6 The respiratory system

The respiratory tract extends from the nostrils to the alveoli but also includes the pulmonary parenchyma and vasculature and the musculosketetal structures required for ventilation. It is often divided for convenience into the upper respiratory tract (URT) which is the nose and pharynx, and the lower respiratory tract (LRT) which consists of the larynx and all distal structures.

The trachea lies in the midline deep to the sternal notch and divides into the left and right main bronchi at the ‘carina’, at about the level of the sternal angle. There are about 25 further divisions before reaching the alveoli.

The right lung has 3 lobes (upper, middle, and lower) whilst the left lung has 2 (upper and lower) to make room for the heart, but the lingular division of the upper lobe is effectively a ‘left middle lobe ‘. Note that the oblique fissures run downwards from the back. Here’s what this means when auscultating (see Fig. 6.1).

The diaphragm slants such that the inferior border of the lungs is at the 6th rib anteriorly but extends down to the 12th posteriorly.

This is a complex system, the outline here is an aide-mémoire only.

Contraction of effector muscles increases thoracic volume and air is drawn in, expiration is largely passive with air being expelled as the lungs recoil under their innate elasticity. During physiological stress, ventilation increases first by increasing tidal volume then by increasing rate: to fit more breaths into a minute, expiration must therefore become active.

Getting enough air in is the first step, but we must also extract oxygen and get rid of carbon dioxide. Anything that impedes gas transfer has clinical implications:

Note that the degree of ventilation–perfusion mismatch will be altered by a patient’s position and cardiac output.

Cough receptors in the pharynx and lower airways initiate a deep inspiration followed by expiration against a closed glottis and a sudden glottal opening. This causes a rapid, forceful expulsion of air.

Larger inhaled particles will impact on airway walls going round the many corners of the respiratory tract. Particles smaller than this might have time to sediment out from the air deep in the lungs (like inhaled medications), before they can be exhaled.

Most of the respiratory tract is lined with mucus secreted from goblet cells that catches these inhaled particles. This is continuously swept upwards like an escalator by cilia, towards the larynx where the mucus is swallowed (yes, we all do it).

In the smaller airways and alveoli, macrophages and a variety of secreted defensive proteins act against microbes at a microscopic level.

Shortness of breath (SOB), or dyspnoea, is the sensation that one has to use an abnormal amount of effort in breathing. Patients may describe ‘breathlessness’, an inability to ‘get their breath’, or being ‘shortwinded’.

This is NOT the same as ‘hypoxia’. A person can be breathless but have normal oxygen levels. Marathon runners crossing the finish-line are breathless but not blue.

‘Tightness’ is often described and may relate to airway narrowing as in asthma or may be chest pain, as in cardiac disease. Tease out exactly what the patient means.

Pleuritic and musculoskeletal chest pain is worse at the height of deep inspiration and patients may say ‘I am not able to get my breath’. Thus, seemingly complaining of breathlessness, their actual problem is pain on inspiration. Ask if they feel unable to breathe deeply and for what reason (is it pain or some other sensation?). If all else fails, ask the patient to take a deep breath and watch what happens.

How quickly did the SOB come on? (see Box 6.1)

Slower onsets are poorly reported. The patient often reports the onset of a worsening of breathlessness or when the breathlessness stopped them doing their benchmark daily activity. Ask when they were last able to run up the stairs and the real duration of breathlessness becomes apparent.

The nature of progression of breathlessness is also crucial: asthma may be long-standing and fluctuate greatly whereas fibrosis inexorably gets worse (often in a step-wise fashion).

Several classifications exist (see Box 6.2) but the key is to quantify in terms of progressive functional impairment whilst trying to keep it in context for the patient, e.g. ‘Can you still mow the lawn without resting?’, ‘Do you have o walk slower than your friends?’, ‘Are you breathless getting washed and dressed in the morning?’

Be sure that activities are restricted by SOB as opposed to arthritic hips, knees, chest pain, or some other ailment.

What makes the breathlessness worse? Can it be reliably triggered by a particular activity or situation? Remember orthopnoea (  104) is not specific for heart failure: breathing whilst lying relies heavily on the diaphragm and also increases perfusion of the upper lobes (usually most badly damaged in COPD) so many people with dyspnoea are more breathless doing this.

What makes the dyspnoea better? Do inhalers or a break from work help?

Dysfunctional breathing, and particularly hyperventilation, is common generally and more so in people with genuine respiratory pathology. Hyperventilation ? blood CO₂ and so increases pH. This leads to symptoms of dyspnoea of rapid onset then:

A common, often overlooked and potentially miserable symptom in respiratory disease, usually caused by upper respiratory tract infection (URTI) and/or smoking. Duration of cough is important, as well as character, exacerbating factors, and whether any sputum is produced. See Tables 6.1a and 6.1b for some causes of cough.

Note that cough may be the only reported symptom of asthma.

This is not particularly useful, however patients are often keen to try to point out where they feel the cough originates.

Beyond the larynx, sensory innervation is such that localization is not possible. Patients often, therefore, point to their throat as the source of the cough.

‘Chronic cough’ is that lasting >8 weeks and is often multi-factorial: common contributors are initial viral infection, asthma, post-nasal drip, gastro-oesophageal reflux disease, and medications (though it can be the first manifestation of interstitial lung disease or even lung cancer).

Smokers will have a chronic cough, particularly in the mornings, so a history of a change is important.

Excess respiratory secretions that are coughed up. Patients will usually understand the term ‘phlegm’ better. Features to glean are:

Attempt to quantify sputum production in terms of well-known objects such as tea-spoons, egg-cups, etc. ‘Mucoid’ sputum is white or clear in colour but can be grey in cigarette smokers. Yellow or green ‘purulent’ sputum is largely caused by inflammatory cells so usually indicates infection; although eosinophils in the sputum of asthmatics also discolour sputum, producing rubbery yellow plugs. See Table 6.2.

The coughing up of blood can vary from streaks to massive, life-threatening bleeds (‘massive’ haemoptysis = >500ml in 24 hours). Establish amount, colour, frequency, and nature of any associated sputum.

Haemoptysis is easily confused with blood originating in the nose, mouth, and GI tract (haematemesis). Ask about, and check for, bleeds in these areas also.

Causes of haemoptysis include infection, bronchiectasis, carcinoma, pulmonary embolus, and pulmonary vasculitis. ‘Infective’ causes will often produce blood-stained sputum as opposed to pure haemoptysis.

This is a whistling ‘musical’ sound emanating from narrow smaller airways. Occurs in inspiration and expiration, but usually louder and more prominent in the latter. Airway calibre is dynamic, and the external pressure in expiration means this is when airways are narrowest and when you’ll hear wheeze. Cause may be any process that ? airway calibre:

A harsh ‘crowing’, predominantly inspiratory, sound with a largely constant pitch. Signals large airway narrowing, usually at the larynx or trachea, (e.g. vocal cord palsy, post intubation stenosis). Can precede complete airway obstruction (e.g. epiglottitis) so is treated as a medical emergency if the cause is unknown.

Chest pain is explored fully in Chapter 5.

Pain arising from respiratory disease may be ‘pleuritic’ in nature: usually arising from the parietal pleura (the lungs have no pain fibres). It is felt as a severe, sharp pain at the height of inspiration or on coughing localized to a small area of chest wall. Note that patients will avoid deep breathing and may complain of ‘breathlessness’.

Pain from lung parenchymal lesions may be dull and constant. This is a sinister sign of malignancy spreading into the chest wall. Remember, though, that the stress placed through the chest wall by increased respiratory effort in other airways disease may cause ill-defined chest wall pain.

Diaphragmatic pain may be felt at the ipsilateral shoulder tip whilst pain from the costal parts of the diaphragm may be referred to the abdomen.

In general, muscular and costal lesions will be tender to touch over the corresponding chest wall and exacerbated by twisting movements—although this is not always the case. Costochondritis is a common cause of pleuritic pain of which Tietze’s syndrome is a specific cause associated with pain and swelling of the superior costal cartilages.

May be due to spinal lesions or herpes zoster.

Sleepy people are often seen by respiratory physicians as the commonest pathological cause (obstructive sleep apnoea) usually requires commencement of nocturnal non-invasive ventilation.

Differentiate sleepiness from fatigue: think of how you feel after exercise and how you feel after being awake a long time (e.g. after a long-haul flight). Quantify how sleepy the patient is (see Epworth Score in Box 6.3).

This is caused by upper airway obstruction in susceptible individuals (overweight/retrognathic/relative macroglossia) as the palatal muscles become flaccid during REM sleep. Partial obstruction causes snoring then brief hypoxia as the obstruction becomes complete. Hypoxia is sensed and the patient wakes enough to return tone to their muscles and open their airway. This cycle is repeated many times per hour (sleepiness), the patient is restless and noisy (sleepy, irritated partner), and blood pressure doesn’t fall at night (can give resistant hypertension).

Severe OSA leads to carbon dioxide retention, worsening somnolence, and early morning headaches.

Narcolepsy is less common than OSA but disabling and the diagnosis is often missed for years. Initially, patients experience weakening at the knees when experiencing sudden emotion (e.g. the punchline of a joke). This ‘cataplexy’ progresses to become more marked and widespread, sleep episodes suddenly occur at any time (e.g. mid-conversation), and dreams intrude into wakefulness. Strong genetic linkage.

Particularly at night may be a sign of infection such as TB, but remember fever is caused by inflammation so may arise from malignancy, PE, or a connective tissue disorder.

A common symptom of cancer, COPD, and chronic infection. Attempt to quantify any loss (how much in how long).

Oedema manifesting as ankle swelling at the end of the day may be a sign of fluid retention due to chronic hypoxaemia ± hypoxia or right heart failure secondary to chronic lung disease (cor pulmonale). Older smokers with COPD often have coexisting cardiac disease.

Many medications can cause respiratory pathology – if unsure consult resources such as Pneumotox (  http://www.pneumotox.com).

Attempt to quantify the habit in ‘pack-years’. 1 pack-year is 20 cigarettes per day for one year. 20 cigarettes is roughly the same risk exposure as 0.5oz (12.5g) of tobacco.

Ask about previous smoking as many will call themselves ex-smokers if they gave up on their way to see you!

Remember to ask about passive smoking.

Alcoholics are at greater risk of chest infections and bingeing may result in aspiration pneumonia.

Animals are a common source of allergens. Remember birds and caged animals. Ask about exposure beyond the home in the form of close friends and relations, and hobbies such as pigeon fancying or horse riding.

Ask about travel (recent or previous) to areas where respiratory infections are endemic. Think particularly about TB. Remember Legionella can be caught from water systems and air-conditioning in developed countries. Pathogens common in other developed countries may be different to those in the UK (e.g. histoplasmosis in the USA) or show extensive antibiotic resistance.

This is hugely important. Individual occupational diseases might be uncommon but collectively they represent a vast number of cases. Be alert to exposure to asbestos, coal, animals, metals and ores, cement dust, and organic compounds.

Trace the occupational history back as there may be a lag of >20 years between exposure and resultant disease. Remember that exposure may not be obvious and the patient may have been unaware of it at the time. Plumbers, builders, and electrical engineers may well have been exposed to asbestos in the past, as might their families, e.g. by washing clothes.

See Health and Safety Executive (HSE) website  http://www.hse.gov.uk for more information.

Respiratory patients may be short of breath and it may be easiest to examine them sitting at the edge of the bed as opposed to the classic position of sitting back at 45°. Choose a position comfortable to you both. They should be undressed to the waist. As ever, make sure you have introduced yourself and have clean hands.

As ever, a surprising amount of information can be obtained by observing the patient before laying on a finger.

Look for evidence of the disease and its severity around the patient:

Watch the patient from the foot of the bed. Or watch them approach your clinic room.

Fingers stained with tar appear yellow/brown where the cigarette is held (nicotine is colourless and does not stain). This indicates smoking but is not an accurate indicator of the number of cigarettes smoked.

This is a bluish tinge to the skin, mucous membranes, and nails, evident when >2.5g/dl of reduced haemoglobin is present (O₂ sat. about 85%). Easier to see in good, natural light.

Central cyanosis is seen in the tongue and oral membranes (severe lung disease, e.g. pneumonia, PE, COPD). Peripheral cyanosis is seen only in the fingers and toes and is caused by peripheral vascular disease and vasoconstriction.

? curvature of the nails. Early clubbing is seen as a softening of the nail bed (nail can be rocked from side to side) but this is very difficult to detect. Progressive clubbing leads to a loss of the nail angle at the base and eventually to a gross longitudinal curvature and deformity.

The most important respiratory causes are carcinoma and lung fibrosis but it is also seen in chronic sepsis (bronchiectasis, abscess, empyema, cystic fibrosis).

Rate, rhythm, character. A tachycardic ‘bounding’ pulse = CO₂ retention.

Pulsus paradoxus. Causes: pericardial effusion, severe asthma (but there should be some other clues to severe asthma!).

See  117. Raised in pulmonary vasoconstriction or pulmonary hypertension and right heart failure. Markedly raised, without a pulsation, in superior vena cava obstruction with distended upper chest wall veins, facial and conjunctival oedema (chemosis).

Examine inside (nasal speculum) and out, looking for polyps (asthma), deviated septum, and lupus pernio (red/purple nasal swelling of sarcoid granuloma).

Look especially for candidiasis (common in those on inhaled steroids or immunosuppressants).

See Chapter 3 for full description of technique. Feel especially the anterior and posterior triangles, the supraclavicular areas. Don’t forget the axillae receive lymph drainage from the chest wall and breasts (Fig. 6.3).

Look at the shape and movement of the chest up-close.

May indicate previous surgery. Look especially in the mid-axillary lines for evidence of past chest drains. Remember a pnemonectomy can be undertaken with a relatively small lateral scar.

Radiotherapy will often cause lasting local skin thickening and erythema. Sites are usually marked with tattoo dots.

Look for unusually prominent surface vasculature suggesting obstructed venous return.

Again, note the rate and depth of breathing as you did at the end of the bed (you only need formally time it once).

Observe chest wall movement during breathing at rest. Also, ask the patient to take a couple of deep breaths in and out and watch closely.

The trachea will shift as the mediastinum is pulled or pushed laterally (e.g. by fibrosis or mass). It should lie in the midline deep to the sternal notch.

You’ll need to push down as well as back otherwise you are just checking the position in the neck: so warn the patient it will be uncomfortable. Use two fingers and palpate the sulci either side of the trachea at the same time. They should feel of identical size (Fig. 6.4).

The trachea often feels central even if there is pathology, but if you do feel a deviation it may be instructive and other signs should be sought.

Normally at the 5th intercostal space in the mid-clavicular line. However, the apex beat is difficult to localize in the presence of hyperexpanded lungs and it may be shifted to the left if the heart is enlarged.

It is important to explain what you are doing here before grabbing hold of the patient’s chest! See also Box 6.4.

Most sources recommend testing lateral expansion at the front and back: this is almost testing the same thing twice but is a good way of ensuring you had the right answer initially.

To test expansion posteriorly it is easiest to ask the patient to lean forward and place your hands on the chest wall with the thumbs pointing down. The procedure can then be repeated.

This is the vibration felt on the chest as the patient speaks. It gives the same information as vocal resonance testing so is now rarely tested.

This takes some practice to master so serves as a sound indicator of how much time a student has spent on the wards (it does also give extremely useful information in clinical practice!).

The aim is to tap the chest and listen to and feel for the resultant vibration (see Figs 6.6 and 6.7). For a right-handed examiner:

Students quickly learn to keep the middle fingernail of their right hand well-trimmed!

The liver is manifested by an area of dullness below the level of the 6th rib anteriorly on the right. This will be lower with hyperinflated lungs.

The diaphragm of the stethoscope should be used except where better surface contact is needed in very thin or hairy patients.

Intrinsic muscle weakness or damaged innervations.

Up to 60% of older people may suffer respiratory symptoms, but less readily see their doctors about them. Lung function declines with age and exertional breathlessness rises, often with concurrent (non-respiratory) illnesses. Careful, thoughtful assessment is therefore vital.