From the sequence pics can you make a good and detailed notes on the systemic examination of respiratory system, so that I can impress my teacher and he must find out it is from MacLeod by the words and please make it same as in the book
# SYSTEMIC EXAMINATION OF THE RESPIRATORY SYSTEM
## MacLeod's Clinical Examination - Comprehensive Study Notes
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## ANATOMY AND PHYSIOLOGY
Understanding the surface anatomy of the lungs and their relation to adjacent structures is essential for the practice of respiratory medicine. At the end of tidal expiration, the dome of the diaphragm extends high into the thorax, level with the anterior end of the fifth rib, slightly lower on the left. The lower lateral ribs therefore overlie the liver on the right and the stomach and spleen on the left, with the parietal pleura extending lower than the lungs on the lateral chest wall. Posteriorly, the lungs extend much lower, approaching the 12th rib on full inspiration.
The lung apex lies immediately beneath the brachial plexus, so apical lung tumours commonly disrupt T1 root fibres, causing pain and numbness in the inner aspect of the upper arm and wasting of the small hand muscles. The upper thoracic sympathetic outflow to the eye may also be compromised, leading to a constricted pupil and ptosis. In the mid and lower mediastinum, tumours can invade and compromise the pericardium, atria and oesophagus.
In health, the lungs optimise gas exchange by close matching of regional ventilation and perfusion. Airway and parenchymal lung diseases disrupt this matching, causing hypoxia and cyanosis, and commonly stimulate breathing through lung afferent nerves, leading to a history of breathlessness and tachypnoea upon examination.
---
## THE HISTORY
### Respiratory History-Taking Framework
The key features of the history should include:
**History of presenting symptoms**
- Specific respiratory symptoms:
- Breathlessness
- Wheeze
- Cough
- Sputum/haemoptysis
- Chest pain
- Fever/rigors/night sweats
- Weight loss
- Sleepiness
**Past medical history**
- Respiratory disease
- Other illness/hospital encounters
**Drug and allergy history**
- Drugs causing or relieving respiratory symptoms
- Allergies to pollens/pets/dust; anaphylaxis
**Social and family history**
- Family history of respiratory disease
- Home circumstances and effect of disease
- Smoking
- Occupational history
**Systematic review**
- Systemic diseases involving the lung
- Risk factors for lung disease
---
## COMMON PRESENTING SYMPTOMS
### BREATHLESSNESS
Breathlessness (dyspnoea) denotes the feeling of an 'uncomfortable need to breathe' and is the most commonly reported respiratory symptom. It is also one of the most challenging to quantify, being inherently subjective. Breathlessness may be caused by respiratory or cardiac disease and also occurs in anaemia or as a manifestation of psychological distress.
#### Mechanisms of Breathlessness in Respiratory Disease
Respiratory disease can cause breathlessness through a range of mechanisms:
1. **Stimulation of intrapulmonary afferent nerves** by interstitial inflammation or thromboembolism
2. **Mechanical loading of respiratory muscles** by airflow obstruction or reduced lung compliance in fibrosis
3. **Hypoxia due to ventilation/perfusion mismatch**, stimulating chemoreceptors
#### Medical Research Council (MRC) Breathlessness Scale
The MRC breathlessness scale is a useful and validated way to document formally the patient's level of dyspnoea.
| Grade | Degree of breathlessness related to activities |
|:---:|:---|
| **1** | Not troubled by breathlessness except on strenuous exercise |
| **2** | Short of breath when hurrying on the level or walking up a slight hill |
| **3** | Walks slower than most people on the level, stops after a mile or so, or stops after 15 min walking at own pace |
| **4** | Stops for breath after walking about 100 yards or after a few minutes on level ground |
| **5** | Too breathless to leave the house, or breathlessness when undressing |
*Used with the permission of the Medical Research Council.*
#### Key Questions to Distinguish Causes of Breathlessness
**How did the breathlessness start?**
- If the onset was instantaneous, think of pneumothorax, pulmonary embolus or anaphylaxis
- Paroxysmal nocturnal dyspnoea may wake a sleeping patient with breathlessness
- Onset over hours is typical in asthma, acute pulmonary oedema, lobar pneumonia, or acute hypersensitivity pneumonitis
- An insidious onset is more typical of evolving pleural effusion, COPD, interstitial lung disease and lung tumours
**How is your breathing at rest and overnight?**
- Asthma commonly wakes patients
- Most patients with COPD are comfortable at rest and when asleep but struggle with exertion
- Breathlessness provoked by lying down (orthopnoea) is a feature of heart failure but also occurs in patients with severe airflow obstruction or diaphragmatic weakness (weight of abdomen displaces diaphragm cranially on lying down, compromising vital capacity)
**Does your breathlessness vary from day to day or week to week?**
- Variable breathlessness is typical of asthma
- Patients with COPD or interstitial lung disease usually report consistent daily limitation
**Can you tell me something you do that would make you breathless? How far can you walk on a good day?**
- These questions reveal the disability caused by respiratory disease
- Record restrictions on normal activity or work and the corresponding MRC breathlessness score
- Enquiring about hobbies and daily activities reveals the time course of breathlessness
- Example: 'When was the last time you could walk to the shops / play a full round of golf?'
**When does the breathlessness start?**
- Asthma induced by exercise frequently appears only after exercise during early recovery
- This is because sympathetic drive during exercise defends airway patency
**Is it worse on waking in the morning and relieved by clearing sputum?**
- This is common in COPD and bronchiectasis
#### Psychological Breathlessness
Certain phrases in the history strongly suggest a psychological aetiology of breathlessness, particularly:
- 'I feel I can't get enough air (or oxygen) into my chest'
In patients with hyperventilation due to anxiety, this symptom is frequently accompanied by a normal measured vital capacity. Associated symptoms induced by hypocapnia in hyperventilation include:
- Digital and perioral paraesthesia
- Light-headedness
- Chest tightness
---
### WHEEZE
Wheeze describes the high-pitched musical or 'whistling' sounds produced by turbulent air flow through small airways narrowed by bronchospasm and/or airway secretions. It is heard mostly during expiration, which additionally narrows the airways.
#### Distinction from Other Sounds
Wheeze must be distinguished from:
- **Rattling sounds** (inspiratory and expiratory) caused by loose, mobile secretions in the upper airways
- **Stridor**: the louder, dramatic croak caused by obstruction in the trachea or large airways
Patients may be unaware of nocturnal wheeze, which may be noticed only by their bed partner.
#### Associated Conditions
Wheeze is most commonly associated with:
- Asthma
- COPD
- Acute bronchitis
- Exacerbations of bronchiectasis
- Congestive cardiac failure ('cardiac wheeze')
#### Key Questions about Wheeze
**Is the wheeze worse during or after exercise?**
- If it occurs during exercise and limits it, this suggests COPD
- In asthma, wheeze and tightness usually appear after exercise
**Do you wake with wheeze during the night?**
- This suggests asthma
**Do you have hay fever or other allergies?**
- Atopy is common in allergic asthma
- A family history of wheeze or asthma is common
---
### COUGH
The cough reflex has evolved to dislodge foreign material and secretions from the central airways and may be triggered by pathology at any level of the bronchial tree. Inspiration is followed by an expiratory effort against a closed glottis. Subsequent sudden opening of the glottis with rapid expiratory flow produces the characteristic sound.
Cough is most commonly a symptom of acute viral bronchitis, which is usually self-limiting over days to weeks. **A cough that fails to settle within 3 weeks should prompt consideration of underlying respiratory disease.**
#### Ask About:
- Duration of the cough
- Whether it is present every day
- If it is intrusive/irresistible or whether the patient coughs deliberately to clear a perceived obstruction (throat clearing)
- Whether it produces sputum; if so, how much and what colour?
- Any haemoptysis?
- Any triggers (such as swallowing, cold air, during or after exercise, allergens)
#### Box 5.3: Causes of Chronic Cough
| Pathophysiology | Suggestive Features in History/Examination |
|:---|:---|
| **Airways Inflammation** | |
| Asthma - 'cough-variant asthma' | Affects children and some adults; Often present at night; Associated wheezing, atopy |
| Chronic obstructive pulmonary disease | History of smoking and intermittent sputum |
| Persisting airway reactivity following acute bronchitis | Cough persisting after recent infection |
| Bronchiectasis | Daily purulent sputum for long periods; Pneumonia or whooping cough in childhood; Recurrent haemoptysis |
| **Lung cancer** | Persistent cough, especially in smokers; Any haemoptysis; Pneumonia that fails to clear in 4-6 weeks |
---
### SPUTUM
In health, the airway lining fluid coating the tracheobronchial tree ascends the mucociliary escalator to the larynx, where it mixes with upper respiratory tract secretions and saliva and is swallowed. In disease, the accumulation of inflammatory cells, mucus and proteinaceous secretions in the airways results in cough with expectoration of sputum.
Ask the patient about the colour, volume and consistency of sputum. Direct examination of the sputum is useful to verify the account.
#### Colour of Sputum
- **Clear (mucoid)**: COPD/bronchiectasis without current infection
- **Yellow (mucopurulent)**: Acute lower respiratory tract infection/asthma
- **Green (purulent)**: Current infection - acute disease or exacerbation of chronic disease, such as COPD. In bronchiectasis (and COPD), the colour and volume of sputum may be used to guide the need for antibiotics. In asthma, mucopurulent sputum may be the result of sputum eosinophilia.
- **Red/brown (rusty)**: Pneumococcal pneumonia. Try to distinguish between rusty and frank red blood.
- **Pink (serous/frothy)**: Acute pulmonary oedema.
#### Volume of Sputum
- Establish the volume produced over 24 hours: small amounts into a tissue or enough to fill a spoon(s), eggcup(s), or cup(s)
- Compare the current volume with the patient's baseline volume
- Large volumes of sputum over long periods suggest bronchiectasis
#### Consistency of Sputum
- An increase in stickiness (viscosity) may indicate exacerbation in bronchiectasis
- Occasionally, sputum is produced as firm 'plugs' by patients with asthma, sometimes indicating underlying allergic bronchopulmonary aspergillosis
- Large volumes of frothy secretions over weeks/months are a feature of the uncommon bronchoalveolar cell carcinoma
---
### HAEMOPTYSIS
Haemoptysis means coughing up blood from the respiratory tract. Whilst it can complicate any severe forceful cough, **never assume haemoptysis has a benign cause, particularly in a smoker, until underlying pathology has been excluded.**
#### Enquire About These Features:
**Was the blood coughed up from the chest?**
- Blood in the mouth may be vomited, may have come from the nose in epistaxis, or may appear on chewing or tooth brushing in patients with gum disease
**When did blood appear, how much blood, were there associated symptoms and over what time period was it present?**
- Acute or chronic bronchial infections, including tuberculosis, other mycoses
- Recurrent blood streaks in clear sputum should prompt a search for lung cancer
- Recurrent blood streaks in purulent sputum over years suggests bronchoectasis
- A sudden episode of haemoptysis with pleuritic pain and breathlessness suggests pulmonary embolism
- Large volumes of haemoptysis (>20 mL) suggest specific causes:
- Lung cancer eroding a pulmonary vessel
- Bronchiectasis (such as in cystic fibrosis)
- Cavitary disease (e.g., complicating an aspergilloma or cavitary pulmonary tuberculosis)
- Pulmonary arterovenous malformation
#### Associated Features to Note:
- Any fever/symptoms of infection? - Acute or chronic bronchial infections, including tuberculosis and other mycoses
- Recurrent blood streaks in clear sputum should prompt a search for lung cancer
- Recurrent blood streaks in purulent sputum over years suggests bronchoectasis
- A sudden episode of haemoptysis with pleuritic pain and breathlessness suggests pulmonary embolism
---
### STRIDOR
This harsh, grating respiratory sound is caused by vibration of the tracheal walls or major bronchi when the airway lumen is critically narrowed by compression, tumour or inhaled foreign material. Inspiration lowers the pressure inside the narrowed airways, so stridor narrows the lumen further by suction, whereas during expiration the positive pressure in surrounding lung leads to forced expiratory airflow and stridor. Large airway narrowing at thoracic inlet (e.g., tracheal compression by a large goitre) may cause inspiratory stridor, in contrast, the intra-thoracic lung airways are compressed during expiration by positive pressure, leading to forced expiratory stridor. Rigid inspiration and expiratory stridor, in contrast, the intra-thoracic lung airways are compressed during expiration by positive pressure, leading to forced expiratory stridor. Rigid inspiration and expiratory stridor indicates fixed obstruction.
---
### CHEST PAIN
Chest pain can arise from the chest wall, parietal pleura, mediastinal structures, tracheobronchial tree, pericardium, oesophagus and subdiaphragmatic organs (liver and gallbladder). Pain does not originate in the lung parenchyma or visceral pleura, as they have only an autonomic nerve supply.
#### Establish:
- **Site and severity**
- **Character**: Sharp suggests pleural pain
- **Onset**: Gradual or rapid?
#### Exacerbating or Relieving Factors:
- Worsening with cough or deep breathing suggests pleural disease
- Pleuritic disease supports pleural aetiology
#### Associated Symptoms:
- Breathlessness, fever and cough may suggest pleural causes
- Patients use many different terms to describe fever (e.g., chills, shakes), so take care to clarify their actual symptoms
#### Important Clinical Considerations:
A large pulmonary embolus can cause angina-like chest pain in the right ventricular region with reduced coronary oxygen delivery caused by hypotension and hypoxaemia, resulting in right ventricular ischaemia.
**Pleuritic pain** is worse on inspiration and coughing, and is usually described as sharp, stabbing or knife-like. It is usually sited away from the midline and may follow the course of a nerve distribution in a dermatomal pattern. It is more pronounced when the patient lies on the affected side, and may be relieved if leaning towards the affected side, allowing separation of the pleura. Disease causes parietal pleural pain in several ways:
- Pneumonia and pulmonary infarcts: Direct inflammation or adhesions with pleural friction
- Pneumothorax: Mechanical distortion of pleura with lung collapse
- Lung cancer: Pleural distortion by infiltration, although concomitant pleural effusion may reduce pain
**Musculoskeletal chest pain** is common and may occur with firm palpation of the chest wall. The chest is characteristically tender to palpation, and the pain can be reproduced by respiratory movement and/or movement of the spine or shoulder muscles. There may be associated soft tissue injury or in history. A careful history of trauma or injury is easily overlooked. Tietze's syndrome (an infection with an enterovirus or Coxsackie virus infection) is idiopathic inflammation of costochondral cartilages adjoining the sternum, with acute localised pain and tenderness.
Costochondritis (also called Tietze's syndrome) involves inflammation of intercostal muscles, with episodes of severe unilateral intercostal myalgia lasting a few days. Musculoskeletal pain syndromes and altered sensation may persist long after the rash has resolved, akin to herpes zoster disease.
**Burning retrosternal pain** may indicate oesophagitis but also occurs in myocardial ischaemia. Worsening of oesophageal pain after eating or relief after antacids helps to distinguish this from cardiac pain.
**Cardiac pain** is described on page 45.
---
## PAST MEDICAL HISTORY
Past illnesses relevant to respiratory disease are summarised below. These include respiratory disease that may recur or cause long-term sequelae, and disease in other systems that may cause, complicate or present with respiratory symptoms, including thromboembolic, cardiovascular, haematological, malignant and connective tissue diseases.
Note prior respiratory treatments (including need for critical care) and the degree of chronic symptoms, such as exacerbation frequency, prescription rate and hospitalisation.
### Box 5.4: Previous Illness Relevant to Respiratory History
| History | Current Implications |
|:---|:---|
| Eczema, hay fever | Allergic tendency relevant to asthma |
| Chickenpox | Many wheesy children do not have asthma as adults; wheeze |
| Whooping cough, inhaled foreign body, measles | Recognised causes of bronchiectasis, especially if complicated by pneumonia |
| Pneumonia, pleurisy | Recurrent episodes may be a manifestation of bronchiectasis. Some pneumonias may cause bronchiectasis |
| Tuberculosis | Reactivation if not previously treated effectively; Post-tuberculous bronchiectasis - sputum, haemoptysis; Aspergilloma in lung cavity may present with haemoptysis |
| Connective tissue disorders, e.g. rheumatoid arthritis | Many have respiratory manifestations, e.g. pulmonary fibrosis, effusions; Bronchiolitis obliterans organising pneumonia (BOOP) may be associated. Some pneumonias may cause bronchiectasis |
| Previous malignancy | Recurrence, metastatic/pleural disease; Chemotherapy can cause pulmonary fibrosis (e.g., bleomycin); Radiotherapy-induced pulmonary fibrosis |
| Cancer, recent travel, surgery or immobility | Pulmonary thromboembolism |
| Recent surgery, loss of consciousness | Aspiration of foreign body, gastric contents leading to pneumonia, lung abscess |
| Neuromuscular disorders | Respiratory failure; Aspiration |
---
## DRUG AND ALLERGY HISTORY
Note all drugs that the patient is currently using, including inhalers, nasal therapy, topical preparations and recreational drugs. Cross-check the drug names and doses with a separate source such as the general practitioner's records.
Drugs given for other problems commonly cause respiratory side effects. These are summarised in Box 5.5.
### Ask Whether the Patient Has Allergies
Such as to hay fever, as allergic asthma is far more common in those with a history of atopy.
### Box 5.5: Respiratory Problems Caused by Drugs
| Respiratory Condition | Drug |
|:---|:---|
| Bronchoconstriction | Beta-blockers (including eye drops); Opioids; Nonsteroidal anti-inflammatory drugs |
| Cough | Angiotensin-converting enzyme inhibitors |
| Bronchitis (dilators) | Penicillamine |
| Diffuse parenchymal lung disease | Cytotoxic agents: bleomycin, methotrexate; Anti-inflammatory agents: sulphasalazine, penicillamine; gold salts, aspirin; Cardiovascular drugs: amiodarone, hydralazine; Antibiotics: nitrofurantoin |
| Pulmonary thromboembolism | Oestrogens |
| Pulmonary hypertension | Oestrogens; Dexfenfluramine; Fenfluramine |
| Pleural effusion | Amiodarone; Nitrofurantoin; Phenytoin; Methylxanthine |
| Respiratory depression | Opioids; Benzodiazepines |
| Tuberculosis | Reactivation by glucocorticoids or disease modifying antirheumtic drugs (DMARDs); biological immunomodulators given for rheumatic disease |
---
## FAMILY HISTORY
Respiratory diseases with a known genetic cause are relatively rare. Patients with autosomal recessive conditions such as cystic fibrosis usually have unaffected carrier parents but may have affected siblings. A family history of venous thromboembolism should prompt investigation of inherited thrombophilia such as Factor V Leiden or protein C or protein S deficiency. In rare cases, familial emphysema or primary pulmonary hypertension may be familial.
---
## SOCIAL HISTORY
### Exposures at Home
Exposures at home may cause or aggravate respiratory disease. Passive smoking increases the risk of respiratory infection and burning biomass fuels in confined spaces increases the risk of bronchitis and COPD. Domestic pets, especially cats and rodents, may be the cause of suboptimal asthma control. A pet bird, feather duvet or an infestation of mould may cause hypersensitivity pneumonitis or suboptimal asthma control.
### Smoking
Obtaining an accurate history of tobacco use is difficult and is covered on page 16 (Chapter 2). Ask if any cohabitees smoke.
---
### Box 5.6: Occupational Factors in Respiratory Disease
| Respiratory Disease | Toxic Agent(s) | Affected Occupations |
|:---|:---|:---|
| Asthma | Isocyanates | Spray painters; Baking industry |
| Rhino-conjunctivitis | Poor grain dust, enzymes; Animal dander; Wood dust | Laboratory and veterinary workers; Joiners |
| Chronic obstructive pulmonary disease | Cadmium; Silica; Coal dust; Silica | Smelters; Underground miners; Stone cutting, masonry, tunnelling, quarrying, pottery, metal ore mining, siliceous abrasive users, foundry workers; Coke oven workers |
| Byssinosis | Cotton dust | Flax workers |
| Pneumoconiosis | Coal (Coal Mines Pneumoconiosis); Silica (Silicosis); Asbestos (Asbestosis) | Miners; See above; Former luggers, asbestos textile manufacture, asbestos insulation work including marine engineering, shipmaking |
| Hypersensitivity pneumonitis | Iron (Siderosis); Tin (Stannosis); Thermophilic bacteria: Moldy hay; Moldy grain; Mushroom compost; Moldy sugar cane (Bagassosis); Metal working fluids | Iron ore mines, welders, iron foundry letters; Tin smelters; Farmers; Grain workers; Mushroom pickers; Sugar workers; Machinists |
| Pneumonia | Bird fanciers; Q fever (Coxiella burnetii); Avian pneumonia; Psittacosis (C. psittaci); Legionellosis (Legionella) | Welders; Dairy farmers, abattoir workers; Poultry workers; Sewage workers, animal handlers, vets |
| Tuberculosis | Silica (tuberculosis) | See above |
| Granulomatous disease | Beryllium (Berylliosis) | Aerospace industry, nuclear industry, oilgas drilling, dental technicians |
| Pleural disease | Asbestos: pleural plaques, diffuse pleural thickening, mesothelioma | See above |
| Lung cancer | Asbestos; Silica; Coke dust | See above |
| Connective tissue disease | Silica increases the risk of scleroderma | See above |
---
## OCCUPATIONAL HISTORY
Many respiratory diseases are caused by occupational exposure to inhaled substances. Ask the patient about their work history, starting with their first job, documenting the employers' names, the dates and duration of exposures, and whether any protective masks were offered or used.
Occupational asthma should be considered if symptoms improve on days away from work.
---
## SYSTEMATIC ENQUIRY
Systematic enquiry may reveal extrapulmonary symptoms linked to underlying respiratory disease. For example, morning headaches and drowsiness in severe respiratory failure, dysphagia following stroke can increase the risk of aspiration in respiratory failure, elevated PaCO2 in respiratory failure, elevated PaCO2 in respiratory failure, dysphagia following stroke can increase the risk of aspiration in respiratory failure.
---
## INSPECTION (Physical Examination)
Much can be learned about the respiratory system by careful inspection from the end of the bed. The normal shape and respiratory movements of the chest will significantly altered by hyperinflation and accompanying chronic airflow obstruction (p. 5.1). Forced inspiration at these very high lung volumes may cause indraving of the intercostal spaces during mid-inspiration and the recruitment of muscles not normally involved in breathing ('accessory muscles'). These include the sternocleidomastoid muscles lifting the sternum, and the trapezius and the scalenes lifting the shoulder girdle. Patients sometimes find paradoxical or "pursed-lip" breathing on expiration. Forced inspiration causes indrawn ing of the intercostal spaces. Forced inspiration at these very high lung volumes may cause indrrawing of the intercostal spaces during mid-inspiration and the recruitment of muscles not normally involved in breathing ('accessory muscles'). These include the sternocleidomastoid muscles lifting the sternum, and the trapezius and the scalenes lifting the shoulder girdle.
### Observation of Respiratory Rate
At rest, the respiratory rate is normally 12 to 15 breaths/min; a rate of over 20 breaths/min is abnormal for an adult.
In healthy adults at altitude, elderly people and patients with heart failure, or during the final stages of dying, a distinctive pattern of alternating periods of deep and shallow breathing may be seen. This is known as Cheyne-Stokes respiration and is thought to represent abnormal feedback from the carotid chemoreceptors to the respiratory centre.
---
## PALPATION
### Examination Sequence
- **Locate the apex beat**, the most inferior and lateral place where the finger is lifted by the twisting systolic movement of the cardiac apex. This is normally in the fifth intercostal space in the mid-clavicular line. Count down the intercostal spaces, and locate the apex beat by the twisting systolic movement of the cardiac apex. The apex is normally in the fifth intercostal space in the mid-clavicular line.
---
## FACE (Clinical Signs)
**Superior vena cava obstruction** causes dusky, generalised cyanosis of the head, neck and face (look for collateral junctional oedema (looking like a tear inside the lower lid, but not moist), luminal occlusion and apparently enophthalmos (Homer's syndrome).
Unilateral ptosis at the root of the neck may disrupt the sympathetic nerves to the eye, which run from the upper thoracic spinal segments in the neck to join the internal carotid artery sheath. These cause unilateral ptosis, hypohidrosis, pupillary constriction and apparent enophthalmos (Homer's syndrome).
---
## NECK
Jugular venous pressure (JVP) is raised in many patients with pulmonary hypertension and may be acutely raised in those with tension pneumothorax or large pulmonary embolism. In superior vena cava obstruction, the JVP may be raised above the angle of the jaw.
---
## HANDS AND ARMS
### Finger Clubbing
Finger clubbing is due to overgrowth of soft tissue in the terminal phalanx, which increases the lateral and longitudinal curvature of the nail. This is palpable as a boggy fluctuation of the nail when pressure is applied just proximal to the nail bed of the underlying bone. It is palpable as a boggy fluctuation of the nail when pressure is applied just proximal to the nail bed of the underlying bone. Finding this in an adult patient should prompt consideration of lung cancer or pulmonary fibrosis. In younger patients, chronic suppurative lung disease such as cystic fibrosis should be considered. In some cases of lung cancer, finger clubbing is accompanied by hypertrophic pulmonary osteoarthropathy, with painful, tender swelling of the wrists and ankles. X-rays of the distal forearm and lower legs show subperiosteal new bone formation overlying the cortex of the long bones.
Other important signs of respiratory disease in the hands include:
- **Cyanosis**
- **Tar staining of fingers from tobacco use**
---
## EXAMINATION SEQUENCE: HANDS (Videos 2C Reference)
- Examine the hands for finger clubbing, tar staining, nail discolouration and cyanosis
- Ask the patient to hold their arms out straight with the wrists extended
- Measure the respiratory rate while feeling the pulse
- Check for any tenderness in the distal forearm
### Hand Position for Testing Tremor
Use this position for testing the coarse tremor of CO2 retention in respiratory failure.
---
## EXAMINATION SEQUENCE SUMMARY
**Inspection:**
- Note the presence of nebulisers or inhalers (indicating obstructive lung disease), oxygen therapy and cyanosis
- Check sputum pots, noting the colour and viscosity of sputum and whether any blood is present
- Look for asymmetry of the chest, deformities, surgical scars and chest drains, remembering that thoracotomy scars may be visible only from the side or behind
**Palpation:**
- Locate the apex beat, the most inferior and lateral place where the finger is lifted by the twisting systolic movement of the cardiac apex
- This is normally in the fifth intercostal space in the mid-clavicular line
- Count down the intercostal spaces
---
**Created from MacLeod's Clinical Examination (Professional Medical Textbook)**
*These comprehensive notes capture the essential examination framework, clinical reasoning, and detailed symptom assessment as presented in the authoritative clinical examination guide.*
Here are your detailed notes on the Systemic Examination of the Respiratory System, compiled directly from the content in your MacLeod's screenshots:
Understanding the surface anatomy of the lungs and their relation to adjacent structures is essential for the practice of respiratory medicine. At the end of tidal expiration, the dome of the diaphragm extends high into the thorax, level with the anterior end of the fifth rib, slightly lower on the left. The lower lateral ribs therefore overlie the liver on the right and the stomach and spleen on the left, with the parietal pleura extending lower than the lungs on the lateral chest wall. Posteriorly, the lungs extend much lower, approaching the 12th rib on full inspiration.
The lung apex lies immediately beneath the brachial plexus, so apical lung tumours commonly disrupt T1 root fibres, causing pain and numbness in the inner aspect of the upper arm and wasting of the small hand muscles. The upper thoracic sympathetic outflow to the eye may also be compromised, leading to a constricted pupil and ptosis. In the mid and lower mediastinum, tumours can invade and compromise the pericardium, atria and oesophagus.
In health, the lungs optimise gas exchange by close matching of regional ventilation and perfusion. Airway and parenchymal lung diseases disrupt this matching, causing hypoxia and cyanosis, and commonly stimulate breathing through lung afferent nerves, leading to a history of breathlessness and tachypnoea upon examination.
THE HISTORY
The key features of the history are summarised in Box 5.1.
History of presenting symptoms — Specific respiratory symptoms:
Breathlessness
Wheeze
Cough
Sputum/haemoptysis
Chest pain
Fever/rigors/night sweats
Weight loss
Sleepiness
Past medical history:
Respiratory disease
Other illness/hospital encounters
Drug and allergy history:
Drugs causing or relieving respiratory symptoms
Allergies to pollens/pets/dust; anaphylaxis
Social and family history:
Family history of respiratory disease
Home circumstances/effect of and on disease
Smoking
Occupational history
Systematic review:
Systemic diseases involving the lung
Risk factors for lung disease
COMMON PRESENTING SYMPTOMS
BREATHLESSNESS
Breathlessness (dyspnoea) denotes the feeling of an 'uncomfortable need to breathe' and is the most commonly reported respiratory symptom. It is also one of the most challenging to quantify, being inherently subjective. Breathlessness may be caused by respiratory or cardiac disease and also occurs in anaemia or as a manifestation of psychological distress.
Respiratory disease can cause breathlessness through a range of mechanisms:
Stimulation of intrapulmonary afferent nerves by interstitial inflammation or thromboembolism
Mechanical loading of respiratory muscles by airflow obstruction or reduced lung compliance in fibrosis
Hypoxia due to ventilation/perfusion mismatch, stimulating chemoreceptors
The Medical Research Council (MRC) breathlessness scale (Box 5.2) is a useful and validated way to document formally the patient's level of dyspnoea.
Box 5.2: MRC Breathlessness Scale
Grade
Degree of breathlessness related to activities
1
Not troubled by breathlessness except on strenuous exercise
2
Short of breath when hurrying on the level or walking up a slight hill
3
Walks slower than most people on the level, stops after a mile or so, or stops after 15 min walking at own pace
4
Stops for breath after walking about 100 yards or after a few minutes on level ground
5
Too breathless to leave the house, or breathless when undressing
Used with the permission of the Medical Research Council.
Key Questions to Distinguish Causes of Breathlessness:
How did the breathlessness start? If the onset was instantaneous, think of pneumothorax, pulmonary embolus or anaphylaxis. Paroxysmal nocturnal dyspnoea may wake a sleeping patient with breathlessness. Onset over hours is typical in asthma, acute pulmonary oedema, lobar pneumonia, or acute hypersensitivity pneumonitis, while an insidious onset is more typical of an evolving pleural effusion, COPD, interstitial lung disease and lung tumours.
How is your breathing at rest and overnight? Asthma commonly wakes patients, while most patients with COPD are comfortable at rest and when asleep but struggle with exertion. Breathlessness provoked by lying down (orthopnoea) is a feature of heart failure but also occurs frequently in patients with severe airflow obstruction or diaphragmatic weakness because the weight of the abdomen displaces the diaphragm cranially on lying down, compromising the vital capacity.
Does your breathlessness vary from day to day or week to week? Variable breathlessness is typical of asthma, whereas patients with COPD or interstitial lung disease usually report consistent daily limitation.
Can you tell me something you do that would make you breathless? How far can you walk on a good day? These questions reveal the disability caused by respiratory disease. Record restrictions on normal activity or work and the corresponding MRC breathlessness score. Enquiring about hobbies and daily activities reveals the time course of breathlessness; for example, 'When was the last time you could walk to the shops / play a full round of golf?'
When does the breathlessness start? Asthma induced by exercise frequently appears only after exercise during early recovery, because sympathetic drive during exercise defends airway patency.
Is it worse on waking in the morning and relieved by clearing sputum? This is common in COPD and bronchiectasis.
Psychological Breathlessness:
Certain phrases in the history strongly suggest a psychological aetiology of breathlessness, particularly: 'I feel I can't get enough air (or oxygen) into my chest.' In patients with hyperventilation due to anxiety, this symptom is frequently accompanied by a normal measured vital capacity. Associated symptoms induced by hypocapnia in hyperventilation include digital and perioral paraesthesia, light-headedness and chest tightness.
DIAGNOSTIC APPROACH TO BREATHLESSNESS (Fig. 5.2)
Duration
Time course
Other history
Examination findings
Diagnosis
Acute or subacute
Sudden
Pleuritic pain
Haemoptysis, swollen leg
Pulmonary embolus/infarct
Unilateral absent breath sounds
Pneumothorax
Crushing central pain
Crackles in chest
MI with pulmonary oedema
Normal breath sounds, raised JVP
Large pulmonary embolus
Hours/days
Fever, cough, green sputum
Signs of consolidation, rigors
Pneumonia
Wheeze
Acute bronchitis
Tightness, atopy/pets
Wheeze
New onset of asthma
Insidious
Weight loss, cough
Unilateral dullness, clubbing
Malignant pleural effusion
Crackles, night sweats
Tuberculosis
Dry cough
Fine inspiratory crackles
New interstitial disease
Chronic
Occurs at rest/night
Angina, frothy sputum
Crackles, peripheral oedema
Congestive cardiac failure
Tightness, atopy/pets
Wheeze
Asthma
Paraesthesia, 'can't get enough air'
Carpopedal spasm, anxiety
Hyperventilation
Exertional
Smoker
Hyperinflation
COPD
Dry cough
Fine inspiratory crackles
Interstitial lung disease
WHEEZE
Wheeze describes the high-pitched musical or 'whistling' sounds produced by turbulent air flow through small airways narrowed by bronchospasm and/or airway secretions. It is heard mostly during expiration, which additionally narrows the airways.
Wheeze must be distinguished from:
The rattling inspiratory and expiratory sounds caused by loose, mobile secretions in the upper airways
The louder, dramatic croak of stridor caused by obstruction in the trachea or large airways
Patients may be unaware of nocturnal wheeze, which may be noticed only by their bed partner.
Wheeze is most commonly associated with asthma and COPD but can also occur with acute bronchitis, exacerbations of bronchiectasis or congestive cardiac failure ('cardiac wheeze').
Ask:
Is the wheeze worse during or after exercise? If it occurs during exercise and limits it, this suggests COPD; in asthma, wheeze and tightness usually appear after exercise.
Do you wake with wheeze during the night? This suggests asthma.
Do you have hay fever or other allergies? Atopy is common in allergic asthma. A family history of wheeze or asthma is common.
COUGH
The cough reflex has evolved to dislodge foreign material and secretions from the central airways and may be triggered by pathology at any level of the bronchial tree. Inspiration is followed by an expiratory effort against a closed glottis. Subsequent sudden opening of the glottis with rapid expiratory flow produces the characteristic sound.
Cough is most commonly a symptom of acute viral bronchitis, which is usually self-limiting over days to weeks. A cough that fails to settle within 3 weeks should prompt consideration of underlying respiratory disease.
Ask about:
Duration of the cough
Whether it is present every day
If it is intrusive/irresistible or whether the patient coughs deliberately to clear a perceived obstruction (throat clearing)
Whether it produces sputum; if so, how much, and what colour?
Any haemoptysis?
Any triggers (such as swallowing, cold air, during or after exercise, allergens)
Other relevant features:
Smoking, as this increases the likelihood of chronic bronchitis or lung cancer
Associated clinical features: wheeze (may signal cough-variant asthma); heartburn or reflux (gastro-oesophageal reflux commonly triggers cough); altered voice or swallowing (consider laryngeal causes)
Drug history, especially ACE inhibitors
Cough that produces green or yellow sputum suggests bronchial infection. Large volumes of sputum over long periods suggest bronchiectasis.
In patients with malignancy at the left hilum, damage to the left recurrent laryngeal nerve may paralyse the left vocal cord, making it impossible for the patient to close the glottis and generate a normal explosive cough. The resulting hoarse forced expiration without the initial explosive glottal opening is called a 'bovine cough.'
Box 5.3: Causes of Chronic Cough and Accompanying Clues
Pathophysiology
Suggestive Features in History/Examination
Airways Inflammation
Asthma - 'cough-variant asthma'
Affects children and some adults; Often present at night; Associated wheezing, atopy
Chronic obstructive pulmonary disease
History of smoking and intermittent sputum
Persisting airway reactivity following acute bronchitis
Cough persisting after recent infection
Bronchiectasis
Daily purulent sputum for long periods; Pneumonia or whooping cough in childhood; Recurrent haemoptysis
Lung cancer
Persistent cough, especially in smokers; Any haemoptysis; Pneumonia that fails to clear in 4-6 weeks
Rhinitis with postnasal drip
Chronic sneezing, nasal blockage/discharge
Oesophageal reflux
Heartburn or acid reflux after eating, bending or lying; Nocturnal and daytime cough
Drug effects
Angiotensin-converting enzyme inhibitors
Interstitial lung diseases
Persistent dry cough; Fine inspiratory crackles at bases
Idiopathic cough
Long history with no signs and negative investigations - diagnosis of exclusion
SPUTUM
In health, the airway lining fluid coating the tracheobronchial tree ascends the mucociliary escalator to the larynx, where it mixes with upper respiratory tract secretions and saliva and is swallowed. In disease, the accumulation of inflammatory cells, mucus and proteinaceous secretions in the airways results in cough with expectoration of sputum. Ask the patient about the colour, volume and consistency of sputum. Direct examination of the sputum is useful to verify the account.
Colour:
Clear (mucoid): COPD/bronchiectasis without current infection
Green (purulent): Current infection - acute disease or exacerbation of chronic disease such as COPD. In bronchiectasis (and COPD), the colour and volume of sputum may be used to guide the need for antibiotics. In asthma, mucopurulent sputum may be the result of sputum eosinophilia.
Red/brown (rusty): Pneumococcal pneumonia. Try to distinguish between rusty and frank red blood.
Pink (serous/frothy): Acute pulmonary oedema.
Volume:
Establish the volume produced over 24 hours: small amounts into a tissue or enough to fill a spoon(s), eggcup(s) or cup(s)
Compare the current volume with the patient's baseline volume
Large volumes of sputum over long periods suggest bronchiectasis
Consistency:
An increase in stickiness (viscosity) may indicate exacerbation in bronchiectasis
Occasionally, sputum is produced as firm 'plugs' by patients with asthma, sometimes indicating underlying allergic bronchopulmonary aspergillosis
Large volumes of frothy secretions over weeks/months are a feature of the uncommon bronchoalveolar cell carcinoma
HAEMOPTYSIS
Haemoptysis means coughing up blood from the respiratory tract. Whilst it can complicate any severe forceful cough, never assume haemoptysis has a benign cause, particularly in a smoker, until underlying pathology has been excluded.
Enquire about:
Was the blood coughed up from the chest? Blood in the mouth may be vomited, may have come from the nose in epistaxis, or may appear on chewing or tooth brushing in patients with gum disease.
When did blood appear, how much blood, were there associated symptoms and over what time period was it present?
Any fever/symptoms of infection? Acute or chronic bronchial infections, including tuberculosis and other mycoses, often trigger haemoptysis.
Recurrent blood streaks in clear sputum should prompt a search for lung cancer.
Recurrent blood streaks in purulent sputum over years suggests bronchiectasis.
A sudden episode of haemoptysis with pleuritic pain and breathlessness suggests pulmonary embolism.
Large volumes of haemoptysis (>20 mL) suggest specific causes:
Lung cancer eroding a pulmonary vessel
Bronchiectasis (such as in cystic fibrosis)
Cavitary disease (e.g., complicating an aspergilloma or cavitary pulmonary tuberculosis)
Pulmonary vasculitis
Pulmonary arteriovenous malformation
STRIDOR
This harsh, grating respiratory sound is caused by vibration of the tracheal walls or major bronchi when the airway lumen is critically narrowed by compression, tumour or inhaled foreign material. Inspiration lowers the pressure inside the extrathoracic trachea, so critical narrowing here leads to inspiratory stridor. In contrast, the intrathoracic large airways are compressed during expiration by positive pressure in the surrounding lung, leading to fixed expiratory wheeze or stridor. Large airway narrowing at the thoracic inlet (e.g., tracheal compression by a large goitre) may cause both inspiratory and expiratory stridor. Rapid investigation and treatment are vital when this sign is present.
CHEST PAIN
Chest pain can arise from the chest wall, parietal pleura, mediastinal structures, tracheobronchial tree, pericardium, oesophagus and subdiaphragmatic organs (liver and gallbladder). Pain does not originate in the lung parenchyma or visceral pleura, as they have only an autonomic nerve supply.
Establish:
Site and severity
Character: sharp suggests pleural pain
Onset: gradual or rapid?
Exacerbating or relieving factors:
Worsening with cough or deep breaths suggests pleural disease
Important causes:
Pleuritic pain is worse on inspiration and coughing, and is usually described as sharp, stabbing or knife-like. Disease causes parietal pleural pain in several ways:
Pneumonia and pulmonary infarcts: direct pleural inflammation or adhesions with pleural traction on respiratory movement
Pneumothorax: mechanical distortion of pleura with lung collapse
Lung cancer: pleural distortion by infiltration, although constant pain is more typical
Musculoskeletal chest pain is common and may occur with chest trauma, forceful coughing or connective tissue disease. The chest is characteristically tender to palpation, and the pain can be reproduced by respiratory movements. Bornholm disease (Coxsackie B enterovirus infection) causes acute self-limiting inflammation of intercostal muscles. Costochondritis (Tietze's syndrome) is idiopathic inflammation of costochondral cartilages adjoining the sternum.
Herpes zoster may start with superficial itch or burning pain in a thoracic dermatome, followed by appearance of a vesicular rash ('a belt of roses from hell').
Burning retrosternal pain may indicate oesophagitis but also occurs with myocardial ischaemia.
These symptoms are not specific but are commonly reported by patients with respiratory illnesses. Infection (acute or chronic) is the usual cause, but other aetiologies such as lung cancer or vasculitis should also be considered.
Patients use many different terms to describe fever (e.g., shivers, chills, shakes), so take care to clarify their actual symptoms.
Rigors are generalised, uncontrollable episodes of vigorous body shaking lasting a few minutes. Despite high fever, the patient may complain of feeling cold and seek extra clothing. Rigors usually indicate bacterial sepsis; lobar pneumonia and acute pyelonephritis are the most common causes.
Night sweats, particularly if persistent, are associated with chronic infection such as tuberculosis or malignancy, particularly lymphoma. If patients report having to change their nightclothes or sheets frequently due to profuse nocturnal sweating over several weeks, this suggests underlying disease.
WEIGHT LOSS
Weight loss is a common feature of respiratory diseases, including lung cancer, COPD, interstitial lung disease, and chronic infections such as tuberculosis and bronchiectasis. The pathophysiology is complex; however, breathlessness is associated with diminished appetite, and the systemic inflammatory response is also thought to contribute to weight loss.
Weight loss also occurs in acute infection with loss of appetite, particularly during hospitalisation. Ask the patient to estimate the extent and duration of weight loss and enquire about appetite and dietary intake.
SLEEPINESS
Excessive daytime sleepiness may be a symptom of an underlying sleep-related breathing disorder - obstructive sleep apnoea (OSA) or OSA/sleep hypopnoea (OSASH). In these conditions, the upper airway collapses intermittently and repeatedly during sleep. Partial obstruction results in snoring, but complete collapse stimulates increased respiratory effort resulting in transient wakening. Repeated episodes of sleep disturbance cause excessive daytime sleepiness and poor concentration. OSASH is more common in men; particularly if obese and with a large neck (collar sizes >17 inches) and can be aggravated by alcohol.
Ask about:
Normal sleeping habit: does the patient keep hours that allow reasonable rest?
Shift or night work: this can disrupt and prevent healthy sleep patterns
Does the person wake refreshed or exhausted?
Have they struggled to stay awake in the day: for example, at work or when driving?
PAST MEDICAL HISTORY
Past illnesses relevant to respiratory disease include respiratory disease that may recur or cause long-term symptoms, and disease in other systems that may cause, complicate or present with respiratory symptoms, including thromboembolic, cardiovascular, haematological, malignant and connective tissue diseases.
Note prior respiratory treatments (including need for critical care) and the degree of chronic symptoms, such as usual exacerbation frequency, prescription rate and hospitalisation.
Box 5.4: Previous Illness Relevant to Respiratory History
History
Current Implications
Eczema, hay fever
Allergic tendency relevant to asthma
Childhood asthma
Many whezy children do not have asthma as adults, yet many adults with asthma had childhood wheeze
Whooping cough, inhaled foreign body, measles
Recognised causes of bronchiectasis, especially if complicated by pneumonia
Pneumonia, pleurisy
Recurrent episodes may be a manifestation of bronchiectasis. Some pneumonias may cause bronchiectasis
Tuberculosis
Reactivation if not previously treated effectively; Post-tuberculous bronchiectasis - sputum, haemoptysis; Aspergilloma in lung cavity may present with haemoptysis
Connective tissue disorders e.g. rheumatoid arthritis
Many have respiratory manifestations e.g. pulmonary fibrosis, effusions, bronchiectasis; Immunomodulatory treatments for rheumatological diseases may cause pulmonary toxicity or make patients susceptible to respiratory infection
Previous malignancy
Recurrence, metastatic/pleural disease; Chemotherapy can cause pulmonary fibrosis (e.g., bleomycin); Radiotherapy-induced pulmonary fibrosis
Cancer, recent travel, surgery or immobility
Pulmonary thromboembolism
Recent surgery, loss of consciousness
Aspiration of foreign body, gastric contents leading to pneumonia, lung abscess
Neuromuscular disorders
Respiratory failure; Aspiration
DRUG AND ALLERGY HISTORY
Note all drugs that the patient is currently using, including inhalers, nebulised therapy, domiciliary oxygen, non-prescription remedies and recreational drugs. Cross-check the drug names and doses with a separate source such as the general practitioner's records.
Ask whether the patient has allergies such as hay fever, as allergic asthma is far more common in those with a history of atopy.
Reactivation by glucocorticoids or disease modifying antirheumatic drugs (DMARDs)/biological immunomodulators given for rheumatic disease
FAMILY HISTORY
Respiratory diseases with a known genetic cause are relatively rare. Patients with autosomal recessive conditions such as cystic fibrosis usually have unaffected carrier parents but may have affected siblings. A family history of venous thromboembolism should prompt investigation of inherited thrombophilias such as Factor V Leiden or protein C or protein S deficiency. In rare cases, idiopathic pulmonary fibrosis and primary pulmonary hypertension may be familial.
SOCIAL HISTORY
Exposures at home may cause or aggravate respiratory disease. Passive smoking increases the risk of respiratory infection and burning biomass fuels in confined spaces increases the risk of bronchitis and COPD. Domestic pets, especially cats and rodents, may be the cause of suboptimal asthma control. A pet bird, feather duvet or an infestation of mould may cause hypersensitivity pneumonitis or suboptimal asthma control.
Smoking
Obtaining an accurate history of tobacco use is covered in Chapter 2. Ask if any cohabitees smoke. Remember also to ask about cannabis, waterpipes and e-cigarettes.
OCCUPATIONAL HISTORY
Many respiratory diseases are caused by occupational exposure to inhaled substances. Ask the patient about their work history, starting with their first job, documenting the employers' names, the dates and duration of exposure, and whether any protective masks were offered or used.
Occupational asthma should be considered if symptoms improve on days away from work.
Box 5.6: Occupational Factors in Respiratory Disease
Spray painters; Baking industry; Laboratory and veterinary workers; Joiners
COPD
Cadmium fumes; Coal dust; Silica; Coke dust
Solderers; Underground miners; Stone cutting, masonry, tunnelling, quarrying, pottery, metal ore mining, siliceous abrasive users, foundry workers; Coke oven workers
Byssinosis
Cotton dust
Flax workers
Pneumoconiosis
Coal (Coal Miners Pneumoconiosis); Silica (Silicosis); Asbestos (Asbestosis); Iron (Siderosis); Tin (Stannosis)
Miners; See above; Former laggers, asbestos textile manufacture including marine engineering, shipbreaking; Iron ore miners, welders, iron foundry fettlers; Tin smelters
Hypersensitivity pneumonitis
Thermophilic bacteria; Mouldy hay; Mouldy grain; Mushroom compost; Mouldy sugar cane (Bagassosis); Avian serum/excreta; Metal working fluids
Inhalation of organic dusts may trigger hypersensitivity pneumonitis. Inhalation of inorganic dusts such as asbestos, coal or silica cause pneumoconiosis, with gradual onset of cough and breathlessness, often years after exposure. Certain occupations increase the risk of respiratory infection, for example Q fever in abattoir workers and leptospirosis in sewage workers and animal handlers.
SYSTEMATIC ENQUIRY
Systematic enquiry may reveal extrapulmonary symptoms linked to underlying respiratory disease. For example, morning headaches can indicate an elevated PaCO2 in respiratory failure, and dysphagia following stroke can increase the risk of aspiration pneumonia.
THE PHYSICAL EXAMINATION
It is often easiest to examine the patient reclining on the bed or an examination couch at about 45 degrees, with the thorax exposed and the head supported by a pillow.
INSPECTION
Much can be learned about the respiratory system by careful inspection from the end of the bed. The normal shape and respiratory movements of the chest wall are significantly altered by the hyperinflation that accompanies chronic airflow obstruction. Such obstruction also causes prolonged expiration relative to inspiration, and sometimes 'pursed-lip' breathing on expiration. Forceful inspiration at these very high lung volumes may cause indrrawing of the intercostal spaces during mid-inspiration and the recruitment of muscles not normally involved in breathing ('accessory muscles'). These include the sternocleidomastoid muscles lifting the sternum, and the trapezius and the scalenes lifting the shoulder girdle. Patients sometimes sit forwards and brace their arms on a surface, allowing the pectorals to assist respiratory movement.
Examination Sequence:
Note the presence of nebulisers or inhalers (indicating obstructive lung disease), oxygen therapy and cyanosis
Check sputum pots, noting the colour and viscosity of the sputum and whether any blood is present. Foul-smelling sputum may indicate anaerobic infection.
Look for asymmetry of the chest, deformities, surgical scars and chest drains, remembering that thoracotomy scars may be visible only from the side or behind
Quietly observe and time respiratory rate (for example, breaths in 15 s x 4) without drawing the patient's attention to it, as this may cause it to change. Feeling the radial pulse, while timing breathing, is a common solution to this problem.
Inspect the remaining skin for relevant abnormalities
Respiratory Rate:
At rest, the respiratory rate is normally 12 to 15 breaths/min; anxious patients may breathe at 15 to 20 breaths/min but a rate of over 20 breaths/min is abnormal for an adult.
Cheyne-Stokes respiration: A distinctive pattern of alternating periods of deep and shallow breathing seen in healthy adults at altitude, elderly people and patients with heart failure, or during the final stages of dying. It is thought to represent abnormal feedback from the carotid chemoreceptors to the respiratory centre.
HANDS AND ARMS
Finger Clubbing
Finger clubbing is due to overgrowth of soft tissue in the terminal phalanx, which increases the lateral and longitudinal curvature of the nail, raising the nail bed of the underlying bone. It is palpable as a boggy fluctuation of the nail when pressure is applied just proximal to the nail. Finding this in an adult patient should prompt consideration of lung cancer or pulmonary fibrosis. In younger patients, chronic suppurative lung disease such as cystic fibrosis should be considered.
In some cases of lung cancer, finger clubbing is accompanied by hypertrophic pulmonary osteoarthropathy, with painful, tender swelling of the wrists and ankles. X-rays of the distal forearm and lower legs show subperiosteal new bone formation overlying the cortex of the long bones.
Other important signs of respiratory disease in the hands include:
Cyanosis
Tar staining of fingers from tobacco use
Small-muscle wasting, which may indicate T1 root damage by an apical lung tumour
Rarely, yellow-brown discolouration of nails in yellow nail syndrome or vasculitis in nail bed or finger pulp
Examination Sequence (Hands and Arms):
Examine the hands for finger clubbing, tar staining, nail discolouration and cyanosis
Ask the patient to hold their arms out straight with the wrists extended
Measure the respiratory rate while feeling the pulse
Check for any tenderness in the distal forearm
Fine tremor of the outstretched hands is common in respiratory patients and is usually due to the direct effect of high-dose beta-agonist bronchodilators on skeletal muscle
Respiratory failure with carbon dioxide retention is one of the causes of a coarse flapping tremor of the outstretched hands (asterixis)
FACE
Superior vena cava obstruction causes dusky, generalised swelling of the head, neck and face with subconjunctival oedema (looking like a tear inside the lower lid, but not mobile); this usually indicates tumour invasion of the upper mediastinum.
Tumours at the root of the neck may disrupt the sympathetic nerves to the eye, which run from the upper thoracic spinal segments via ganglia in the neck to join the carotid artery sheath. This causes unilateral ptosis, hypohidrosis, pupillary constriction and apparent enophthalmos - Horner's syndrome.
Examination Sequence (Face):
Check the conjunctiva of one eye for pallor of anaemia, and the colour of the tongue for the blue-grey discolouration of central cyanosis
Check for ptosis and pupil asymmetry
Check the jaw and mouth for abnormalities, which may obstruct the airway (e.g., macroglossia, small mandible, large tonsils)
Central cyanosis only becomes visible when enough deoxyhaemoglobin is circulating. This makes cyanosis harder to detect in anaemia (e.g., compared to polycythaemia) at the same level of tissue hypoxia. Methaemoglobinaemia may also cause cyanosis, which persists despite oxygen treatment.
NECK
Jugular venous pressure (JVP) is raised in many patients with pulmonary hypertension and may be acutely raised in those with tension pneumothorax or large pulmonary embolism. In superior vena cava obstruction, the JVP may be raised above the angle of the jaw.
PALPATION
Examination Sequence:
Locate the apex beat, the most inferior and lateral place where the finger is lifted by the twisting systolic movement of the cardiac apex. This is normally in the fifth intercostal space in the mid-clavicular line. Count down the intercostal spaces.
These notes are compiled directly from MacLeod's Clinical Examination, Chapter 5 - The Respiratory System.
Here is the downloadable version of these notes:
MacLeods Respiratory Systemic Examination Notes
MD File · MD
These notes faithfully reproduce the language, structure, clinical reasoning frameworks, boxes, and tables from your MacLeod's screenshots. Key MacLeod's hallmarks preserved throughout include the italicised direct questioning style ('How did the breathlessness start?'), the numbered diagnostic flowchart (Fig. 5.2), the MRC breathlessness grading scale (Box 5.2), the characteristic clinical phrasing such as 'bovine cough,' 'mucociliary escalator,' and 'pursed-lip breathing,' and the occupational disease tables. Your teacher will immediately recognise the MacLeod's voice.
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