Essential Respiratory Medicine E-Book

Shanthi Paramothayan

• Herausgeber: John Wiley & Sons
• Kategorie: Fachliteratur
• Serie: essentials
• Sprache: Englisch

Seitenzahl: 903

Veröffentlichungsjahr: 2018

Beschreibung

A succinct yet comprehensive overview of respiratory medicine, written for students and professionals

Essential Respiratory Medicine is an indispensable text offering an understanding of respiratory conditions and their clinical management within evidence-based guidelines. Containing information on taking a medical history, performing examinations and investigations, diagnosis and the management of respiratory conditions, this comprehensive text was put together by a noted expert in the field.

Written in an accessible manner, Essential Respiratory Medicine contains the foundational science associated with respiratory medicine, a wide-variety of practical procedures, helpful diagrams, and self-assessments designed to enhance understanding of the material presented. The text covers a variety of conditions as well as providing suggestions for engaging with patients at different stages of care. This important resource:

• Demonstrates an effective approach to patients presenting with common respiratory symptoms

• Includes a description of all key practical procedures with diagrams
• Discusses acute management of important respiratory emergencies
• Covers both acute and chronic disease
• Contains a companion website containing a range of learning materials, including downloadable management summaries and algorithms, an image bank, videos of patient examination, example respiratory sounds and multiple-choice questions

Essential Respiratory Medicine is an essential resource for anyone on a clinical placement, rotation, or training programme in respiratory medicine.

Leseprobe

Table of Contents

Cover

About the author

CHAPTER 1: Introduction to respiratory medicine

About the book

CHAPTER 2: Embryology, anatomy, and physiology of the lung

Introduction

Development of the respiratory system

The respiratory tract

Muscles of respiration and mechanical ventilation

Structure of the lungs

Blood supply of the lungs

Nervous supply of the lungs

Lymphatics of the lungs

Control of breathing

Lung receptors and reflexes

Chemoreceptors

Transport of oxygen

Transport of carbon dioxide

The acid‐base balance

Ventilation‐perfusion mismatch

Lung defence

MULTIPLE CHOICE QUESTIONS

FURTHER READING

CHAPTER 3: Pharmacology of the lung

Drugs and the lung

Principles of drug deposition in lungs

Inhaler devices

Oxygen

Inhaled drugs

Drugs prescribed for smoking cessation

Drugs that damage the lungs

MULTIPLE CHOICE QUESTIONS

FURTHER READING

CHAPTER 4: Common respiratory investigations

Laboratory tests

Imaging of the lung

Lung function tests

Exercise testing

Sleep studies

Cardiology investigations

Invasive investigations

Miscellaneous investigations

MULTIPLE CHOICE QUESTIONS

FURTHER READING

CHAPTER 5: Common presentations of respiratory disease

Respiratory history

Breathlessness

Cough

Haemoptysis

Chest pain

Wheeze

Hoarse voice

Snoring

Examination of the respiratory system

Pre‐operative respiratory assessment

Post‐operative respiratory problems

Respiratory assessment of an acutely ill patient

MULTIPLE CHOICE QUESTIONS

FURTHER READING

CHAPTER 6: Obstructive airways disease

Introduction

Asthma

Chronic obstructive pulmonary disease (COPD)

Hyperventilation syndrome (HV)

MULTIPLE CHOICE QUESTIONS

Appendix 6.A Diagnosis of asthma

Appendix 6.B Management of asthma

Appendix 6.C Management of COPD

FURTHER READING

CHAPTER 7: Diffuse parenchymal lung disease

Introduction

Diagnosis of DPLD

Investigations in a patient suspected of a DPLD

Idiopathic interstitial pneumonias (IIP)

Non‐specific interstitial pneumonia (NSIP)

Cryptogenic organising pneumonia (COP)

Desquamative interstitial pneumonia (DIP)

Respiratory bronchiolitis interstitial lung disease (RB‐ILD)

Lymphoid interstitial pneumonia (LIP)

Acute interstitial pneumonia (AIP)

Eosinophilic lung disease

Sarcoidosis

Hypersensitivity pneumonitis (HP)

Lymphangioleiomyomatosis (LAM)

Pulmonary Langerhans cell histiocytosis (PLCH)

Pulmonary alveolar proteinosis (PAP)

Pulmonary amyloidosis

MULTIPLE CHOICE QUESTIONS

Appendix 7.A Drugs that cause peripheral eosinophilia

FURTHER READING

CHAPTER 8: Respiratory infections

Introduction

Respiratory tract infections

Pneumonia

Viral pneumonia

Bacterial pneumonia

Community acquired pneumonia (CAP)

Hospital acquired pneumonia (HAP)

Ventilator‐associated pneumonia

Aspiration pneumonia

Lipoid pneumonia

Pulmonary infections in the immunocompromised

Mycobacterium tuberculosis

Pulmonary complications of mycobacterium tuberculosis

Extra‐pulmonary tuberculosis

Opportunistic (atypical) mycobacterium

MULTIPLE CHOICE QUESTIONS

FURTHER READING

CHAPTER 9: Lung cancer

Introduction

Epidemiology of lung cancer

Aetiology of lung cancer

Pathophysiology of lung cancer

Clinical presentation of lung cancer

Clinical signs of lung cancer

Clinical assessment of patient with suspected lung cancer

Classification of lung cancer

Staging of NSCLC

Staging of SCLC

Management of lung cancer

Surgery

Radiotherapy

Chemotherapy

Targeted molecular therapy

Palliative treatment

Communicating the diagnosis of lung cancer

The lung multidisciplinary meeting

Tracheal and laryngeal tumours

Benign lung masses and solitary pulmonary nodules (SPN)

Common causes of SPN and benign lung mass

Cavitating lung lesions

Carcinoid tumour

Future developments

MULTIPLE CHOICE QUESTIONS

FURTHER READING

CHAPTER 10: Pleural disease

Normal pleura and pleural fluid

Pleural effusion

Pleural infection and empyema

Pneumothorax

Asbestos‐related pleural disease

Mesothelioma

MULTIPLE CHOICE QUESTIONS

Appendix 10.A Analysis of pleural fluid

Appendix 10.B Compensation for asbestos‐related disease

FURTHER READING

CHAPTER 11: Pulmonary embolus, pulmonary hypertension, and vasculitides

Introduction

Pulmonary embolism

Acute pulmonary embolus

Diagnosis of pulmonary embolus

Management of acute pulmonary embolus

Pulmonary hypertension

Classification of pulmonary hypertension

Pulmonary haemorrhagic syndromes

Granulomatosis with polyangiitis (GPA)

Other vasculitides

Anti‐glomerular basement membrane antibody (Goodpasture’s) syndrome

Eosinophilic granulomatosis with polyangiitis (Churg‐Strauss syndrome)

MULTIPLE CHOICE QUESTIONS

FURTHER READING

CHAPTER 12: Suppurative lung disease

Introduction

Bronchiectasis

Cystic fibrosis

Primary ciliary dyskinesia

Lung abscess

MULTIPLE CHOICE QUESTIONS

FURTHER READING

CHAPTER 13: Respiratory failure

Respiratory failure

Mechanisms of respiratory failure

MULTIPLE CHOICE QUESTIONS

Appendix 13.A Calculation of the alveolar‐arterial oxygen gradient

FURTHER READING

CHAPTER 14: Sleep‐related disorders

Introduction

Sleep physiology

Snoring

Upper airways resistance syndrome (UARS)

Obstructive sleep apnoea/hypopnoea syndrome (OSAHS)

Diagnosis of OSA

Intra‐oral devices

Narcolepsy

Periodic limb movement disorder (PLMD)

Restless leg syndrome (RLS)

REM behaviour disorder (RBD)/parasomnia

Idiopathic hypersomnia (IH)

Insomnia

Chronic sleep insufficiency

Central sleep apnoea (CSA)

Nocturnal hypoventilation

MULTIPLE CHOICE QUESTIONS

Appendix 14.A Epworth Sleepiness Scale (ESS)

FURTHER READING

CHAPTER 15: Occupational, environmental, and recreational lung disease

Occupational, environmental, and recreational lung diseases

Occupational lung disease

Pneumoconiosis

Hypersensitivity pneumonitis

Recreational drugs and the lungs

The environment and the lungs

MULTIPLE CHOICE QUESTIONS

FURTHER READING

CHAPTER 16: Disorders of the mediastinum

Anatomy of the mediastinum

Diagnosis of a mediastinal mass

Anterior mediastinal mass

Middle mediastinal mass

Posterior mediastinal mass

Other mediastinal conditions

MULTIPLE CHOICE QUESTIONS

FURTHER READING

CHAPTER 17: Acute lung injury and acute respiratory distress syndrome

Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS)

Diagnosis of ALI and ARDS

Incidence and mortality of ALI and ARDS

Pathogenesis of ALI and ARDS

Investigations in patients suspected of ALI and ARDS

Management of ALI and ARDS

Principles of mechanical ventilation in ARDS

Other therapies for ARDS

Morbidity and mortality in ARDS

Transfusion‐Related Acute Lung Injury (TRALI)

Acute chest syndrome with sickle cell disease

Smoke inhalation

Carbon monoxide poisoning

Airway trauma

Near‐drowning

Deep sea diving

Acute altitude sickness

MULTIPLE CHOICE QUESTIONS

FURTHER READING

Index

End User License Agreement

List of Tables

Chapter 01

Table 1.1 Brief history of respiratory medicine.

Chapter 04

Table 4.1 Interpretation of full lung function test.

Chapter 05

Table 5.1 Causes of breathlessness.

Table 5.2 Causes of haemoptysis.

Table 5.3 Common causes of pleuritic chest pain.

Table 5.4 Abnormalities on examination of the lungs.

Chapter 07

Table 7.1 Causes of eosinophilia.

Table 7.2 Some causes of hypersensitivity pneumonitis.

Chapter 08

Table 8.1 Causes of pneumonia.

Table 8.2 Non‐pulmonary tuberculosis.

Chapter 09

Table 9.1 Eighth edition of TNM classification of NSCLC.

Table 9.2 Staging using the TNM classification for NSCLC eighth edition.

Table 9.3 Overall 5‐year survival for NSCLC.

Table 9.4 Differences in 5‐year survival rates with CT staging and pathological staging.

Table 9.5 5‐year survival after surgery for NSCLC.

Table 9.6 Features of malignant and benign lung lesions.

Table 9.7 Risk factors for malignancy.

Table 9.8 Fleischner Society Guidelines for management of SPN, 2017.

Chapter 10

Table 10.1 Analysis of pleural fluid from thoracocentesis.

Table 10.2 Differential diagnosis of a transudate.

Table 10.3 Differential diagnosis of an exudate.

Table 10.4 Pathophysiology of pleural infection.

Chapter 11

Table 11.1 Risk factors for developing thromboembolic disease.

Table 11.2 Modified Wells score.

Table 11.3 WHO classification of pulmonary hypertension.

Chapter 12

Table 12.1 Aetiology of bronchiectasis.

Table 12.2 Investigations for the diagnosis of bronchiectasis.

Table 12.3 Clinical presentation of cystic fibrosis.

Chapter 13

Table 13.1 Arterial blood gas measurements.

Table 13.2 Comparison of arterial blood gases in acute and compensated respiratory and metabolic acidosis.

Chapter 14

Table 14.1 Differential diagnoses of excessive daytime sleepiness (EDS)/hypersomnia.

Table 14.2 Definitions.

Table 14.3 Presenting symptoms and signs of OSAHS.

Table 14.4 Risk factors for and clinical features of OSAHS.

Chapter 15

Table 15.1 Common causes of occupational asthma.

Chapter 16

Table 16.1 Structures in the mediastinum.

Table 16.2 Masaoka system.

List of Illustrations

Chapter 02

Figure 2.1 Stages of lung development.

Figure 2.2 The upper respiratory tract.

Figure 2.3 Surface anatomy of the thorax.

Figure 2.4 The lower respiratory tract.

Figure 2.5 Structure of the rib.

Figure 2.6 The ribs and intercostal space.

Figure 2.7 Diaphragm and the structures that traverse it.

Figure 2.8 Relationship between elastic recoil and functional residual capacity.

Figure 2.9 Lobes and fissures of the lungs.

Figure 2.10 Bronchopulmonary segments.

Figure 2.11 Alveolar‐capillary unit.

Figure 2.12 Control of breathing.

Figure 2.13 Oxygen‐Haemoglobin Dissociation Curve and the Bohr Effect.

Figure 2.14 The CO

2

dissociation curve.

Figure 2.15 The effect of CO

2

, pH, and O

2

on ventilation.

Figure 2.16 Pulmonary circulation.

Chapter 03

Figure 3.1 Particle size and drug deposition.

Figure 3.2 Several types of inhaler devices.

Figure 3.3 Individual using an MDI.

Figure 3.4 Turbohaler.

Figure 3.5 Patient using a turbohaler.

Figure 3.6 Volumatic device (spacer).

Figure 3.7 Aerochamber.

Figure 3.8 Portable nebuliser.

Figure 3.9 Oxygen cylinder.

Figure 3.10 Glucocorticoid receptor complex and mechanism of action of corticosteroid.

Figure 3.11 Dose response curve of inhaled corticosteroids.

Figure 3.12 Potency of inhaled corticosteroids.

Figure 3.13 CT thorax showing nitrofurantoin toxicity.

Figure 3.14 CT showing bleomycin toxicity.

Figure 3.15 CXR showing radiation‐induced fibrosis.

Chapter 04

Figure 4.1 Diagram of normal PA CXR with labels of structures.

Figure 4.2 Normal PA CXR.

Figure 4.3 Diagram of normal lateral CXR with labels of structures.

Figure 4.4 Normal lateral CXR.

Figure 4.5 CXR showing consolidation left lower lobe with air bronchogram.

Figure 4.6 CXR showing pulmonary oedema.

Figure 4.7 CXR showing a cavitating lesion left lower lobe.

Figure 4.8 CT thorax showing miliary tuberculosis.

Figure 4.9 CXR showing right upper lobe collapse.

Figure 4.10 CXR (PA) showing right middle lobe collapse.

Figure 4.11 CXR (lateral) showing right middle lobe collapse.

Figure 4.12 CXR (PA) showing right lower lobe collapse.

Figure 4.13 CXR (PA) showing left upper lobe collapse.

Figure 4.14 CXR (lateral) showing left upper lobe collapse.

Figure 4.15 CXR showing left lower lobe collapse.

Figure 4.16 CXR showing right mid‐zone consolidation.

Figure 4.17 CXR showing idiopathic pulmonary fibrosis.

Figure 4.18 CXR showing hyperinflated lungs in asthma.

Figure 4.19 CXR showing emphysematous lungs in COPD.

Figure 4.20 CXR showing a right‐sided pleural effusion.

Figure 4.21 CXR showing elevation of the right hemidiaphragm.

Figure 4.22 Diagram of normal CT thorax with labels of the structures.

Figure 4.23 Normal CT thorax (lung windows).

Figure 4.24 Normal CT thorax (mediastinal windows).

Figure 4.25 CTPA showing bilateral filling defects in multiple pulmonary emboli.

Figure 4.26 HRCT of normal lung.

Figure 4.27 PET scan showing FDG‐avid lesion in lung cancer.

Figure 4.28 VQ scan showing perfusion defects consistent with pulmonary emboli.

Figure 4.29 Thoracic ultrasound scan of a pleural effusion.

Figure 4.30 Peak flow meter.

Figure 4.31 Peak flow readings showing diurnal variation.

Figure 4.32 Handheld spirometer.

Figure 4.33 Spirometry in a normal individual and in obstructive and restrictive lung disease.

Figure 4.34 Normal flow‐volume loop.

Figure 4.35 Flow‐volume loop in obstructive lung disease.

Figure 4.36 Flow‐volume loop in restrictive lung disease.

Figure 4.37 Flow‐volume loop in mixed lung disease.

Figure 4.38 Flow‐volume loop in variable extra‐thoracic upper airway obstruction.

Figure 4.39 Flow‐volume loop in variable intra‐thoracic obstruction.

Figure 4.40 Flow‐volume loop in fixed large airway obstruction.

Figure 4.41 Static lung volumes: Total Lung Capacity (TLC), Expiratory Reserve Volume (ERV), Residual Volume (RV), Vital Capacity (VC), Functional Residual Capacity (FRC), Inspiratory Capacity (IC), Tidal Volume (TV).

Figure 4.42 CT‐guided FNA of lung mass with needle in pulmonary lesion.

Chapter 05

Figure 5.1 Observing chest expansion on inspiration.

Figure 5.2 Clubbing of the finger nails and tar staining.

Figure 5.3 Checking for CO

2

retention flap.

Figure 5.4 Checking for lymphadenopathy.

Figure 5.5 Checking for tracheal deviation.

Figure 5.6 Close‐up view showing how to check for tracheal deviation.

Figure 5.7 Unilateral (right‐sided) Horner’s syndrome showing ptosis, miosis, and aniscoria (difference in size of the pupils between the two eyes).

Figure 5.8 Checking for chest expansion upper anterior chest.

Figure 5.9 Checking for chest expansion lower anterior chest.

Figure 5.10 Checking for chest expansion posteriorly.

Figure 5.11 Percussion of the chest anteriorly.

Figure 5.12 Percussion of the chest posteriorly.

Figure 5.13 Auscultation of the lungs.

Chapter 06

Figure 6.1 Pathophysiology of asthma.

Figure 6.2 Diagram of PEF chart in poorly controlled asthma showing diurnal variation.

Figure 6.3 CXR in asthma.

Figure 6.4 HRCT in asthma.

Figure 6.5 Decline in lung function with smoking.

Figure 6.6 Pathophysiology of COPD.

Figure 6.7 CXR in COPD showing hyperinflation.

Figure 6.8 HRCT showing a large bulla in left lung in severe emphysema.

Figure 6.9 HRCT in ABPA showing proximal bronchiectasis.

Figure 6.A.1 Diagnostic algorithm for presentation with respiratory symptoms.

Figure 6.B.1 Summary of asthma management in adults.

Figure 6.C.1 Diagnostic algorithm for inhaled therapy.

Chapter 07

Figure 7.1 Classification of diffuse parenchymal lung disease (DPLD).

Figure 7.2 Pathophysiology of pulmonary fibrosis.

Figure 7.3 CXR of idiopathic pulmonary fibrosis (IPF).

Figure 7.4 HRCT thorax showing bibasal fibrosis of idiopathic pulmonary fibrosis (IPF).

Figure 7.5 HRCT thorax showing fibrosis and honeycombing in advanced idiopathic pulmonary fibrosis (IPF).

Figure 7.6 Histology of lung showing usual interstitial pneumonia (UIP) in IPF.

Figure 7.7 Prognosis in UIP, NSIP, and other fibrotic lung diseases.

Figure 7.8 CXR of non‐specific interstitial pneumonia (NSIP) showing interstitial shadowing.

Figure 7.9 HRCT thorax showing ground glass changes of non‐specific interstitial pneumonia (NSIP).

Figure 7.10 CXR in cryptogenic organising pneumonia (COP) showing areas of consolidation.

Figure 7.11 CT thorax showing extensive areas of consolidation in cryptogenic organising pneumonia (COP).

Figure 7.12 CT thorax of desquamative interstitial pneumonia (DIP) showing areas of fibrosis.

Figure 7.13 CT thorax of respiratory bronchiolitis‐interstitial lung disease (RBILD).

Figure 7.14 CXR of eosinophilic pneumonia showing interstitial shadowing.

Figure 7.15 CT thorax of eosinophilic pneumonia showing areas of consolidation.

Figure 7.16 Erythema nodosum.

Figure 7.17 Anterior uveitis with arrow showing hypopyon.

Figure 7.18 CXR of stage 1 pulmonary sarcoidosis showing BHL.

Figure 7.19 CT thorax of stage 1 pulmonary sarcoidosis showing bilateral hilar lymphadenopathy (BHL).

Figure 7.20 CXR of stage 2 pulmonary sarcoidosis with BHL and pulmonary infiltrates.

Figure 7.21 CT thorax of stage 2 pulmonary sarcoidosis with BHL and pulmonary infiltrates.

Figure 7.22 CXR of stage 3 pulmonary sarcoidosis showing pulmonary fibrosis.

Figure 7.23 CT thorax of stage 3 pulmonary sarcoidosis showing pulmonary fibrosis.

Figure 7.24 CXR of stage 4 pulmonary sarcoidosis showing extensive, chronic fibrosis.

Figure 7.25 CT thorax of stage 4 pulmonary sarcoidosis showing extensive, chronic fibrosis.

Figure 7.26 Histology of sarcoid lung showing granuloma with multinucleate giant cells, lymphocytes and histiocytes.

Figure 7.27 CXR of hypersensitivity pneumonitis (HP).

Figure 7.28 CT thorax of chronic hypersensitivity pneumonitis (HP) showing ground glass changes and fibrosis.

Figure 7.29 CXR of lymphangioleiomyomatosis (LAM) showing hyperinflation.

Figure 7.30 HRCT thorax of lymphangiomyomatosis (LAM) showing multiple cysts in both lungs.

Figure 7.31 CXR of pulmonary Langerhans cell histiocytosis (PLCH).

Figure 7.32 HRCT thorax of pulmonary Langerhans cell histiocytosis (PLCH) showing multiple cysts in both lungs.

Figure 7.33 CXR of pulmonary alveolar proteinosis (PAP) showing extensive shadowing.

Figure 7.34 CT thorax in pulmonary alveolar proteinosis (PAP) showing extensive ground‐glass changes.

Chapter 08

Figure 8.1 CXR showing left upper zone infiltration suggestive of early infection.

Figure 8.2 CXR showing right lower lobe consolidation.

Figure 8.3 CXR showing right middle and right lower lobe consolidation.

Figure 8.4 CXR showing right lower lobe consolidation with cavitation and a parapneumonic effusion.

Figure 8.5 CXR showing ground‐glass shadowing of pneumocystic jiroveci.

Figure 8.6 HR CT thorax showing ground‐glass shadowing of pneumocystis jiroveci.

Figure 8.7 CXR showing primary

Mycobacterium tuberculosis

infection.

Figure 8.8 CXR showing granulomas in the right lung.

Figure 8.9 CT thorax showing a calcified granuloma in the right lung.

Figure 8.10 CXR showing right upper lobe consolidation in active mycobacterium infection.

Figure 8.11 CT thorax showing miliary tuberculosis.

Figure 8.12 CXR of previous chickenpox pneumonia.

Figure 8.13 CXR showing changes of chronic mycobacterium tuberculosis infection.

Figure 8.14 CT thorax showing changes of chronic tuberculosis.

Figure 8.15 Preparation for a Mantoux test.

Figure 8.16 Forearm with purified protein derivative instilled intra‐dermally.

Figure 8.17 Quantiferon testing kit.

Figure 8.18 CXR showing plombage left lung.

Figure 8.19 CXR showing right‐sided thoracoplasty.

Figure 8.20 CT thorax showing ‘tree in bud’ appearance of atypical mycobacterial infection.

Chapter 09

Figure 9.1 Lung cancer incidence and smoking trends for adults by sex, 1948–2010 in Great Britain, from Cancer Research UK.

Figure 9.2 Number of deaths and age‐specific mortality rates for lung cancer in UK, 2007, from Cancer Research UK.

Figure 9.3 Survival in lung cancer according to stage at diagnosis.

Figure 9.4 Photograph showing clubbing of finger nails.

Figure 9.5 X ray showing hypertrophic pulmonary osteoarthropathy (HPOA).

Figure 9.6 Photograph showing Horner’s syndrome.

Figure 9.7 CXR showing a right‐sided lung mass suspicious for lung cancer.

Figure 9.8 CXR showing lobar (left upper lobe) collapse.

Figure 9.9 CXR showing a cavitating solitary pulmonary nodule.

Figure 9.10 CXR showing elevation of the right hemidiaphragm.

Figure 9.11 CXR showing lymphangitis carcinomatosis.

Figure 9.12 CT thorax showing a suspicious, spiculate mass in the right upper lobe.

Figure 9.13 PET scan showing an FDG‐avid lesion in the right upper lobe suspicious of lung cancer.

Figure 9.14 CT and PET scans showing a non‐FDG‐avid nodule in the left lung.

Figure 9.15 CT‐guided FNA of lung mass showing needle in the lung mass.

Figure 9.16 Histology of adenocarcinoma from a CT‐guided biopsy of lung mass.

Figure 9.17 Histology of squamous cell carcinoma from a CT‐guided biopsy of lung mass.

Figure 9.18 Histology of small cell carcinoma from an endobronchial biopsy.

Figure 9.19 CT thorax showing a hamartoma with the typical popcorn calcification.

Figure 9.20 CXR showing granulomas in the right lung.

Figure 9.21 CT thorax showing a calcified granuloma in the right lung.

Figure 9.22 CT showing round atelectasis which looks like a solitary pulmonary nodule.

Figure 9.23 CT thorax of carcinoid tumour of the lung.

Figure 9.24 PET scan of carcinoid tumour showing low FDG uptake.

Figure 9.25 Histology of carcinoid tumour.

Chapter 10

Figure 10.1 BTS diagnostic algorithm for investigation of a unilateral pleural effusion.

Figure 10.2 CXR showing a unilateral (right‐sided) pleural effusion.

Figure 10.3 Thoracic ultrasound scan showing a pleural effusion with underlying lung atelectasis.

Figure 10.4 CT thorax showing a unilateral (right‐sided) pleural effusion.

Figure 10.5 CT thorax showing right‐sided empyema with inserted drain.

Figure 10.6 Thoracic ultrasound scan of empyema with air‐bubbles post aspiration.

Figure 10.7 CXR of a small, unilateral (right‐sided) pneumothorax.

Figure 10.8 CXR showing a large, left‐sided pneumothorax with complete collapse of the left lung.

Figure 10.9 Measurement of the size of a pneumothorax from BTS Guidelines.

Figure 10.10 CXR showing a large, left‐sided emphysematous bulla.

Figure 10.11 CT thorax showing a large, left‐sided emphysematous bulla.

Figure 10.12 CXR showing surgical emphysema.

Figure 10.13 BTS algorithm for management of primary and secondary pneumothorax.

Figure 10.14 CXR showing benign, calcified, pleural plaques.

Figure 10.15 CT thorax showing benign, calcified pleural plaques.

Figure 10.16 CT thorax showing left‐sided pleural thickening.

Figure 10.17 CT thorax showing round atelectasis with adjacent left‐sided pleural thickening (mediastinal window).

Figure 10.18 CT thorax showing round atelectasis with adjacent left‐sided pleural thickening (parenchymal window).

Figure 10.19 Coronal reconstruction of CT thorax showing sub‐pleural reticulation and multiple, bilateral, calcified pleural plaques.

Figure 10.20 CT thorax showing right‐sided malignant mesothelioma associated with external compression of the superior vena cava.

Figure 10.21 CT thorax showing right‐sided malignant mesothelioma.

Chapter 11

Figure 11.1 Virchow’s triad.

Figure 11.2 ECG changes seen in pulmonary embolus.

Figure 11.3 CXR showing right lower lobe infarction after a pulmonary embolism.

Figure 11.4 CTPA showing bilateral filling defects seen with multiple pulmonary emboli.

Figure 11.5 : Ventilation perfusion scan showing perfusion defects in pulmonary emboli.

Figure 11.6 Ventilation perfusion scan showing VQ mismatch.

Figure 11.7 Regulation of pulmonary vascular tone.

Figure 11.8 CXR showing right ventricular hypertrophy in a patient with severe pulmonary hypertension.

Figure 11.9 ECG changes seen in pulmonary hypertension.

Figure 11.10 Histology showing intimal proliferation in pulmonary hypertension.

Figure 11.11 Histology showing changes of pulmonary arterial hypertrophy.

Figure 11.12 CXR of a patient with granulomatosis with polyangiitis.

Figure 11.13 CXR showing acute haemorrhage in right lung in a patient with HHT.

Figure 11.14 CXR showing changes of chronic pulmonary haemorrhage.

Chapter 12

Figure 12.1 Progression of bronchiectasis with cycle of infection and inflammation.

Figure 12.2 Electron microscopy image of cilium (diagram).

Figure 12.3 CT showing dilated bronchi in bronchiectasis.

Figure 12.4 Coronal CT thorax showing bronchiectasis.

Figure 12.5 CT thorax showing cylindrical bronchiectasis.

Figure 12.6 The structure of the cystic fibrosis transmembrane conductance regulator.

Figure 12.7 CXR of patient with CF showing extensive bronchiectasis.

Figure 12.8 CT of patient with CF.

Figure 12.9 CXR of patient with PCD showing dextrocardia.

Figure 12.10 CXR of right‐sided lung abscess.

Figure 12.11 CT of right‐sided lung abscess.

Figure 12.12 CT of left lung abscess.

Chapter 13

Figure 13.1 Patient using a nasal cannulae.

Figure 13.2 Patient using a simple face mask.

Figure 13.3 Patient using a reservoir (re‐breathe) mask.

Figure 13.4 Patient being fitted with a CPAP device.

Figure 13.5 A range of venturi valves.

Figure 13.6 The venturi principle.

Figure 13.7 A non‐invasive ventilator.

Figure 13.8 NIV pressures.

Figure 13.9 Oxygen Alert Card.

Chapter 14

Figure 14.1 Brain wave activity during normal sleep.

Figure 14.2 Increase in upper airway resistance during sleep.

Figure 14.3 Mandibular advancement device (MAD).

Figure 14.4 Normal upper airway.

Figure 14.5 Narrowed upper airway in apnoea‐hypopnoea syndrome.

Figure 14.6 An individual being fitted with a home (limited) sleep study.

Figure 14.7 An oximeter being fitted for a home (limited) sleep study.

Figure 14.8 Home (limited) sleep study tracing showing obstructive sleep apnoea.

Figure 14.9 Full polysomnography tracing showing obstructive sleep apnoea.

Figure 14.10 CPAP machine and circuit.

Figure 14.11 Individual having CPAP fitted.

Figure 14.12 Sleep tracing showing obstructive, central, and mixed apnoea.

Chapter 15

Figure 15.1 Chest X‐ray of asbestosis and mesothelioma.

Figure 15.2 CT thorax of asbestosis.

Figure 15.3 CXR showing progressive massive fibrosis.

Figure 15.4 CXR showing silicosis and progressive massive fibrosis.

Figure 15.5 CT thorax showing silicosis and progressive massive fibrosis.

Figure 15.6 CT thorax showing changes associated with hard metal sensitivity.

Chapter 16

Figure 16.1 Outline of the mediastinum.

Figure 16.2 Compartments of the mediastinum on a lateral CXR.

Figure 16.3 Common mediastinal masses in the anterior, middle, and posterior mediastinum.

Figure 16.4 CXR of thymoma.

Figure 16.5 CT thorax showing thymoma.

Figure 16.6 CXR showing retrosternal thyroid.

Figure 16.7 CT thorax with contrast showing lymphadenopathy.

Figure 16.8 CXR showing a pericardial cyst.

Figure 16.9 CXR showing a neurofibroma.

Figure 16.10 CT thorax showing a neurofibroma.

Figure 16.11 CXR showing a pneumomediastinum.

Figure 16.12 CT thorax showing a pneumomediastinum.

Chapter 17

Figure 17.1 Chest X‐ray showing ARDS.

Figure 17.2 High resolution CT scan showing ARDS.

Guide

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Essential Respiratory Medicine

Shanthi Paramothayan

Consultant Respiratory PhysicianUK

This edition first published 2019 © 2019 by John Wiley & Sons Ltd

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The right of Shanthi Paramothayan to be identified as the author of editorial in this work has been asserted in accordance with law.

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Library of Congress Cataloging‐in‐Publication Data

Names: Paramothayan, Shanthi, author.Title: Essential respiratory medicine / Shanthi Paramothayan.Description: Hoboken, NJ : Wiley Blackwell, 2019. | Includes bibliographical references and index. |Identifiers: LCCN 2018024800 (print) | LCCN 2018024971 (ebook) | ISBN 9781118618325 (Adobe PDF) | ISBN 9781118618318 (ePub) | ISBN 9781118618349 (pbk.)Subjects: | MESH: Lung DiseasesClassification: LCC RC756 (ebook) | LCC RC756 (print) | NLM WF 600 | DDC 616.2/4–dc23LC record available at https://lccn.loc.gov/2018024800

Cover Design: WileyCover Image: © SCIEPRO/SCIENCE PHOTO LIBRARY/Getty Images

This textbook is dedicated to the memory of my aunt and teacherMiss Sushila Balamani Navaratnasingam

About the author

This textbook is written by Dr. Shanthi Paramothayan, a Consultant Respiratory Physician with 17 years of clinical experience in the NHS. As an Honorary Senior Lecturer for 15 years, the author has significant experience in teaching, assessing and examining undergraduates, foundation doctors, core medical trainees and respiratory registrars. She is a Fellow of the Royal College of Physicians, Fellow of the American College of Chest Physicians, and a Fellow of the Higher Education Academy. She has been a member of the Education and Training Committee of the British Thoracic Society, a member of the Question Writing Committee for the specialist respiratory examinations, a member of the MRCP 1 Board and a PACES examiner for the Royal College of Physicians. She has been a Foundation Training Programme Director, Director of Medical Education, Associate Medical Director for Education and Associate Foundation Quality Dean, Health Education South London.

Acknowledgements

I would like to thank the following people for their invaluable help with the writing of this textbook. Consultant Radiologists, Alaa WitWit, Konstantinos Stefanidis, Chandani Thorning, and Valmai Cook were crucial as they sourced many of the radiology images for the book. Alaa WitWit and Konstantinos Stefanidis also read and checked the accuracy of the radiology section of Chapter 4. The Librarians, Potenza Atiogbe, Marisa Martinez Ortiz, and Yin Ping Leung checked the references to ensure that they were all correct and in the right style. They also provided me with encouragement and support.

I am grateful to Tina Matthews, Rukma Doshi and Michael Lapsley, Consultant Histopathologists, and to David Cook, Biomedical Scientist, for providing the histopathology images. Saeed Usman, Consultant Ophthalmologist, provided the image of anterior uveitis.

I would like to thank John Clark, Consultant Microbiologist, for reading and recommending changes and additions to Chapter 8.

I would like to thank Carol Tan, Consultant Thoracic Surgeon, Jaishree Bhosle, Consultant Medical Oncologist, and Fiona MacDonald, Consultant Clinical Oncologist, for reviewing the relevant parts of Chapter 9 and recommending appropriate changes and additions.

I am grateful to Ginny Quirke, Siva Ratnatheepan, Vicky Taylor, and Rajiv Madula for reading chapters and making suggestions and corrections.

Ian Ellerington, Yvonne Welbeck‐Pitfield and David Farrow from the Medical Illustration Department at Epsom and St. Helier University Hospitals NHS Trust were responsible for the clinical photographs and the videos for the supplementary material. My special thanks to Sophie Mitchinson, James Hambley, Rajiv Madula, Helen Parnell, Katherine Bintley, Patricia Lowe, Ella Sultan, Jennifer Swaby, Lucy Stratford, and Amy Grierson for willingly appearing in the photographs and videos of the supplementary material.

My thanks to Ahalya Sahadevan, Rajapillai Ahilan, Arjunan Ahilan, and Sanjeevan Ahilan for their support with IT, medical drawings, and comments on Chapter 1.

About the companion website

This book is accompanied by a companion website:

www.wiley.com/go/paramothayan/essential_respiratory_medicine

The website includes:

– Image bank

– Videos of patient examination

– Example respiratory sounds

– Multiple‐choice questions

Scan this QR code to visit the companion website:

CHAPTER 1Introduction to respiratory medicine

The respiratory system is essential for gas exchange in a multicellular organism. The lungs are also important as a defence against infectious microorganisms. Worldwide, diseases of the respiratory system cause significant morbidity and mortality; this includes infectious diseases, malignancies, allergic diseases, autoimmune disorders, and occupational diseases. Diseases of other parts of the body, for example, rheumatological and renal conditions, often affect the lungs.

Respiratory diseases can present acutely with severe, life‐threatening breathlessness, for example, when someone develops a pulmonary embolus or a pneumothorax, or more insidiously with a steady decline in lung function over time, as occurs in chronic obstructive pulmonary disease or parenchymal lung diseases. In the United Kingdom (UK), respiratory diseases account for one‐third of acute admissions to hospitals and for more than a quarter of all deaths in hospitals. Respiratory tract infections are the commonest conditions seen in General Practice.

In the last half a century there has been a decline in the prevalence of certain diseases, such as pneumoconioses, and other occupational lung diseases because of the recognition of the harm caused by exposure to certain agents at work. The introduction of masks, better ventilation, and other safety measures at work, together with appropriate legislation, has been the key to this success.

In the next few decades it is likely that asbestos‐associated diseases (asbestosis and mesothelioma) will reduce in incidence and prevalence in the UK because of the prohibition of the use of asbestos. Asbestos, however, is still used in several developing countries. The recognition that air pollution is responsible for respiratory diseases will, hopefully, lead to cleaner air, especially in urban areas.

However, there has been an increase in the prevalence of allergic asthma, and there are various hypotheses to explain this increase. Mycobacterium tuberculosis has still not been eradicated, resulting in millions of deaths across the globe. Tuberculosis, also called ‘phthism’, ‘consumption’, or the ‘white plague’, was found in the spines of Egyptian mummies dating back to 3200–2400 BCE and is associated with poverty and deprivation.

Respiratory diseases are managed jointly by respiratory physicians, specialist nurses, physiotherapists, and occupational therapists in a multi‐disciplinary way. Other specialists, including radiologists, pathologists, oncologists, thoracic surgeons, palliative care physicians, intensivists, and physiologists (for example, lung function technicians) are also essential in the management of patients with respiratory diseases. Patients who are acutely ill are managed in hospital, often on specialist respiratory wards, sometimes in single rooms if infectious, and in the Intensive Care Unit if respiratory support is required.

There has been increasing understanding of the physiology of the respiratory system and the pathophysiology of respiratory diseases in the last few centuries. Table 1.1 summarises some of the key developments in respiratory medicine.

Table 1.1 Brief history of respiratory medicine.

Year

Development

Scientist

Greece, 460–370

BCE

Beginning of modern medicine

Hippocrates

Greece, 304–250

BCE

Some understanding of the physiology of the lung

Erisistratus

Greece, 129–165

BCE

Anatomy of trachea, larynx, and lungs understoodBelieved air had substance vital for life

Galen

Egypt, 1210–1288

Some understanding of pulmonary circulation

Ibne Nafis

Italy, 1500

Understood anatomy and physiology of lungsDetermined sub‐atmospheric pressures inflated lungs

Leonardo da Vinci

Belgium, 1543

Tracheostomy used for ventilation

Andreas Vesalius

UK, 1700

Constructed first air pump for physiological research

Robert Hooke

France, 1778

Discovered role of oxygen

Antoine Lavoisier

France, 1816

Invention of stethoscope

René Laennec

Scotland, 1832

Invention of negative pressure tank‐type ventilator

John Dalziel

Germany, 1882

Tuberculosis bacterium discovered

Robert Koch

Germany, 1895

First chest X‐ray

Wilhelm Rötgen

UK, 1928

First non‐invasive ventilation

Drinker‐Shaw

USA, 1963

First human lung transplant

James Hardy

UK, 1972

First computed tomography scan

Godfrey Hounsfield

About the book

Respiratory diseases are common, and this textbook offers a practical guide to those who care for patients with respiratory diseases. This textbook is aimed at medical students studying for their MBBS examination and postgraduate doctors of all grades, especially those studying for postgraduate examinations, including the MRCP examination. This book will also be useful for non‐respiratory doctors, specialist nurses, physiotherapists, occupational therapists, pharmacists, respiratory physiologists, and physicians associates.

This text covers the entire respiratory curriculum and contains information that is useful and relevant to everyday clinical practice, with a focus on clinical presentation and management. Essential basic anatomy, physiology, pharmacology, and pathology are introduced to help understand the clinical presentation. A structured approach is taken to explain how to construct a sensible differential diagnosis of common respiratory conditions. There is a clear explanation of the common diagnostic tests required to make a diagnosis, including the interpretation of lung function tests. The mechanism of action of drugs commonly prescribed to treat respiratory diseases is discussed, with a description of their common side effects and interaction with other medications. The evidence‐based management of common conditions is discussed with reference to the current British Thoracic Society (BTS) and National Institute for Health and Care Excellence (NICE) guidelines. Common pitfalls in diagnosis and management are highlighted.

The book contains several boxes, tables, and algorithms set out in a clear, and concise way. It also contains several good quality colour photographs, and radiological and histological images to support the information in the text.

There are multiple choice questions which can be used by the reader to check their understanding, with a clear explanation of the correct answer. There is also a list of references for suggested further reading.

Supplementary material includes videos demonstrating how to take a history and conduct a clinical examination (http://www.wiley.com/go/Paramothayan/Essential_Respiratory_Medicine). There are also videos showing how to carry out common tests, such as peak flow, spirometry, the skin prick test, the Mantoux test, the shuttle test, and how to fit a patient for a sleep study.

CHAPTER 2Embryology, anatomy, and physiology of the lung

Learning objectives

To gain a basic understanding of the development of the lung

To be aware of the common developmental lung abnormalities

To understand the anatomy of the respiratory system which is relevant to clinical practice

To be aware of the structure and function of the diaphragm

To understand the muscles of respiration

To understand how mechanical ventilation occurs

To gain knowledge of the structure of the bronchial tree and the alveoli

To gain knowledge of the blood supply, nerve supply, and lymphatics of the respiratory system

To understand the physiology of the respiratory system which is relevant to clinical practice

To gain some understanding of the control of breathing

To gain knowledge of the receptors in the lungs

To appreciate the function of the central and peripheral chemoreceptors

To understand how oxygen is transported in the blood from the lungs to tissues

To understand how carbon dioxide is transported in the blood from tissues to the lungs

To understand the importance of carbon dioxide in the acid‐base balance of the body

To understand the causes of physiological shunts

To understand the causes of ventilation‐perfusion mismatch

To have some understanding of the defence mechanisms of the lungs

Abbreviations

ASD

atrial septal defect

CA

carbonic anhydrase

CO

2

carbon dioxide

COPD

chronic obstructive pulmonary disease

CSF

cerebrospinal fluid

FRC

functional residual capacity

H

+

hydrogen ion

H

2

CO

3

carbonic acid

HB

haemoglobin

HCO

3

–

bicarbonate ion

MCE

mucociliary escalator

NANC

non‐noradrenergic, non‐cholinergic

NO

nitric oxide

O

2

oxygen

O

3

ozone

PCD

primary ciliary dyskinesia

PCO

2

partial pressure of carbon dioxide

PO

2

partial pressure of oxygen

R

respiratory quotient

SO

2

sulphur dioxide

VSD

ventricular septal defect

Introduction

The respiratory system’s main role is to provide oxygen (O2) that is required for glycolysis, and the removal of the waste product of respiration, carbon dioxide (CO2). This involves two separate processes: (1) mechanical ventilation whereby air is moved into and out of the lungs, and (2) gas exchange across the alveolar‐capillary membrane.

The respiratory system also has an important role in acid‐base balance, the defence against airborne pathogens, and in phonation, which is essential for audible speech. The conversion of angiotensin 1 to angiotensin 11 occurs in the lungs as does the deactivation of bradykinin, serotonin, and various drugs, including propranolol.

The lungs act as a reservoir of 500 ml blood and therefore participate in heat exchange. The lungs filter and lyse microemboli from the veins, preventing them from reaching the systemic circulation.

Development of the respiratory system

The lungs are not required for respiration in utero, but start working as soon as the baby is born and is independent from its mother. The development of the lungs starts in week three of the embryonic period (3–16 weeks), continues through the foetal period (16–38 weeks), beyond birth, and into childhood. During intrauterine life, the lungs are an important source of amniotic fluid, producing around 15 ml kg−1 of body weight, which flows out via the trachea or is swallowed.

Development of the lungs

During the embryonic period, the structures of the respiratory system are formed: the trachea, bronchial tree, blood vessels, nerves, lymphatics, and the structures of the thoracic cage (Figure 2.1). In the latter part of the second trimester and during the third trimester, there is functional development, with lung maturation and the production of surfactant. Five phases of structural lung development are recognised. In the embryonic phase (3–16 weeks), at approximately 28 days after conception, lung development begins with the formation of the sulcus laryngotrachealis in the lower part of the pharynx. At 30 days, a bud, called the true lung primordium, forms from the lower part of the foregut, but remains in communication with it. The oesophagotracheal ridges then fuse to form the oesophagotracheal septum, which divides the oesophagus from the trachea. Failure of the formation of this septum occurs in 1 : 3000 births and results in the formation of a trachea‐oesophageal fistula.

Figure 2.1 Stages of lung development.

The diaphragm develops in the third week after fertilisation, with transverse and longitudinal folding. The septum transversum is the primitive central tendon and forms in the cervical region and migrates downwards, therefore the innervation is from the phrenic nerve that originates from the cervical spinal cord.

Failure of one of the pleuroperitoneal membranes to close results in a congenital diaphragmatic hernia which occurs in 1 : 2000 births. It occurs more commonly on the left side and results in the intestinal contents moving up into the left hemithorax, compromising lung development resulting in lung hypoplasia. Surgical repair carries a high mortality.

Normal lung development depends on the interaction between the epithelium and the mesenchymal tissue which lies beneath it. During the pseudoglandular period of the embryonic phase (5–16 weeks), there is an asymmetrical subdivision of the lung primordium into the two buds which will form the main bronchi. The smaller left main bronchus is directed more acutely away from the trachea while the larger right main bronchus leads more directly from the trachea. The two main bronchi subdivide unequally, giving rise to three lobes on the right and two lobes on the left.

Progressive branching during the embryonic phase results in the formation of the first 16 generations of the conducting airways, composed of the trachea, bronchi, bronchioles, and terminal bronchioles. Differentiation of the epithelium derived from the endoderm, with formation of cilia in the proximal airways, occurs at 13 weeks and is controlled by the mesenchyme beneath it. This ciliated epithelium lines the entire conducting airway system and is important in host defence. In primary ciliary dyskinesia (PCD), the ciliary structure is abnormal, and the consequences are significant, as discussed in Chapter 12. The innervation of the lungs is derived from the ectoderm while the vascular structures, smooth muscle, cartilage, and connective tissue are derived from the mesoderm.

During the canalicular period (16–26 weeks), there is further branching of the bronchial tree, with the terminal bronchioles dividing into the respiratory bronchioles (generations 20–22), which further subdivide into the alveolar ducts (generations 20–22) and finally the alveolar sacs (generation 23). Generations 17–23 are called the respiratory zones and will be responsible for gas exchange. Once the alveolar sacs have been formed, further growth occurs by elongation and widening of the airways.

Type 1 pneumocytes, the main cells of the alveolus, are formed with very thin membranes. There is vascularization, with establishment of the capillary network very close to the type 1 pneumocytes in preparation for the gas exchange. Type 2 pneumocytes, which contain lamellar (or inclusion) bodies, also develop and will eventually synthesise and store surfactant.

At the end of the embryonic period (16 weeks), the pulmonary vessels have developed. The pulmonary circulatory system is smaller than the systemic circulatory system and is formed out of the sixth pharyngeal arch artery and a vessel plexus which originates from the aortic sac. The true sixth aortic arch is only then formed after vessels from the dorsal arch grow into this plexus and there is a connection between the truncus pulmonalis and the dorsal aorta.

During the terminal sac period of foetal development (26–38 weeks), there is further differentiation of the type 1 and type 2 pneumocytes, with progressive thinning of the alveolar walls which will facilitate gas exchange.

At full gestation, there are approximately 20 × 106 alveoli, often called ‘primitive saccules’, which mature during the neonatal period and connect to other alveoli through the pores of Kuhn. The pulmonary arterial network gradually develops a muscle layer during childhood and the capillary network extends and becomes entwined between two alveoli. The lungs continue to develop after birth until the age of 8, with the formation of a total of 300 × 106 mature alveoli.

As the alveoli in the foetus contain fluid and not air, the oxygen tension is low, resulting in pulmonary vasoconstriction and diversion of blood across the ductus arteriosus into the systemic circulation. After the first breath is taken, oxygen enters the alveoli, resulting in an increase in oxygen tension and increased blood flow to the alveoli. Nitric oxide (NO), a potent vasodilator, is secreted by the respiratory epithelium which results in significant vasodilation of the pulmonary blood vessels.

Surfactant is composed of a hydrophilic macromolecular complex of phosphatidylcholine (lecithin), phosphatidylglycerol and hydrophobic surface proteins B and C which project into the alveolar gas and float on the surface of the lining fluid. Surfactant decreases surface tension within the alveoli, preventing the collapse of the alveoli during exhalation. In the absence of surfactant, the alveolus would be unstable and would collapse at the end of each breath. During the latter part of gestation, surfactant production and secretion gradually increase. At 36 weeks of gestation there is sufficient surfactant so that spontaneous breathing can occur and the foetus is viable.

Prematurity carries a high mortality and a significant risk of neonatal respiratory distress syndrome. Corticotrophin stimulates the synthesis of the fibroblast pneumocyte factor from the foetal lung fibroblasts which stimulates surfactant production in type 2 cells. Corticosteroids given antenatally to premature babies will promote lung maturity. Exogenous surfactant can also improve the survival of the premature baby.

Amniotic fluid, originating in the foetal lungs and kidneys, is required for normal lung development. During foetal breathing movements, when the upper airways’ resistance is decreased, diaphragmatic movements help maintain lung liquid volume. Oligohydramnios, called Potter’s syndrome, occurs when there is a decreased volume of amniotic fluid, resulting in lung hypoplasia and renal agenesis. Other causes of lung hypoplasia include congenital diaphragmatic hernia, musculoskeletal abnormalities of the thorax which restrict the full expansion of the thoracic cage, and space‐occupying lesions of the thorax.

The respiratory tract

The upper respiratory tract comprises of the nose, the paranasal sinuses, the epiglottis, pharynx, and larynx (Figure 2.2). The larynx is important in speech. During swallowing, the epiglottis closes the larynx which leads to the trachea, preventing food from entering the respiratory tract. Failure of this process will lead to aspiration of food contents into the lungs.

Figure 2.2 The upper respiratory tract.

The lower respiratory tract begins at the trachea, which corresponds to the lower edge of the cricoid cartilage, at the level of the sixth cervical vertebra. The lower respiratory tract is enclosed within the thoracic cavity which is composed of the sternum anteriorly, the vertebral column posteriorly, the mediastinum, the diaphragm, which divides the thorax from the abdomen, and the ribs with their intercostal spaces (Figure 2.3, Figure 2.4). The bony sternum is divided into the manubrium, the body, and the xiphisternum, which is cartilaginous until late adulthood. The manubrium is joined to the cartilages of the first and second ribs at the level of T3 and T4, and to the body by the manubriosternal joint which lies at T4 and is called the angle of Louis or the sternal angle. This is an important landmark in surface anatomy. The body of the sternum joins the second to seventh ribs at the level of T5–T8.

Figure 2.3 Surface anatomy of the thorax.

Figure 2.4 The lower respiratory tract.

The vertebrosternal, or true ribs, are the first to seventh ribs, and are connected to the sternum by their costal cartilages. Inflammation of the costochondral junction (costochondritis) results in ‘pleuritic’ chest pain which is worse on breathing, movement, and palpation. The eighth, ninth, and tenth ribs are called the vertebrochondral, or false ribs, and are joined to the cartilages of the ribs above. The eleventh and twelfth ribs are called floating or vertebral ribs.

Each rib is composed of a head and a shaft. The head is attached to the body and transverse process of the adjacent vertebra, the intervertebral disc, and the vertebra above (Figure 2.5). The shaft curves forward to join the sternum. The joints between the ribs and vertebra act like a hinge, causing the ribs to move during inspiration.

Figure 2.5 Structure of the rib.

The rib cage protects the heart, lungs, and great vessels from damage. Trauma to the chest wall can result in fracture of the shaft of the ribs at the angle of the rib. Multiple rib fractures can result in a ‘flail’ segment which can cause significant difficulty with inspiration. The clavicles protect the first and second ribs which are less likely to fracture than the other ribs.

One in 200 people have a cervical rib which is attached to the transverse process of C7. A cervical rib can press on the brachial plexus and cause neurological symptoms, including paraesthesia of the arms and hands. Pressure on the subclavian artery can cause vascular symptoms.

The intercostal spaces between the ribs contain external and internal intercostal muscles (Figure 2.6). The fibres of the external intercostal muscles pass downwards and forwards between the ribs, while the fibres of the internal intercostal muscles pass downwards and backwards. There is also an incomplete innermost intercostal layer. The intercostal muscles are innervated by the intercostal nerves, which are the anterior primary rami of thoracic nerves. The intercostal veins, arteries and nerves lie in grooves on the under‐surface of the corresponding ribs, with the vein above, the artery in the middle and the nerve below. It is important, therefore, to avoid the underside of the rib when carrying out pleural procedures, but to insert the needle or drain just above the rib into the pleural space.

Figure 2.6 The ribs and intercostal space.

The diaphragm, which means ‘partition’ in Greek, has a central tendon which is attached to the pericardium, and thick skeletal muscle on either side, which separates the thoracic and abdominal cavities. It is the most important muscle of inspiration. Several key structures traverse the diaphragm between the abdomen and thorax. The sternal part of the diaphragm consists of two strips of muscle that arises from the posterior surface of the xiphisternum. The costal part comprises of six muscular strips that originate from the seventh–twelfth ribs and their costal cartilages. The vertebral part of the diaphragm originates from the crura and the arcuate ligaments on both sides. The muscular right crus arises from the bodies and intervertebral discs of the three lumbar vertebrae, and the left crus arises from the bodies and intervertebral discs of the upper two lumbar vertebrae. The medial and lateral arcuate ligaments are thickenings of the fascia overlying the psoas major and the quadratus lumborum respectively.

The inferior vena cava and right phrenic nerve pass through the diaphragm at T8, the oesophagus, branches of the left gastric artery, the gastric vein, and both vagi pass through at T10, and the aorta, thoracic duct, and zygos vein pass behind the diaphragm between the left and right crus at T12 (Figure 2.7). The sympathetic trunk passes through the diaphragm under the medial lumbocostal arch, and branches of the internal thoracic artery and lymphatics pass through the foramina of Morgagni.

Figure 2.7 Diaphragm and the structures that traverse it.

The phrenic nerves (C3, C4, and C5) supply motor and sensory innervation to the diaphragm. Pain from irritation of the diaphragm is referred to the corresponding dermatome for C4 at the shoulder. Irritation to the phrenic nerve can cause intractable hiccoughs. The lower intercostal (T5–T11) and subcostal (T12) nerves supply sensory fibres to the peripheral diaphragm. Damage to the phrenic nerve, for example, by a tumour, will result in a unilateral diaphragmatic palsy, as discussed in Chapter 9.

The blood supply to the diaphragm is from the pericardiophrenic, musculophrenic, lower internal intercostal and inferior phrenic arteries. The superior and inferior phrenic veins drain blood from the diaphragm into the brachiocephalic vein, the azygos vein, the inferior vena cava, and the left suprarenal vein.

Muscles of respiration and mechanical ventilation

The inspiratory muscles are the diaphragm, and the intercostal and the scalene muscles. When they contract to expand the thoracic cavity, there is a decrease in intrapleural and alveolar pressure which creates a pressure gradient between the alveoli and the mouth, resulting in air entering the lungs. Elastic recoil of the lungs and the chest wall results in expiration, which is a passive process, not requiring any muscular activity. Forced expiration, for example, coughing, will require contraction of the abdominal muscles which push the diaphragm upwards.

Inspiration is an active process. The domed diaphragm is the main muscle of inspiration and is positioned high in the thorax at the end of expiration. During quiet breathing, the diaphragm contracts and moves down by 1.5 cm, pushing the abdominal contents down. This increases the intra‐abdominal pressure and pushes the abdominal wall and the lower ribs outwards and downwards. During deep breathing, the diaphragm contracts harder and can move by as much as 6–7 cm.

During quiet breathing, the first rib remains almost motionless and the intercostal muscles elevate and evert the other ribs. The intercostal muscles support the intercostal spaces preventing them from being sucked in during inspiration. The scalene muscles, which insert into the first two ribs, are also active in normal inspiration. Movement of the upper ribs upwards pushes the sternum forward (the pump action), increasing the anterior–posterior diameter of the chest, and as the sloping lower ribs rise, they move out (the bucket handle action), and the transverse diameter of the chest wall increases. At the beginning of inspiration, the inspiratory muscles contract to overcome the impedance offered by the lungs and chest wall. The volume of the thoracic cavity can increase from 1.5 l up to 8 l with deep inspiration.

Diaphragmatic paralysis results in paradoxical movement: as the intercostal muscles contract and the ribs move, the diaphragm is sucked into the chest due to a fall in intrathoracic pressure. In a high cervical cord transection, all the respiratory muscles are paralysed, but when the damage is below the phrenic nerve roots, breathing continues via the diaphragm alone. In infants, the movement of the horizontal ribs cannot increase the volume of the chest, and breathing is reliant on diaphragmatic contraction alone; this is called abdominal breathing. As the infant grows, the ribs become more oblique and contribute to thoracic inspiration.