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Oxford Handbook of Clinical Examination > The Respiratory System > Flashcards

The Respiratory System Flashcards

1
Q

Respiratory history: What is dyspnoea?

A

Shortness of breath, the sensation that one has to use an abnormal amount of effort in breathing.
‘Breathlessness’, inability to ‘catch their breath’, ‘short-winded’.
Not hypoxia- normal oxygen levels. Check not pleuritic chest pain.

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2
Q

Respiratory history: Causes of abrupt onset dyspnoea

A

Pulmonary embolus.
Pneumothorax.
Acute exacerbation of asthma.

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3
Q

Respiratory history: Causes of dyspnoea, onset over days/weeks

A

Asthma exacerbation.
Pneumonia.
Congestive heart failure.

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4
Q

Respiratory history: Causes of dyspnoea, onset over months

A

Pulmonary fibrosis.

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5
Q

Respiratory history: Causes of dyspnoea, onset over years

A

COPD.

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6
Q

Respiratory history: Severity of breathlessness

A

Quantify in terms of progressive functional impairment.
Can you still mow the lawn without resting? Do you have to walk slower than your friends? Are you breathless getting washed and dressed in the morning?

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7
Q

Respiratory history: Exacerbating and relieving factors for breathlessness

A

What makes the breathlessness worse?
Can it be reliably triggered by a particular activity or situation?
Orthopnoea?
What makes the dyspnoea better? Do inhalers or a break from work help?

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8
Q

Respiratory history: Hyperventilation

A

Dysfunctional breathing is common generally and more so in people with genuine respiratory pathology.
Hyperventilation decreases blood CO2, so increases pH.
This leads to symptoms of dyspnoea of rapid onset then: early = paraesthesia in lips and fingers, light headedness, chest pain or ‘tightness’; prolonged episode = bronchospasm, post episode hypoxia.

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9
Q

Respiratory history: Cough overview

A

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 sputum production.

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10
Q

Respiratory history: Chronic cough

A

Lasting >8 weeks.
Often multifactorial.
Common contributors are initial viral infection, asthma, post-nasal drip, GORD, medications.
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.

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11
Q

Character of a cough caused by laryngitis

A

Cough with a hoarse voice

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12
Q

Cause of a cough with a hoarse voice

A

Laryngitis

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13
Q

Character of a cough caused by tracheitis

A

Dry and very painful

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14
Q

Cause of a dry and very painful cough

A

Tracheitis

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15
Q

Character of a cough caused by epiglottitis

A

‘Barking’

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16
Q

Cause of a ‘barking’ cough

A

Epiglottitis

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17
Q

Character of a cough caused by LRTI

A

Purulent sputum, perhaps with pleuritic chest pain

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18
Q

Cause of a cough with purulent sputum, perhaps with pleuritic chest pain

A

LRTI

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19
Q

Cause of white/grey sputum

A

Smoking

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20
Q

Causes of green/yellow sputum

A

Bronchitis, bronchiectasis

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21
Q

Causes of green and offensive sputum

A

Bronchiectasis, abscesses

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22
Q

Cause of sticky, rusty sputum

A

Streptococcus pneumoniae infection

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23
Q

Cause of frothy, pink sputum

A

Congestive heart failure

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24
Q

Cause of 3 layers (mucoid, watery, rusty) sputum

A

Severe bronchiectasis

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25
Q

Cause of very sticky, often yellow sputum

A

Asthma

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26
Q

Cause of sticky, yellow sputum with large plugs

A

Allergic bronchopulmonary aspergillosis

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27
Q

Colour of sputum caused by smoking

A

White/grey

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28
Q

Colour of sputum caused by bronchitis

A

Green/yellow

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29
Q

Colour of sputum caused by bronchiectasis

A

Green/yellow, offensive, 3 layers if severe (mucoid, watery, rusty)

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30
Q

Colour of sputum caused by abscesses

A

Green and offensive

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31
Q

Colour of sputum caused by Streptococcus pneumoniae infection

A

Sticky, rusty

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32
Q

Colour of sputum caused by congestive heart failure

A

Pink, frothy

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33
Q

Colour of sputum caused by asthma

A

Very sticky, often yellow

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34
Q

Colour of sputum caused by allergic bronchopulmonary aspergillosis

A

Sticky, yellow, with large plugs

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35
Q

Respiratory history: Sputum

A

Excess respiratory secretions that are coughed up; ‘phlegm’.
How often?
How much?
How difficult is it to cough up?
Colour.
Consistency and smell.
‘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.

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36
Q

Respiratory history: Haemoptysis overview

A

The coughing up of blood can vary from streaks to massive, life-threatening bleeds (‘massive’ haemoptysis = >500mL in 24hrs).
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 too.

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37
Q

Respiratory history: Haemoptysis causes

A 
Infection.
Bronchiectasis.
Carcinoma.
Pulmonary embolus.
Pulmonary vasculitis.
'Infective' causes will often produce blood-stained sputum as opposed to pure haemoptysis.
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38
Q

Respiratory history: Wheeze

A

A whistling ‘musical’ sound emanating from narrow smaller airways.
Occurs in inspiration and expiration, but usually louder and more prominent in expiration.
Airway calibre is dynamic, and the external pressure in expiration means this is when airways are narrowest and when you’ll hear wheeze.

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39
Q

Respiratory history: Wheeze causes

A

Cause may be any process that decreases airway calibre.
Airway muscle contraction: asthma.
Reduced airway support tissue: COPD.
Airway oedema: heart failure.
Airway inflammation/mucus: bronchiectasis.

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40
Q

Respiratory history: Stridor

A

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.

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41
Q

Respiratory history: Pleuritic chest pain

A

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 localised to a small area of chest wall.
Patient will avoid deep breathing and may complain of ‘breathlessness’.

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42
Q

Respiratory history: Lung parenchymal chest pain

A

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

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43
Q

Respiratory history: Diaphragmatic chest pain

A

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.

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44
Q

Respiratory history: Musculoskeletal chest pain

A

In general, muscular and costal lesions will be tender to touch over the corresponding chest wall and exacerbated by twisting movements- 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.

45
Q

Respiratory history: Nerve root chest pain

A

May be due to spinal lesions or herpes zoster.

46
Q

Respiratory history: Somnolence

A

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

47
Q

Respiratory history: Somnolence, obstructive sleep apnoea (OSA)

A

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.

48
Q

Respiratory history: Somnolence, narcolepsy

A

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.

49
Q

Respiratory history: Fever

A

Particularly at night may be a sign of infection such as TB.

Fever is caused by inflammation so may arise from malignancy, PE, or a connective tissue disorder.

50
Q

Respiratory history: Weight loss

A

A common symptom of cancer, COPD, and chronic infection.

Attempt to quantify any loss (how much in how long).

51
Q

Respiratory history: Peripheral oedema

A

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.

52
Q

Respiratory history: Past medical history

A

Vaccination for respiratory illnesses, particularly BCG.
Previous respiratory infections, especially TB before 1950 when surgery may have been performed resulting in lifelong deformity.
X-ray abnormalities previously mentioned to the patient.
Childhood (a ‘chesty child’ may have had undiagnosed asthma.
Previous respiratory high dependency or ITU admissions and NIV.
Multisystem disorders that affect the chest, e.g. rheumatoid.

53
Q

Respiratory history: Drug history

A

Many medications cause respiratory pathology.
What inhalers are used and how often? Check inhaler technique.
Previous unsuccessful use of bronchodilators and steroids.
Immunosuppressives including oral steroids predispose to (often atypical) infection.
ACE inhibitors cause a dry cough.
If O2 therapy- cylinders or concentrator? how many hours per day?
Illicit drug use (cannabis causes emphysema, many others are associated with respiratory disease).

54
Q

Respiratory history: Family history

A

Asthma, eczema, and allergies.
Inherited conditions (e.g. alpha-1-antitrypsin deficiency).
Family contacts with TB.

55
Q

Respiratory history: Smoking

A

Quantify the habit in pack years. 1 pack year = 20 cigarettes/day for 1 year.
Ask about previous smoking.
Ask about passive smoking.

56
Q

Respiratory history: Alcohol

A

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

57
Q

Respiratory history: Social history, pets

A

Animals are a common source of allergens.
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.

58
Q

Respiratory history: Social history, travel

A

Ask about recent and previous travel to areas where respiratory infections are endemic.
Think particularly about TB.
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 US) or show extensive antibiotic resistance.

59
Q

Respiratory history: Social history, occupation

A

Exposure to asbestos, coal, animals, metals and ores, cement dust, and organic compounds?
Plumbers, builders, and electrical engineers may have been exposed to asbestos in the past, as might their families, e.g. by washing clothes.

60
Q

Respiratory examination: General appearance and introductions

A

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 degrees.
Choose a position comfortable to you both.
They should be undressed to the waist.
Introduce yourself and clean your hands.

61
Q

Respiratory examination: General inspection, bedside clues

A

Look for evidence of disease and its severity around the patient.
Inhalers? which ones? spacer device?
Nebuliser? NIV machine?
Is the patient receiving O2 therapy? how much and by what method (i.e. face mask, nasal cannula, etc)?
Sputum pot? -look inside!
Any mobility aids nearby?
Look for cigarettes, lighter, or matches at the bedside or in a pocket.

62
Q

Respiratory examination: General inspection, respiration

A

Watch the patient from the foot of the bed.
Do they appear out of breath at rest? or after undressing/walking in?
Count the respiratory rate. At rest, it should be <15/minute.
Pretend to be checking the pulse if you think your observation is changing the patient’s breathing patterns.
Are the breaths of normal volume? patients with neuromuscular or fibrotic disease have more shallow and rapid breathing.
Expiration should be shorter than inspiration (2:1), but this will be reversed in obstructive lung diseases as the patient tries to prevent airway collapse from external pressure.
Are they breathing through pursed lips? increasing the end-expiratory pressure, an indication of COPD.
Patients with airway obstruction have a high residual volume (increased airway radial traction/ incomplete expiration due to airway collapse).
Are they using the accessory respiratory muscles (e.g. sternomastoids) or bracing their arms to splint their chest? tripod?
Does the abdomen move out on inspiration? or is a weakened diaphragm being drawn up and hence the abdomen inward (abdominal paradox)?

63
Q

Respiratory examination: General inspection, abnormal breathing patterns

A

Kussmaul’s respiration: deep, sighing breaths; systemic acidosis.
Cheyne-Stokes breathing: a waxing and waning of breath amplitude and rate; due to failure of the normal respiratory regulation in response to blood CO2 levels; commonly seen after cerebral insult (poor prognostic sign) or in heart failure (patient often relatively well).
Other characteristic neurogenic ventilation patterns are described but are far less common.

64
Q

Respiratory examination: General inspection, listen before ‘auscultating’

A

Is the speech limited by their breathlessness? can they complete a full sentence?
Listen for hoarseness as well as the gurgling of excess secretions.
A nasal voice may indicate neuromuscular weakness.
Listen for coughing and stridor or wheeze.

65
Q

Respiratory examination: Skills station model technique, examine this patient’s respiratory system

A

Clean your hands.
Introduce yourself and check patient details.
Explain the purpose of the examination, obtain informed consent.
Ask for any painful areas that you should avoid.
Note the patient’s general appearance and demeanour.
Note any bedside clues.
Ask the patient to undress to the waist and sit comfortably at 45 degrees.
Measure the patient’s respiratory rate and breathing pattern.
Examine the hands: note staining, cyanosis, clubbing, radial pulse; assess for tremor, asterixis.
Offer blood pressure.
Examine the JVP.
Look in the nose, mouth, and eyes.
Feel for cervical, supraclavicular, and axillary lymph nodes.
Inspect the chest.
Palpate for mediastinal position (trachea, apex beat) and chest expansion, front and back.
Percuss front and back, comparing sides.
Auscultate front and back, comparing sides.
Consider other bedside tests such as PEFR or simple spirometry.
Thank the patient and help them redress if necessary.

66
Q

Respiratory examination: Hands, face, and neck

A 
Temperature
Staining
Cyanosis
Digital clubbing
Pulse
Tremor, asterixis
Blood pressure
JVP
Nose
Mouth
Eyes
Lymph nodes
67
Q

Respiratory examination: Hands, face, and neck- Temperature

A

Cold fingers indicate peripheral vasoconstriction or heart failure.
Warm hands with dilated veins are seen in CO2 retention.

68
Q

Respiratory examination: Hands, face, and neck- Staining

A

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 accurate to the number of cigarettes smoked.

69
Q

Respiratory examination: Hands, face, and neck- Cyanosis

A

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.

70
Q

Respiratory examination: Hands, face, and neck- Digital clubbing

A

Increased 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.
Respiratory causes: carcinoma and lung fibrosis, chronic sepsis (bronchiectasis, abscess, empyema, cystic fibrosis).

71
Q

Respiratory examination: Hands, face, and neck- Pulse

A

Rate, rhythm, and character.

A tachycardia, bounding pulse = CO2 retention.

72
Q

Respiratory examination: Hands, face, and neck- Tremor

A 
Fine tremor = caused by use of beta-agonist drugs, e.g. salbutamol.
Flapping tremor (asterixis) = late sign of CO2 retention.
73
Q

Respiratory examination: Hands, face, and neck- Blood pressure

A

Pulsus paradoxus.

Causes: pleural effusion, severe asthma.

74
Q

Respiratory examination: Hands, face, and neck- JVP

A

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).

75
Q

Respiratory examination: Hands, face, and neck- Nose

A

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

76
Q

Respiratory examination: Hands, face, and neck- Mouth

A

Look especially for candidiasis (common in those on inhaled steroids or immunosuppressants).
Look for central cyanosis.
Look for tar staining.

77
Q

Respiratory examination: Hands, face, and neck- Eyes

A

Conjunctiva: evidence of anaemia?
Horner’s syndrome: caused by compression of the sympathetic chain in the chest cavity (tumour, e.g. Pancoast’s, sarcoidosis, fibrosis).
Iritis: TB, sarcoidosis.
Conjunctivitis: TB, sarcoidosis.

78
Q

Respiratory examination: Hands, face, and neck- Lymph nodes

A 
Feel especially the anterior and posterior triangles, the supraclavicular areas.
Submental
Submandibular
Anterior cervical/ jugular chain
Supraclavicular
Posterior cervical chain
Pre auricular
Post auricular
Occipital
79
Q

Respiratory examination: Inspection of the chest

A

Surface markings
Shape
Breathing pattern
Movement

80
Q

Respiratory examination: Inspection of the chest- Surface markings

A

Scars: may indicate previous surgery; look especially in the mid-axillary lines for evidence of past chest drains, pneumonectomy scar.
Radiotherapy: often causes lasting local skin thickening and erythema; sites usually marked with tattoo dots.
Veins: look for unusually prominent surface vasculature suggesting obstructed venous return.

81
Q

Respiratory examination: Inspection of the chest- Shape

A

Deformity: any asymmetry of shape? check the spine for scoliosis or kyphosis.
Surgery: TB patients from the 40s and 50s may have had operations resulting in lasting and gross deformity (thoracoplasty).
Barrel chest: a rounded thorax with increased AP diameter; hyperinflation, a marker of COPD.
Pectus carinatum: ‘pigeon chest’; sternum and costal cartilages are prominent and protrude from the chest; can be caused by increased respiratory effort when the bones are still malleable in childhood- asthma, rickets.
Pectus excavatum: ‘funnel chest’’ sternum and costal cartilages appear depressed into the chest; developmental defect, not usually clinically significant.
Surgical emphysema: air in the soft tissues will appear as a diffuse dwelling in the neck or around a chest drain site and will be ‘crackly’ to the touch.

82
Q

Respiratory examination: Inspection of the chest- Breathing pattern

A

Note the rate and depth of breathing as you did at the end of the bed.

83
Q

Respiratory examination: Inspection of the chest- Movement

A

Observe chest wall movement during breathing at rest.
Ask the patient to take a couple of deep breaths in and out and watch closely.
Look for asymmetry. Decreased movement usually indicates lung disease on that side.
Harrison’s sulcus is a depression of the lower ribs just above the costal margins and is occasionally seen in the context of severe childhood asthma.

84
Q

Respiratory examination: Palpation- Mediastinal position, trachea

A

The trachea will shift as the mediastinum is pulley’s for pushed laterally (e.g. by fibrosis or mass).
It should lie in the midline deep to the sternal notch.
Push down and back, warning the patient that it will be uncomfortable.
Use 3 fingers and palpate the sulci either side of the trachea at the same time.
They should feel the identical size.
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.

85
Q

Respiratory examination: Palpation- Mediastinal position, apex beat

A

Normally at the 5th intercostal space in the mid-clavicular line.
Difficult to localise in the presence of hyper expanded lung, may be shifted to the left if heart is enlarged.

86
Q

Respiratory examination: Palpation- Chest expansion

A

Explain.
Antero-posterior diameter: put both hands lightly on the chest wall above the nipples, fingers towards the clavicles; ask the patient to breathe all the way out, then take a deep breath in- your hands should move equally.
Lateral diameter (from the front): place both hands on the chest wall just below the level of their nipples, anchoring your fingers laterally at the sides; extend your thumbs so that they touch in the midline when the patient is in full expiration; ask the patient to take a deep breath in; your thumbs should move apart equally; any reduction in movement on one side should be visible.
Test lateral expansion on the back too.

87
Q

Respiratory examination: Palpation

A

Mediastinal position (trachea, apex beat).
Chest expansion.
(Tactile vocal fremitus).

88
Q

Respiratory examination: Percussion, technique

A

Tap the chest and listen to and feel for the resultant vibration.
Place one hand on the chest wall, fingers separated and middle finger lying between the ribs.
Press the middle finger firmly against the chest.
Use the middle finger of he other hand to strike the middle phalanx of the middle finger of the first hand.
Move the striking finger away again quickly to avoid muffling the noise.
Keep the striking finger flexed and move from the wrist.
Percuss each area of the lung, comparing right then left each time. Areas: apices, 2nd rib, nipple, axillae. 4 sites on L and R, front and back.
Percuss the apices directly on the clavicle.
If an area of dullness is heard or felt, this should be percussed in more detail so as to map out the borders of the abnormality.

89
Q

Respiratory examination: Percussion, findings

A

Normal lung sounds ‘resonant’.
‘Dullness’ is heard/felt over areas of increased density (consolidation, collapse, alveolar fluid, pleural thickening, peripheral abscess, neoplasm).
‘Stony dullness’ is the unique extreme dullness heard over a pleural effusion.
‘Hyper-resonance’ indicates areas of decreased density (emphysematous bullae or pneumothorax).
COPD can create a globally hyper-resonant chest.
Normal dull area: there should be an area of dullness our the heart which may be diminished in hyper-expansion state (e.g. COPD or asthma).
The liver is manifested by an area of dullness below the level of the 6th rib anteriorly to the right. This will be lower with hyper-inflated lungs.

90
Q

When might ‘dullness’ be heard in respiratory percussion?

A 
Consolidation
Collapse
Alveolar fluid
Pleural thickening
Peripheral abscess
Neoplasm
Areas of increased density.
91
Q

When might ‘stony dullness’ be heard in respiratory percussion?

A

Pleural effusion.

92
Q

When might ‘hyper-resonance’ be heard in respiratory percussion?

A

Emphysematous bullae
Pneumothorax
COPD
Areas of decreased density.

93
Q

Respiratory examination: Auscultation, technique

A

Ask the patient to take deep breaths in and out through their mouth.
Listen to the whole of both inspiration and expiration.
Listen over the same areas percussed, comparing left and right: apices with bell, then 2nd rib, nipple, axillae (front and back).
If an abnormality is found, examine more carefully and define borders.
Listen for the breath sounds and any added sounds- and note at which point in the respiratory cycle they occur.

94
Q

Respiratory examination: Auscultation, findings

A

Normal breath sounds: vesicular, produced by airflow in the large airways and larynx and altered by passage through the small airways before reaching the stethoscope; ‘rustling’.
Reduced sound: if local = effusion, tumour, pneumothorax, pneumonia, lung collapse; if global = COPD, asthma
Bronchial breathing: caused by increased density of matter in the peripheral lung allowing sound from the larynx to the stethoscope unchanged; hollow, blowing quality; heard equally in inspiration and expiration (Darth Vader); heard over consolidation, lung abscess in the chest wall, dense fibrosis.
Added sounds: wheeze, crackles, rub.

95
Q

What are normal breath sounds?

A

Vesicular, produced by airflow in the large airways and larynx and altered by passage through the small airways before reaching the stethoscope; ‘rustling’.

96
Q

What causes reduced breath sounds?

A

If local = effusion, tumour, pneumothorax, pneumonia, lung collapse.
If global = COPD, asthma

97
Q

What is bronchial breathing, and what causes it?

A

Caused by increased density of matter in the peripheral lung allowing sound from the larynx to the stethoscope unchanged.
Hollow, blowing quality.
Heard equally in inspiration and expiration, often with a pause in between.
(Darth Vader).
Heard over consolidation, lung abscess in the chest wall, dense fibrosis.

98
Q

What is a wheeze (added sound on respiratory auscultation)?

A

Rhonchi.
Musical whistling sounds caused by narrowed airways.
Heard in expiration.
Different calibre airways = different pitch note.
Asthma and COPD can cause a chorus of notes, ‘polyphonic wheeze’.
Monophonic wheeze indicates a single airway is narrowed, usually by a foreign body or carcinoma.

99
Q

What causes a polyphonic wheeze?

A

Asthma.

COPD.

100
Q

What causes a monophonic wheeze?

A

Monophonic wheeze indicates a single airway is narrowed, usually by a foreign body or carcinoma.

101
Q

What are crackles (added sound on respiratory auscultation)?

A

Crackles (crepitations, rales).
Caused by air entering collapsed airways and alveoli producing an opening snap or by mucus moving.
Heard in inspiration.
‘Coarse’ crackles made by larger airways opening and sound like the snap and pop of Rice Crispies. Caused by fluid or infection.
‘Fine’ crackles occur later in inspiration. They sound like the tear of velcro and can also be reproduced by rolling the hair at your temples between the thumb and forefinger. Usually fluid or fibrosis.
The ‘deciduous’ crackles of bronchiectasis are of predominantly coarse type but fall away in volume and depth of note on inspiration.
Crackles are often a normal finding at the lung bases. If so, they will clear after asking the patient to cough.

102
Q

What causes coarse crackles?

A

Fluid, infection.

103
Q

What causes fine crackles?

A

Fluid, fibrosis.

104
Q

What is a rub (added sound on respiratory auscultation)?

A

Creaking sound likened to the bending of new leather or the crunch of a footstep in fresh snow.
Heard best at the height of inspiration.
May be very well localised.
Caused by inflamed pleural surfaces rubbing against each other.
Causes: pneumonia, pulmonary embolism with infarction.

105
Q

What causes a respiratory rub?

A

Caused by inflamed pleural surfaces rubbing against each other.
Causes: pneumonia, pulmonary embolism with infarction.

106
Q

Respiratory examination: Auscultation, vocal resonance

A

Auscultatory equivalent of vocal fremitus.
Sound transmitted through the solid material (consolidated or collapsed lung) travels much better than through healthy air-filled lung, so phonation is more clearly heard.
Ask the patient to say ‘ninety-nine’ and listen over the same areas as before.
Lower pitched sounds transmit particularly well so create a vocal ‘booming’ quality.
Marked increased resonance, such that a whisper can be clearly heard, is termed ‘whispering pectoriloquy’.

107
Q

Where do you auscultate for the upper lobes?

A

Anteriorly, nipple level and above.

108
Q

Where do you auscultate for the right middle lobe/ left ingula?

A

Anterolaterally.

109
Q

Where do you auscultate for the lower lobes?

A

Posteriorly.

Oxford Handbook of Clinical Examination (13 decks)

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