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2 History and examination
Insomnia
HIV
CBT
OHCS
FBC, ESR
LFT,
TFT
PBC)HIV
CKD
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This is trivial— until we ourselves have a few sleepless nights. Then sleep becomes the most desirable thing imaginable, and bestowing it the best thing we
can do, like relieving pain. But don’t give drugs without looking for a cause.
• Self- limiting: jet l ag, st ress, s hift w ork, hosp ital admissi on.
• Mental health: de pressi on, an xiety, m ania, psychomot or agi tatio n/ psychosis.
• Organic:
• Sensory disturbance: pain, tinnitus, itch.
• Breathlessness: asthma, orthopnoea, obstructive sleep apnoea (p
• Movement: dystonia, restless legs (p
• Dementia.
• Drugs: eg diu retics , steroid s, dopamine a gonist s, coc aine, alcoh ol.
• Rare: encephalitis (West Nile virus), encephalopathy (Whipple’s, pellagra,
688
, check ferritin).
188
).
), fatal
familial insomnia.
Sleep hygiene No daytime naps, regular bedtime routine. Stop caeine and nico-
tine. Avoid late exercise, screen time, and alcohol. Look for patterns and possible
modification in a sleep diary. Music and relaxation may make sleep more restorative and augment personal resources.
Hypnotic drugs Do not induce natural sleep. SE: daytime somnolence, rebound
insomnia, addiction. Warn about driving/ machine use.
Parasomnias,
p
739
; narcolepsy, p
688
.
is better.
Pruritis (itch)
Ask What provokes it? eg after a bath 8 polycythaemia rubra vera (p
Exposure, eg to animals (atopy) or contact (irritant eczema). Are any others
aected? eg scabies. Causes are shown in
table 2.2.
362
Examine
• Skin: scabies burrows in finger webs, lice on hair shafts, knee and elbow blisters
(dermatitis herpetiformis), wheals (urticaria).
• Systemic: jaun dice, splen omega ly (p54, p59), lymphadenopathy, thyroid (p78)?
Investigate
Table 2.
2
Aetiology of pruritus
Primary skin disease Secondary causes
Eczema, atopy, urticaria
Scabies
Lichen planus Malignancy (eg lymphoma) Diabetes mellitus
Dermatitis herpetiformis Polycythaemia rubra vera Thyroid disease
Dry skin Iron deficiency anaemia
, glucose,
kidney function, ferritin,
Liver disease (bile salts, eg
Uraemia (eg
)
.
seroconversion
Drugs (eg opioids)
Tre at Cause, emollien ts, emollient bath oi ls, antihista mine (for s leep if not for itch).
31
).
Non- specific symptom pathways
A concern for both patients and physicians is that non- specific symptoms herald
an underlying malignancy. Although non- specific symptoms have a low predictive value for individual cancers, the overall risk of harbouring cancer of any
type is higher, and non- specific symptoms (including unexplained weight loss, fatigue, atypical abdominal pain, and persistent nausea) are present in a significant
proportion of cancer diagnoses.
As non- specific symptoms can be caused by a range of conditions of which
cancer is only one possible diagnosis amongst many, identifying the appropriate
diagnostic tests and referral route for non- specific symptoms is challenging.
There are emerging data to support dedicated referral pathways for patients
presenting with non- specific and concerning symptoms, who do not qualify for
an appropriate tumour- specific urgent referral pathway (
p
517
).
2 History and examination
Method and order for physical examination
SVC
GTN
SLE
DM
IX, X, XII
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32
The aim of physical examination is to confirm, exclude, or define the diagnosis revealed in the history. Conventional examination starts with a visual survey of the
patient and the patient’s environment. It then moves from the hand, up the arm, to
the face and neck, and then down the body to include cardiac, respiratory, and abdominal examinations. The whole body is then revisited with central and peripheral
neurological examinations. With experience, physical examination gets quicker as
the patient’s story directs your approach.
Practice is key.
1
Visual survey
• General wellbeing: are they well or sick? Could they be sicker than they look?
• Appearance: does this suggest a diagnosis, eg acromegaly, Cushing’s syndrome,
hypopituitarism (
p
osis (
drome (
• Pain: do es this makes t hem lie sti ll (perito nitis) or writhe a bout (coli c)?
• Breathing: laboured, rapid, shallow, irregular?
• Mood/ aect? Appropriate or not (p72)?
• Look for clues: oxygen,
p
548
), Turner’s (p
p
524
). Cachexia? Obesity?
226
), hyper/ hypothyroidism (p
143
), neurofibromatosis (p
spray, ast hma in haler , gluc ose mo nitor, walki ng aid.
2
Hands
212, 214
), Marfan’s, systemic scler-
510
), Parkinsonism (p
• Signs of systemic disease in the hands, see p74.
• Nails: clubbing, koilonychia (iron deficiency), onycholysis (psoriasis), nail fold infarcts
(small vessel vasculitis), splinter haemorrhage (trauma, endocarditis).
• Joints: swelling, deformity, Heberden’s/ Bouchard’s nodes (osteoarthritis).
• Skin: jaundice, palmar erythema, scleroderma, lesions (psoriasis, vasculitic changes,
xantho mata, telangiectasia, tophi, neurofibromatosis).
• Muscle: wasting, fasciculation.
• Palpati on: Dupu ytren’s contra cture (fig
ease, hypercalcaemia).
• Capillary refill: if well perfused <2s.
2.24
, p58), calcinosis (connective tissue dis-
490
),
syn-
• Radial and brachial pulses, see p40.
• Blood pressure: trend may be more important than a single value, see p
• Arteriovenous fistulae (p
• Appearance: Bell’s palsy (p
• Colour:
• Blue/ purple: cyanosis (p
• Yellow: jaundice, uraemia, pernicious anaemia, carotenaemia. If the sclera are
also yellow it is jaundice.
• Pal lor: n on- specific. Anaemia may be better assessed from palmar skin creases
(when spread) and conjunctivae (
• Hyperpigmentation: haemochromatosis (slate- grey), amiodarone, minocycline.
• Rash: malar flush (mitral valve disease), butterfly rash (
• Eyes: ptosis (Horner’s (fig
arcus senilis, cataract (myotonic dystrophy,
• Mouth: systemic sclerosis (p
osis, pigmentation (Addison’s,
• Smell: hepatic fetor (p
3
Arm
302
), venous access (chronic/ recurrent IV treatme nt).
4
498
270
), ketosis, alcohol, cannabis.
Fac e
), exophthalmos (p79).
48
, fig
2.15
).
fig
8.18, p32 5
).
2.18
, p48, and p69), myasthenia gravis), heliotrope rash,
548
), telangiectasia (Osler– Webe r– Rendu, p
p
220
),
), xanthelasma.
ner ve les ions (p66), candida.
).
108
694
.
), cyan-
2 History and examination
5
JVP
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• Carotid pulse, see p40.
• Jugular venous pressure (
• Trac he a: tu g, p os it io n.
• Scars: tracheostomy, central venous access (critical illness, dialysis).
• Goitre (p78): palpate from behind. Moves with swallowing. Auscultate for bruit.
• Lymphadenopathy: supraclavicular (Virchow’s node), submandibular, post-
auricular.
• Cardiovascular examination, see p38.
• Respiratory examination, see p48.
• Breast examination (p80) if indicated (chaperone for all intimate examinations, and
whenever requested).
• Check for axillary lymphadenopathy.
• Abdominal examination, see p58. Lie patient flat (one pillow).
• Check for inguinal lymphadenopathy.
• Consider rectal examination and urine output.
• Gynaecological examination if indicated.
• Vasc ular dis ease (p82): absence of hair, shiny skin, pulseless feet, varicosities (p83),
ulcers, gangrene.
• Skin disease: erythema nodosum.
• Other: musculoskeletal, eg tibial bowing (Paget’s disease, check also for enlarge-
ment of the skull), Charcot’s (neuropathic) joint.
Neck
), see p41. Ensure patient is at 45°.
6
Chest
7
Abdomen
8
Legs
33
• Examination of the central nervous system, see p66.
• Examination of the peripheral nervous system, see p62, p64.
• Mental state examination, see p72.
• Musculoskeletal examination of the hand, see p76.
Temperature
• Strictly speaking not ‘observation’, but traditionally included with examination.
• Varies during the day with a 95% reference range of 35.7– 37.3°C.
• Rectal temperatures are approximately 0.6°C above oral temperatures.
• Te mp e ra t ur e f a ll s by –
pronounced with age.
• Core temperature <35°C = hypothermia. Specific low- reading thermometers
may be required.
9
Neurological examination
10
Other
0.021
°C for every decade, so fever may not be so
2 History and examination
Non- specific signs
EBV, HIV, CMV
SLE
OHCS
ALL, CLL, AML
COPD
PE,
VSD
ACTH
ACTH
OCP
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34
Non- specific signs can be caused by a range of conditions, and do not conveniently
direct the physician to a diagnosis.
Changes in colour
Cyanosis
Peripheral:
dusky blue skin, usually fingers. Will occur with central cyanosis but
can also be due to peripheral changes, eg cold, hypovolaemia, arterial disease.
Central: blue discolouration of the mucous membranes (check the tongue).
50
Requires
g/ L of deoxyHb. Central cyanosis therefore indicates hypoxaemia,
but do not assume that absence of cyanosis means adequate oxygenation.
Acute cyanosis is an emergency.
Causes
• Lung disease: luminal obstruction, asthma,
dema, pneumothorax. May be corrected by iinspired O
• Congenital cyanotic heart disease: a r ight- to- left shunt allows deoxygenated blood
to reach the systemic circulation, eg transposition of the great arteries,
Eisenmenger’s syndrome (
• Rare: methaemoglobinaemia, globin gene mutations.
Pallor
May not be pathological. Possible pathologies: anaemia, hypotension, Stokes– Adams
p
456
, pale first, then flushing), hypothyroidism, hypopituitarism, albinism.
(
Anaemia is haemoglobin concentration <
pregnant women (
creases. Koilonychia and stomatitis (
jaundice suggests haemolysis. If pallor in just one limb/ digit, consider emboli.
Other colour changes
• Genetic.
• Irradiation, scarring.
• i
which cross- reacts with melanin receptors: Addison’s (p
drome after adrenalectomy for Cushing’s (
• Sallow colouration in chronic kidney disease with uraemia (p
• Melasma due to increase in melanin and melanocytes. Can be triggered by
pregnancy. No longer called chloasma (= green), which is a misnomer.
• Biliary cirrhosis, malabsorption.
• Haemochromatosis (‘bronzed diabetes’).
• Carotenaemia.
• Drugs: chlorpromazine, busulfan, amiodarone, gold.
Lymphadenopathy
Can be reactive or infiltrative:
Reactive
Infective:
• Bacterial: eg pyogenic, TB, brucella, syphilis.
• Viral:
• Others: toxoplasmosis, trypanosomiasis.
, infectious hepatitis.
Non-infective:
Sarcoidosis, berylliosis, connective tissue disease (eg rheumatoid,
pathic lymphadenitis, drugs (eg phenytoin).
Infiltrative
• Amyloidosis.
• Histiocytosis (
• Lipoidoses.
• Cancer:
p
• Haematological: lymphoma, leukaemias (
• Metastatic: breast, lung, bowel, prostate, kidney, head and neck cancers.
, pneumonia,
.
2
p
148
). Will not be reversed by iinspired O2.
130
p
324
). It may be assessed from the conjunctivae and skin
g/ L in men and <
pulmonary oe-
120
g/ L in non-
p58) suggest iron deficiency. Anaemia with
220
sec retion .
298
354
).
), Nelson’s syn-
).
848
p75), ectopic
).
, p
with
and
), dermato-
2 History and examination
Oedema
DVT
EBV
SLE
OHCS
TFT, CXR
AIDS
TB
BMI
IHD.
BP.
SARS- CoV-
BMI
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Pitting oedema
Due to increased hydrostatic pressure (eg
oncotic pressure due to low concentrations of plasma proteins (eg cirrhosis, nephrotic syndrome, protein- losing enteropathy). Though the pathophysiology of oedema is not completely understood.
Periorbital oedema
Eyelid skin is very thin and susceptible to small fluid shifts. Causes include:
• Contact dermatitis: eye make- up.
• Angioedema: hereditary or acquired.
• Infection: orbital cellulitis can be life- threatening and needs urgent treatment.
.
Also
• If there is proptosis, think Graves’ disease (p78).
• Connective tissue disease: dermatomyositis,
• Always dip the urine to exclude nephrotic syndrome.
Non- pitting oedema
Lym phoe dema du e to poo r ly mpha tic drai nage is non - indentable. Causes include
radiotherapy, malignant infiltration, infection, filariasis, or rarely primary lymphoedema
(Milroy disease,
p
692
).
Weight
Wei ght los s
A symptom (reported by the patient) and a sign (identified by physician).
Causes include:
• Malnutrition/ malabsorption.
• Chronic infection, eg TB.
• Depression.
• Cancer.
• Endocrine disorders: diabetes mellitus, hyperthyroidism.
• Degenerative neurological disease.
• Cardiac failure (cardiac cachexia), though right heart failure may mask weight loss
by the scales.
• Anorexia nervosa (
• Advanced chronic kidney disease.
Unintentional weight loss should ring alarm bells— assess patients carefully.
Investigations: blood glucose,
Cachexia
General muscle wasting from deating (neurological disease: stroke, dementia; anorexia nervosa), malabsorption (enteropathic
Whipple’s), icatabolism (neoplasia,
Obesity
=
>30kg/ m2. Most not due to metabolic disease.
Associated health risks:
• Type 2 dia betes mel litus (p
•
• Dyslipidaemia.
• i
• Osteoarthritis.
• Cancer.
• Non- alcoholic fatty liver disease.
• Infection, eg
Treatment: lifestyle change is key— increase energy expenditure and reduce in-
p
238
). Medication ± surgery is considered if
take (
with significant disease that could improve with weight loss. Non- surgical meas-
2.
ures should be tried first. Surgical and anaesthetic risks should be considered.
Rare secondary causes of obesity include genetic conditions (Prader– Willi,
Lawrence– Moon) and endocrine conditions (hypothyroidism, Cushing’s, hypothalamic damage, eg tumour or trauma l damage to satiety regions).
p
746
).
200
, right heart failure) or reduced
, sarcoid, amyloid.
, and as directed by history/ examination.
). Also poverty/ famine.
, slim disease, Cryptosporidium,
).
>40 kg/ m2, or >35 kg/ m2
35
2 History and examination
The cardiovascular system: history
GTN
NB: GI
SVT
AF
TSH
ECG
ECG
NYHA
BP
SOCRATES
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36
Table 2.
3
Presenting symptoms and questions to ask
Presenting
symptoms
Chest pain
(see
pp86– 7
p
764
and
Direct questions
Site: eg central
Onset: what was the patient doing when it started?
)
Character: ask patient to describe pain (crushing? heavy?)
Radiation: ask specifically if moves to arm, neck, or jaw
Associations: ask specifically about shortness of breath, nausea, sweating
Timing: will help interpret investigations, eg troponin
Exacerbating and alleviating factors: ischaemic pain may be relieved by
. Worse on inspiration and better if sitting forwards suggests peri-
carditis. Worse with respiration or movement is less likely to be angina
Severity: out of
Is patient known to have angina or chest pain? Better/ worse/ same as
usual pain? More frequent? Decreasing exercise tolerance?
lying flat, or associated with dysphagia
Palpitations ‘Are you aware of your own heartbeat?’ When and how did it start/
stop? Sudden/ gradual onset? Duration? Associated with pre- syncope/
syncope/ chest pain/ dyspnoea? Lifestyle trigger, eg caeine?
Regular fast palpitations may be paroxysmal supraventricular tachycardia (
Irregular fast palpitations may be paroxysmal
with variable block
Dropped or missed beats related to rest, recumbency, or eating may
be atrial or ventricular ectopics
Regular pounding may be normal or due to anxiety
Slow palpitations may be due to rate- controlling drugs, eg - blockers.
Also bigeminy (
Check
corder, if available, may be better than a
Dyspnoea
p48
(see
and p
765
Dizziness/
blackouts
pp
(see
Claudication
Duration? On exertion or at rest? Determine exercise tolerance (and any
other reason for limitation, eg arthritis).
when lying flat (orthopnoea, ask how many pillows the patient sleeps
)
with)? Does the patient ever wake up in the night gasping for breath
(paroxysmal nocturnal dyspnoea), and how often? Any ankle swelling?
Dizziness: a loose term, try to clarify what your patient means
Syncope: did they lose consciousness, and for how long (short
456– 8
)
duration suggests cardiovascular cause may be more likely than
epilepsy)? Any warning (pre- syncope)? What was patient doing at
the time? Sudden/ gradual? Associated symptoms? Tongue biting
pp
456– 7
(
eg confusion? How long did it take to feel ‘normal’? Witnessed?
Vertigo: the illusion of rotation of either the patient or their surroundings ± diculty walking/ standing (
Imbalance: diculty in walking, without vertigo. Causes include
neurological (peripheral nerve, posterior column, cerebellar or other
central nerve disorder) and musculoskeletal disease
Faintness: ‘light- headedness’. Seen in anaemia, d
sion, hypoglycaemia, carotid sinus hypersensitivity, epilepsy
long can patient walk before onset of pain? Is there rest pain?
10
cause more likely if ‘burning’, onset after eating/ drinking, worse
) or ventricular tachycardia (VT)
fig
3.39
, p
125
. Consider a 24h
)
(Holter monitor, p
, or atrial flutter
121
). An event re-
24
h
classification (p
135
)? Worse
) and incontinence suggest seizure. Any residual symptoms,
p
458
)
, postural hypoten-
? Foot/ calf/ thigh/ buttock? ‘Claudication distance’, ie how
2 History and examination
Presenting problem
BOX
ECG
CABG
GTN
ACE-
ARB
SGLT
CVD
BP
ACTH
BP.
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Presenting symptoms and useful questions to ask are shown in table
Past history
Ask specifically about:
• History of cardiovascular disease: angina, heart attack, stroke.
• Cardiovascular risk factors (see
• Rheumatic fever.
• Previous tests/ procedures:
cardiac scintigraphy, coronary artery bypass grafts (
Drug history
Particularly note cardiovascular medications: aspirin/ anti- platelet,
i/
, diuretics, statin,
Fam i ly hi st o ry
Enquire specifically if any 1st- degree relatives have cardiovascular disease/ events.
Any sudden/ unexplained death?
Social history
Smoking, impact of symptoms on daily life, alcohol (clarify number of units), exercise.
Ischaemic heart disease risk factors
• Hypertension.
• Smoking.
• Diabetes mellitus.
• Fami l y h i st or y of pr em a tu re
• Hyperlipidaemia.
• Pregnancy- induced hypertension, pre- eclampsia/ eclampsia.
Postural hypotension
This is an important cause of falls and faints, particularly in the elderly. It is
defined as a drop in systolic
3
min vs lying.
for
Causes Hypovolaemia (early sign). Drugs: antihypertensives, nitrates, diuretics,
antipsychotics. Hypocortisolaemia: Addison’s (
Autonomic disease: neuropathy (
After a marathon run, peripheral resistance is low for some hours!
Tre at me nt
• Postural hypotension is not a diagnosis, merely a description of a physical sign.
Search for the underlying diagnosis to determine the best management.
• Consider referral to a ‘falls clinic’, where special equipment is available for assess-
ment under various tilts.
• Generic management:
• Lie down if feeling faint.
• Stand slowly (with escape route: don’t move away from the chair too soon).
• iWater and salt ingestion, eg
salt has its problems).
• Physical measures: leg crossing, squatting, elastic compression stockings
(check dorsalis pedis pulse is present), and careful exercise may help.
• If post- prandial dizziness, eat little and often: dcarbohydrate and alcohol
intake.
• Head- up tilt of the bed at night (
• Drug options:
• Fludrocortisone:
Monitor weight, beware in heart failure, kidney impairment, or dalbumin as
fludrocortisone worsens oedema.
• Other: sympathomimetics, eg midodrine; pyridostigmine (if underactive
bladder too).
50– 100
‘Is chaem ic hea rt dis ease ri sk fac tors’) .
, angiogram, angioplasty/ stents, echocardiogram,
2
inhibitor, anticoagulant, anti- arrhythmic.
(ag e ≤60).
>20mmHg or diastolic >10mmHg after standing
p
501
), multisystem atrophy (p
9
g salt (3.6g/
10
°) irenin release, so may istanding
mcg/ day PO, then up to
S).
p
220
), hypopituitarism (d
490
150
mmol sodium) per day (but
300
mcg/ day if tolerated.
2.3
.
, - blocker,
). Idiopathic.
37
).
2 History and examination
JVP/ CVP
CVP
CVP
CABG
GTN
(ASD).
The cardiovascular system: examination
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38
Introduce yourself, obtain consent to examine, and position sitting up at 45°. Expose
to the waist (for female patients delay until examining the praecordium). Explain
throughout.
1
Inspection
• General Ill o r well ? In pain?
• Breathing pattern Short of breath?
• Colour Pale , cyanos ed, flu shed?
• Scars Media n stern otomy ( fig
2.3
)—
, valve
replacement, congenital heart disease. Pacemaker/
internal cardiac defibrillator.
• Listen Au dible prosth etic v alve cl ick.
• Clues Oxygen ,
• Colour Cyanosis (fig
• Perfusi on Tempera ture, c apill ary refi ll tim e.
• Fingers Arachnodactyly (Marfan’s), polydactyly
spray.
2.4
), tobacco staining.
2
Hands
Fig 2.
3
Sternotomy scar.
• Nails Clubbing (p74, cyanotic heart disease, endocarditis), splinter haemorrhages (endocarditis).
• Nail bed Nail fold infarcts (vasculitis), nail bed
pulsations (Quincke’s sign of aortic regurgitation).
• Other Osler’s nodes (tender nodules, eg in
finger pulps, endocarditis), Janeway lesions (red
macules, endocarditis), tendon xanthomata
Fig 2.
4
Peripheral cyanosis.
Reproduc ed from Bal l G, et al.
(eds). Oxford Textbook of Vasculitis
(
2014
), with permission from Oxford
(hyperlipidaemia).
3
• Radial (fig
2.5
) Rate, rhythm (AF, p
Pulse (pp40– 1)
126
); radio-
radial delay (palpate radial pulses simultaneously
bilaterally, aortic arch aneurysm), radio- femoral
delay (palpate ipsilateral pulses simultaneously,
coarctation).
• Collapsing pulse
1 Identify radial pulse then wrap your fingers
around wrist.
2
Before elevating arm check for pain.
3
Lift arm straight up, collapsing pulse is felt as
‘waterhammer’ pulsation.
• Brachial Wave form ch aracte r.
Fig 2.
5
Radial pulse.
Reproduced from Thomas J, et al.
(eds). Oxford Handbook of Clinical
Examination and Practical Skills
(
2014
), with permission from
Oxford University Press.
University Press.
• Systolic (1st Korotko sound) and diastolic (5th Korotko sound = silence)
Hypertension (p
• Pulse pressure Dierence between systolic and diastolic pressures. Narrow in
108
aortic stenosis, volume depletion; wide in aortic regurgitation, arteriosclerosis.
Top tip
The han d can be used as a mano meter to es timate
neck properly (eg central line in situ). Hold the hand palm down below the level of
the heart until the veins dilate (patient must be warm!), then lift slowly, keeping the
arm horizontal. The veins should empty as the hand is raised. Empty veins below the
level of the heart suggest a low
4
Blood pressure
), postural hypotension (p37).
, if they remain full it suggests a normal/ high
if you cannot see the
.
2 History and examination
5
JVP
JVP.
ASD, VSD,
MR
RV
ASD
COPD
S
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•
(p41) Height above manubriosternal angle (not sternal notch) at
Neck
45o (fig
2.6
Waveform. Hepatojugular reflux: venous distension
with pressure on liver (right heart incompetence).
• Carotid pulse Inspect: Corrigan's sign (excess
pulsations due to aortic regurgitation). Palpate:
volume and character on one side, then the other.
Fig 2.
6
The
and Practical Skills (
Reproduced from Thomas J, et al. (eds). Oxford Handbook of Clinical Examination
2014
), with permission from Oxford University Press.
6
Fac e
• Colour Malar flush (mitral stenosis), central cyanosis.
• Eyes Corneal arcus (may suggest hyperlipidaemia, fig
xanthelasma (eyelid xanthomata), exophthalmos
(arrhythmia due to Graves’ disease,
pallor (anaemia).
• Dysmorphia Mar fan’s (ao rtic d issec tion) , Down’s (
), Turner’s (coarctation), Williams’ (AS, p
p78), conjunctival
143
7
The praecordium
).
2.7
),
Fig 2.
7
Corneal arcus.
• ‘Heaves’ and ‘thrills’ Place heel of hand flat on chest to left then right of sternum.
Heave: sustained thrusting usually felt at left sternal edge (=
pulmonary stenosis, cor pulmonale,
• Apex beat Lowermost lateral pulsation normally felt in 5th intercostal space,
mid- clavicular line (sternal notch =
ment (cardiomegaly), impalpable (dextrocardia/
). Thrill: pa lpabl e murm ur felt as vibrat ion.
2
nd intercostal space). Lateral displace-
enlargement, eg
), tapping (palpable
mitral stenosis), thrusting (volume overload), double impulse (hypertrophic
cardiomyopathy).
• Auscultation Palpate the carotid pulse s imult an-
eously. Identify
normal? Listen for
murs
1
Mitral area (apex). Listen with diaphragm for
mitral regurgitation, a pansystolic murmur
radiating to the axilla. Ask patient to, ‘Roll
to your left side, breathe out, and hold’ then
listen with the bell for
rumbling mid- diastolic murmur.
2
Tricuspid area (lower left sternal edge) and
3
Pulmonary area (left of manubrium in the 2nd
intercostal space). If you suspect a right- sided
murmur, listen with the patient’s breath held in inspiration.
4
Aortic area (right of manubrium in 2nd intercostal space). Listen for aortic
stenosis
5
Finally, sit the patient forwards and listen at the lower left sternal edge in
expiration for
1
st and 2nd heart sounds. Are they
added sounds (p42) and mur-
(p44) in all valve areas (fig
2.8
):
Fig 2.
mitral stenosis, a
, an ejection systolic murmur radiating to the carotids.
aortic regurgitation, an early diastolic murmur.
8
Valve areas.
Reproduced from Thomas J, et al.
(eds). Oxford Handbook of Clinical
Examination and Practical Skills
(
2014
), with permission from
Oxford University Press.
39
).
in
1
• Palpate for sacral/ ankle oedema (fig
• Lung bases: i nspira tory cr epitat ions, pleura l eusions.
• Abdomen: pulsatile liver, ascites (righ t- sided
heart failure)
aneurysm
• Fundo scop y fo r Roth's spots (in fectiv e endo cardit is).
• Periphe ral pul ses and bruits (p82), urinalysis, BP, tem-
perature, oxygen saturation, urinalysis.
, splenomegaly (endocarditis), aortic
.
8
Complete the examination
2.9
).
Fig 2.
9
Oedema ‘pits’
after firm pressure for a
few seconds.
2 History and examination
Pulses
LVF
H(O)CM
e.g. aortic regurgitation
https://t.me/med1917
40
The radial pulse is used to determine rate and rhythm. A collapsing pulse is felt
at the radial (or brachial) artery when the patient’s arm is elevated above their
fig
2.10
head (
brachial) arteries.
Rate Is the pulse fast (≥
). Other character and volume changes are assessed at the carotid (or
100
bpm, p
122
) or slow (≤60bpm, p
120
)?
Rhythm An irregularly irregular pulse occurs in AF and with ectopics. A regularly
2
irregular pulse occurs in
° heart block and ventricular bigeminy.
Character (waveform) and volume
• Bounding pulse: CO2 rete ntion , live r failu re, sep sis.
• Small volume pulse: aortic stenosis, shock, pericardial eusion.
• Collapsing (‘waterhammer’) pulse: aortic regurgitation, AV malformation, patent
ductus arteriosus.
• Anacrotic (slow- rising) pulse: aor tic ste nosis .
• Bisferiens pulse: combined aortic stenosis and regurgitation.
• Pulsus alternans: alternating strong and weak beats.
stenosis.
• Jerky pulse:
• Pulsus paradoxus: (>10mmHg) fall in systolic pressure with inspiration. Cardiac
.
, cardiomyopathy, aortic
tamponade, pericardial constriction, severe asthma, tension pneumothorax.
Other pulses: see peripheral vascular examination,
p82.
Waterhammer pulse
The waterhammer was a vacuum tube toy half- filled with water. On inversion,
the whoosh of water produced a hammer- blow as it rushed from end to end.
This is the alternative name for Corrigan’s collapsing pulse: the upstroke is abrupt and steep, reaching an early peak (felt as a flick), before a rapid downstroke
(felt across all four fingers placed on the patient’s pulse) as blood whooshes back
into the left ventricle through an incompetent aortic valve.
Normal
Fig 2.
10
Arterial pulse waveforms.
Reproduc ed from Thoma s J, et al. (eds). Oxford Handbook of Clinical Examination and Practical Skills (
Slow rising e.g. aortic stenosis
Bisferiens e.g. aortic stenosis
mixed with
aortic regurgitation
Collapsing
with permission from Oxford University Press.
2014
),
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