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2 History and examination
Jugular venous pressure (
JVP
JVP
JVP
JVP
JVP
JVP
JVP
SVC
JVP
JVP
JVP
a
Diastole
systole
a
closure of tricuspid valve, not
JVP
JVP
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The internal jugular vein acts as a capricious manometer of right atrial pressure.
examination is dicult so do not be downhearted when the skill eludes you.
Observe the height and the waveform of the pulse. Concomitantly palpate the arterial pulse to help decipher patterns.
Distinguishing the venous pulse
• Usually impalpable and obliterated by finger pressure on the vessel.
• Rises transiently with pressure on abdomen (abdominojugular reflux)1 or liver
(hepatojugular reflux).
• Changes with posture and respiration: disappears/ falls when patient sits upright.
• Usually has a double pulse for every arterial pulse (fig
v
c
y
x
Ventricular
Fig 2.
11
The jugular venous pressure wave. The
because the right atrium is no longer contracting. This means that the pressure in the right atrium
is dropping and this is reflected by the
After Clinical Examination, Macleod, Churchill and Aids to Undergraduate Medicine, J Burton, Churchill.
Height
Observe the patient at 45°
with their head turned
slightly to the left and neck
relaxed. Good lighting and
correct positioning are key.
Look for the right internal
jugular vein as it passes just
medial to the clavicular head
of the sternocleidomastoid,
behind the angle of the jaw
fig
2.12
). The
(
by measuring the vertical
height of the top of the pulse
above the manubriosternal
angle (not the sternal notch). Pressure at zero (the sternal angle) is
the height of the
sure above
Abnormalities of the
• Raised
• Fixed raised
• Large a wave: pulmonary hypertension, pulmonary stenosis.
• Cannon a wave: when the right atrium contracts against a closed tricuspid valve,
large ‘cannon’ a waves result. Seen in complete heart block, single chamber ventricular
pacing, ventricular arrhythmias/ ectopics.
• Absent a wave: atrial fibrillation.
• Large v waves: tricuspid regurgitation, look for earlobe movement.
• Constrictive pericarditis: high plateau
with deep x and y descents.
• Absent
tory volume (eg volume depletion, haemorrhage) the
1
This sign was first described by Pasteur in
is assessed
to obtain the right heart filling pressure in cm of water. A pres-
9
cm (4cm above the manubriosternal angle at 45°) is elevated.
with normal waveform: flui d overl oad, r ight h eart fa ilure.
with absent pulsation:
: when lying flat, the jugular vein should be filled. If there is reduced circula-
Diastole
.
Fig 2.
12
The jugular venous system.
1885
in the context of tricuspid incompetence.
)
2.11
).
a wave:
atrial systole
c wave:
normally visible
fall in atrial pressure during
x descent:
ventricular systole
atrial filling against a closed
v wave:
tricuspid valve
opening of tricuspid valve
y descent:
drops (X descent) during ventricular systole
5
cm, so add 5 to
obs truct ion (p
which ri ses on i nspirat ion (Kussmaul’s sign)
524
).
may b e abse nt.
41
2 History and examination
Heart sounds
PR
VSD
VSD
VSD),
JVP
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42
Listen systematically: heart sounds then murmurs. While listening, palpate the
carotid artery: the carotid upstroke corresponds to systole (
Heart sounds The 1st and 2nd sounds are usually clear. Confident pronouncements
about other sounds and soft murmurs may be dicult. Even senior colleagues may
disagree with one another, before deferring to an echocardiogram.
The 1st heart sound (S1) represents mitral (M1) and tricuspid (T1) valve closure.
• Loud S1 occurs in mitral stenosis. The narrowed valve orifice limits ventricular filling so
there is no gradual decrease in flow towards the end of diastole. The valves are, therefore, at their maximum excursion at the end of diastole, and so shut rapidly leading to
a loud and palpable (the ‘tapping’ apex) S
ened, eg if the
• Soft S1 oc cur s if th e di ast oli c fi lli ng t ime is pro lon ged , eg pro lo nge d PR interval, or when
the mitral valve leaflets fail to close properly in mitral incompetence.
• Variab le in tens ity S1 in AV blo ck, AF, and nodal and ventricular tachycardias.
• Splitting of S1 may be heard in inspiration. It is normal and due to physiological asyn-
int erval i s shor t, and in tac hycardi a.
chrony in the closure of mitral and tricuspid valves.
The 2nd heart sound (S2) represents aortic (A2) and pulmonary valve (P2) closure.
• Soft A2 occ urs in aorti c steno sis.
• Loud A2 can occur in tachycardia, hypertension, and transposition, though diagnostic
discrimination is limited in clinical practice.
• P2 is loud i n pulm onary hypert ensio n and soft in pulmonary stenosis.
• Splitting of S2 is best heard in the pulmonary area:
• Normal splitting in inspiration due to the variation of right heart venous return
with respiration, delaying the pulmonary component.
• Wide splitting occurs in right bundle branch block, pulmonary stenosis, deep in-
spiration, mitral regurgitation, and ventricular septal defects (
• Wide fixed splitting o ccurs with at rial s eptal defects.
• Reversed splitting (ie A
curs in left bundle branch block, aortic stenosis, patent ductus arteriosus, and right
ventricular pacing.
• Single S
occurs in Fallot’s tetralogy, severe aortic or pulmonary stenosis, pul-
2
monary atresia, Eisenmenger’s syndrome (
Additional sounds
• 3rd heart sound (S3) occurs just after S2, due to rapid ventricular filling. This can be due
to increased volume load (mitral regurgitation,
cardiomyopathy), or physiology (pregnancy). It is low pitched and best heard with the
bell. It can be distinguished from the ‘pericardial knock’ of constrictive pericarditis or
restrictive cardiomyopathy as this is higher pitched and associated with constrictive
changes in the
• 4th heart sound (S4) occurs just before S1. Always abnormal, it represents atrial con-
(p41).
traction against a ventricle made sti by any cause, eg aortic stenosis or hypertensive
heart disease.
• Trip le a nd ga l lo p r hy th ms : a 3rd or 4th heart sound occurring with a sinus tachycardia
may give the impression of galloping hooves. An S
‘Ken- tucky’, whereas an S
occur in a tachycardia, eg with pulmonary embolism, they may summate and appear
as a single sound, a summation gallop.
• An ejection systolic click is heard early in systole with a bicuspid aortic valve, and in
hypertension. Equivalent lesions in the right heart may also cause clicks.
• Mid- systolic clicks occur in mitral valve prolapse (p
• An opening snap precedes the mid- diastolic murmur of mitral (and tricuspid) stenosis.
It indicates a pliable (non- calcified) valve.
• Prosthetic sounds are caused by non- biological valves opening and closing: rumbling
8
ball and cage valves, eg Starr– Edwards; single clicks 8 tilting disc valves, eg
sounds
single disc (Bjork- Shiley), bileaflet (St. Jude— often quieter). Prosthetic mitral valve
clicks occur with S
and aorti c valve s clic k in ti me with S2.
1
fig
2.13
).
. S1 is also lou d if dia stol ic fi llin g ti me i s sho rt-
1
S).
following P2, with splitting increasing on expiration) oc-
2
p
148
), and with a large
ventricular dysfunction (dilated
gallop has the same rhythm as
138
3
).
gal lop has t he sa me rhy thm a s ‘Tenn e- ssee’. When S3 and S4
4
.
2 History and examination
QRS
Pressure (mmHg)Left ventricular volume (mL)
r
4
= Isovolumetric ventricular relaxation
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43
Fig 2.
130
13
110
P
4
th
T
2
nd
3
1
st
rd
A P
50
0
End-diastolic
volume
65
Open
Open
End-systolic
volume
DiastoleDiastole Systole
1123 4
1
= Ventricular filling
2
= Isovolumetric ventricular contraction
3
= Ventricular ejection
The cardiac cycle.
Open
ECG
Heart
sounds
Aortic pressure
Left atrial pressure
Left ventricular pressure
Left ventricular volume
Position of atrioventricula
valves
Position of aortic and
pulmonary valves
Phase of cardiac cycle
2 History and examination
Cardiac murmurs
NB:
ESM
ESM
H(O)CM
PSM
EDM
EDM
EDM
MDM
MDM
ESM
ESM
PSM
H(O)CM
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44
Think: ‘What do I expect to hear?’ Be guided by symptoms and signs before aus-
cultation (but not dictated to: don’t let your expectations determine auscultation).
Use the stethoscope correctly: remember that the bell is good for low- pitched
sounds (eg mitral stenosis) and should be applied gently. The diaphragm filters out
low pitches, making higher- pitched murmurs easier to detect (eg aortic regurgita-
a bell applied tightly to the skin becomes a diaphragm.
tion).
Consider any murmur in terms of character, timing, intensity, area where loudest,
radiation, and accentuating manoeuvres.
When in doubt, rely on echocardiography rather than disputed sounds (but
continue to enjoy the challenge!).
Character and timing (fig 2.
• An ejection- systolic murmur (
the outflow tract and waxes and wanes with intraventricular pressure.
innocent in children and are not due to valve disease in high- output states (eg tachycardia, pregnancy). Pathological causes include aortic stenosis and sclerosis, pulmonary stenosis, and
• A pansystolic murmur (
pathological and heard with mitral or tricuspid regurgitation (S
these), or a ventricular septal defect (
systolic murmur ± mi d- systolic click.
• An early diastolic murmur (
sence of silence’ in early diastole. An
gitation. If pulmonary regurgitation is secondary to pulmonary hypertension resulting
from mitral stenosis, then the
• A mid- diastolic murmur (
osis (accentuated presystolically if in sinus rhythm). If due to rheumatic thickening of
the mitral valve =
context of aortic regurgitation due to the fluttering of the anterior mitral valve cusp by
the regurgitant stream.
• Continuous murmurs are present throughout the cardiac cycle and occur with a pa-
tent ductus arteriosus, arteriovenous fistula, or ruptured sinus of Valsalva.
Carey Coombs’ murmur. An Austin Flint murmur is an
Intensity All murmurs are graded on a scale of 1– 6 (table
diastolic murmurs, being less loud, are only graded
the severity of a lesion: an
Area where loudest Though there are no guarantees, mitral murmurs tend to be
loudest over the apex, aortic murmurs over the right
monary over the left
sternal edge (
Radiation The
fig
2.8
, p39).
of aortic stenosis classically radiates to the carotids. The
mitral regurgitation radiates to the axilla.
Accentuating manoeuvres
• Movements that bring the relevant part of the heart closer to the stethoscope accen-
tuate murmurs: lean forward for aortic regurgitation, left lateral position for mitral
stenosis.
• Expiration increases blood flow to the left side of the heart and therefore accentuates
left- sided murmurs.
• Valsal va mano euvr e (forced expiration against a closed glottis) decreases systemic
venous return, accentuating mitral valve prolapse and
gurgitation and aortic stenosis.
ates the murmur of mitral stenosis.
Non- valvular added sounds
A pericardial friction rub may be heard in pericarditis. It is a superficial scratching
sound, not confined to systole or diastole.
)
, crescendo– decrescendo) usually originates from
S may be
.
) is of uniform intensity and merges with S2. It is usually
p
148
). Mitral valve prolapse may produce a late
) is high pitched and easily missed: listen for the ‘ab-
occurs in aortic and pulmonary (rare) regur-
is c alled a Graham Steell mu rmur.
) is low p itched and rumb ling. They occur i n mitral ste n-
1– 4
may be inaudible in severe aortic stenosis.
2
nd intercostal space, and tricuspid murmurs at the lower left
may also be soft in
1
in the
2.4
), though in practice
. Intensity is a poor guide to
2
nd intercostal space, pul-
Inspiration acc entuat es rig ht- sided murmurs.
, but softening mitral re-
Squatting has the opposite eect. Exercise accentu-
of
2 History and examination
S
1
S
1
S
2
S
1
S
1
S
2
S
Ejection-systolic eg: aortic stenosis
Early diastolic eg: aortic regurgitation
Pansystolic eg: mitral regurgitation Mid-diastolic eg: mitral
ESM
ESM
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1
S
2
Fig 2.
14
Typical waveforms of common heart murmurs.
45
Opening
S
1
S
1
S
2
snap
Presystolic
accentuation
S
1
Grading intensity of heart murmurs
The following grading is commonly used for murmurs: systolic murmurs from
1
to 6 and diastolic murmurs from 1 to 4 (as they cannot reach grading 5 or 6).
Table 2.
4
Grading of heart murmurs.
Grade Description
1/ 6
2/ 6
3/ 6
4/ 6
5/ 6
6/ 6
Very soft, only heard after listening for a while
Soft, but detectable immediately
Clearly audible, but no thrill palpable
Clearly audible, palpable thrill
Audible with stethoscope only partially touching chest
Can be heard without placing stethoscope on chest
Prosthetic valve murmurs
Prosthetic valves Created either from synthetic material (mechanical pros-
thesis, see prosthetic sounds,
p42) or from biological tissue (bioprosthesis). The
choice of prosthesis is determined by the anticipated lifespans of the patient and
the graft, and the risks of anticoagulation (including plans for pregnancy). Three
mechanical valve designs exist: the caged ball valve, the tilting disc single leaflet
valve, and the bileaflet valve. Tissue valves are made from porcine valves or bovine pericardium.
Prosthetic aortic valves All produce a degree of outflow obstruction and thus
have an
. The intensity of this murmur increases as the valve fails. Ball and
cage valves (eg Starr– Edwards) and tissue valves do close completely in diastole
and so a diastolic murmur warrants assessment for valve failure.
Prosthetic mitral valves B all a nd c age v alve s pro ject into the left vent ricl e an d can
cause a low- intensity
and bileaflet valves can also have a low- intensity diastolic murmur. Consider any
as they interfere with the ejected stream. Tissue valves
systolic murmur of loud intensity to be a sign of regurgitation and failure.
Eponymous signs of aortic regurgitation
• de Musset’s sign: head nodding in time with the pulse.
• Müller’s sign: systolic pulsations of the uvula.
• Corrigan’s sign: visible carotid pulsations due to a rapid systolic rise and a rapid
diastolic collapse.
• Quincke’s sign: capillary nailbed pulsation in the fingers.
• Traube’s sign: ‘pistol shot’ femorals, a booming sound heard over the femorals.
• Duroziez’s sign: to- and- fro diastolic murmur heard when compressing the
femorals proximally with the stethoscope.
2 History and examination
The respiratory system: history
TB
CXR
SLE
ACE
TB
PND
JVP,
NYHA
TB
OHCS
SOCRATES
COPD
LV
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46
Table 2.
5
Presenting symptoms and questions to ask
Presenting
symptoms
Dyspnoea
table 2.6 and
(
p
765
)
Cough (
Haemoptysis
table 2.7)
(
Hoarseness
p
(
Wheeze (
stridor(
Chest pain
(
p86, p
History Ask about current symptoms (table
bronchitis,
surgery, myopathy/ neurological disorders, connective tissue disorders/ symptoms,
eg rheumatoid,
Direct questions and possible causes
Duration? Exercise tolerance: steps climbed/ distance walked?
classification (
about circumstances in which dyspnoea occurs (eg occupational
allergen exposure)
p47) Duration? Character (eg barking/ dry)? Nocturnal (≈ asthma, ask
about other atopic symptoms, eg eczema, hay fever)? Exacerbating
factors? Sputum (colour? how much?). Haemoptysis?
Always consider risk factors for
night sweats (
suggest pulmonary embolism, trauma, or bleeding into a lung cavity.
Melaena can occur if enough blood is swallowed
Laryngitis, recurrent laryngeal nerve palsy, Singer’s nodules, or
418
)
laryngeal tumour
Wheeze is common in asthma but also foreign body, congestive
p51)/
heart failure, malignancy, and any lesion causing airway narrowing
p47)
764
)
involvement
, atopy (asthma/ eczema/ hay fever), previous
.
p
135
)? Diurnal variation (≈ asthma)? Ask specifically
p30), smoking). Blood not mixed with sputum may
(see p36), ‘pleuritic’ (worse on inspiration) suggests pleural
and malignancy (weight loss,
2.5
) and past history: pneumonia/
abnormalities, lung
Drug history Respiratory medications: bronchodilators, corticosteroids? Any medi-
cations with respiratory side eects, eg
- i, cytotoxics, - blockers, amiodarone?
Fam i ly hi st o ry Atopy? Emphysema? TB?
Social history Quantify smoking in ‘pack- years’ (20 cigarettes/ day for 1 year = 1
pack- year). Occupation: farming, mining, asbestos. Pets? Recent travel/
Dyspnoea
Subjective sensation of shortness of breath, often exacerbated by exertion.
Speed of onset may aid diagnosis (
• Lung disease: air way and inte rsti tial disea se. M ay be hard t o dierentiate from car-
diac causes. Asthma: nocturnal cough, early morning dyspnoea & wheeze.
• Cardiac disease: left ventricular failure of any cause. Orthopnoea (dyspnoea worse
on lying down; ‘How many pillows?’) and paroxysmal nocturnal dyspnoea (
dyspnoea waking one up). Also peripheral oedema, i
• Anatomical: diseases of the chest wall (p50), muscles, pleura. Ascites can cause
breathlessness by splinting the diaphragm and restricting its movement.
• Other: shock— dyspnoea may be shock’s presenting feature (p
Metabolic acidosis with respiratory compensation, eg ketoacidosis, salicylate
table 2.6). Causes include:
crepitations (p51).
599
, p
770
poisoning. Dyspnoea at rest unassociated with exertion may be psychogenic.
Prolonged hyperventilation causes respiratory alkalosis, and a fall in ionized calcium
leading to peripheral/ perioral paraesthesiae ± carpopedal spasm. Physiological
breathlessness of pregnancy (breathe deeper, not faster).
Table 2.
6
Aetiology of dyspnoea by timing of onset
Acute Subacute Chronic
Foreign body
Pneumothorax (
Pulmonary embolus
Acute pulmonary oedema
p
733
, fig
16.44
Asthma
)
Pneumonia
Eusion
Interstitial lung disease
dysfunction
Anaemia
contacts?
). Anaemia.
;
2 History and examination
Haemoptysis
TB
IV
FBC, INR/ APTT
IV
, TB
SARS- CoV
ANCA
GBM
SLE
DIC
ACE
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Haemoptysis is blood that is coughed up: frothy, alkaline, and bright red, often in
a context of known lung disease (
Table 2.
7
Causes of haemoptysis
Infective
Neoplastic
Vas cula r
Paren chymal
Pulmonary
hypertension
Coagulopathy
Tra um a/ foreign body
Pseud o- haemoptysis
table 2.7). (NB: Vomit ed blood is ac idic and d ark.)
Pneumonia, pneumonitis, bronchiectasis, bronchitis, abscess.
Can be bacterial (pneumococcus
viral (influenza,
Primary or secondary
Lung infarction (PE), vasculitis (
disease,
arteriovenous malformation
Interstitial lung disease, sarcoidosis, haemosiderosis, cystic
fibrosis
Idiopathic, thromboembolic, congenital cyanotic heart
disease (
Any, eg thrombocytopenia (p
Always exclude underlying pathology
Includes following intubation
Oropharyngeal bleeding, aspirated haematemesis.
Red pigment (prodigiosin) from Serratia marcescens.
Munchausen’s (
), hereditary haemorrhagic telangiectasia,
p
148
)
p
), fungal (aspergillosis),
- 2), and helminths (schistosomiasis)
- associated, anti-
342
),
, warfarin toxicity.
694
)
Rare causes refuse to be classified neatly: vascular causes may have infective
origins, eg hydatid cyst may count as a foreign body and infection and vascular
if it fistulates with the aorta; ditto for infected (mycotic) aneurysm rupture, or
aortitis. Infective causes may cause coagulopathy: dengue; leptospirosis. If
monthly haemoptysis, consider lung endometriosis.
Tre at me nt If massive (eg trauma, TB, hydatid cyst, cancer, AV malforma-
tion): prepare (
access, blood gas,
by interventional radiology, bronchoscopic (stent/ balloon) tamponade, or cardiothoracic surgery (lobe resection).
inoperable malignancy.
, crossmatch) for embolization
morphine if distressed by symptoms, eg
Cough
Coughing is relatively non- specific, resulting from irritation anywhere from the
pharynx to the lungs. The character of a cough may, however, give clues as to the
underlying cause:
• Loud, brassy: pressure on the trachea, eg tumour.
• Hollow, ‘bovine': recurr ent laryngea l nerve palsy.
• Barking: laryngotracheobronchitis (croup).
• Chronic: TB, foreign body, asthma (nocturnal), pertussis.
• Dry, chronic: oeso phage al reflu x, sid e eect of
- i.
Do not ignore a change in character of a chronic cough; it may signify a new
problem, eg infection, malignancy.
Stridor
Inspiratory
• Within the lumen: foreign body, tumour, bilateral vocal cord palsy.
• Within the airway wall: oedema (eg anaphylaxis), laryngospasm, epiglottitis, laryn-
• Extrin sic to the airway: goitre (p
If gas exchange is impaired, manage as an emergency (p
sound due to partial obstruction of upper airways. Obstruction may be:
gotracheobronchitis (croup), amyloidosis.
78
), oesophagus, lymphadenopathy.
756
).
47
2 History and examination
The respiratory system: examination
T
TB
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48
Introduce yourself, obtain consent to examine, and position sitting up at 45°.
Expose to the waist (for female patients delay until examining the chest). Explain
throughout.
1
Inspection
• General Ill or well? Respiratory distress (p49)?
p47)? Short of breath (p46)? Accessory
Stridor (
muscle use? Cachexia (
• Chest wall Movement: ask patient to take a deep
breath (pathology is on the restricted side).
Deformities of chest wall (
tattoos from radiotherapy, chest drain insertion.
• Respiratory rate and breathing pattern See p50. Paradoxical respiration: ab-
domen sucked in with inspiration in diaphragmatic paralysis (
• Colour Pale, cyanosed (fig
• Clues Oxygen, inhaler, peak flow meter, nebulizer.
p35)?
p50). Scars: skin thickening/
2.15
), flushed.
2
Hands
Fig 2.
15
Cyanosis.
p
496
• Inspect Peri pheral cyan osis, clubbing (p74),
systemic disease (sclerosis, rheumatoid arthritis),
tremor (- agonist use), tobacco staining (
muscle wasting (
p
694
osteoarthropathy in cancer).
• Asterixis Ask the patient to hold their hands out
and cock their wrists back: CO
• Pulse Pulsus paradoxus (respiratory distress, p40), bounding (CO2 retention).
• Trachea Sternal notch (fig
1
lesions, eg Pancoast’s tumour,
), tender wrists (hypertrophic pulmonary
3
Neck
2.17
fig
2.16
retention.
2
)— is trachea devi-
),
Fig 2.
16
Tar stains.
ated towards collapse or away from pleural eusion/ tension pneumothorax? (A slight deviation
to right is normal.) Assess cricosternal distance:
3
cm is hyperexpansion. Feel for tracheal tug: des-
<
cent of trachea with inspiration due to severe airflow limitation.
• Lymph ade nopa thy Sit patient forward and examine
• JVP See p41. Raised in cor pulmonale, fixed and
from behind (
, malignancy, sarcoid).
Fig 2.
17
Sternal notch.
raised in superior vena cava obstruction.
).
• Eyes Horner’s syndrome: ptosis, miosis, anhidrosis,
enophthalmos (
• Mouth Central cyanosis (ask patient to stick out
fig
tongue), pursed lip breathing.
Top tips
• Whispering pectoriloquy is a classic and specific sign of consolidation.
• Expose the chest so not to miss small scars, eg from video thoracoscopy.
• If you see Horner’s syndrome (fig
of the hand.
4
Fac e
2.18
, and p69). Conjunctival pallor.
2.18
), check for wasting of the small muscles
Fig 2.
18
Horner’s syndrome.
2 History and examination
ANTERIOR
Lateral basalLateral basal
POSTERIOR
5
COPD
COPD
COPD
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• Apex beat Impalpable due to
Chest
/ pleural eusion/ dextrocardia?
Complete the next steps on the front of the chest before sitting the patient forward
to perform again on the back of the chest.
1 Expansion Horizontal: place hands as positioned
fig
2.19
in expiration (‘Breathe all the way
in
out’), note movement of thumbs from midline.
Vertical: place finger tips on clavicles in expiration
and note symmetry of movement in inspiration.
2
Ta c ti l e v oc a l f re m i tu s Palpate the chest with the
lateral surface of your hand asking the patient to
99
’ each time they feel your hand. Compare
say ‘
right to left. Often omitted (in clinical practice, but
not in exams) in preference for vocal resonance.
3
Perc ussion Percuss all respiratory segments,
comparing right and left (
fig
2.20
). Dull: collapse,
consolidation, pleural thickening, eusion (‘stony
dull’). Cardiac dullness detectable on the left side.
Liver dullness usually extends to
mid- clavicular line; hyperinflation (eg asthma,
) may push liver down. Hyperresonance:
pneumothorax or hyperinflation (
4
Auscultation With diaphragm, from apices to
bases, comparing right and left (
5
Vocal reso nance Repeat auscultation, asking patient to say (whisper) ‘99’
5
th rib, right
).
fig
2.23
Fig 2.
testing expansion: anchor fingers with thumbs free- floating.
, table
2.8
, p51).
19
Hand placement for
Reproduced from Thomas J,
et al. (eds). Oxford Handbook
of Clinical Examination and
Practical Skills (
2007
permission from Oxford
), with
University Press.
each time they feel the stethoscope. iResonance with whispering (‘whispering pectoriloquy’) is a sensitive sign for consolidation.
6
• Palpate for sacral and ankle oedema (fig
• Observation chart for temperature and O2 sat uratio n.
• Examine the sputum pot (p50) and check peak flow.
Complete the examination
2.9, p39
).
49
Apical
Anterior
Posterior
Lateral
middle
Medial
Anterior
middle
basal
Fig 2.
20
The respiratory segments supplied by the segmental bronchi.
Signs of respiratory distress
• Tachypnoea.
• Nasal flaring.
• Tracheal tug: pulling of thyroid cartilage towards sternal notch in inspiration.
• Accessory muscle use: sternocleidomastoid, platysma, and infrahyoid.
• Recession: intercostal, subcostal, and sternal.
• Pulsus paradoxus (p40).
Apical
Anterior
Inferior
lingular
Superior
lingular
terior
An
bas
al
Apical
+
Posterior
Apical
(lower lobe)
Posterior
basal
Lateral basal
Apical
Posterior
Apical
(lower lobe)
Posterior
basal
Lateral
basal
2 History and examination
COPD
OHCS
ICP
ZN
ALGrawany
https://t.me/med1917
50
The respiratory system: important presentations
Chest deformities
• Barrel chest iDiameter, dchest expansion. Seen in hyperinflation (asthma/
• Pectus cari natum ( pigeon chest) Prominent sternum (fig
• Pectus excavat um (fun nel che st) Depression of sternum (fig
• Kyphosi s iAP tho racic s pine c urvatu re.
• Scoliosis Latera l curva ture (
Fig 2.
21
Pectus carinatum. Prominent sternum
from lung hyperinflation while bony thorax develops, eg chronic childhood asthma. Often seen
with Harrison’s sulcus: groove deformity due to
indrawing of lower ribs at diaphragm attachment. Usually no significance for function, may
have psychological eects.
Image courtesy of Prof Eric Fonkalsrud.
p
480
).
Fig 2.
22
atic, but may cause displacement of the heart
to the left, and restricted ventilatory capacity
± mild air- trapping. Associations: scoliosis;
Marfan’s; Ehlers– Danlos.
Breathing patterns
Hyperventilation Rapid (tachypnoea >20 breaths/ min) or deep (hyperpnoea
(itidal volume)) breathing. In the absence of lung disease consider:
• Hyperventilation syndrome: a panic attack associated with hyperventilation.
Associated symptoms include: palpitations, dizziness, tinnitus, chest pain/ tightness,
perioral/limb paraesthesiae (plasma dCa
breathing into a paper bag (iinspired CO
• Kussmaul respiration: deep, sighing breaths in severe metabolic acidosis (blow-
• Neurogenic hyperventilation is produced by pontine lesions.
), eg diabetic or alcoholic ketoacidosis, kidney failure, aspirin overdose
ing o CO
2
p
825
).
(
2
+
). Treatment: relaxation techniques and
cor rects t he alka losis ).
2
Cheyne– Stokes breathing Breaths get deeper and deeper, then shallower (± epi-
sodic apnoea) in cycles. Caused by brainstem lesions/ compression, eg stroke,
). If cycle is long (eg 3min), there may be a long lung- to- brain circulation time
i
(eg chronic pulmonary oedema or dcardiac output). Enhanced by opioids.
2.21
).
2.22
Pectus excavatum. Often asymptom-
Image courtesy of Prof Eric Fonkalsrud.
).
).
Sputum examination
Inspect sputum as part of routine respiratory examination. Send for culture,
Gram stain (auramine/
• Black carbon specks sug gest s mokin g: com mones t cause of inc reased sputu m.
• Yell ow / green sputum suggests infection, eg bronchiectasis, pneumonia.
• Pink frothy sputum suggests pulmonary oedema.
• Bloody sputum (haemoptysis) may b e due to mal igna ncy, TB, infection, trauma, pul-
monary vasculitis. Always requires investigation (
• Clear sputum is probably saliva.
stain if indicated), and cytology.
p47).
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