertension the origin of the respiratory cycle. Their activity is modulated by multiple occurs when vessels are destroyed by emphysema, obstructed by external inputs in health and in disease (see Fig. 17.9): thrombus, involved in interstitial inammation or thickened by pulmonary vascular disease. The right ventricle responds by hypertrophy, with right  Central chemoreceptors in the ventrolateral medulla sense the pH of axis deviation and P pulmonale (tall, peaked p waves) on the electrocar- the cerebrospinal uid (CSF) and are indirectly stimulated by a rise in diogram (ECG), and clinical features of right heart failure; the term ‘cor arterial PCO2 pulmonale’ is often used for these ndings.  The carotid bodies sense hypoxaemia but are mainly activated by Changes in respiratory function associated with old age are shown in arterial PO2 values below 8 kPa (60 mmHg). They are also sensitised Box 17.1 to hypoxia by raised arterial PCO2  Muscle spindles in the respiratory muscles sense changes in Lung defences Reading mechanical load.  Vagal sensory bres in the lung may be stimulated by stretch, Upper airway defences inhaled toxins or disease processes in the interstitium. Large airborne particles are trapped by nasal hairs, and smaller par-  Cortical (volitional) and limbic (emotional) inuences can override the ticles settling on the mucosa are cleared towards the oropharynx by automatic control of breathing. the columnar ciliated epithelium that covers the turbinates and septum  484  RESPIRATORY MEDICINE 17.1 Respiratory function in old age M  Reserve capacity: a signicant reduction in function can occur with ageing with only minimal effect on normal breathing, but the ability to combat acute disease is reduced.  Decline in FEV1: the FEV1/FVC (forced expiratory volume/forced vital capacity) ratio falls by around 0.2% per year from 70% at the age of 40–45 years, due to a decline in elastic recoil in the small airways with age. Smoking accelerates this decline threefold on average. Symptoms usually occur only when FEV 1 drops below 50% of predicted. C  Increasing ventilation perfusion mismatch: the reduction in elastic recoil causes a tendency for the small airways to collapse during expiration, particularly in dependent areas of the lungs, thus reducing ventilation.  Reduced ventilatory responses to hypoxia and hypercapnia: older people may be less tachypnoeic for any given fall in PaO2 or rise in PaCO2  Impaired defences against infection: due to reduced numbers of glandular epithelial cells, which lead to a reduction in protective mucus. Fig. 17.3 The mucociliary escalator. Scanning electron micrograph of the respiratory  Decline in maximum oxygen uptake: due to a combination of impairments epithelium showing large numbers of cilia (C) overlaid by the mucus ‘raft’ (M). in muscle, and the respiratory and cardiovascular systems. This leads to a reduction in cardiorespiratory reserve and exercise capacity.  Loss of chest wall compliance: due to reduced intervertebral disc spaces and ossication of the costal cartilages; respiratory muscle strength and endurance Investigation of respiratory disease also decline. These changes become important only in the presence of other respiratory disease. A detailed history, thorough examination and basic haematological and biochemical tests usually indicate the likely diagnosis and differential. A number of other investigations are normally required to conrm the diag- (Fig. 17.3). During cough, expiratory muscle effort against a closed nosis and/or monitor disease activity. glottis results in high intrathoracic pressure, which is then released explosively. The exible posterior tracheal wall is pushed inwards by Imaging the high surrounding pressure, which reduces tracheal cross-section and thus maximises the airspeed to achieve effective expectoration. The ‘plain’ chest X-ray The larynx also acts as a sphincter, closing to protect the airway during swallowing and vomiting. The chest X-ray (CXR) is one of the initial investigations performed on the majority of patients suspected of having respiratory disease. A pos- Lower airway defences teroanterior (PA) lm provides information on the lung elds, heart, medi- The structure and function of the lower airways are maintained by close astinum, vascular structures and thoracic cage (Fig. 17.4). A lateral lm cooperation between the innate and adaptive immune responses. may provide additional information, particularly if pathology is suspected Traditionally, the healthy lower respiratory tract was considered to be behind the heart or deep in the diaphragmatic sulci. An approach to sterile. However, molecular analysis has established that it harbours a interpreting the chest X-ray is given in Box 17.2; common abnormalities diverse resident microbial population (the lung microbiome); understand- are listed in Box 17.3 ing of the interactions between the immune system and the lung micro- Increased shadowing may represent accumulation of uid, lobar biome, and its role in health and disease, is in its infancy. collapse or consolidation. Uncomplicated consolidation should not The innate response in the lungs is characterised by a number of change the position of the mediastinum and the presence of an air non-specic defence mechanisms. Inhaled particulate matter is trapped bronchogram means that proximal bronchi are patent. Collapse (imply- in airway mucus and cleared by the mucociliary escalator. Tobacco ing obstruction of the lobar bronchus) is accompanied by loss of vol- smoke increases mucus secretion but reduces mucociliary clearance ume and displacement of the mediastinum towards the affected side and predisposes towards lower respiratory tract infections, including (Fig. 17.5). pneumonia. Defective mucociliary transport is also a feature of several The presence of ring shadows (thickened bronchi seen end-on), tram- MCQ rare diseases including cystic brosis, primary ciliary dyskinesia and line shadows (thickened bronchi side-on) or tubular shadows (bronchi Young syndrome, which are characterised by repeated sino-pulmonary lled with secretions) suggests bronchiectasis. The presence of pleural infections and bronchiectasis. uid is suggested by a dense basal shadow, which, in the erect patient, Airway secretions contain an array of antimicrobial peptides (AMPs, ascends towards the axilla. In a large pulmonary embolism, relative olig- such as defensins and lysozyme), immunoglobulin A (IgA), antiprotein- aemia may cause a lung eld to appear abnormally dark. ases and antioxidants. Many assist with the opsonisation and killing of bacteria and the regulation of the proteolytic enzymes secreted Computed tomography by inammatory cells. In particular, α1-antitrypsin regulates neutrophil elastase, and deciency of this may be associated with premature Computed tomography (CT) provides detailed images of the pulmonary SBA emphysema. parenchyma, mediastinum, pleura and bony structures. The displayed Macrophages engulf microbes, organic dusts and other particulate range of densities can be adjusted to highlight different structures matter. They cannot digest inorganic agents such as asbestos or silica, such as the lung parenchyma, the mediastinal vascular structures or which cause their death and lead to the release of powerful proteolytic bone. Cross-sectional formatting allows recognition of the axial distri- enzymes that damage the lung. Neutrophil numbers in the airway are low bution of the disease, while coronal reformation displays the cranio- but the pulmonary circulation contains a marginated pool that may be caudal distribution. In cases of suspected lung cancer, CT is central recruited rapidly in response to bacterial infection. to both diagnosis and staging, and facilitates percutaneous needle Adaptive immunity is characterised by a specic response and immu- biopsy. CT identies the extent and appearance of pleural thickening nological memory. Lung dendritic cells facilitate antigen presentation to (see Fig. 17.64) and reliably differentiates pleural and pericardial fat SBA T and B lymphocytes. from pathology. High-resolution thin-section scanning provides detailed  Investigation of respiratory disease  485 images of the pulmonary parenchyma and is superior to chest X-ray for assessment of diffuse parenchymal lung disease (see Fig. 17.55), identi- 17.2 How to interpret a chest X-ray fying airway thickening, bronchiectasis (see Fig. 17.29) and emphysema (see Fig. 17.27). The relative contribution of competing pathologies to Name, date, orientation Films are posteroanterior (PA) unless marked a breathless patient may be assessed. Prone imaging may be used to AP to denote that they are anteroposterior differentiate the gravity-induced posterobasal attenuation seen in supine Lung elds Equal translucency? scans. CT pulmonary angiography (CTPA) has become the investiga- Check horizontal ssure from right hilum to SBA tion of choice in the diagnosis of pulmonary thromboembolism (see sixth rib at the anterior axillary line Fig. 17.67), when it may either conrm the suspected embolism or high- Masses? Consolidation? Cavitation? light an alternative diagnosis. CTPA has largely replaced the radioiso- Lung apices Check behind the clavicles. Masses? tope-based ventilation–perfusion (V /Q˙ ) scan for this purpose. CT may Consolidation? Cavitation? assist in identifying cavitation and other features of infection (e.g. air Trachea Central (midway between the clavicular creascent and halo signs in aspergillosis). Finally, CT may be used to heads)? monitor disease progression in established disease and for screening in Paratracheal mass? Goitre? certain high-risk populations. Heart Normal shape? Cardiothoracic ratio (should be < half the Positron emission tomography intrathoracic diameter) Retrocardiac mass? Positron emission tomography (PET) scanners employ the radiotracer Hila Left should be higher than right 18 F-uorodeoxyglucose (FDG) to quantify the rate of glucose metabolism Shape (should be concave laterally; if convex, by cells. The 18FDG is rapidly taken up by metabolically active tissue, consider mass or lymphadenopathy)? where it is phosphorylated and ‘trapped’ in the cell. The assessment of Density? 18 FDG uptake may be qualitative (visual analysis) or semi-quantitative, Diaphragm Right should be higher than left using the standardised uptake value (SUV) (Fig. 17.6). FDG-PET is useful Hyperination (no more than 10 ribs should be in the staging of mediastinal lymph nodes and distal metastatic disease visible posteriorly above the diaphragm)? in patients with lung cancer and in the investigation of pulmonary nod- ules. Co-registration of PET and CT (PET-CT) enhances localisation and Costophrenic angles Acute and well dened (pleural uid or thickening, if not)? characterisation of metabolically active deposits (see Fig. 17.6). FDG- PET may also differentiate benign from malignant pleural disease and Soft tissues Breast shadows in females can be used to assess the extent of extrapulmonary disease in sarcoido- Chest wall for masses or subcutaneous sis. However, 18FDG uptake by a lesion is affected by a large number emphysema of parameters, including equipment used, the physics, and biological Bones Ribs, vertebrae, scapulae and clavicles 17 factors such as amount of body fat and brown fat uptake and the blood Any fracture visible at bone margins or glucose level. lucencies? ★ Metabolic activity of tumor cell is seen by PET scan Clavicular heads symmetrical Lung apex Trachea either side of spine – no rotation Indication of PET scan : *Staging of metastatic disease & mediastinal Medial border lymph node of scapula *Inv. of pulmonary nodule Aortic arch *Differentiate benign from Right hilum Left hilum mallignat pleural disease *Assess the extent of extra pulmonary disease in Right atrial Left ventricular border border sarcoidosis *PET -CT enhance Cardiac apex localisation & Right characterization of costophrenic metabolically active angle deposit Right hemidiaphragm Left hemidiaphragm (normally lower than right) Right cardiophrenic angle Gastric air bubble Fig. 17.4 The normal chest X-ray. The lung markings consist of branching and tapering lines radiating out from the hila. Where airways and vessels turn towards the lm, they can appear as open or lled circles (see upper pole of right hilum). The scapulae may overlie the lung elds; trace the edge of bony structures to avoid mistaking them for pleural or pulmonary shadows. To check for hyperination, count the ribs; if more than 10 are visible posteriorly above the diaphragm, the lungs are hyperinated. From Innes JA. Davidson’s Essentials of medicine. Edinburgh: Churchill Livingstone, Elsevier Ltd; 2009.  486  RESPIRATORY MEDICINE Left 17.3 Common chest X-ray abnormalities ★★★★★ upper lobe Pulmonary and pleural shadowing  Consolidation: infection, infarction, inammation and, rarely, bronchoalveolar cell carcinoma  Lobar collapse: mucus plugging, tumour, compression by lymph nodes  Solitary nodule  Multiple nodules: miliary tuberculosis (TB), dust inhalation, metastatic malignancy, healed varicella pneumonia, rheumatoid disease  Ring shadows, tramlines and tubular shadows: bronchiectasis MCQ/SBA  Cavitating lesions: tumour, abscess, infarct, pneumonia (Staphylococcus/ Lingula Klebsiella), granulomatosis with polyangiitis (GPA)  Reticular, nodular and reticulonodular shadows: diffuse parenchymal lung disease, infection  Pleural abnormalities: uid, plaques, tumour Increased translucency  Bullae Remember : BOP  Pneumothorax  Oligaemia Hilar abnormalities  Unilateral hilar enlargement: TB, lung cancer, lymphoma Left lower  Bilateral hilar enlargement: sarcoidosis, lymphoma, TB, silicosis Most common is lobe Other abnormalities Sarcoidosis & TB  Hiatus hernia  Surgical emphysema Magnetic resonance imaging Right Conventional magnetic resonance imaging (MRI) of the lung parenchyma upper is seldom useful, although the technique is being used increasingly in lobe distinguishing benign from malignant pleural disease and in delineating SBA invasion of the chest wall or diaphragm by tumour. SBA The use of hyperpolarized 3He MRI is a developing method of assess- ing the distribution of ventilation within the lung. Ultrasound Transthoracic ultrasound is a point-of-care investigation used to Right SBA assess the pleural space (see Fig. 17.15). In the hands of an experi- middle enced operator it can distinguish pleural uid from pleural thickening, lobe identify a pneumothorax and, by directly visualising the diaphragm and solid organs such as the liver, spleen and kidneys, may be used to guide pleural aspiration, biopsy and intercostal chest drain insertion. It is also used to guide needle biopsy of supercial lymph node or chest wall masses and provides useful information on the shape and move- ment of the diaphragm. Endoscopic examination Right lower lobe Laryngoscopy The larynx may be inspected directly with a breoptic laryngoscope in SBA cases of suspected intermittent laryngeal obstruction (ILO), when par- adoxical movement of the vocal cords may mimic asthma. Left-sided lung tumours may involve the left recurrent laryngeal nerve, paralysing SBA the left vocal cord and leading to a hoarse voice and a ‘bovine’ cough. Continuous laryngoscopy during exercise tests allows the identication Fig. 17.5 Radiological features of lobar collapse caused by bronchial of exercise-induced ILO. obstruction. The dotted line in the drawings represents the normal position of the diaphragm. The dark pink area represents the extent of shadowing seen on the X-ray. Bronchoscopy in the bronchial lumen or wall can be biopsied, and bronchial brushings, The trachea and the rst 3–4 generations of bronchi may be inspected washings or aspirates can be taken for cytological or bacteriological using a exible breoptic bronchoscope. This is usually performed under examination. Small biopsy specimens of lung tissue, taken by forceps - local anaesthesia with sedation, on an outpatient basis. Abnormal tissue passed through the bronchial wall (transbronchial biopsies), may be Gold standard for Sarcoidosis & Diffuse Mallignancy  Investigation of respiratory disease  487 A B C Fig. 17.6 Computed tomography and positron emission tomography combined to reveal intrathoracic metastases. (CT = computed tomography; FDG = 18F-uorodeoxyglucose; PET = positron emission tomography) (A–C) From http://radiology.rsnajnls.org helpful in the diagnosis of bronchocentric disorders such as sarcoidosis the serum. IgG enzyme immunoassay or identication of serum precip- and diffuse malignancy but are generally too small to be of diagnostic itins (antibodies that form visible lines of precipitated glycoprotein when value in other diffuse parenchymal pulmonary disease. they encounter their specic antigen in an agarose gel) can be used to Rigid bronchoscopy requires general anaesthesia and is reserved for spe- identify a reaction to fungi such as Aspergillus or to antigens involved in MCQ cic situations, such as massive haemoptysis or removal of a foreign body hypersensitivity pneumonitis, such as farmer’s lung or bird fancier’s lung. (see Fig. 9.2), and can facilitate endobronchial laser therapy and stenting. The presence of pneumococcal antigen in sputum, blood or urine may be of diagnostic importance in pneumonia. Respiratory viruses can be detected in nose/throat swabs by immunouorescence and Legionella SBA Endobronchial ultrasound infection may diagnosed by detection of a Legionella antigen in urine. Endobronchial ultrasound (EBUS) allows directed needle aspiration ß-1,3-D-glucan detection (in blood) is a marker of fungal infection (see SBA from peribronchial nodes and is used increasingly to stage lung cancer. Chapter 13) and Aspergillus galactomannan (in blood and bronchial lav- It may also be useful in non-malignant conditions, such as mediastinal age uid) is used to diagnose invasive aspergillosis. Interferon-gamma MCQ lymphadenopathy caused by tuberculosis or sarcoidosis. Lymph nodes release assays are useful in the detection of latent tuberculosis. SBA 17 down to the main carina can also be sampled using a mediastinoscope passed through a small incision at the suprasternal notch under general Cytology and histopathology anaesthetic. Lymph nodes in the lower mediastinum may be biopsied via the oesophagus using an oesophageal endoscope equipped with an Cytological examination of exfoliated cells in pleural uid or bronchial ultrasound transducer and biopsy needle (endoscopic ultrasound). brushings and washings, or of ne needle aspirates from lymph nodes or pulmonary lesions, can support a diagnosis of malignancy. A larger tissue biopsy is often necessary, however, as this allows immunohis- Thoracoscopy tochemistry and genetic testing to characterise the tumor and guide Thoracoscopy, which involves the insertion of an endoscope through the variant-specic therapy. Histopathology may also allow identication chest wall, facilitates biopsy under direct vision and is the gold standard of microorganisms using conventional staining or NAATs. Differential for the evaluation of the pleural surfaces, characterisation of complex cell counts in bronchial lavage uid may help to distinguish pulmonary SBA pleural effusion, and identication of exudate and haemorrhage. It is also changes due to sarcoidosis, idiopathic pulmonary brosis or hypersen- used for accurate staging of apical tumours. sitivity pneumonitis. Microbiological investigations Respiratory function testing Sputum, pleural uid, throat swabs, blood, and bronchial washings and Respiratory function tests are used to aid diagnosis, quantify functional aspirates can be examined for bacteria, fungi and viruses. The use of impairment and monitor treatment or progression of disease. Airway hypertonic saline to induce expectoration of sputum may obviate the narrowing, lung volume and gas exchange capacity are quantied and need for more invasive procedures such as bronchoscopy. Molecular compared with normal values adjusted for age, gender, height and ethnic tests (nucleic acid amplication tests, NAATs) are being used increasingly origin. In diseases characterised by airway narrowing (e.g. asthma, bron- SBA as rst-line diagnostic tests for respiratory viruses (including inuenza chitis and emphysema), maximum expiratory ow is limited by dynamic and coronaviruses such as SARS-CoV-2), as well as bacterial patho- compression of small intrathoracic airways, some of which may close gens (e.g. Legionella, Mycoplasma), for which they have largely replaced completely during expiration, limiting the volume that can be expired paired serology and antigen-based tests. NAATs are also gaining an (‘obstructive’ defect). This causes hyperination of the chest, which can SBA increased role as rst-line diagnostic tests for tuberculosis and for rapid become extreme if elastic recoil is also lost due to parenchymal destruc- identication of antimicrobial drug resistance. tion, as in emphysema. In contrast, diseases that cause interstitial inam- mation and/or brosis lead to progressive loss of lung volume (‘restrictive’ Immunological and serological tests defect) with normal expiratory ow rates. Typical laboratory traces are illustrated in Figure 17.7 SBA The presence of atopy can be detected by demonstrating an elevated level of immunoglobulin E (IgE), and the measurement of IgE directed Reading Measurement of airway obstruction against specic antigens. This can be useful to support the diagnosis of asthma and in identifying triggers. Many autoimmune diseases pres- Airway narrowing is assessed by asking patients to breathe in fully, ent with pulmonary involvement and autoantibodies may be identied in then blow out as hard and fast as they can into a peak ow meter or  488  RESPIRATORY MEDICINE a spirometer. Peak ow meters are useful for home monitoring of peak Transfer factor '/#. condition ) -#%0 '/#1#2 /%"? expiratory ow (PEF) in the detection and monitoring of asthma but results are effort-dependent. More accurate and reproducible meas- To measure the capacity of the lungs to exchange gas, patients inhale ures are obtained by maximum forced expiration into a spirometer. The a test mixture of 0.3% carbon monoxide, which is taken up avidly by forced expired volume in 1 second (FEV 1) is the volume exhaled in the rst haemoglobin in pulmonary capillaries. After a short breath-hold, the rate second, and the forced vital capacity (FVC) is the total volume exhaled. of disappearance of CO into the circulation is calculated from a sample Airow obstruction is dened as a FEV 1/FVC ratio of less than 70%. In of expirate, and expressed as the TL CO or carbon monoxide transfer fac- this situation, spirometry should be repeated following inhaled short- tor. Helium is also included in the test breath to allow calculation of the acting β2-adrenoceptor agonists (e.g. salbutamol); an increase of > 12% volume of lung examined by the test breath. Transfer factor expressed and > 200 mL in FEV1 or FVC indicates signicant reversibility. A large per unit lung volume is termed K CO. Common respiratory function abnor- improvement in FEV1 (> 400 mL) and variability in peak ow over time are malities are summarised in Box 17.4 features of asthma. Large airway narrowing (e.g. tracheal stenosis or compression; see Arterial blood gases and oximetry Fig.20.12) can be distinguished from small airway narrowing through plot- ting spirometry data as ow/volume loops. These display ow in relation to The measurement of hydrogen ion concentration, PaO2 and PaCO2, and lung volume (rather than time) during maximum expiration and inspiration, derived bicarbonate concentration in an arterial blood sample is essential and the pattern of ow reveals the site of airow obstruction (Fig. 17.7B). for assessing the degree and type of respiratory failure and for measuring acid–base status. This is discussed in detail on pages 496 and 630 (see Box 17.16). Interpretation of results is facilitated by blood gas diagrams Lung volumes (Fig. 17.8), which indicate whether any acidosis or alkalosis is due to acute Spirometry can measure only the volume of gas that can be exhaled; or chronic respiratory derangements of PaCO2 or to metabolic causes. it cannot measure the gas remaining in the lungs after a maximal expi- Pulse oximeters provide a continuous estimation of arterial oxygen sat- SBA ration. All the gas in the lungs can be measured by rebreathing an inert uration (SaO2, or SpO2 if measured by pulse oximetry) (see p.177), thus non-absorbed gas (usually helium) and recording how much the test allowing a real-time assessment of a patient’s response to oxygen therapy. gas is diluted by lung gas at equilibrium. This measures the volume of intrathoracic gas that mixes freely with tidal breaths. Alternatively, lung SBA Exercise tests volume may be measured by body plethysmography (see Chapter 9), which determines the pressure/volume relationship of the thorax. This Resting measurements may be unhelpful in early disease or in patients method measures total intrathoracic gas volume, including poorly venti- complaining only of exercise-induced symptoms. Spirometry testing lated areas such as bullae. The terms used to describe lung volume are before and after exercise can help to reveal exercise-induced asthma. shown in Figure 17.7C Walk tests include the self-paced 6-minute walk and the externally A Volume B Expiration Flow FVC FEV1 Volume 1 sec Time Inspiration C Volume Normal COPD Fibrosis Tracheal obstruction 4 5 1 Total lung capacity 2 Functional residual capacity 3 Residual volume 4 Inspiratory capacity 1 2 3 5 Vital capacity Time Fig. 17.7 Respiratory function tests in health and disease. brosis. COPD causes slow, prolonged and limited exhalation. In brosis, forced expiration results in rapid expulsion of a reduced forced vital capacity (FVC). Forced expiratory volume (FEV1 volume measurement. Volume/time graphs during quiet breathing with a single maximal breath in and out. COPD causes hyperination with increased residual volume. Fibrosis causes a proportional reduction in all lung volumes.  Obstructive : FEV1 '-3( /%" ,Ratio /%" ,TLC ,RV -#%0 Presenting problems in respiratory disease  489 Restrictive : FVC '-3( /%" , Ratio -#%0 -# normal 1#%/ , TLC, RV /%" smoke or perfumes. Distinguishing characteristics of various causes of Exam 17.4 How to interpret respiratory function abnormalities cough are detailed in Box 17.5 The explosive quality of a normal cough is lost in patients with respira- night Asthma Chronic Emphysema Pulmonary tory muscle paralysis or vocal cord palsy. Paralysis of a single vocal cord topic bronchitis brosis gives rise to a prolonged, low-pitched, inefcient ‘bovine’ cough accom- FEV1 ↓↓ ↓↓ ↓↓ ↓ panied by hoarseness. Coexistence of an inspiratory noise (stridor) FVC ↓ ↓ ↓ ↓↓ indicates partial obstruction of a major airway (e.g. laryngeal oedema, FEV1/FVC ↓ ↓ ↓ →/↑ tracheal tumour, scarring, compression or inhaled foreign body) and requires urgent investigation and treatment. Sputum production is com- TLCO → → ↓↓ ↓↓ mon in patients with acute or chronic cough, and its nature and appear- KCO →/↑ → ↓ →/↓ ance can provide clues to the aetiology. TLC →/↑ ↑ ↑↑ ↓ Aetiology RV →/↑ ↑ ↑↑ ↓ Acute transient cough is most commonly caused by viral tracheo- (RV = residual volume; TLC = total lung capacity; see text for other abbreviations) bronchial infection, post-nasal drip resulting from rhinitis or sinusitis, aspiration of a foreign body, or throat-clearing secondary to laryngitis or pharyngitis. When cough occurs in the context of more serious diseases, such as pneumonia, aspiration, congestive heart failure or pulmonary 7.0 100 embolism, it is usually easy to diagnose from other clinical features. 5 10 15 20 25 90 Patients with chronic cough present more of a challenge and should [HCO3– ] mmol/L be assessed with history, physical examination, chest X-ray and lung 7.1 80 30 sis function studies. o 70 acid Adults with chronic cough and a history of tobacco exposure should ry 7.2 ato be considered for CT scanning if they have either an abnormal chest 60 pir 40 M cid res X-ray or a normal X-ray and other symptoms that might suggest lung eta os a 50 ute cidosis bo is 7.3 Ac a cancer. iratory lic ic resp 7.4 40 Chron In the context of normal respiratory examination and investigations, Met extra-thoracic causes of cough need to be considered such as post- 7.5 is 30 alos alkaabolic nasal drip secondary to nasal or sinus disease, gastro-oesophageal pH alk losi 7.6. s reux disease or cough hypersensitivity. Use of angiotensin-converting 20 sp Re [H+] nmol/L enzyme (ACE) inhibitors can result in a chronic dry cough, taking up to 10 6 months to resolve following cessation. Bordetella pertussis infection in 17 0 adults can result in cough lasting up to 3 months. 0 2 4 6 kPa8 12 10 The prescence of ne inspiratory crackles and a dry cough should prompt investigation for the possibility of an interstitial lung disease. SBA clue 0 15 mmHg 30 45 60 75 90 Arterial PaCO2 Breathlessness Reference range Breathlessness or dyspnoea is dened as the feeling of an uncom- 95% Confidence limits fortable need to breathe. It is unusual among sensations, as it has no dened receptors, no localised representation in the brain, and multiple Fig. 17.8 Changes in blood [H+], PaCO2 and plasma [HCO3−] in acid–base causes both in health (e.g. exercise) and in diseases of the lungs, heart disorders. The rectangle indicates normal limits for [H +] and PaCO2. The bands or muscles. represent 95% condence limits of single disturbances in human blood. To determine the likely cause of an acid–base disorder, plot the values of [H +] and PaCO2 from Pathophysiology an arterial blood gas measurement.. The diagram indicates whether any acidosis or alkalosis results primarily from a respiratory disorder of PaCO2 or from a metabolic Stimuli to breathing resulting from disease processes are shown in Figure derangement. From Flenley D. Lancet 1971; 1:1921, with permission from Elsevier. 17.9. Respiratory diseases can stimulate breathing and dyspnoea by:  stimulating intrapulmonary sensory nerves (e.g. pneumothorax, paced incremental ‘shuttle’ test, where patients walk at increasing interstitial inammation and pulmonary embolus) pace between two cones 10 m apart. These provide simple, repeatable  increasing the mechanical load on the respiratory muscles (e.g. assessments of disability and response to treatment. Cardiopulmonary airow obstruction or pulmonary brosis) bicycle exercise testing, with measurement of metabolic gas exchange,  causing hypoxia, hypercapnia or acidosis, which stimulate ventilation and ECG changes, is useful for quantifying exercise limitation chemoreceptors. and detecting occult cardiovascular or respiratory limitation in a breath- less patient. In cardiac failure, pulmonary congestion reduces lung compliance and can also obstruct the small airways. Reduced cardiac output also limits oxygen supply to the skeletal muscles during exercise, causing Presenting problems in respiratory disease early lactic acidaemia and further stimulating breathing via the central chemoreceptors. Cough Breathlessness and the effects of treatment can be quantied using a symptom scale. Patients tend to report breathlessness in propor- SBA Cough is the most frequent symptom of respiratory disease and is tion to the sum of the above stimuli to breathing. Individual patients caused by stimulation of sensory nerves in the mucosa of the pharynx, differ greatly in the intensity of breathlessness reported for a given set larynx, trachea and bronchi. Acute sensitisation of the normal cough of circumstances, but breathlessness scores during exercise within reex occurs in a number of conditions and it is typically induced by individuals are reproducible and can be used to monitor the effects changes in air temperature or exposure to irritants, such as cigarette of therapy. 490  RESPIRATORY MEDICINE 17.5 Cough SBA Clue Origin Common causes Clinical features Pharynx Post-nasal drip History of chronic rhinitis Larynx Laryngitis, tumour, whooping cough, croup Voice or swallowing altered, harsh or painful cough Paroxysms of cough, often associated with stridor Trachea Tracheitis Raw retrosternal pain with cough Bronchi Bronchitis (acute) and chronic obstructive pulmonary Dry or productive, worse in mornings disease (COPD) Asthma Usually dry, worse at night Eosinophilic bronchitis Features similar to asthma but airway hyper-reactivity absent Lung cancer Persistent (often with haemoptysis) Lung parenchyma Tuberculosis Productive (often with haemoptysis) Pneumonia Dry initially, productive later Atypical pneumonias including COVID-19 often present with a dry cough Bronchiectasis Productive, changes in posture induce sputum production Pulmonary oedema Often at night (may be productive of pink, frothy sputum) Interstitial brosis Dry and distressing Drug side-effect Angiotensin-converting enzyme (ACE) inhibitors Dry cough Aspiration Gastro-oesophageal reux disease (GORD) History of acid reux, heartburn, hiatus hernia Obesity Adapted from Munro JF, Campbell IW. Macleod’s Clinical examination, 10th edn. Edinburgh: Churchill Livingstone, Elsevier Ltd; 2000. ★★★ Breathlessness Cortical drive Limbic drives (emotion) IX Central chemoreceptors Carotid body ( CSF pH) ( PaO2, PaCO2) Spinal Vagal lung afferents afferents Type II respiratory failure, PaCO2 + acidosis Pulmonary Altered V/Q embolus Hypoxaemia Airway obstruction  Asthma  Emphysema Interstitial disease  Inflammation Pulmonary  Infection Increased fibrosis