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62 • THE CARDIOVASCULAR SYSTEM
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• occur from the onset of diastole (no gap between S2and
murmur) but with a distinct gap between the end of the
murmur and S
• begin later in diastole with a distinct gap between S
(early diastolic murmur)
1
and
2
the onset of the murmur (mid-diastolic murmur)?
• Quality and pitch. This is somewhat subjective but ask
yourself whether the murmur is:
• a coarse or harsh sound akin to noises generated from the
back of the mouth such as clearing the throat (typical of
ejection systolic murmurs)?
• a blowing sound akin to noises generated from the front of
the mouth with lips parted such as an unsuccessful
whistle (typical of regurgitant systolic murmurs)
• a low-pitched, rumbling sound akin to noises generated
from the back of the mouth with lips closed like a gentle
growl (typical of mitral stenosis)?
• Intensity. Ask yourself how easily the murmur is heard and
whether there is an associated thrill then grade according to
Box 4.17.
• Location and radiation. Ask yourself the following questions:
• At what sites on the precordium is the murmur audible?
• At what site is the murmur most easily heard/loudest?
• Is the murmur audible at any other site, e.g. over the ca-
rotids or in the axilla?
Heart sounds
First heart sound
The first heart sound (S1), ‘lub’, is caused by closure of the mitral
and tricuspid valves at the onset of ventricular systole. It is best
heard at the apex. In mitral stenosis the intensity of S
increased due to elevated left atrial pressure (Box 4.18).
Second heart sound
The second heart sound (S2), ‘dub’, is caused by closure of the
pulmonary and aortic valves at the end of ventricular systole and
is best heard at the left sternal edge. It is louder and higherpitched than the S
louder than the pulmonary component.
Physiological splitting of S
contraction ends slightly before that of the right ventricle so that
the aortic valve closes before the pulmonary valve. This splitting
increases on inspiration (‘lub d-dub’) because increased venous
filling of the right ventricle further delays pulmonary valve closure.
The separation disappears on expiration (‘lub dub’; Fig. 4.19).
‘lub’, and the aortic component is normally
1
occurs because left ventricular
2
1
4.18 Abnormalities of intensity of the first heart sound
Quiet
• Low cardiac output
• Poor left ventricular function
• Rheumatic mitral regurgitation
Loud
• Increased cardiac output
• Large stroke volume
Variable
• Atrial fibrillation
• Extrasystoles
Wide splitting of S
, but with normal respiratory variation, oc-
2
curs in conditions that delay right ventricular emptying, such as
right bundle branch block or pulmonary hypertension. Wide and
fixed splitting of S
, with no variation in respiration, is almost
2
always due to an atrial septal defect (Fig. 4.20). In this condition,
shunting of blood from the left atrium to the right atrium causes
is
• Long P–R interval (first-degree
heart block)
• Mitral stenosis
• Short P–R interval
• Atrial myxoma (rare)
• Complete heart block
it
n;
4.17 Grades of intensity of murmur
Grade Description
1 Heard by an expert in optimum conditions
2 Heard by a non-expert in optimum conditions
3 Easily heard; no thrill
4 A loud murmur, with a thrill
5 Very loud, often heard over a wide area, with thrill
6 Extremely loud, heard without a stethoscope
Fig. 4.19 Physiological and pathological splitting of the second heart
sound.
The physical examination • 63
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Additional clinical findings
Right parasternal heave*
Loud pulmonary component of
second heart sound*
4
S
1
Ejection systolic murmur
(pulmonary flow murmur) with
fixed splitting of second sound
Fig. 4.20 Atrial septal defect. The increased blood flow through the right heart resulting from the left to right shunt produces a pulmonary flow murmur, best
heard in the pulmonary area (left parasternal edge, second intercostal space).
right ventricular stroke volume to be significantly larger than the
left throughout the respiratory cycle.
Reversed splitting of S
on expiration; Fig. 4.19) occurs when left ventricular emptying is
delayed so that the aortic valve closes after the pulmonary valve.
Examples include left bundle branch block and severe aortic
stenosis.
The aortic component of S
calcific aortic stenosis. A loud pulmonary component of S
important sign of pulmonary hypertension.
Third heart sound
The third heart sound (S3) is a low-pitched early diastolic sound
best heard with the bell at the apex. It results from a brief period
of rapid ventricular filling immediately after opening of the atrioventricular valves and is therefore heard after the second heart
sound as ‘lub dub-dum’. It may be a normal physiological fi nding
in children and young adults or during fever or pregnancy.
However, after the age of 40 years, it is usually due to left ventricular failure or mitral regurgitation, with the rapid ventricular
filling a consequence of high left atrial pressure at the onset of
diastole. In patients presenting to hospital with acute breathlessness, the presence of an S
creases the likelihood of heart failure but its absence does not
help to rule out heart failure. In the context of heart failure, S
typically accompanied by a tachycardia and referred to as a
‘gallop’ rhythm.
Fourth heart sound
A fourth heart sound (S4) is less common than an S3and less
useful in modern clinical practice. It is soft and low-pitched, best
heard with the bell at the apex. It occurs just before S
dub). It is caused by forceful atrial contraction against a noncompliant or stiff ventricle, most often with left ventricular hypertrophy due to hypertension, aortic stenosis or hypertrophic
cardiomyopathy. It cannot occur when there is atrial fibrillation.
Additional sounds
An opening snap is commonly heard in mitral (rarely, tricuspid)
stenosis. It results from sudden opening of a stenosed valve and
A
2P2
(‘lub dub’ on inspiration; ‘lub d-dub’
2
is sometimes quiet or absent in
2
, on examination, strongly in-
3
2
(da-lub-
1
*If pulmonary hypertension
has developed
occurs early in diastole, just after the S
heard with the diaphragm at the apex.
Ejection clicks are high-pitched sounds best heard with the
diaphragm. They occur early in systole just after the S
is an
is
3
Fig. 4.21 ‘ Added sounds’ on auscultation.
(Fig. 4.21A). It is best
2
,in
1
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patients with congenital pulmonary or aortic stenosis (see
Fig. 4.21B). The mechanism is similar to that of an opening snap.
Ejection clicks do not occur in calcific aortic stenosis because the
cusps are rigid.
Mid-systolic clicks are high-pitched and best heard at the apex
with the diaphragm. They occur in mitral valve prolapse (see
Fig. 4.21C) where they are often associated with a late systolic
murmur.
A pericardial (friction) rub is a coarse scratching sound that is
typically biphasic, with both systolic and diastolic components. It
is best heard using the diaphragm with the patient holding their
breath in expiration. It may be audible over any part of the precordium but is often localised, varying in intensity over time and
with the position of the patient. It is highly specific for pericarditis
and present in 35–85% of cases. It is an important sign in
contemporary practice because it is one of four criteria (along
with characteristic chest pain, suggestive electrocardiogram
(ECG) changes and new or worsening pericardial effusion) used
to diagnose acute pericarditis; at least two of the four criteria
need to be present.
Prosthetic valve sounds
Mechanical heart valves can make a sound when they close or
open. The closure sound is normally louder, especially with
modern valves. The sounds are high-pitched, with a ‘metallic’
quality, are often heard without a stethoscope, and may even be
palpable. A mechanical mitral valve replacement makes a metallic
S
and a sound like a loud opening snap early in diastole (see
1
Fig. 4.21D). Mechanical aortic valves have a loud, metallic S
an opening sound like an ejection click at the start of systole (see
Fig. 4.21E); they are normally associated with a flow murmur.
Heart sounds arising from bioprosthetic valves usually sound
similar to those of normal valves.
and
2
Murmurs
Heart murmurs are produced by increased velocity of flow
through a normal valve or by turbulent flow across an abnormal
valve, septal defect or outflow obstruction.
Systolic murmurs
Causes of systolic murmurs are shown in Box 4.19.
‘Innocent’ murmurs occur when stroke volume is increased,
as in pregnant women, athletes with resting bradycardia or patients with fever or anaemia. They tend to be low in intensity
(grade 2), short in duration and best heard at the left sternal edge
with no radiation.
The murmur of aortic stenosis is often audible all over the
precordium with radiation to the suprasternal notch and carotid
arteries (Fig. 4.22). It is a harsh, ejection systolic murmur that is
usually loud and there may be a thrill. The absence of an ejection
systolic murmur makes clinically significant aortic stenosis
extremely unlikely. In the presence of an ejection systolic
murmur, several clinical signs support the diagnosis (see
Fig. 4.22) and moderate to severe stenosis is highly likely if three
or more of these are present.
Aortic sclerosis (thickening and calcification of the aortic valve
without obstruction) produces a similar quality of murmur but it is
4.19 Causes of systolic murmurs
Ejection systolic murmurs
• High cardiac output state: severe anaemia, fever, athletes (bradycardia
/ large stroke volume), pregnancy, thyrotoxicosis, liver cirrhosis,
arteriovenous fistula.
• Pulmonary flow murmur from increased RV stroke volume: atrial septal
defect; pulmonary regurgitation
• Aortic flow murmur from increased LV stroke volume: aortic
regurgitation
• Valvular stenosis: aortic stenosis; pulmonary stenosis
• Other valve abnormalities: mechanical aortic or pulmonary valve; aortic
sclerosis (turbulent flow without significant pressure gradient)
• Subvalvular obstruction: hypertrophic obstructive cardiomyopathy;
subaortic membrane
Pansystolic murmurs
• Mitral regurgitation
• Tricuspid regurgitation
• Ventricular septal defect
Late systolic murmurs
• Mitral valve prolapse
less likely to radiate and is not associated with a thrill or other
signs of aortic stenosis.
Mitral regurgitation is the most common cause of a pansystolic
murmur and tends to have a ‘blowing’ quality. The most helpful
feature in distinguishing it from other causes is its location
(Fig. 4.23): a murmur that extends from the apex to the anterior
axillary line – but is only audible below the third intercostal space
– strongly suggests mitral regurgitation. With mitral valve prolapse, regurgitation begins in mid-systole, producing a late systolic murmur (see Fig. 4.23).
The murmur of tricuspid regurgitation is another common
cause of a pansystolic murmur. Localisation to the lower left
sternal edge (only audible below the third intercostal space or
lateral to the mid-clavicular line (Fig. 4.24 ), strongly supports the
diagnosis, as does an increase in its intensity with inspiration,
which increases blood flow through the right heart. Notably, the
absence of a murmur does not exclude tricuspid regurgitation.
Ventricular septal defects also cause a pansystolic murmur.
Small congenital defects produce a loud murmur audible at the
left sternal border, radiating to the right sternal border and often
associated with a thrill. Rupture of the interventricular septum
can complicate myocardial infarction, producing a harsh pansystolic murmur, typically accompanied by major haemodynamic
compromise.
Diastolic murmurs
The murmur of aortic regurgitation (Fig. 4.25) may last
throughout most, or even all of diastole, but is usually termed an
‘early diastolic murmur’ because it is loudest in early diastole. It is
best heard at the left sternal edge with the patient leaning forwards in held expiration. Significant aortic regurgitation increases
The physical examination • 65
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Additional clinical findings
Slow rising pulse*
Reduced pulse volume*
Narrow pulse pressure
Apical heave
Thrill in aortic region
Reduced or absent second
heart sound over aortic area*
EC
S
1
Lean patient forward with
breath held in expiration to feel
thrill and hear murmur best
S
2
Radiation of murmur to
carotid artery*
*In patients with an ESM, 3 or more
of these features make moderate to
severe aortic stenosis highly likely
Fig. 4.22 Aortic stenosis. There is a systolic pressure gradient across the stenosed aortic valve. The resultant high-velocity jet tends to be widely audible
throughout the praecordium, though it is best heard with the diaphragm in the aortic area. Alternatively, the bell may be placed in the suprasternal notch. In
patients with bicuspid aortic valve, the ejection systolic murmur follows an ejection click (EC).
Apical pansystolic murmur
radiates to axilla
Additional clinical findings
Displaced apex beat
Third heart sound
S
1
S2S
3
Variant: mid-systolic click/
late systolic murmur
(mitral valve prolapse)
4
S1MSC S2S
Fig. 4.23 Mitral regurgitation. The murmur is best heard at the apex with radiation to the axilla and is usually audible only below the third intercostal space. It
typically begins at the moment of valve closure and may obscure the first heart sound. It varies little in intensity throughout systole. In mitral valve prolapse the
murmur begins in mid- or late systole and there is often a mid-systolic click (MSC).
S
1
Pansystolic murmur.
The murmur intensity
increases with inspiration.
Fig. 4.24 Tricuspid regurgitation. The murmur is usually heard only in the tricuspid area (left sternal edge, fourth intercostal space) and not at the other common
sites of auscultation. It typically begins at the moment of valve closure and varies little in intensity throughout systole. JVP, Jugular venous pressure.
3
Additional clinical findings
Elevated JVP with systolic
cv wave
Pulsatile hepatomegaly
Right parasternal heave*
Loud pulmonary component of
S
2
second heart sound*
*If pulmonary hypertension
has developed
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Additional clinical findings
Large volume pulse
Collapsing pulse
Wide pulse pressure
Prominent carotid pulsations
(Corrigan’s sign)
S
1
S
2
Displaced apex beat
Lean patient forward with
breath in held expiration
to hear murmur best
Fig. 4.25 Aortic regurgitation. There is an early diastolic murmur, best heard along the left sternal edge, with the diaphragm during held expiration. An
associated systolic murmur is common because of the increased flow through the aortic valve in systole.
left ventricular stroke volume so there is usually an associated
systolic flow murmur – which may be more obvious than the
diastolic murmur. Rarely, impingement of the regurgitant jet on
the anterior mitral valve leaflet can produce a mid-diastolic
murmur akin to that of mitral stenosis (‘Austin Flint’ murmur),
but this sign has negligible value in contemporary practice.
Pulmonary regurgitation produces a similar murmur to aortic
regurgitation but is far less common.
Mitral stenosis causes a low-pitched, rumbling mid-diastolic
murmur that may follow an opening snap (Fig. 4.26). The
cadence sounds like ‘lup-ta-ta-rru’: ‘lup’ is the S
‘ta-ta’ the S
and opening snap, and ‘rru’ the mid-diastolic
2
(typically loud),
1
murmur. If the patient is in sinus rhythm, left atrial contraction
causes presystolic accentuation of the murmur. The murmur is
often difficult to hear but is best appreciated with the bell (using
light pressure) at the apex with the patient positioned on their left
side; it can be accentuated by exercise such as touching the
toes or raising the legs up and down on the bed several times.
The murmur of tricuspid stenosis is similar but very rare.
Loud
S
1
S
2
OS
Loud
S
2
Roll patient towards left
to hear murmur best
Continuous murmurs
Continuous murmurs are rare in adults. The most common
cause is a patent ductus arteriosus. In the fetus this connects the
upper descending aorta and pulmonary artery, and normally
closes just after birth. The murmur is best heard at the upper left
sternal border and radiates over the left scapula. Its continuous
character is ‘machinery-like’; as aortic pressure always exceeds
pulmonary pressure, there is continuous ductal flow, with the
greatest pressure difference in systole, resulting in a louder
systolic component.
Interpretation of the findings
Serious cardiac pathology such as ischaemic heart disease can
occur in the absence of any clinical signs, so a clear history
(combined with ECG and other basic tests) is vital to accurate
diagnosis.
Additional clinical findings
Low volume pulse
Tapping apex beat
Loud S1
Opening snap
Right parasternal heave*
Loud pulmonary component
of second heart sound*
*If pulmonary hypertension
has developed
Fig. 4.26 Mitral stenosis. There is a pressure gradient across the mitral valve, giving rise to a low-pitched mid-diastolic murmur that is heard best with the bell
at the apex. Occasionally, an opening snap (OS) can arise due to the sharp movement of the tethered anterior cusp of the mitral valve at the time when the flow
commences.
Investigations • 67
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Identifying clinical signs of cardiac congestion – most notably
an elevated JVP – is critical to the diagnosis, assessment,
monitoring and treatment of cardiac failure, as well as other
conditions such as cardiac tamponade.
Despite the availability of echocardiography, auscultation remains an important clinical skill: the detection of abnormal signs
is required to guide appropriate investigation, and some diagnostically useful auscultatory signs, such as a pericardial friction
rub, have no direct equivalent on echocardiography.
Clinical examination also permits opportunistic detection of
asymptomatic but potentially important cardiovascular disease,
such as atrial fibrillation, valvular heart disease, and abdominal
aortic aneurysm (AAA), which can then be assessed further by
appropriate investigation.
Investigations
Haematology and clinical chemistry
As anaemia can unmask angina or exacerbate heart failure, a full
blood count is useful and helps guide the safe use of antiplatelet
therapies and anticoagulants. Thyroid function should be
assessed since thyroid disorders can cause or exacerbate most
cardiac conditions. Urea and electrolytes are measured and liver
function tests performed prior to starting therapies that may have
impact upon renal function or cause hepatotoxicity.
Blood glucose and a lipid profile help identify patients with
diabetes mellitus and assess cardiovascular risk. In patients with
acute chest pain, cardiac troponin is measured to determine
whether there is myocardial injury or infarction.
Electrocardiography
In performing a standard 12-lead electrocardiogram (ECG;
Fig. 4.27), the patient must be resting supine and relaxed to
avoid muscle tremor. Good contact between the electrode and
skin is important and it may be necessary to shave the chest.
The electrodes must be positioned correctly to obtain recordings
made from the six precordial electrodes (V
cordings from the limb electrodes (left arm, right arm and left leg).
The right leg electrode is used as a reference. Confirm that the
ECG is calibrated using a 1 mV signal prior to recording. The
ECG plays an indispensable role in the diagnosis of acute coronary syndromes (most notably, ST segment-elevation
myocardial infarction; Fig 4.27C), cardiac arrhythmias, acute
pericarditis and inherited heart conditions such as cardiomyopathies or congenital long QT syndrome.
Ambulatory ECG monitoring
Continuous ECG recording over 24–48 hours can be used to
identify symptomatic or asymptomatic rhythm disturbances in
patients with palpitation or syncope. If symptoms are less
frequent, it may be necessary to use patient-activated recorders
) and six re-
1–V6
that record the heart rhythm only when the patient is symptomatic; the device is activated by the patient (Fig. 4.28).
Exercise ECG
An exercise ECG is useful in the diagnosis and functional
assessment of patients with suspected coronary artery disease.
Down-sloping ST segment depression, particularly when it occurs during minor exertion, or ST segment elevation, is of
prognostic significance and helps inform the need for invasive
investigation with coronary angiography.
Ambulatory blood pressure monitoring
A portable device can be worn by the patient at home that takes
at least two BP measurements per hour. It is used to confirm the
diagnosis of hypertension and provide a more reliable assessment of response to treatment.
Chest X-ray
The maximum width of the heart divided by the maximum width
of the thorax on a posteroanterior chest x-ray (the cardiothoracic
ratio) should normally be less than 0.5. An increased cardiothoracic ratio is common in heart failure and some valvular lesions. In the former this is often accompanied by distension of
the upper lobe pulmonary veins, diffuse shadowing within the
lungs due to pulmonary oedema, and Kerley B lines (horizontal,
engorged lymphatics at the periphery of the lower lobes;
Fig. 4.29A). A widened mediastinum may indicate a thoracic
aortic aneurysm.
Echocardiography
Echocardiography uses high-frequency sound waves to evaluate cardiac structure and function. It permits measurements of
chamber size and wall thickness, assessment of regional and
global ventricular systolic funct ion and detection of abnormal
valve morphology or motion. In addition, Doppler echocardiography, through visualisation of blood flow and measurement
of blood velocity, enables detection and quantification of
valvular stenosis or regurgitation and other lesions such as
intracardiac shunts. Most echocardiography scans are performed through the anterior chest wall (transthoracic;
Fig. 4.29B). Transoesophageal echocardiography requires
sedation but gives high resolution of posterior structures
such as the left atrium, mitral valve and descending aorta,
and is useful in detecting valvular vegetations in infective
endocarditis.
Radionuclide studies
Technetium-99 is injected intravenously and detected using a
gamma camera to assess left ventricular function. Thallium and
sestamibi are taken up by myocardial cells and indicate
myocardial perfusion at rest and exercise.
4
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A
aV
R
B
C
N
P wave:
atrial activation
PQS
P wave
QRS width
(< 0.12 s)
P–R interval
(< 0.20 s)
aV
L
aV
F
R
QRS complex: ventricular
activation
(< 0.12 s)
(< 0.42 s at rate of 60/min)
V
1
T wave: ventricular
repolarisation
Q–T interval
V
6
V
5
V
4
V
3
V
2
T
Fig. 4.27 Electrocardiography (ECG). A 12-lead ECG lead placement. B Normal PQRST complex. C Acute anterior myocardial infarction. Note the ST
elevation in leads V
1–V6
and aVL, and ‘reciprocal’ ST depression in leads II, III and aVF.
Investigations • 69
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**
Fig. 4.28 Printout from a 24-hour ambulatory electrocardiogram recording, showing complete heart block. Arrows indicate visible P waves. At times, these are
masked by the QRS complex or T wave (*).
LV
LA
4
A
CX
LM
LAD
CD
Fig. 4.29 Cardiovascular imaging. A Chest X-ray in heart failure. This shows cardiomegaly with patchy alveolar shadowing of pulmonary oedema and Kerley
B lines (engorged lymphatics, arrow) at the periphery of both lungs.
ventricular apex. This is the site of a recent anterior myocardial infarct. LA, Left atrium; LV, left ventricle.
occlusion of the proximal left anterior descending artery. CX, circumflex; LAD, left anterior descending; LM, left main. D Cardiac magnetic resonance imaging.
Gadolinium enhancement image demonstrates regional uptake of gadolinium (white arrows) consistent with myocardial fibrosis in the territory of the LAD.
B
B Transthoracic echocardiogram in an apical two-chamber view, showing thinning of the left
C Coronary angiography. The arrow indicates an abrupt
A
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Cardiac catheterisation
A fine catheter is introduced under local anaesthetic via a peripheral artery (usually the radial or femoral) and advanced to the
heart under x-ray guidance. Although measurements of intracardiac pressures, and therefore estimates of valvular and cardiac function, are possible, the primary application of this
technique is imaging of the coronary circulation using contrast
medium. This is performed to inform and guide revascularisation,
either by coronary angioplasty or bypass grafting (see
Fig. 4.29C).
Computed tomography and magnetic
resonance imaging
Computed tomography (CT), combined with cardiac gating
permits high resolution imaging of the coronary arteries including
coronary atheroma and calcification. CT is particularly useful for
ruling out obstructive coronary artery disease (and thereby
angina) in patients with chest pain who are deemed to be at low
to moderate risk of coronary disease. It can also reduce the need
for invasive investigation in patients with a low probability of
occlusive coronary disease who require valve surgery. Magnetic
resonance imaging (MRI; Fig. 4.29D) provides superior spatial
resolution to echocardiography, together with an unrestricted
viewing plane. It is the most accurate method of measuring
cardiac volumes and ventricular ejection fraction and is the imaging modality of choice for investigating the aetiology of heart
muscle diseases (cardiomyopathy).
Carotid artery
Subclavian artery
Brachial artery
orta
Radial artery
Ulnar artery
Femoral artery
Popliteal artery
Posterior tibial artery
Dorsalis pedis artery
Fig. 4.30 The arterial system.
PERIPHERAL ARTERIAL SYSTEM
Anatomy and physiology
See Fig. 4.30.
The history
Common presenting symptom s
Leg pain
Asymptomatic ischaemia
PAD is recognised as a worldwide public health challenge with a
concerning increase in prevalence over recent decades in both
high- and low- income countries. Studies from Scotland suggest
around 5% of men and women over 55 years of age experience
intermittent claudication and a further 25% had evidence of
asymptomatic PAD. The underlying pathology is usually atherosclerosis affecting large and medium-sized vessels. PAD affects
the legs eight times more commonly than the arms. This is partly
because the lower limb arteries are more frequently affected by
atherosclerosis, but also because the arterial supply to the legs is
less well developed in relation to the muscle mass. Haemodynamically significant lower limb ischaemia is defined as an ankleto-brachial pressure index (ABPI) of less than 0.9 at rest (p. 76).
The Fontaine classification describes the progression of symptoms that occurs as the atherosclerotic burden increases and
the blood supply to the limb diminishes (Box 4.20).
4.20 Fontaine classification of lower limb ischaemia
Stage Description
I Asymptomatic
II Intermittent claudication
III Night/rest pain
IV Tissue loss (ulceration/gangrene)
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Whilst the risk of limb loss is low even in patients with intermittent claudication (1–2% per year), PAD carries additional
clinical importance because it has a very strong association with
coronary and cerebrovascular atherosclerotic disease. There is
an elevated risk of major adverse cardiovascular events in both
symptomatic and asymptomatic patients with PAD, and the
mortality is double that of the age-matched population. Atherosclerosis is a systemic disease, and it is therefore important that
patients with PAD are identified and treated similarly to those
patients presenting with coronary and cerebrovascular events.
Remember that many patients with PAD may be asymptomatic either because they choose not to walk very far, or because
their exercise tolerance is limited by other comorbidities such as
cardiac disease.
Intermittent claudication
Intermittent claudication is pain felt in the legs on walking due to
arterial insufficiency and is the most common symptom of PAD. It
is important to distinguish claudication due to arterial insufficiency
from other causes of lower limb pain, which include osteoarthritis,
neurogenic claudication and venous claudication (Box 4.21).
Patients with intermittent claudication describe tightness or
‘cramp-like’ pain that develops after a relatively constant distance;
the distance is often shorter if walking uphill. The pain disappears
completely within a few minutes of rest but recurs on walking. The
‘claudication distance’ is how far patients say they can walk before
the pain comes on. The ‘total walking distance’ is how far they can
walk before the pain is so bad that they have to stop.
The pain is felt in major muscle groups and its location depends on the level at which the arteries are diseased. The calf
muscle is most commonly affected due to femoropopliteal disease, while pain in the thigh or buttock suggests common
femoral or aortoiliac obstruction. Male patients who have bilateral
common iliac or internal iliac artery occlusion may develop Leriche’s syndrome, involving buttock claudication and erectile
dysfunction.
Claudication is not in itself limb-threatening, although it is a
marker for widespread atherosclerotic disease. With best medical therapy and supervised exercise programmes, 50% will
improve, 30% will remain stable and only 20% will deteriorate
further.
Any intervention for claudication is performed purely for the
purpose of symptomatic relief, since only a small minority of
patient’s progress to critical limb ischaemia. The patient’s age,
occupation and comorbidities are important in determining the
extent to which claudication limits their lifestyle. A postal worker
who is only able to walk 100 metres is seriously limited, but an
elderly person who simply wants to cross the road to the shops
may cope well. While absolute distances are important, it may be
more helpful to ask specific questions about how symptoms
affect the patient’s lifestyle:
• Can you walk to the clinic from the bus stop or car park
without stopping?
• Can you do your own shopping?
• What are you unable to do because of the pain?
4
4.21 The clinical features of arterial, neurogenic and venous claudication
Pathology Stenosis or occlusion of major lower limb
Site of pain Muscles, usually the calf but may involve
Laterality Unilateral or bilateral Often bilateral Nearly always unilateral
Onset Gradual after walking the ‘claudication
Relieving features On stopping walking, the pain
Colour Normal or pale Normal Cyanosed
Temperature Normal or cool Normal Normal or increased
Oedema Absent Absent Always present
Pulses Reduced or absent Normal Present but may be difficult to feel owing to
Straight-leg
raising
Arterial Neurogenic Venous
arteries
thigh and buttocks
distance’
disappears completely in 1–2 minutes
Normal May be limited Normal
Lumbar nerve root or cauda equina
compression (spinal stenosis)
Ill-defined
Whole leg
May be associated with numbness
and tingling
Often immediate on walking or
standing up
Bending forwards and stopping
walking
Patient may sit down for full relief
Obstruction to the venous outflow of the leg due
to iliofemoral venous occlusion
Whole leg
‘Bursting’ in nature
Gradual, from the moment walking starts
Leg elevation
Often visible varicose veins
oedema
ALGrawany
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