2 Respiratory Examination Notes

Jack’s Notes CLINICAL SKILLS
Respiratory Examination
RESPIRATORY EXAMINATION
SEQUENCE
1. Introduction/ Explanation/ 5. Face
Consent and Hand Wash a. Face, Nose, Sinuses
a. Patient Positioned sitting b. Mouth and Throat
up on edge of the bed, 6. Neck
chest exposed 7. Chest (Anterior & Posterior)
2. General Appearance a. Inspect, Palpate,
3. Vital Signs Percuss, Auscultate
a. Pulse, Resp, BP, Temp, 8. Abdomen
BMI 9. Legs
4. Hands/ Arms a. Inspect, Palpate
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INTRODUCTION/ EXPLANATION/ CONSENT

• Introduce self and explain procedure
• Gain consent
• Wash Hands
• Patient is positioned sitting over edge of bed with chest adequately
exposed
GENERAL APPEARANCE
• Dyspnoeic
o Use of accessory muscles
o Intercostal indrawing/ recession
o Hallowing of supraclavicular fossa during inspiration – delayed
increase in lung volume despite the generation of large negative
pleural pressures
o Tripoding – leaning forward, arms on knees pushes abdomen and
diaphragm up to improve inspiration
o Pursed lipped breathing
o Nasal flaring
o Tracheal tug
• Speaking in full sentences (Alert & Orientated)
o SOB severe causing inability to speak in full sentences
§ Severe asthma, ARDs
o Hoarseness of voice (dysphonia) – laryngitis, use of ICS in asthma,
hypothyroidism and recurrent laryngeal nerve palsy (carcinoma of lung
or laryngeal carcinoma)
• Cyanotic
• Plethora
o Reddish erythema complex – CO2 retention, chronic hypoxia
(Secondary Polycythaemia)
• Coughing
o Sputum production
o Wheeze
o Characteristics of cough; Duration; Severity; Dry/Productive
§ Lack of usual explosive beginning – Bovine Cough (Vocal cord
paralysis)
§ Muffled, wheezy ineffective cough – COPD
§ Very loose productive cough – excessive bronchial secretions
such as acute/chronic bronchitis, pneumonia, bronchiectasis,
bacterial COPDIE
§ Dry, irritating cough - chest infection, asthma, carcinoma, HF,
ILD, ACEi induced
§ Barking, croupy cough – upper airway issue such as pharynx,
larynx (URTI – pharyngitis/ laryngitis, croup, epiglottitis,
tracheitis) or pertussis infection (Whooping Cough)
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• Stridor
o Foreign body, Anaphylaxis, Croup,
Cancer, Tracheitis, Epiglottitis, Ludwig’s
Angina, Retropharyngeal abscess
• Surrounding environment
o NP, O2 mask, e.g.
o Puffers on table
o Sputum cup close-by
• Mucous Production
o White and translucent – viral infection and bronchitis/ atypical
pneumonia
o White and foamy/ frothy slightly pink – pulmonary oedema, ARDs
caused by surfactant + blood
o Yellow-green – bacterial infection (mucopurulent, mucous)
o Green – Pseudomonal infection or longstanding infection
o Rusty Sputum – reddish, brown, blood-stained classic for
Streptococcal pneumoniae, either Lobar or Bronchopulmonary. Also
seen in PE, Lung Cancer or TB
o Scanty-Watery – atypical pneumonia
o Foul smelling sputum – anaerobic infections, aspiration/ lung
abscess/ necrotizing pneumonia
o Red-Jelly/ Dark Red – Klebsiella pneumoniae
o Greyish – Pneumoconiosis, waning bacterial infection
o Blackish-Brown – possibly old blood that should be investigated; can
be incidental
o Friable – TB
o Haemoptysis
§ Cancer – Bronchogenic carcinoma
§ Severe lung inflammation – bronchiectasis, bronchitis,
pneumonia, TB, aspergilloma, CF
§ Pulmonary Vascular Disorder – PE, Pulmonary HTN (mitral
stenosis), Severe HF with APO
§ Airway – trauma, foreign body, iatrogenic
§ Coagulopathy, Vasculitides
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VITALS
• Pulse
o Rate – tachycardia, bradycardia
o Rhythm – regular, irregular
o Character & Volume – weak/thready, bounding pulse (CO2 retention)
• Respirations
o Rate
§ Normal: 12-25 RR
§ Tachypnoea: >26 RR
§ Bradypnea: <12 RR
• Respiratory Depression (Respiratory Acidosis)
o Rhythm
§ See below
o Depth – shallow/ deep

§ Inspiratory and Expiratory Phase
• Prolonged Expiratory in COPD/Asthma
§ Hyperventilating (deep and fast) / Hypoventilating (shallow and
slow)
o Dyspnoea – laboured breathing, increased effort to breath

§ SOB – sensation of physical distress/ inability to breath with or
without physical impairment
§ Use of accessory muscles
• COPD, Asthma, Pneumonia, Pneumothorax, PE, HF
§ Pursed lip breathing – Severe COPD; aids in providing
continuous positive airway pressure to prevent airway collapse
§ Nasal flaring
§ Tripoding – leaning forward, arms on knees pushes abdomen
and diaphragm up to improve inspiration
• Severe asthma, COPD, ARDs, Epiglottitis
§ Tracheal tug – increased diaphragmatic movements may cause
downward displacement of the trachea
• Severe asthma, COPD, ARDs
§ Intercostal recession
• ARDs, Pneumonia, Bronchiolitis, Anaphylaxis, Croup,
Epiglottitis, Foreign body
§ Orthopnoea and PND
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o Stridor – High pitched, over the trachea due to narrowing or

obstruction of extra thoracic airway. Usually audible without
stethoscope.
§ Inspiration (inspiratory
stridor) – obstruction of the
extra-thoracic airways; above
the level of vocal cords due to
collapse of soft tissues
(pharynx) with negative pressure
during inspiration
§ Epiglottitis
§ Croup
§ Foreign Body above vocal cords
§ Aspiration
§ Bilateral vocal cord palsy
§ Ludwig’s Angina
§ Cancer in pharynx
• Expiration (expiratory stridor): obstruction of the intrathoracic
airways; similar to wheezing but more severe
§ Asthma
§ COPD
§ Obstruction at the level of bronchi
§ Retropharyngeal abscess
• Inspirational and Expiration Stridor (Biphasic Stridor):
obstruction at the level of the glottis
§ Foreign Body at level of glottis
§ Tracheitis
§ Cancer
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• Abnormal Breathing Patterns

o Obstructive Breathing – prolonged expiration phase, seen in COPD
o Kussmaul Breathing – deep laboured breathing, can be normal rate
or rapid due to acidosis in DKA. NOT in HONK.
§ Metabolic acidosis – DKA, uraemia
o Cheyne-Stokes Respirations – Cyclic tachypnoea of crescendo-
decrescendo (waxing/waning) pattern with intermittent period of
apnoea
§ Damage to Respiratory Centre (stroke, TBI, tumours), Central
sleep apnoea, Heart Failure (EF <40%), Deaths Door, CO
poisoning, Morphine
o Ataxic (Biot) Respirations – Unpredictable irregular breathing
followed by regular or irregular periods of apnoea
§ Increased intracranial pressure, stroke, opioids, meningitis
o Agonal Breathing – Slow laboured breaths, gasping, myoclonus and
grunting, often prior to terminal apnoea and death; can last seconds-
hours
§ Cardiac arrest – NOT considered BREATHING!
• Caused by hypoxia induced contractions of diaphragm,
usually starting 15-60sec post Cardiac arrest (Brain stem
reflex for survival)
o Rapid, Shallow Breathing – rapid shallow breaths with low tidal
volume
§ Pain, Post exubation, pneumonia, PE, Asthma, COPDE, Anxiety
(Panic Attack)
o Orthopnoea/ PND/ Apnoea/ e.g.
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• O2 Saturations
o Hypoxic: <95% SpO2
o Severe Hypoxia: <85% SpO2
SIGNS OF HYPOXIA
Early Hypoxia - RAT Late Hypoxia Signs - BED C
• Restlessness • Bradycardia
• Anxiousness • Extreme Restlessness
• Tachycardia and Tachypnoea • Dyspnoea
• Cyanosis
Causes of Hypoxia
• Hypoxaemia - see below
• Anaemia
• CO poisoning and other chemicals (shock)
• Ischaemia - atherosclerosis, impeded venous return
• Decreased CO - HF, Aortic Stenosis, shock (all types - septic, anaphylaxis,
neurogenic, obstructive, cardiogenic, chemicals) increased peripheral
vasoconstriction causing peripheries slowed blood flow thus by the time
reached peripheries, Hb O2 offloading has excessively occurred causing
hypoxia (cyanosis) at peripheries
Causes of Hypoxaemia
Divided into Normal A-a Gradient and High A-a Gradient
NORMAL A-a Gradient with Hypoxia - AH! - both PAO2 and PaO2 is reduced
equally due to overall O2 availability due to high altitude or overall depressed
respirations
A - Altitude
• Lower amount of O2 available overall thus reduced partial O2 in the alveolar
and capillary equally; although hypoxic
H - Hypoventilation - NAILED, except for Lung Pathology!

• Depressed breathing (Hypoventilation) causes both Respiratory Acidosis due
to accumulated PaCO2 as well as reduced breathing in of O2 thus overall, the
O2 is reduced equally in the alveolar and capillaries. Cause Type II
Respiratory Failure (pump) failure.
NAI-ED
• Neuromuscular Disorders - poliomyelitis, Guillain Barre, ALS, Myasthenia
gravis, Muscular Dystrophy
• Airway Obstruction
• ICP Raised, Meningitis, e.g.
• Epilepsy
• Drugs (opioids, benzos, alcohol, e.g.)
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HIGH A-a Gradient - VSD

A large difference between the alveolar and arteriole O2 partial pressures signifies an
impairment in gas exchange – something is 'blocking' O2 exchange from the
alveolar into the capillaries
Causes are broken into 3 categories: VSD

• Think of Fick's Law and factors that are inhibiting gas exchange
o Surface area of alveoli/capillaries - COPD, atelectasis/pneumothorax
o Thickness (fluid, interstitial disease, pneumocystis, early Pulmonary
Oedema limited to interstitials only)
o Partial Pressure mismatches - PE, shunting
V - Ventilation/Perfusion (V/Q) Mismatch

Ø High V/Q = Good Ventilation with Poor Perfusion
Ø Low V/Q Poor Ventilation with Good Perfusion (Alveolar hypoventilation)
Usually, areas of V/Q mismatch undergo hypoxic vasoconstriction to direct blood
supply to healthier alveoli. In this instance, the excess CO2 can typically be removed
in healthy lung tissue although the oxygenation capacity has a threshold of maximum
saturation of O2 binding in the capillaries. As such, classically causes Type I
Respiratory Failure. O2 supplementation may improve PaO2 up until this threshold
of maximum oxygen saturation is met. This threshold is increased as the perfusion to
healthier alveoli increases, thus more blood is present to saturate O2. Once this limit
is met, O2 supplementation does not fix PaO2. There is a CO2 offloading threshold
although it is much higher. As such, if these cases are severe enough, then Type II
Respiratory Failure will occur, as the increased perfusion to healthy tissue is still not
enough to offload the excess CO2.
• Pneumonia - fluid in alveoli – perfusion with reduced ventilation (Low VQ)

• APO - fluid in alveoli – perfusion with reduced ventilation (Low V/Q)
• Atelectasis/Pneumothorax – perfusion with reduced ventilation (Low V/Q)
• COPD and Bronchitis – ventilation without perfusion (emphysema (High
V/Q)); or perfusion with reduced ventilation (obstruction/ bronchitis (Low V/Q)
• Asthma - perfusion without ventilation (obstruction/ bronchospasm) (Low V/Q)
S - Shunt
• Intrapulmonary/ Physiological Shunting - directly bypassing alveoli thus
oxygenation within the lungs is bypassed OR due to complete alveolar loss of
ventilation OR perfusion. Physiological shunt is the extreme degree of V/Q
Mismatch and thus these processes poorly respond to O2 supplemental
therapy. (High V/Q)
o PE - good ventilation with poor/ no perfusion due to blockage in
pulmonary artery
o Severe pneumonia, ARDS, severe pulmonary oedema/atelectasis,
e.g. - consolidation causes no alveolar ventilation
o Pulmonary arteriovenous malformation - bypassing capillaries thus
no gas exchange at the alveoli occurs
o Bronchial veins physiological shunt - some bronchial veins drain
directly into pulmonary veins, bypassing alveolar capillary thus gas
exchange entirely.
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• Extrapulmonary Shunt - bypassing alveoli thus oxygenation outside the lungs

o Ventricular/Atrial Septic defect - mixing of venous/arterial blood
through patent septic defect (right to left shunt)
o Patent Foramen Ovale - as above
o Patent Ductus Arteriosus - aortic oxygenated blood is shunted into
the pulmonary circuit, increasing pulmonary blood supply and
'recycling' already oxygenated blood
D - Diffusion Problem - thickness issue limiting exchange between alveoli and

capillary. Similar to Low V/Q mismatch although the alveoli are not hypoventilated,
rather the O2 just cannot cross into the capillaries. Corrects with O2 supplementation
as healthier areas of lung tissue are able to compensate greater gas exchange.
• Interstitial Lung disease (genetic/acquired)
• Environmental Lung asbestos, Pneumoconiosis (Silicosis)
• Early Acute Pulmonary Oedema where fluid is limited to interstitium initially
• Pneumocystis Pneumonia
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• Blood Pressure
o Normotensive: 90-119/60-79
o Hypotensive: <90/<60
o Hypertensive: >120/>80
o Pulsus Paradoxus – inspiratory fall of systolic BP ≥10mmHg and
pulse pressure fall during inspiration
• Severe Asthma
• Cardiac Tamponade/ Constrictive Pericarditis/ Pericardial
Effusion
• Tension Pneumothorax
• Large PE, large pleural effusion, acute MI, SVC obstruction,
diaphragmatic hernia, volvulus of stomach
• Temperature
o Afebrile: 36.4-36.9o C
o Febrile: >37.5 o C
§ Pneumonia, IECOPD
o Hypothermia: <35 o C
• BMI – Body Mass Index
o Normal: 18.5-24.9
o Underweight: <18.5
o Overweight: 25-29.9
o Obese: >30
§ Class I: 30.0-34.9
§ Class II: 35-39.9
§ Class III: >40
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HANDS
NAILS
• Clubbing – 80% caused by Respiratory Causes
o Lovibond’s Angle – angle between the meeting of the proximal nail
fold and the nail plate
§ Normal: <160o
§ Clubbing: ≥180o
o Curth’s Angle – angle of the DIP joint
§ Normal: 180o (straight)
§ Clubbing: <180o (bent inwards)
o Shamroth’s Window (Diamond Test) – placing two fingers together
shows a small diamond window gap
• Clubbing: If NOT present
• HPOA – Wrist Tenderness; squeeze wrists to elicit tenderness
o Clubbing is often associated with Hypertrophic Pulmonary
Osteoarthropathy (HPO) which is characterised by the presence of
periosteal inflammation (swelling and tenderness) at the distal ends
of the long bones; the wrist, ankles and metacarpal/tarsals.
o HPO is a syndrome of excessive proliferation of the skin and bone,
which can thus cause clubbing, triggered by one or more factors
(megakaryocytes, e.g.) are shunted into systemic circulation and
become deposited in the peripheries stimulating growth.
§ Normally, the lung’s pulmonary capillaries break down factors,
including megakaryocytes and larger platelets, preventing
access into the systemic circuit
§ When there is HPO there is always clubbing; when there is
clubbing there is not always HPO!!!
o Factors that stimulate growth include PDGF, bradykinin, VEGF causing
vascular hyperplasia and proliferation of periosteal layers
o HPO is caused by
§ Primary Lung Carcinoma and Pleural Fibromas
§ Congenital heart defects
o Clubbing Causes:
§ Lung Disease – Lung Ca, ILD, TB, CF, bronchiectasis
§ Heart Disease – Endocarditis, Chronic hypoxia, Cyanotic
congenital diseases
§ GI Disorders – Cirrhosis, Crohn’s
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• CRT – Capillary Refill Time

o Normal: ≤2 sec
o ↓ peripheral perfusion from ↑ SNS vasoconstriction or reduced driving
pressure from poor CO/inotropy – severe dehydration, hypovolaemia, PVD,
HF, obstruction (embolus), shock, septic shock (imbalance of
vasoconstrictors/dilators and endothelial dysfunction)
§ Especially useful in children – >3 sec refill implies >100mL/kg
fluid deficit
• Peripheral Cyanosis
o Causes by slowing of blood flow to peripheries resulting in increased
O2 extraction thus increased deoxy Hb concentration at the peripheries
§ Cold exposure, decreased CO (e.g. shock (except distributive), HF),
Raynaud’s; Causes of Central Cyanosis
• Tar Staining of Fingers

o Caused by tar from cigarettes; nicotine is actually colourless
PALMS
• Temperature
o Warm
§ Hypercapnia – CO2 retention, distributive shock
§ Feverish
o Cold
§ Poor perfusion – shock, ARDs, severe pneumonia/asthma, e.g.
• Wasting of hand muscles (thenar/hypothenar)
o Peripheral Lung tumour (adenocarcinoma/ malignancy) of lower trunk
(T1) of Brachial plexus resulting in muscle atrophy due to loss of
innervation and weakness in finger abduction
• Finger Abduction Test
o Peripheral Lung tumour (adenocarcinoma/ malignancy) of lower trunk
(T1) of Brachial plexus resulting in muscle atrophy due to loss of
innervation and weakness in finger abduction
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ARMS
• Asterixis (CO2 Narcosis)
o Dorsiflexion of the wrists with the arms outstretched and fingers
abducted
o POSITIVE – flapping tremor with a 2-3 second cycle in severe CO2
retention
§ Severe COPD
• Accompanied with dyspnoea, headache, confusion,
lethargy, coma, wide pulse pressure (bounding pulse)
§ Liver Failure (Hepatic Flap) – encephalopathy
§ Renal Failure – Uraemia
o Exact mechanism unknown – dysfunction in diencephalon and motor
centres involved in agonism/antagonistic control of muscles
• Pemberton’s Sign – Arms in full abduction for approx. 1 min causes

flushing, plethora of face (erythema), congestion of face, cyanosis,
dyspnoea, inspiratory stridor, JVP elevation Occurs due to Lung tumour
(adenocarcinoma)/ Retrosternal Goitre pressing on SVC (SVC Obstruction)
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FACE
FACE
• Facial Plethora
o SVC obstruction
o Pulmonary HTN
o Chronic hypoxia induced
polycythaemia
• Leathery Skin – chronic smoker and sun
exposure
• Signs of Sleep Apnoea
o Marks from apnoea mask
o Puffiness around eyes
o Obese
o Short thick neck
o Small pharynx
o Retracted neck
EYES
• Sub-conjunctival haemorrhage
o Severe coughing, trauma, conjunctivitis (associated with URTI), contact lens use
• Horner’s Syndrome
o Apical Peripheral Lung Cancer pressing on sympathetic trunk;
unilateral
(Pancoast’s
Tumour)
§ Ptosis –
drooping
eyelid
§ Miosis –
pupillary
constriction
§ Anhidrosis –
absence of
sweating
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NOSE
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Inspection
• Discharge (Rhinorrhoea)
o Caused by excess mucus production in the mucous membranes of
nasal cavity, sinuses and naso/oropharynx – inflammation, infection,
allergy
o Thin, mucus fluid usually clear
§ Allergies, Sinusitis, common cold, crying, cocaine abuse, opioid
withdrawal
• Swelling – red, swollen nose, orbital swelling
o Chronic sinusitis, Common cold, Allergies
o Constant rubbing due to rhinorrhoea
• Nasal Deviation
o Best observed from behind the patient and looking down
§ Impact trauma (fracture), Congenital, Compression of nose
during birth, Saddle Nose (Wegner’s)
§ Only severe nasal deviation will cause symptoms
• Recurrent infections/ sinusitis, snoring, sleep apnoea,
sneezing, mouth breathing, reduced smell, dyspnoea
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• Inside the Nares – Tilt the patients head backwards and press the tip of the
nose upwards with the thumb and inspect inside the nares with a light
o Deviated Septum
o Polyps – jelly-like overgrowths of the lining of the nasal mucosa, looks
like a grape on the end of a stalk
§ Asthma (usually allergic to aspirin and NSAIDs)
§ Chronic sinusitis
§ CF
o Enlarged turbinates
§ Allergies/ Chronic sinusitis
o Discharge (Rhinorrhoea)
§ Caused by excess mucus production in the mucous membranes
of nasal cavity, sinuses and naso/oropharynx – inflammation,
infection, allergy
§ Thin, mucus fluid usually clear
• Allergies, Sinusitis, common cold, crying, cocaine abuse,
opioid withdrawal
Palpation
• Feel for any swelling, tenderness or deformity
• Block each nostril and test for breathing
o Congestion (URTI, Sinusitis)
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SINUSES
There are 4 sinuses however only 2 can be palpated. The non-palpable sinuses
are the Ethmoid sinuses and the Sphenoid sinuses.
The palpable sinuses; test for Sinusitis

• Frontal
o Test for tenderness by pressing upwards with thumbs just below the
medial edge of eyebrows or by percussing with one finger over the
brow
• Maxillary
o Test for tenderness by pressing upwards with thumbs on inferior
aspect of Zygomatic Process or by percussing with one finger over the
maxilla
o Transilluminate Maxillary Test
§ Shine light from otoscope over the infraorbital rum and observe
the inside of the mouth for illumination of the hard palate
• If light is NOT present – suggests obstruction
(congestion)
• Requires dark room
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MOUTH/ THROAT
Gums/ Teeth
• Dentition and Decay
• Infection
• Periodontal disease
o Broken or rotten tooth; may predispose to lung abscess
Tongue
• Central Cyanosis – Purple/bluish discolouration of tongue, lips and membranes
due to the tissues near the skin surface having low O2 saturation of Hb. Blue
tinge from excessive deoxyhaemoglobin instead of O2Hb
o Key aspect of Central Cyanosis is that deoxygenated blood is leaving the
heart – that is, deoxygenated blood is somehow present in the arterial
circuit due to low O2 saturation and/or abnormal haemoglobin
o Causes
§ Cardiac – 5 T’s & 2 E’s of Congenital disease – Transposition of
great arteries, ToF, Tricuspid atresia, Truncus arteriosus, Total
anomalous pulmonary venous return, Ebstein’s anomaly,
Eisenmenger physiology
§ Respiratory – V/Q mismatch (pneumonia, ARDs, COPD, Severe
Asthma, Severe PR e.g.), hypoventilation
§ Haematological – methemoglobinemia, sulfamoglobinaemia
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Oral/ Mucosa/ Palate
• Hydration
o Dry/ Wet mucous membranes
• Fetor Orris (bad breath)
o Tonsilitis, tooth infection, gum infection
Inspect oropharynx and uvula by asking patient to say “Ah!” with a tongue
depressor
• Tonsil enlargement (Tonsilitis) – 3 Tonsils: Palatine, Pharyngeal
(adenoid), Lingual
o With or without coating of pus (bacterial)
o Kissing Tonsils – so enlarged the two tonsils meet
o Tonsilloliths (Tonsil stones)
• Pharyngitis – reddened, inflamed, swollen, sore
o URTI – viral vs bacterial (Strep Throat)
o Crowding of the Pharynx
§ Sleep Apnoea – reduction in the size of the velopharyngeal
lumen; the space between the soft palate, tonsils and back of
the tongue
• Tongue
o Candidiasis
• Uvula
o Deviation
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NECK
TRACHEA
• Use of Accessory Muscles – any acute respiratory distress
§ SCM
§ Scales
o Chronic COPD (Pink Puffers) may have generalised muscle atrophy
with maintained tone/musculature in SCM, scalene and other
accessory muscles
• Trachea Midline/ Displaced
o Hold two fingers against each sternoclavicular joint and have centre
finger press into the jugular notch space and feel for trachea; if
trachea is displaced, you will feel the edge of the trachea rather than
the middle
§ Tension Pneumothorax – away from side of lesion
§ Pneumothorax – towards side of lesion
§ Atelectasis and pneumonia of upper lobe – towards side of
lesion
§ Massive Pleural effusion – away from side of lesion
§ Upper lobe cancers/ lymphomas/ retrosternal goitre
• Tracheal Tug
o Increased diaphragmatic and accessory muscle movements with gross
overexpansion of the chest may cause downward displacement of the
trachea
o Rest a finger on the trachea and feel if trachea moves inferiorly with
inspiration
§ Severe asthma, COPD, ARDs
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LYMPH NODES
• Palpate the Cervical Lymph Nodes
Assessment of lymph nodes

• Site – assess the lymph node’s location in relation to other anatomical
structures
• Size – assess the size
• Shape – borders to determine if they feel regular or irregular
• Consistency – determine if nodes feel soft, hard or rubbery
• Tenderness – note if the lymph node is tender (sore/ painful) on palpation
• Mobility – assess if the lymph node feels mobile or is tethered to other
structures
• Overlying Skin Changes – note any overlying skin changes such as
oedema, swelling, erythema, pain, infection, e.g.
Classic Interpretation
• Benign Lymph Nodes
o <1cm, smooth, round, non-tender, mobile
• Reactive Lymph Node (fever, infection)
o May be enlarged (>1cm), smooth, round, tender, mobile and
associative infectious symptoms (fever, URTI, e.g.)
• Lymphadenopathy associated with Haematological Malignancy
o Widespread enlarged rubbery lymph nodes
• Lymphadenopathy associated with Metastatic Cancer
o Regional lymphadenopathy in the node groups draining that affected
organ
o Hard, firm, irregular and often tethered to local structures thus immobile
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Cervical Lymph Nodes – order of palpation, not of the image below!

1. Submental – directly under chin
2. Submandibular – below angle of
jaw
3. Pre Auricular – in front of ears
4. Post Auricular – behind ears
5. Occipital – occipital protuberance
region
6. Jugular Chain – anterior to SCM
7. Posterior Triangle – posterior to
SCM, over traps region
8. Supraclavicular – patient has
shoulders shrugged and palpate in
the supraclavicular foassa’s
Chin à Jaw à Ear à Occipital à in front and

behind SCM à supraclavicular
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SITE • Assess the lymph node’s location in relation to other anatomical

structures – consider drainage of potential malignancies
o Epitrochlear; Axilla; Cervical & Occipital; Supraclavicular;
Para-aortic (rarely palpable); inguinal; popliteal
SIZE • Assess the size
o >1cm is abnormal; palpable or non-palpable
o <1cm but palpable is usually benign
CONSISTANCY • Borders to determine if they feel regular or irregular

& SHAPE o Smooth – normal
o Rough – malignancy deposits; extracapsular
• Determine if nodes feel soft, hard or rubbery
o Hard – carcinoma from other malignancy deposits
o Soft – normal, reactive/inflammatory
o Rubbery – lymphoma
TENDERNESS • Note if the lymph node is tender (sore/ painful) on palpation
o Tenderness – classically implies infection/ reactive
o Non-tender – carcinoma or lymphoma
FIXATION • Assess if the lymph node feels mobile or is tethered to other

structures
o Mobile - normal
o Fixed to underlying structures – carcinoma/ lymphoma
OVERLYING • Note any overlying skin changes such as tethering, bulging,

SKIN oedema, swelling, erythema, pain, infection, e.g.
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CHEST
RIGHT LOBE
• 3 Lobes – Superior, Middle, Inferior
o Inferior border of the lung anteriorly lies at the level of the 6th rib in
the midclavicular line
§ As you move laterally around the chest, this becomes the 8th rib
at the mid axillary line and at T10 spinous process
posteriorly
• 2 Fissures
o Transverse Fissure
§ Anteriorly, runs close to the 4th rib and meets the oblique fissure
in the mid axillary line near the 5th rib
o Oblique Fissure
§ Runs obliquely from T4 posteriorly to the 6th rib in the
midclavicular line anteriorly. Have patient put hand on head
and the medial border of scapular shapes the Oblique fissure
ling towards the 6th rib laterally-anteriorly.
LEFT LOBE
• 2 Lobes – Superior and Inferior
o Inferior border of the lung anteriorly lies at the level of the 6th rib in
the midclavicular line
§ As you move laterally around the chest, this becomes the 8th rib
at the mid axillary line and at T10 spinous process posteriorly
• 1 Fissure – Oblique Fissure
o Runs obliquely from T4 posteriorly to the 6th rib in the midclavicular
line anteriorly
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POSTERIOR CHEST
Examine the posterior chest (back) first.
INSPECT
Shape and Symmetry
• Deformities – potential Restrictive Lung
Disease
o Kyphosis – exaggerated forward
curvature of spine
o Scoliosis – lateral bowing of spine
o Kyphoscoliosis
• Shape
o Barrel Chest – Increased AP diameter
of chest
§ Severe COPD due to
hyperinflation
§ Severe Asthma – not seen as much anymore due to
management
o Cachectic – cancer, anorexia
• Lesions
o Bruising
o Scaring – previous surgeries, chest
drains, e.g.
o Trauma
o Radiation injury – erythema,
thickening of skin
• Chest Wall Expansion Symmetry
o Inspect rise and fall of clavicles for upper lobe expansion
§ Only unequal when severe –
• Unilateral: localised lung fibrosis, consolidation, collapse
(atelectasis/pneumothorax), pleural effusion, tension
pneumothorax (affected side), flail chest, trauma
• Bilateral: neuropathy (Guillain Barre), COPD, diffuse ILD,
pleuritic chest pain, kyphoscoliosis
40
PALPATE
• Chest Expansion
o Place hands firmly on chest wall with fingers around the side of the
chest; grab some pull of skin and hold firmly. Have thumbs meet in the
midline and not be in contact with skin
o Ask patient to take a deep breath and the thumbs should move
symmetrically outwards
§ At least 5cm is normal
§ Unequal Expansion – The affected side may show delayed or
decreased movement
• Unilateral: localised lung fibrosis, consolidation, collapse
(atelectasis/pneumothorax), pleural effusion, tension
pneumothorax (affected side), flail chest, trauma
• Bilateral: neuropathy (Guillain Barre), COPD, diffuse
ILD, pleuritic chest pain, kyphoscoliosis
• Bony Tenderness
o Palpate spine and Press sternum and spine together
§ Rib fractures/ bruising
§ Costochondritis
§ Prolonged/ Chronic coughing
§ Osteosarcoma and Bone malignancy (Lung, Prostate, Breast,
Multiple myeloma, Hodgkin’s and Non-Hodgkin’s, Ovarian
Cancer, thyroid, bladder, RCC, melanoma)
• Subcutaneous Emphysema
o Crackling sensation felt on palpating the skin of the chest or neck
often accompanied by diffuse swelling
§ Caused by air/gas tracking from the lungs usually due to
pneumothorax/ tension pneumothorax, ruptured oesophagus
(Boerhaave's), pneumomediastinum or some traumas
(barotrauma).
41
• Palpate the 5 Axilla Lymph Nodes – lung malignancy, infection

o Raise the patients arm and using your left hand for the right side, push
your fingers as high as possible into the axilla; then bring the patients
arm down to rest on your forearm and ask him/her to relax, allowing
you to take the weight
5 AXILLA LYMPH NODES

1. Central
a. Start first and feel deep in the centre of axilla, and as they relax their
arm down palpate into the axilla fossa
2. Lateral
a. Above and lateral to the head of humerus
3. Pectoral
a. Medial, against the palpable anterior pectoralis major muscle
4. Subscapular
a. Palpate against the subscapular fossa and Latissimus Dorsi muscle
5. Infraclavicular
a. Palpate along, under the clavicle
42
• Tactile (Vocal) Fremitus

Ask patient to hug themselves to move scapular away – Using ulnar edge of hands, press
firmly against the chest bilaterally and ask patient to say “99”.
Fremitus is the manner in which various voice frequencies are transmitted through
tissue and fluid.
When a person speaks, airflow from the lungs causes the vocal cords in the larynx to
vibrate. These vibrations, which are also known as vocal fremitus, are transmitted down the
tracheobronchial tree and through the lung tissue to the chest wall, where they can be
felt by the hand as a palpable vibration.
The assessment of tactile fremitus is based on the principle that sound vibrations are
conducted better through solid or fluid mediums, as opposed to air, which causes a
decay in sound transmission. As a result, areas of increased lung tissue density are
better conductors of sound, and generally present a more noticeable fremitus than normal
air-filled lung tissue. Thus, fremitus is best appreciated at the level between the scapular.
Conversely, an excessive amount of air within the lungs may cause impaired sound
transmission, leading to a decreased or absent tactile fremitus, as in lung peripheries
where it is moderately decreased normally.
Decreased intensity of tactile fremitus may occur as a result of excessive amounts of air in
the lungs (also known as hyperinflation). Hyperinflation can be seen in individuals with
pulmonary emphysema, chronic obstructive pulmonary disease (COPD), asthma, or severe
airway obstruction.
Additionally, decreased or absent tactile fremitus may also occur when there is an
increased distance between the lungs and the chest wall. For instance, excess fluid or air
can collect in the pleural space; the thin fluid-filled cavity that forms between the two layers
of serous membrane between the lungs and the chest wall. The build-up of excess fluid in
the pleural space is known as a pleural effusion, whereas accumulation of air in the pleural
space is known as a pneumothorax.
Finally, tactile fremitus may also have decreased intensity in individuals with obesity or
increased muscular mass, due to increased thickness of the chest wall.
Assessing for equal vibrations (fremitus)

• Decreased Fremitus – vibration is decreased in bigger areas of air, fat, fluid
increases length of vibration transmission thus reduced
o COPD/ Asthma – hyperinflation increases length thus reduces
transmission capacity
o Pleural Effusion – acts like a wall of fluid blocking transmission of
sound; increasing length of transmission
o Pneumothorax – loss of transmission due to tissue collapse
o Obesity
• Increased Fremitus – often localised and very difficult to identify with
palpation/tactile. Better appreciated with Vocal Fremitus or Resonance
o Pneumonia/ Consolidation – Consolidation occurs when air in the
alveoli is replaced with inflammatory exudate, blood, pus.
Consolidation augments lower frequencies (human voice) and thus is
likely to be felt as a stronger vibration
o Pulmonary oedema – fluid enhances lower frequencies
o ILD/ Atelectasis/ Tumour – increased tissue density enhances
transmission (some say decreases; may be due to size)
43
Percussion
Percuss the symmetrical areas of the anterior, posterior, superior, middle and
inferior and axillary regions. Also percuss the supraclavicular fossa as well as the
clavicles directly. Do not percuss over the scapular; ask patient to hug themselves
to move scapular more laterally.
With your left hand on the patient’s chest wall and fingers slightly separated and
aligned with the patients ribs, press your middle finger firmly against the patients
chest. Use the pad of your right middle finger to strike firmly the middle
phalanx of the middle finger of the left hand. Remove finger quickly so that the note
generated is not dampened by the pressure of the percussing finger.
• The percussing finger must be held partly flexed and a loose swinging
movement should come from the wrist and not the forearm
The percussion note is as important as the sound.

The NOTE of percussion is affected by thickness of the chest wall as well as
underlying structures
• NORMAL/ RESONANT: Percussion over normal lung produces a resonant
note
• DULL: Over a solid structure, liver or consolidation, or over collapsed lung
tissue (atelectasis), dampens normal resonance of the lung fields, thus dull
note – quieter and lower pitched
o Pneumonia (consolidation)
o Haemothorax
o Lung Fibrosis (ILD)
o Atelectasis
o Tumour (difficult to appreciate)
o Pulmonary oedema
• STONY DULL: Percussion over a large fluid filled area produces an
extremely dull note – stony dull
o Pleural effusion
• HYPER-RESONANT: Percussion over a hollow structure enhances
transmission thus produces a hyper-resonant note – louder and higher
pitched
o Pneumothorax
o Tension Pneumothorax
o COPD – hyperinflation/ Usually normal if not severe
o Asthma – hyperinflation (chronic)/ Usually Normal
• Liver Dullness
o 5, 7, 9
§ 5th rib midclavicular line anteriorly; below is Liver
§ 7th rib mid axillary line; below is Liver
§ 9th rib posteriorly; below is Liver
o DECREASED LVER DULLNESS – Liver Ptosis due to hyperinflation
causes liver to be pushed down thus normal resonance is heard;
typically liver itself is NOT enlarged, just pushed down.
• Cardiac Dullness
o Left side of the chest mainly; normal to have slight dullness due to
superficial cardiac fullness
• If not dull – Hyperinflated lung
44
45
AUSCULTATE
Listen to breath sounds with the diaphragm (firm pressure) of the stethoscope in
the same stepladder symmetrical regions of the lung. Listen to the axilla regions
with the bell (light pressure). Utilise land markings to determine lobe areas in order
to begin identifying approximate region of lung pathology if abnormal sounds are
heard.
Ask the patient to hug themselves and take a deep breath, through their mouth.
46
BREATH SOUNDS
Vesicular Breath Sounds

• Soft and low-pitched sound transmitted from airflow turbulence in the localised
lobar, segmental and smaller peripheral airways in inspiration
o Louder and longer sound in inspiration with no gap between I and E
§ Vesicular sounds are mainly produced in inspiration; expiration
sounds are thought to be distant transmissions from the bronchi
rather than the distant bronchioles themselves
o Alveoli ‘filter’ the turbulence of intense airflow thus the sound is soft
and not harsh/ intense like bronchial breath sounds, although vesicular
sounds themselves do not arise from the alveoli, rather the distant
bronchioles
o Called Vesicular, as the alveoli is the viscera of the lung
Bronchial Breath Sounds

• Loud, harsh and intense high pitched sound that are heard over the sternum/
manubrium (main bronchi)
o Hollow, blowing sound
• Similar duration of I and E although E is louder, due to greater pressures
pushing out of bronchi causing more turbulence
o Also heard in
§ Areas of Consolidation (pneumonia, atelectasis, tumour,
localised fibrosis) or just above a massive pleural effusion
• The area of solid lung (consolidated) prevents the alveoli
from ‘filtering’ the harsh high pitched sounds thus not
enabling vesicular sounds to occur – furthermore, the
consolidation of fluid enhances the higher frequency of
bronchial breath sounds therefore producing ‘bronchial’
transmission in the peripheries
• Pneumonia can cause Bronchial Breath sounds or
Reduced sounds overall – see Intensity of Breath Sounds
Tracheal Breath Sounds
• Very loud, high pitched harsh/ intense sounds heard over the trachea
o Greater turbulence and movement of air
o Heard over the neck
Bronchovesicular
• Intermediate intensity and pitch, through both I and E
• Heard over 1st and 2nd intercostal spaces
47
Healthy lung tissue and alveolar air usually surround the bronchi and bronchioles,
acting as a low frequency filter or muffler. This allows transmission of low-frequency
sounds (100-200Hz) but filters higher frequencies (30-500Hz). Consolidation,
oedema and pleural fluids are better at transmitting higher frequencies thus results in
the altered transmission (bronchial breath sounds) as well as the other respiratory
signs such as increased vocal resonance and fremitus.
48
INTENSITY OF BREATH SOUNDS
Refers to the loudness of breath sounds audible. Intensity of flow (sound energy)
as well as Transmission of sound through the lungs and chest wall influences
overall intensity of breath sounds.
Normal Intensity – normal lung sounds
Reduced Intensity – soft/ low intensity (reduced) breath sounds

• Asymmetrical reduction in intensity
o Bronchial obstruction – carcinoma or foreign body – blocks airflow
past the area of occlusion in bronchi thus no air transmission
o Haemothorax (reduced/absent)
• Generalised Reduced Intensity
o COPD (and Severe Asthma)
§ Emphysema and hyperinflation store excess reserved volumes
of air, reducing transmission capability as well as reducing
amount of air able to be inspired
o Pleural Effusion – muffled or absent breath sounds
§ Decreased expansion and ventilation to area of hemithorax due
to effusion as well as fluid wall blocking transmission of sound
• In pleural effusions, bronchial breath sounds may be
heard just above the fluid level due to enhanced
conduction of sound
o Pneumonia – determined by the patency of the airways in whether
you get reduced breath sounds or bronchial breath sounds
§ Decreased breath sounds – if the consolidation in the alveoli
blocks off airways that are also surrounded by consolidation,
then there will be no flow of air thus no sound
§ Bronchial breath sounds (increased intensity) – if the underlying
airways are patent and surrounded by consolidation material
then the bronchial breathing is heard as bronchial breath sounds
are transmitted
o Large cancer or foreign body – sound cannot transmit past
obstruction
o Pneumothorax/ Tension Pneumothorax – absent breath sounds
o Neuromuscular/ Respiratory Depression – reduces overall
inspiratory effort thus reduces intensity of air flow
o Obesity – increased transmission length thus vibrations die out before
reaching chest wall
49
50
ADDED (ADVENTITIOUS) BREATH SOUNDS – PATHOLOGICAL BREATH

SOUNDS
CRACKLES (rales/ crepitations) – Discontinuous, intermittent popping sounds.

There is terminology confusion as in the past low-pitched crackles were called rales and
high-pitched crackles were crepitations. Best approach is to call ALL as crackles and
instead describe their timing and pitch.
Crackles are caused by loss of stability in peripheral airways (alveoli) with high
inspiratory pressure causing rapid air entry causing abrupt opening of alveoli and of
small-medium sized bronchioles containing secretions in the regions of the lung deflated
to residual volume. More compliant (distensible) areas open up first followed by increasingly
stiff areas. The negative pressure of inspiration causes airways that have previously
collapsed to ‘pop’ open. Once open, there is a sudden equalisation of pressure on either
side of the obstruction, causing vibrations, which create the sound.
Crackles can be present in normal people although will always clear with coughing.
Fine: soft, high-pitched and usually late or pan-inspiratory
• Caused by the sudden opening of small airways (Velcro being separated)

usually heard mid-late inspiration, uninfluenced by cough, gravity or body
position. Due to sticky fibrotic regions causing localised atelectasis
o Interstitial Pneumonia
o Pulmonary Fibrosis (IDL) and Sarcoidosis – fine, mid-late, sparse
Coarse: loud, low-pitched – Produced by pockets of air passing through the

airways as they open and close intermittently. Tends to occur early during
inspiration and throughout expiration with popping quality
• COPD (Chronic Bronchitis) – produced by previously collapsed mucus

bronchioles opening up
o Early inspiratory crackles; end before end of inspiration
• Pulmonary Oedema/ Congestive Heart Failure and Atelectasis
o Middle-Late or Pan inspiratory medium crackles
• Pneumonia
o Mid/Late inspiratory
o Acute Stage – Early/Mid inspiratory, long crackles. Infiltration of
consolidation (pus, cells, oedema) fill smaller airways and alveoli, and
thus inspiration abruptly opens them up
o Late/ Resolving Stage – End inspiratory, short. Oedema decreased but
inflammatory cells are still present thus the lungs become drier, leading
to reduced compliance causing segmental airway collapse
• Asthma
o Early inspiratory crackles; end before end of inspiration
§ Secretion and collapse of smaller airways (bronchioles) causes
crackles upon inspiration as smaller, sticky airways open
• Bronchiectasis
o Mid-inspiratory – destruction of bronchiole wall (muscular/ elastic) can
cause them to collapse at the end of expiration
51
52
WHEEZE
Continuous oscillation of air from opposing airway walls producing a musical quality,
and implies significant airway narrowing. Occur at the end of inspiration and
become louder on expiration; because airways are more narrowed in expiration
with a higher force of airflow pressure being forced out.
Frequency (pitch) of wheeze varies and is determined by the velocity of the air jet
and is not related to the length of the airway
• High Pitched – Sibilant wheezing – produced in smaller bronchi
• Low Pitched – Rhonchi – larger airways
• Monophonic Wheeze
o Single note that starts and ends at different points in time. The pitch
and timing is fixed as the obstruction itself is static
§ Tumour in the bronchi
§ Foreign body in bronchi
• Polyphonic Wheeze
o A wheeze with several different tones starting and finishing at the same
time. It is heard when a fixed compression occurs in multiple bronchi at
the same time. It is caused by second or third order bronchi closing at
the same time at the end of expiration, as the pressures within the
airway keeping them patent are reduced
§ COPD (Chronic Bronchitis) and Acute Bronchitis
§ Asthma (and Cardiac Asthma)
The longer and more high pitched the wheeze, the more severe the obstruction is
generally. However, wheeze should NOT be used as an indicator of severity.
Wheeze implies that there is enough air movement to produce a sound (wheeze).
Beware of the wheezing patient becoming silent; this implies the air movement is so
low that a wheeze cannot be produced (Severe Asthma) and may mean respiratory
arrest may be imminent.
Sibilant Wheezing – musical, prolonged (High Pitched) – smaller bronchi

• Asthma - polyphonic
• Cardiac Asthma - polyphonic
o Widespread interstitial oedema and congestion of lung with bronchial
oedema causing constriction with reflexive irritative bronchospasm
• Neoplasm
o Fixed, localised obstruction causing sibilant monophonic wheeze
Rhonchi – Sonor Wheezing – low pitched continuous or expiratory – larger airways

• Secretions – bronchial pneumonia/ respiratory tract infection
o CF, Bronchiectasis, pneumonia
• Acute Bronchitis
• COPD exacerbation – mucosal secretions, may be cleared with coughing
o Usually COPD on its own does not produce a wheeze; secondary to
bronchial spasm, mucosal oedema during exacerbations
53
STRIDOR
High pitched, over the trachea due to narrowing or obstruction of extra thoracic
airway. Usually audible without stethoscope.
• Inspiration (inspiratory stridor) – obstruction of the extra-thoracic
airways; above the level of vocal cords due to collapse of soft tissues
(pharynx) with negative pressure during inspiration
• Epiglottitis
• Croup
• Foreign Body above vocal cords
• Aspiration
• Bilateral vocal cord palsy
• Ludwig’s Angina
• Cancer in pharynx
• Expiration (expiratory stridor): obstruction of the intrathoracic
airways; similar to wheezing but more severe
• Asthma
• COPD
• Obstruction at the level of bronchi
• Retropharyngeal abscess
• Inspirational and Expiration Stridor (Biphasic Stridor):
obstruction at the level of the glottis
• Foreign Body at level of glottis
• Tracheitis
• Cancer
54
PLEURAL FRICTION RUB

Scratchy, high-frequency sound. Occurs when thick, roughened pleural surfaces
rub together as the lungs expand and contract.
• Pleurisy – inflammation/infection of pleura itself
o May be secondary to
§ Pulmonary infarct (severe PE)
§ severe Pneumonia
§ Lung Cancer and Mesothelioma
§ RA, SLE, Sjoegren
§ TB
55
Vocal Resonance
Verbal Fremitus – refers to vibration intensity whilst Vocal resonance is the speech
Auscultation over the chest wall while the patient speaks “99” also aids in giving
information about the lungs ability to transmit sound.
Normal Lung
• Low-pitched components of speech are heard with a booming quality as low
pitched sound is transmitted best through lung parenchyma and high pitched
sounds are filtered out
o The sound is therefore muffled as the higher pitched frequencies
are lost
Increased Vocal Resonance – Consolidation – Increased density – fluid, pus,

cells, blood, tissue that transmits sound greater
• Transmits both low and higher frequency sounds thus the speech heard has a
bleating quality (e in bee will sound like a as in bay) and is crisp/ audible
• The speech (99) will be clearer and more audible due to greater transmission
of sound waves from the consolidation
o If vocal resonance is increased, bronchial breath sounds are likely
to be heard in these areas with inspiration
o Sometimes vocal resonance can be increased so much that whispered
speech can be distinctly heard
• Pneumonia (consolidation) – crisp, clear voice
• Haemothorax
• Tumour
• Atelectasis
• ILD
Reduced Vocal Resonance: Presence of fluid or air within the lung blocks
transmission of sound, either due to increased distance thus reduced, or the physical
properties of blocking.
• Pleural Effusion – absence/ very muffled and quiet
• Pneumothorax – increased air
• COPD
• Asthma
• Obesity
56
ANTERIOR CHEST
INSPECT
Shape and Symmetry
• Deformities
o Pectus Excavatum (funnel chest)
§ Developmental defect involving a
localised depression of the lower end of
the sternum
§ Problem is usually aesthetic although if
severe can cause Restrictive lung
o Pectus Carinatum (pigeon chest)

§ Localised prominence; outward bowing
of the sternum and costal cartilages
§ May be manifestation of chronic
childhood respiratory illness where
repeated forceful contractions of the
diaphragm when the thorax is still
pliable. It can also occur in rickets.
• Intercostal Recession
• Prominent Veins – SVC obstruction, thoracic inlet
obstruction from tumour, lymphoma, retrosternal goitre, tension pneumothorax
• Chest wall Lesions

o Flail chest
§ Occurs when there are two or more adjacent ribs that
are fractured in two or more places, leaving a plate like
of free ribs. It is usually caused by high impact trauma
with other associated thoracic injuries.
§ The flail part of the ribs, the free broken parts, move
paradoxically with the normal chest movements
(opposite).
§ When inspiration occurs and the normal thoracic cage
expands and rises, the flail part will get sucked into the
thoracic cavity and thus that area will depress. Thus, in expiration, the
normal thoracic cage will depress and decrease in volume. This will
cause the flail part to rise up and does not follow the typical chest
depression.
§ Almost always associated with other thoracic injuries e.g. heart and/or
lung contusion, laceration, haemothorax/pneumothorax
o Bruising
o Scarring
o Trauma
57
PALPATE
• Chest expansion the same but anterior of chest
o Hoover’s Sign
§ Place your hands along the costal margins with your thumbs
close to the xiphisternum
• Normally, inspiration causes them to separate however in
COPD, when the chest becomes severely hyperinflated,
the diaphragm often becomes stretched. As a
consequence, contraction of the diaphragm at inspiration
results in an inward movement, bringing the costal
margins with it, as opposed to normal downward,
separating movement.
TACTILE FREMITUS, PERCUSSION & AUSCULTATION

The same as above but for anterior chest.
58
ABDOMEN
• Palpate and Percuss the Liver
o Ptosis
§ Liver is dragged down due to hyperinflation; thus may be
palpable although it is NOT enlarged
o Hepatomegaly – liver metastasis from Lung Ca
LOWER EXTREMITIES
• Oedema
• Clubbing
• Capillary Refill
• Temperature
• Signs of DVT
o Swelling, redness, pain/ tenderness
o Homan’s Sign
§ Raise the straightened leg to 10o and actively or ask patient
to dorsiflex the foot
• Deep calf pain upon dorsiflexion may indicate DVT
o Usually, unilateral
o May dislodge the clot so be careful. POOR
specificity
59
CARDIOVASCULAR EXAM
• Integral part of Respiratory exam and both are typically done together
o JVP – RV failure, Pulmonary HTN, PE, Chronic COPD (Cor
Pulmonale), Tension Pneumothorax
o Heart Sounds/ Thrills/ Palpations
§ Pulmonary HTN – Loud P2, parasternal impulse, tricuspid
regurgitation (pansystolic)
o Apex Beat Palpation
§ Displacement towards the side of the lesion can be caused by
collapse of the lower lobe or by localised ILD
§ Displacement away from the side of the lesion can be caused
by massive pleural effusions or tension pneumothorax
§ Apex is often im-palpable in COPD due to hyperinflation
60
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APPENDIX
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CROUP
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Jack’s Notes CLINICAL SKILLS

INTRODUCTION/ EXPLANATION/ CONSENT

o Depth – shallow/ deep

o Dyspnoea – laboured breathing, increased effort to breath

o Stridor – High pitched, over the trachea due to narrowing or

• Abnormal Breathing Patterns

H - Hypoventilation - NAILED, except for Lung Pathology!

HIGH A-a Gradient - VSD

Causes are broken into 3 categories: VSD

V - Ventilation/Perfusion (V/Q) Mismatch

• Pneumonia - fluid in alveoli – perfusion with reduced ventilation (Low VQ)

• Extrapulmonary Shunt - bypassing alveoli thus oxygenation outside the lungs

D - Diffusion Problem - thickness issue limiting exchange between alveoli and

• CRT – Capillary Refill Time

• Tar Staining of Fingers

• Pemberton’s Sign – Arms in full abduction for approx. 1 min causes

The palpable sinuses; test for Sinusitis

Oral/ Mucosa/ Palate

Assessment of lymph nodes

Cervical Lymph Nodes – order of palpation, not of the image below!

Chin à Jaw à Ear à Occipital à in front and

SITE • Assess the lymph node’s location in relation to other anatomical

CONSISTANCY • Borders to determine if they feel regular or irregular

FIXATION • Assess if the lymph node feels mobile or is tethered to other

OVERLYING • Note any overlying skin changes such as tethering, bulging,

• Palpate the 5 Axilla Lymph Nodes – lung malignancy, infection

5 AXILLA LYMPH NODES

• Tactile (Vocal) Fremitus

Assessing for equal vibrations (fremitus)

The percussion note is as important as the sound.

Vesicular Breath Sounds

Bronchial Breath Sounds

INTENSITY OF BREATH SOUNDS

Normal Intensity – normal lung sounds

Reduced Intensity – soft/ low intensity (reduced) breath sounds

ADDED (ADVENTITIOUS) BREATH SOUNDS – PATHOLOGICAL BREATH

CRACKLES (rales/ crepitations) – Discontinuous, intermittent popping sounds.

Fine: soft, high-pitched and usually late or pan-inspiratory

• Caused by the sudden opening of small airways (Velcro being separated)

Coarse: loud, low-pitched – Produced by pockets of air passing through the

• COPD (Chronic Bronchitis) – produced by previously collapsed mucus

Sibilant Wheezing – musical, prolonged (High Pitched) – smaller bronchi

Rhonchi – Sonor Wheezing – low pitched continuous or expiratory – larger airways

PLEURAL FRICTION RUB

Increased Vocal Resonance – Consolidation – Increased density – fluid, pus,

o Pectus Carinatum (pigeon chest)

• Chest wall Lesions

TACTILE FREMITUS, PERCUSSION & AUSCULTATION

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