#3 Clinical - Examination 101-150

CHAPTER 7 Correlation of physical signs and cardiovascular disease 101
Systole Diastole
Raised left atrial
Presystolic accentuation pressure displaces
is present only if the patient atrial septum
is in sinus rhythm
Left atrium dilated
Turbulent flow
in diastole
Mitral valve
leaflets thickened
S1 A2 P2 S1 Chordae often thickened
Loud (S2) Opening snap

Doming in diastole
This distance is inversely
proportional to the
severity of the stenosis
a b
Figure 7.6 Mitral stenosis, at the apex: (a) murmur; (b) anatomy
long as there is a gradient); diastolic thrill at the ● Palpation: the apex beat is displaced, diffuse
apex; signs of pulmonary hypertension. and hyperdynamic; a pansystolic thrill is
● Causes of mitral stenosis: (1) rheumatic occasionally present at the apex; a parasternal
(following acute rheumatic fever); (2) congenital impulse may be present (due to left atrial
parachute valve (all chordae insert into one enlargement behind the right ventricle—the left
papillary muscle—rare). atrium is often larger in mitral regurgitation
than in mitral stenosis and can be enormous).
MITRAL REGURGITATION (CHRONIC) ● Auscultation (see Figure 7.7): soft or absent S1
A regurgitant mitral valve allows part of the left (by the end of diastole, atrial and ventricular
ventricular stroke volume to regurgitate into the pressures have equalised and the valve cusps
left atrium, imposing a volume load on both the left have drifted back together); left ventricular S3,
atrium and the left ventricle. which is due to rapid left ventricular filling in
● Symptoms: dyspnoea (increased left atrial early diastole and, when soft, does not imply
pressure); fatigue (decreased cardiac output). severe regurgitation; pansystolic murmur
● General signs: tachypnoea. maximal at the apex and usually radiating
● Pulse: normal, or sharp upstroke due to rapid towards the axilla.
Copyright © 2013. Elsevier Health Sciences APAC. All rights reserved.
left ventricular decompression; atrial fibrillation ● Signs indicating severe chronic mitral
is relatively common. regurgitation: small volume pulse; enlarged
Systole Diastole
High velocity flow
throughout systole
Left atrium often

dilated
S1 A2 P2 S1
Loud (S2) Left ventricle may
Diastolic flow be dilated
murmur and S3
(only severe lesion)
a b
Figure 7.7 Mitral regurgitation: (a) murmur, at the apex; (b) anatomy
Talley, N. J. O. S. (2013). Clinical Examination. Chatswood: Elsevier Health Sciences APAC. Retrieved from http://ebookcentral.proquest.com/lib/unda/detail.action?docID=1723115
Created from unda on 2017-03-15 15:29:59.
102 SECTION 2 The cardiovascular system
left ventricle; loud S3; soft S1; A2 is early, MITRAL VALVE PROLAPSE (SYSTOLIC-
because rapid left ventricular decompression CLICK MURMUR SYNDROME)
into the left atrium causes the aortic valve
to close early; early diastolic rumble; signs This syndrome can cause a systolic murmur or click,
of pulmonary hypertension; signs of left or both, at the apex. The presence of the murmur
ventricular failure. indicates that there is some mitral regurgitation
● Causes of chronic mitral regurgitation: present.
(1) mitral valve prolapse; (2) ‘degenerative’— ● Auscultation (see Figure 7.8): typically there
associated with ageing; (3) rheumatic; is a midsystolic click followed by a middle and
(4) papillary muscle dysfunction, due to left late systolic murmur that extends to the second
ventricular failure or ischaemia; (5) cardio- heart sound. It often has a blowing quality.
myopathy—hypertrophic, dilated or restrictive There may, however, be a click and no murmur
cardiomyopathy; (6) connective tissue disease (suggests little or no regurgitation) or a typical
(e.g. Marfan’s syndrome, rheumatoid arthritis, murmur without an audible click.
ankylosing spondylitis); (7) congenital ● Dynamic auscultation: murmur and click occur
(e.g. atrioventricular canal defect). earlier and may become louder with the Valsalva
manoeuvre and with standing (unlike the ejection
click of aortic or pulmonary stenosis), but with
ACUTE MITRAL REGURGITATION squatting and isometric exercise both murmur
In this case patients can present with pulmonary and click occur later and may become softer.
oedema and cardiovascular collapse. The murmur ● Causes of mitral valve prolapse: (1) myxo-
may be softer and lower pitched than that of severe matous degeneration of the mitral valve tissue—it
chronic mitral regurgitation. It tends to be short is very common, especially in women, and the
and may be decrescendo (i.e. declines in intensity severity may increase with age, particularly in
towards the end of systole) because atrial pressure men, so that significant mitral regurgitation may
is increased. supervene; (2) may be associated with atrial septal
With anterior leaflet chordae rupture the murmur defect (secundum), hypertrophic cardiomyopathy
radiates to the axilla and back; with posterior leaflet or Marfan’s syndrome.
rupture the murmur radiates to the cardiac base and
carotids. AORTIC STENOSIS
● Causes of acute mitral regurgitation: The normal area of the aortic valve is more than
(1) myocardial infarction (dysfunction or 2 cm2. Significant narrowing of this valve restricts
rupture of papillary muscles); (2) infective left ventricular outflow and imposes a pressure load
endocarditis; (3) trauma or surgery; on the left ventricle.
(4) spontaneous rupture of a myxomatous ● Symptoms: exertional chest pain (50% do
cord (sometimes during exercise). not have coronary artery disease), exertional
dyspnoea and exertional syncope.
Systole Diastole High velocity flow

during middle and
late systole
Left atrium often

dilated
Posterior leaflet prolapse
S1 A2 P2 S1
Left ventricle may
Loud (S2) be dilated
Click
a b
Figure 7.8 Mitral valve prolapse (MVP; Barlow’s 1 syndrome): (a) murmur, at the apex; (b) anatomy
● General signs: usually there is nothing ● Auscultation (see Figure 7.9): a narrowly split or
remarkable about the general appearance. reversed S2 because of delayed left ventricular
● Pulse: there may be a plateau or anacrotic pulse, ejection; a harsh midsystolic ejection murmur,
or the pulse may be late peaking (tardus) and of maximal over the aortic area and extending
small volume (parvus).5 into the carotid arteries (see Figure 7.10), is
● Palpation: the apex beat is hyperdynamic and characteristic. However, it may be heard widely
may be slightly displaced; systolic thrill at the over the praecordium and extend to the apex.
base of the heart (aortic area). The murmur is loudest with the patient sitting
Systole Diastole
Mild
S1 A2 P2 S1
Ejection click (S2)
(Suggests congenital AS) Normal
Moderate
S1 S2 S1
Single
Severe
S1 P2 A2 S1
Reversed
a
Ascending aorta may

be dilated
Valve cusps often

thickened and calcified
Left ventricle may be
hypertrophied
Figure 7.9 Aortic stenosis (AS): (a) murmur, at the aortic area; (b) anatomy
GOOD SIGNS GUIDE 7.2

Severe aortic stenosis
Sign LR+ LR–
Delayed carotid upstroke 9.2 0.56
Diminished carotid pulse on 2.0 0.64
palpation
Absent or decreased A2 7.5 0.5
Murmur over right clavicle 3.0 0.1
Any systolic murmur 2.6 0
Murmur radiates to the right carotid 8.1 0.29
artery
(Etchells E, Glenns V, Shadowitz S et al. A bedside clinical
prediction rule for detecting moderate or severe aortic stenosis.
J Gen Intern Med 1998; 13(10):699–704.)
where there is narrowing of the ascending aorta

or a fibrous diaphragm just above the aortic
valve—this is rare and may be associated with
a characteristic facies (a broad forehead, widely
set eyes and a pointed chin); there is a loud A2
and often a thrill in the area of the sternal notch;
(2) subvalvular obstruction, where there is a
Figure 7.10 Aortic stenosis: listening over the carotid membranous diaphragm or fibrous ridge just
(Courtesy of Glenn McCulloch)
below the aortic valve—aortic regurgitation is
associated and is due to a jet lesion affecting
the coronary cusp of the valve; (3) dynamic
up and in full expiration; associated aortic left ventricular outflow tract obstruction may
regurgitation is common; in congenital aortic occur in hypertrophic cardiomyopathy—here
stenosis where the valve cusps remain mobile there may be a double apical impulse. Atrial
and the dome of the valve comes to a sudden contraction into a stiff left ventricle may be
halt, an ejection click may precede the murmur— palpable before the left ventricular impulse
the ejection click is absent if the valve is calcified (only in the presence of sinus rhythm, of
or if the stenosis is not at the valve level but course).

above or below it (supra or subvalvular stenosis). Aortic sclerosis presents in the elderly; there are
● Signs indicating severe aortic stenosis (see none of the peripheral signs of aortic stenosis. The
Good signs guide 7.2; valve area less than 1 cm2, diagnosis implies the absence of a gradient across
or valve gradient greater than 50 mmHg): the aortic valve despite some thickening and a
plateau pulse, carotid pulse reduced in force; murmur.
thrill in the aortic area; length of the murmur
and lateness of the peak of the systolic murmur; AORTIC REGURGITATION
soft or absent A2; left ventricular failure (very The incompetent aortic valve allows regurgitation
late sign); pressure-loaded apex beat. These of blood from the aorta to the left ventricle during
signs are not reliable for distinguishing between diastole for as long as the aortic diastolic pressure
moderate and severe disease. It is important to exceeds the left ventricular diastolic pressure.7,8
remember that the signs of severity of aortic ● Symptoms: occur in the late stages of disease
stenosis are less reliable in the elderly.6 and include exertional dyspnoea, fatigue,
● Causes of aortic stenosis: (1) degenerative palpitations (hyperdynamic circulation) and
calcific aortic stenosis, particularly in elderly exertional angina.
patients; (2) calcific in younger patients, usually ● General signs: Marfan’s syndrome, ankylosing
on a congenital bicuspid valve; (3) rheumatic. spondylitis or one of the other seronegative
● Other types of aortic outflow obstruction are arthropathies or, rarely, Argyll Robertson pupils
also possible: (1) supravalvular obstruction, may be obvious.
● Pulse and blood pressure: the pulse is regurgitant jet from the aortic valve causes the
characteristically collapsing, a ‘water hammer’h anterior mitral valve leaflet to shudder). It can
pulse (see Table 7.2); there may be a wide be distinguished from mitral stenosis because
pulse pressure. This sign is most obvious if S1 (the first heart sound) is not loud and there
the clinician raises the patient’s arm while is no opening snap. Many other signs have been
feeling the radial pulse with the web spaces of described, but they are interesting rather than
the lifting hand. A bisferiens pulse (from the helpful (see Table 7.2 and Good signs guide 7.3).
Latin, to beat twice) may be a sign of severe ● Signs indicating severe chronic aortic
aortic regurgitation or of combined aortic regurgitation: collapsing pulse; wide pulse
regurgitation and aortic stenosis. It is best pressure (systolic pressure 80 mmHg more
assessed at the carotid artery, where two beats than the diastolic); long decrescendo diastolic
can be felt in each cardiac cycle. It is probably murmur; left ventricular S3 (third heart sound);
caused by a Venturi effect in the aorta related to soft A2; Austin Flint murmur; signs of left
rapid ejection of blood and brief in-drawing of ventricular failure.
the aortic wall, leading to a diminution of the ● Causes of aortic regurgitation: disease may
pulse followed by a rebound increase. It was a affect the valvular area or aortic root, and may
particular favourite of Galen’s.i be acute or chronic.
● Neck: prominent carotid pulsations (Corrigan’s ● Causes of chronic aortic regurgitation:
sign). (1) valvular—rheumatic (rarely the only
● Palpation: the apex beat is characteristically murmur in this case), congenital (e.g. bicuspid
displaced and hyperkinetic. A diastolic thrill valve; ventricular septal defect—an associated
may be felt at the left sternal edge when the prolapse of the aortic cusp is not uncommon),
patient sits up and breathes out. seronegative arthropathy, especially ankylosing
● Auscultation (see Figure 7.11): A2 (the aortic spondylitis; (2) aortic root dilation (murmur
component of the second heart sound) may may be maximal at the right sternal border)—
be soft; there is a decrescendo high-pitched Marfan’s syndrome, aortitis (e.g. seronegative
diastolic murmur beginning immediately after arthropathies, rheumatoid arthritis, tertiary
the second heart sound and extending for a syphilis), dissecting aneurysm.
variable time into diastole—it is loudest at the ● Acute aortic regurgitation: presents differently—
third and fourth left intercostal spaces; a systolic there is no collapsing pulse (blood pressure is
ejection murmur is usually present (due to low) and the diastolic murmur is short.
associated aortic stenosis or to torrential flow ● Causes of acute aortic regurgitation:
across a normal diameter aortic valve). Aortic (1) valvular—infective endocarditis; (2) aortic
stenosis is distinguished from an aortic flow root—Marfan’s syndrome, dissecting aneurysm
murmur by the presence of the peripheral signs of the aortic root.
of significant aortic stenosis, such as a plateau
pulse. However, the harsher and louder the

murmur (and especially if there is a thrill), the
more likely it is aortic stenosis. An Austin Valve diseases of the right heart
Flint murmur j should also be listened for. This
TRICUSPID STENOSIS
is a low-pitched rumbling mid-diastolic and
presystolic murmur audible at the apex (the This is very rare.
● JVP: raised; giant a waves with a slow y descent
may be seen.
● Auscultation: a diastolic murmur audible at
h
This Victorian children’s toy consisted of a sealed tube half-filled with the left sternal edge, accentuated by inspiration,
fluid, with the other half being a vacuum. Inversion of the tube caused
the fluid to fall rapidly without air resistance and strike the other end very similar to the murmur of mitral stenosis
with a noise like a hammer blow. It is not easy to imagine a child today except for the site of maximal intensity and the
being entertained by this for very long.
i
Claudius Galen (130–200 AD). Born in Pergamum, he worked as a
effect of respiration (louder on inspiration);
gladiator’s surgeon but moved to Rome in 164 AD to become the tricuspid regurgitation and mitral stenosis are
city’s most famous physician. He was the first to describe the cranial often present as well; no signs of pulmonary
nerves. He never performed dissection on human bodies, but his
often erroneous anatomical teachings were regarded as infallible for hypertension.
15 centuries. ● Abdomen: presystolic pulsation of the liver,
j
Austin Flint (1812–1886), New York physician and professor of medi- caused by forceful atrial systole.
cine at the New Orleans Medical School, described this murmur in
1862. Author of The principles and practice of medicine. He was very
● Cause of tricuspid stenosis: rheumatic heart
much opposed to the naming of signs after people. disease.
TABLE 7.2 Eponymous signs of aortic regurgitation

Quincke’s sign Capillary pulsation in the nail beds—it is of no value, as this sign occurs normally.
Corrigan’s sign Prominent carotid pulsations; the Corrigan water hammer pulse sign is present when the patient
lies supine with the arms beside the body; the radial pulse is compressed until it disappears, the
arm is then lifted perpendicular to the body and the pulse becomes palpable again even though
the same pressure has been maintained on the radial artery.
De Musset’s sign Head nodding in time with the heartbeat.
Hill’s sign Increased blood pressure (>20 mmHg) in the legs compared with the arms.
Mueller’s sign Pulsation of the uvula in time with the heartbeat.
Duroziez’s sign Systolic and diastolic murmurs over the femoral artery on gradual compression of the vessel.
The vessel is compressed with the diaphragm of the stethoscope. A systolic murmur will always
be heard. As the compression is increased a diastolic murmur will be heard in patients with
significant aortic regurgitation and is due to retrograde flow of blood back towards the heart in
diastole. Tilting the diaphragm towards the patient’s head will make the diastolic bruit softer if
the patient has aortic regurgitation but louder if the bruit is due to an increased cardiac output
(e.g. due to thyrotoxicosis).
Traube’s sign A double sound heard over the femoral artery on compressing the vessel distally; this is not a
‘pistol shot’ sound that may be heard over the femoral artery with very severe aortic
regurgitation.
Mayne’s sign A decrease in diastolic pressure of 15 mmHg when the patient’s arm is held above the head
compared with that when the arm is at the level of the heart.
Rosenbach’s liver Pulsation of the liver in time with the heartbeat (in the absence of tricuspid regurgitation).
pulsation sign
Austin Flint murmur Short rumbling diastolic murmur, thought by Flint to be due to functional mitral stenosis caused
by impinging of the aortic regurgitant jet on the anterior mitral valve leaflet.
Becker’s sign Accentuated retinal artery pulsations.
Gerhard’s sign Pulsatile spleen.
Landolfi’s sign Prominent alternating constriction and dilation of the pupils (hippus, from the Greek hippos—
‘horse’—and its rhythmical galloping).
Lincoln’s sign (see Exaggerated movement of the ankle when one leg is crossed over the other; said to have been
Figure 7.11(c)) described by Abraham Lincoln from a photograph of himself (he did not know the cause).
Sherman’s sign An easily palpable dorsalis pedis pulse in a patient over the age of 75 years.
Watson’s water See page 105.
hammer pulse
Ashrafian’s sign Pulsatile pseudo proptosis.
Note: These signs are amusing, but not often helpful. The signs were named after the following people: Heinrich Quincke (1842–1922),
German neurologist; Dominic Corrigan (1802–80), Edinburgh graduate who worked in Dublin and is credited with discovering aortic
regurgitation; Alfred de Musset, 19th-century French poet who suffered from aortic regurgitation (the sign was noticed by his brother, a
physician); Sir Leonard Hill (1866–1952), English physiologist who also described the physiology of the cerebral circulation; Frederick Von
Mueller (1858–1941), German physician who also noted an increase in metabolism in exophthalmic goitre; Paul Duroziez (1826–97),
French physician; Ludwig Traube (1818–76), Hungarian physician who worked in Germany; Otto Heinrich Becker (1828–1890), professor
of ophthalmology, University of Heidelberg, who also described this sign in patients with Graves’ disease; Lincoln’s sign is like de
Musset’s sign in being named after the patient with the condition; Thomas Watson, English physician, who described this sign in 1844;
Hutan Ashrafian, cardiothoracic surgeon, St Mary’s Hospital, London, who described this sign in 2006—proof that the hunt for more
signs of aortic regurgitation goes on.
(Babu AN, Kymes SM, Carpenter Fryer SM. Eponyms and the diagnosis of aortic regurgitation: What says the evidence? Ann Intern Med
2003: 138:736–745.)
TRICUSPID REGURGITATION ● Auscultation: there may be a pansystolic

(see Figure 7.12) murmur maximal at the lower end of the
sternum that increases on inspiration, but
● JVP: large v waves; the JVP is elevated if right the diagnosis can be made on the basis of the
ventricular failure has occurred. peripheral signs alone.
● Palpation: right ventricular heave (parasternal ● Abdomen: a pulsatile, large and tender liver is
impulse). usually present and may cause the right nipple
Systole Diastole
S1 S2 S1
Flow murmur Length of murmur is
proportional to the
severity of the lesion
Aortic root
Diastolic murmur begins

immediately after closure
of aortic valve c
Figure 7.11 Aortic regurgitation: (a) murmur, at the

Left ventricle dilated left sternal edge; (b) anatomy; (c) Lincoln’s sign: left
foot is blurred by motion
b
to dance in time with the heart beat; ascites,

GOOD SIGNS GUIDE 7.3
Moderate or worse aortic regurgitation oedema and pleural effusions may also be
present.
Finding LR+ LR– ● Legs: dilated, pulsatile veins.
Typical murmur 4.0–8.3 0.1 ● Causes of tricuspid regurgitation:k
Grade 1 murmur (moderate to 0.0 NA (1) functional (no disease of the valve leaflets)—
severe AR) right ventricular failure; (2) rheumatic—only
Grade 2 murmur (moderate to 1.1 NA
very rarely does rheumatic tricuspid
severe AR) regurgitation occur alone, usually mitral valve
disease is also present; (3) infective endocarditis
Murmur grade 3 or more 4.5 NA
(moderate to severe AR) (right-sided endocarditis in intravenous
drug addicts); (4) tricuspid valve prolapse;
Pulse pressure
(5) right ventricular papillary muscle infarction;
>80 mmHg 10.9 (6) trauma (usually caused by a steering wheel
Other signs—distinguishing mild from moderate to injury to the sternum); (7) congenital—Ebstein’s
severe AR anomaly.l
Duroziez’s sign, pistol shot NS NS
femorals, water hammer pulse
AR = aortic regurgitation; NS = not significant; NA = not k
Doppler echocardiography has shown that trivial tricuspid regurgitation
applicable.
is very common and is then considered physiological. Christian
(Adapted from Simel DL, Rennie D. The rational clinical
Doppler (1803–1853) was an Austrian physicist and mathematician.
examination: evidence-based diagnosis. New York: McGraw- l
Wilhelm Ebstein (1836–1912), professor of medicine at Göttingen in
Hill, 2009, Table 32-3.)
Germany, who invented and developed palpation.
ejection systolic murmur, heard best in the

pulmonary area and with inspiration, is typically
present; right ventricular S4 may be present
Superior
vena cava
(due to right atrial hypertrophy). It is not well
heard over the carotid arteries.
● Abdomen: presystolic pulsation of the liver may
be present.
TR jet
● Signs of severe pulmonary stenosis: an ejection
systolic murmur peaking late in systole; absence
of an ejection click (also absent when the
pulmonary stenosis is infundibular i.e. below
the valve level); presence of S4; signs of right
Inferior
vena cava ventricular failure.
● Causes of pulmonary stenosis: (1) congenital;
(2) carcinoid syndrome (rare).
Left PULMONARY REGURGITATION
ventricle
Right This is an uncommon pathological condition;
ventricle trivial pulmonary regurgitation is often found at
echocardiography and is considered physiological.
Figure 7.12 Tricuspid regurgitation (TR): anatomy
● Auscultation: a decrescendo diastolic murmur
that is high-pitched and audible at the left
sternal edge is characteristic—this typically
PULMONARY STENOSIS (IN ADULTS) but not always increases on inspiration (unlike
(see Figure 7.13) the murmur of aortic regurgitation). It is
● General signs: peripheral cyanosis, due to a low called the Graham Steell murmurm when it
cardiac output, but only in severe cases. occurs secondary to pulmonary artery dilation
● Pulse: normal or reduced if cardiac output is caused by pulmonary hypertension. (Note: If
low. there are no signs of pulmonary hypertension,
● JVP: giant a waves because of right atrial a decrescendo diastolic murmur at the left
hypertrophy; the JVP may be elevated. sternal edge is more likely to be due to aortic
● Palpation: right ventricular heave; thrill over regurgitation than to pulmonary regurgitation.)
the pulmonary area. ● Causes of pulmonary regurgitation:
● Auscultation: the murmur may be preceded (1) pulmonary hypertension; (2) infective
by an ejection click; a harsh and usually loud endocarditis; (3) following balloon valvotomy
for pulmonary stenosis or surgery for

pulmonary atresia; (4) congenital absence of
the pulmonary valve.
PROSTHETIC HEART VALVES

The physical signs with common types of valves
Main pulmonary
are presented in Table 7.3. Mechanical prosthetic
artery valves should have a crisp sound. Muffling of the
mechanical sounds may be a sign of thrombotic
obstruction of the valve or chronic tissue ingrowth
(pannus). After replacement of the aortic valve the
presence of audible aortic regurgitation may indicate
a paravalvular leak, often through a stitching hole
Right ventricular in the valve sewing ring. As tissue valves age and
hypertrophy degenerate they may develop signs of regurgitation
or stenosis, or both.
m
Graham Steell (1851–1942), Manchester physician, described this
Figure 7.13 Valvar pulmonary stenosis: anatomy murmur in 1888.
TABLE 7.3 Prosthetic heart valves: physical signs

Type Mitral Aortic
Ball valve (e.g. Starr-Edwards)* Sharp mitral opening sound after S2, Sharp aortic opening sound
sharp closing sound at S1 Systolic ejection murmur (harsh), no
Systolic ejection murmur, no diastolic diastolic murmur unless a paravalvular
murmur leak has occurred, early diastolic
murmur indicates AR usually due to
a paravalvular leak**
Disc valve (e.g. Bjork-Shiley)† Sharp closing sound at S1, soft systolic Sharp closing sound at S2, systolic
ejection murmur and diastolic rumble ejection murmur (soft)
(diastolic murmur occasionally)
Porcine or bovine pericardial Usually sound normal, diastolic rumble Closing sound usually heard, systolic
valve‡ mitral opening sound occasionally ejection murmur (soft), no diastolic
murmur
Bileaflet valve (e.g. St Jude) — Aortic valve opening and closing sounds
common, soft systolic ejection
murmur common
Homograft (human) valve Normal heart sounds, occasional soft —
systolic murmur; early diastolic murmur
if AR has occurred
*Modern mechanical valves (e.g. St Jude) make softer opening and closing sounds than older valves. The Starr-Edwards valve is often
very noisy and sounds like a ball rattling around in a cage (which is what it is). The valve sounds may be audible to everyone in the room
when things are quiet.
**An aortic regurgitation murmur present after aortic valve replacement suggests regurgitation of the valve ring. It is not uncommon.
Less often, a mitral regurgitation murmur suggests the same problem with a prosthetic mitral valve.
†
Severe prosthetic dysfunction causes absence of the opening or closing sounds. Ball and cage valves cause more haemolysis than
other types and make the most noise, while disc valves are more thrombogenic.
‡
Bioprosthetic obstruction or patient–prosthetic mismatch causes diastolic rumbling. These valves are used less often in the mitral
position because they often have a very limited life there. A degenerated bioprosthetic valve may cause murmurs of regurgitation or
stenosis, or both.
AR = aortic regurgitation.
(Modified from Smith ND, Raizada V, Abrams J. Auscultation of the normally functioning prosthetic valve. Ann Intern Med 1981; 95:594.)
Cardiomyopathy
HYPERTROPHIC CARDIOMYOPATHY
(see Figure 7.14) Aorta
This is abnormal hypertrophy of the muscle in the
left ventricular or right ventricular outflow tract, or

both. It can obstruct outflow from the left ventricle
late in systole when the hypertrophied area contracts. 2
1
Systolic displacement of the mitral valve apparatus
into the left ventricular outflow tract also occurs, 3
causing mitral regurgitation and contributing to the
outflow obstruction. Although the outflow tract is 4
narrowed by the hypertrophied septum, the major
contribution to the dynamic increase in obstruction
comes from the systolic movement of the mitral
valve. Variants of hypertrophic cardiomyopathy
may involve the mid-ventricle or apex with varying
degrees of obstruction.
● Symptoms: dyspnoea (increased left ventricular 1 Systolic anterior motion
end-diastolic pressure due to abnormal diastolic of anterior mitral valve leaflet
compliance), angina, syncope or sudden death 2 Jet of mitral regurgitation
3 Left ventricular outflow tract
(secondary to ventricular fibrillation or a
4 Septal hypertrophy
sudden increase in outflow obstruction).
● Pulse: sharp rising and jerky or double
(bisferiens). Rapid ejection by the hypertrophied Figure 7.14 Hypertrophic cardiomyopathy anatomy
ventricle early in systole is followed by Acyanotic congenital heart

obstruction caused by the displacement of the
mitral valve into the outflow tract. This is quite disease
different from the pulse of aortic stenosis. VENTRICULAR SEPTAL DEFECT
● JVP: there is usually a prominent a wave, In this condition one or more holes are present in the
due to forceful atrial contraction against a membranous or muscular ventricular septum.
noncompliant right ventricle. ● Palpation: hyperkinetic displaced apex if the
● Palpation: double or triple apical impulse, due defect is large; and a thrill at the left sternal edge.
to presystolic expansion of the ventricle caused ● Auscultation (see Figure 7.15): a harsh
by atrial contraction.
pansystolic murmur maximal at, and almost
● Auscultation: late systolic murmur at the
confined to, the lower left sternal edge with
lower left sternal edge and apex (due to the
a third or fourth heart sound—the murmur
obstruction) and a pansystolic murmur at
is louder on expiration; sometimes a mitral
the apex (due to mitral regurgitation); S4.
regurgitation murmur is associated. There is
● Dynamic manoeuvres: the outflow murmur
often a palpable systolic thrill. The murmur
is increased by the Valsalva manoeuvre, by
is often louder and harsher when the defect is
standing and by isotonic exercise; it is decreased
by squatting and isometric exercise. small.
● Causes of hypertrophic cardiomyopathy:
● Causes of ventricular septal defect:
(1) autosomal dominant (sarcomeric heavy (1) congenital; (2) acquired (e.g. myocardial
chain or troponin gene mutation) with variable infarction involving the septum).
expressivity; (2) idiopathic; (3) Friedreich’s
ataxian (page 475). ATRIAL SEPTAL DEFECT
There are two main types: ostium secundum (90%),
DILATED CARDIOMYOPATHY where there is a defect in the part of the septum that
This heart muscle abnormality results in a global does not involve the atrioventricular valves, and
reduction in cardiac function. Coronary artery ostium primum, where the defect does involve the
disease is excluded as a cause by definition. (Ischaemic atrioventricular valves.
cardiomyopathy is a term often used to describe ● Palpation: normal or right ventricular
severe myocardial dysfunction secondary to recurrent enlargement.
ischaemic events.) The signs are those of congestive ● Auscultation (see Figure 7.16): fixed splitting
cardiac failure, including those of mitral and tricuspid of S2; the defect produces no murmur directly,
regurgitation. The heart sounds themselves may be but increased flow through the right side of
very quiet. Ventricular arrhythmias are common. It the heart can produce a low-pitched diastolic
is a common indication for cardiac transplantation. tricuspid flow murmur and more often a
● Causes of dilated cardiomyopathy: pulmonary systolic ejection murmur—these are

(1) idiopathic and familial; (2) alcohol; both louder on inspiration.
(3) post-viral; (4) postpartum; (5) drugs ● Signs: the signs of an ostium primum defect
(e.g. doxorubicin); (6) dystrophia myotonica; are the same as for an ostium secundum defect,
(7) haemochromatosis. but associated mitral regurgitation, tricuspid
regurgitation or a ventricular septal defect may
RESTRICTIVE CARDIOMYOPATHY be present. The left ventricular impulse is often
This causes similar signs to those caused by impalpable.
constrictive pericarditis, but Kussmaul’s sign is more
common and the apex beat is usually easily palpable. PATENT DUCTUS ARTERIOSUS
● Causes of restrictive cardiomyopathy: (see Figure 7.17)
(1) idiopathic; (2) eosinophilic endomyocardial This is a persistent embryonic vessel that connects
disease; (3) endomyocardial fibrosis; the pulmonary artery and the aorta. The shunt
(4) infiltrative disease (e.g. amyloid); is from the aorta to the pulmonary artery unless
(5) granulomas (e.g. sarcoid). pulmonary hypertension has supervened.
● Pulse and blood pressure: a collapsing pulse
with a sharp upstroke (due to ejection of a large
n
volume of blood into the empty aorta with
Nikolaus Friedreich (1825–82), German physician, described this
disease in 1863. He succeeded Virchow as professor of pathological systole); low diastolic blood pressure (due to
anatomy at Würzburg at the age of 31. rapid decompression of the aorta).
Systole Diastole
Membranous ventricular
septal defect
S1 P2 A2 S1 Right ventricle
may be dilated Muscular ventricular
Harsh (S2) septal defect
High velocity jet

from left to right
a b
Figure 7.15 Ventricular septal defect (VSD): (a) murmur, at the left sternal edge; (b) anatomy
Systole Diastole
1
Right atrium
2
Left atrium
3
S1 A2 P2 S1 Tricuspid valve Mitral valve

Pulmonary artery (S2) Tricuspid annulus
flow murmur (Fixed) flow murmur Right ventricle Left ventricle
dilated
1 Sinus venosus
2 Secundum
3 Primum
a b
Figure 7.16 Atrial septal defect (ASD): (a) murmur, at the left sternal edge; (b) anatomy
● Palpation: often there is a hyperkinetic apex

beat.
● Auscultation: if the shunt is of moderate size
a single second heart sound is heard, but if the
shunt is of significant size reversed splitting of
the second heart sound occurs (due to a delayed
A2 because of an increased volume load in the
left ventricle); a continuous loud ‘machinery’
murmur maximal at the first left intercostal
space is usually present; flow murmurs through
the left side of the heart, including a mitral mid-
diastolic murmur, may be heard.
COARCTATION OF THE AORTA

(see Figure 7.18)
This is congenital narrowing of the aorta usually
Figure 7.17 Patent ductus arteriosus: anatomy just distal to the origin of the left subclavian artery.
LIST 7.2 Classification of congenital heart

disease
Acyanotic
WITH LEFT-TO-RIGHT SHUNT
Ventricular septal defect
Atrial septal defect
Patent ductus arteriosus
WITH NO SHUNT
Bicuspid aortic valve, congenital aortic stenosis
Coarctation of aorta
Dextrocardia
Pulmonary stenosis, tricuspid stenosis
Ebstein’s anomaly
Cyanotic
Eisenmenger’s syndrome (pulmonary hypertension
and a right-to-left shunt)
Tetralogy of Fallot
Ebstein’s anomaly (if an atrial septal defect and
Figure 7.18 Coarctation of the aorta: anatomy right-to-left shunt are also present)
Truncus arteriosus
Transposition of the great vessels
Tricuspid arteria
It is more common in males. The underlying cause Total anomalous pulmonary venous drainage
is uncertain but seems related to abnormal place-
ment of tissue involved in the closing of the ductus
arteriosus. There is an association with bicuspid
reactive pulmonary hypertension so that pulmonary
aortic valve and Turner’s syndrome.
pressures eventually exceed systemic pressures.
● Signs: the upper body may be better developed
When that happens, the systemic to pulmonary (left
than the lower; radiofemoral delay is present, and
to right) shunt will reverse. This right-to-left shunt
the femoral pulses are weak; hypertension occurs
leads to deoxygenated blood being mixed in the
in the arms but not in the legs; a midsystolic
systemic circulation, resulting in cyanosis. This is
murmur is usually audible over the praecordium
called Eisenmenger’s syndrome.o
and the back, due to blood flow through collateral
chest vessels and across the coarct itself.
EISENMENGER’S SYNDROME
EBSTEIN’S ANOMALY (PULMONARY HYPERTENSION AND
This is a very rare lesion. The abnormality is a A RIGHT-TO-LEFT SHUNT)

downward displacement of the tricuspid valve ● Signs: central cyanosis; clubbing; polycythaemia;
apparatus into the right ventricle so that the right signs of pulmonary hypertension.
atrium becomes very large and consists partly It may be possible to decide at what level the shunt
of ventricular muscle, while the right ventricle occurs by listening to the second heart sound (S2).
becomes small. An atrial septal defect is commonly If there is wide fixed splitting, this suggests an atrial
associated. Characteristically, multiple clicks occur septal defect. If a single second heart sound is present,
due to asynchronous closure of the tricuspid valve. this suggests truncus arteriosus or a ventricular septal
Tricuspid regurgitation is usually present. defect. A normal or reversed S2 suggests a patent
ductus arteriosus.
Cyanotic congenital heart
TETRALOGY OF FALLOTp
disease There are four features that are due to a single
This is a difficult area. The causes of congenital developmental abnormality: (1) ventricular septal
heart disease are listed in List 7.2. The important defect; (2) right ventricular outflow obstruction,
point to determine is whether or not signs of
pulmonary hypertension are present. Congenital
o
heart disease in which a shunt from the left to Victor Eisenmenger (1864–1932), German physician. He described
this syndrome in 1897.
the right side of the circulation occurs leads to an p
Etienne-Louis Fallot (1850–1911), professor of hygiene, Marseilles,
increase in pulmonary blood flow. This can cause described this in 1888.
which determines the severity of the condition, Mustard procedure. In this abnormality, the
and can be at the pulmonary valve or infundibular pulmonary artery is connected to the left ventricle
level; (3) an aorta that overrides the ventricular and the aorta to the right ventricle. Thus the systemic
septal defect and is responsible for the cyanosis; and pulmonary circulations are in parallel. This is
and (4) right ventricular hypertrophy secondary to not compatible with life unless some connection
outflow obstruction. between the two circulations is present. Neonates
● Signs: central cyanosis—this occurs without with the condition will have an atrial septal defect
pulmonary hypertension because venous created soon after birth with a catheter-based
mixing is possible at the ventricular level, where balloon (balloon septostomy). This allows mixing of
pressures are balanced. The aorta overrides the circulations. Later, ‘baffles’ are created surgically
both ventricles and so receives right and left in the atria to direct blood returning from the body
ventricular blood. Clubbing and polycythaemia into the right atrium across the atrial septal defect
are usually present. There may be evidence of and into the left atrium, where it is pumped into
right ventricular enlargement—a parasternal the pulmonary artery and into the lungs. Blood
impulse at the left sternal edge. A systolic thrill returning from the lungs into the left atrium is
caused by pulmonary valve or right ventricular directed across into the right atrium and into the
outflow obstruction may be present. There is morphological right ventricle and on into the aorta.
no overall cardiomegaly. On auscultation the This means that the morphological right ventricle is
second heart sound is single and there are no working as the systemic ventricle. This arrangement
signs of pulmonary hypertension; a pulmonary works very well, but there are long-term concerns
systolic ejection murmur is present. about the ability of the right ventricle to cope with
systemic workloads.
● Symptoms: symptoms that commonly
‘Grown-up’ congenital heart occur include palpitations caused by
disease supraventricular arrhythmias, dizziness caused
Patients who have been treated for serious congenital by bradycardias and breathlessness related to
cardiac conditions now frequently survive into adult failure of the systemic ventricle. Occasionally,
life. Many of the surgical procedures undertaken obstruction of the baffles may occur. The most
for these conditions, especially 20 years ago, were common problem is with the superior vena
palliative rather than curative. The patients present caval baffle, which leads to facial swelling and
with specific symptoms and signs. flushing.
● Signs: include the usual scar, facial flushing
TETRALOGY OF FALLOT and oedema, cyanosis, peripheral oedema from
Patients who have had repair of this condition in inferior caval baffle obstruction and signs of
infancy may present with particular problems. Repair tricuspid regurgitation. On auscultation there
may be a gallop rhythm and the murmurs of
of the right ventricular outflow obstruction and

enlargement of the pulmonary valve annulus may mitral and tricuspid regurgitation.
leave severe pulmonary regurgitation. This may lead
eventually to exertional dyspnoea. The surgery itself
has, until recently, required a right ventriculotomy T&O’C essentials
(cutting into the right ventricle). This leaves a scar that
can be associated with cardiac rhythm abnormalities 1. Careful examination of the heart can lead to an
in later life. Patients may present with palpitations accurate diagnosis in most cases of valvular
heart disease.
or syncope.
2. Proper history taking and examination will
● Signs: may include a median sternotomy prevent the ordering of expensive and
scar, a long diastolic murmur of pulmonary inappropriate cardiac tests.
regurgitation and signs of right ventricular 3. It is not necessary to memorise the entire list of
enlargement (parasternal impulse) and later of eponymous signs of aortic regurgitation (in fact,
tricuspid regurgitation (big v waves in the neck you can forget them all).
and a pulsatile liver). 4. The presence of specific signs of heart failure
(e.g. a third heart sound and abnormal apex
beat) makes the diagnosis almost certain; their
TRANSPOSITION OF THE GREAT absence does not rule out heart failure.
ARTERIES 5. There are few specific signs of myocardial
infarction and the diagnosis depends on the
Most adults who have had surgery for this abnor- history and ECG.
mality have had a palliative operation called a
OSCE example References

CARDIOVASCULAR EXAMINATION 1. Stevenson LW, Perluff JK. The limited reliability
of physical signs for estimating hemodynamics in
Please examine this 75-year-old woman with chronic heart failure. JAMA 1989; 261:884–888.
dyspnoea and suspected heart failure. Physical signs poorly predict haemodynamic changes
1. Wash your hands. in heart failure. However, some signs are useful.
2. Khot U, Jia G, Moliterno DJ et al. Prognostic
2. Introduce yourself to the patient and explain the value of physical examination for heart failure
purpose and nature of the examination. (e.g. ‘I’m
in non-ST elevation acute coronary syndromes.
going to examine your heart if that is all right?’)
JAMA 2003; 290:2174–2181. This analysis of
3. Stand back to look for breathlessness and the Killip classification for patients with acute
tachypnoea, cyanosis, elevated JVP, use of coronary syndromes expands the relevance of the
supplementary oxygen. Does the patient look classification from its original use for patients with
unwell? ST elevation infarction in the pre-thrombolytic era.
4. Position the patient at 45°, and loosen the 3. Klompas M. Does this patient have an acute thoracic
patient’s gown to allow access to the front of the dissection? JAMA 2002; 287(17):2262–2272.
chest but keep a female’s breasts covered. 4. Turnbull JM. Is listening for abdominal bruits useful
in the evaluation of hypertension? The rational
5. Take the patient’s pulse (consider rate and
clinical examination. JAMA 1995; 274:16. If an
possible AF).
abdominal bruit extends into diastole, this has a
6. Take the blood pressure. high predictive value for a clinically important bruit.
7. Look at the JVP again (especially big v waves). The pitch and intensity are not helpful.
Perform abdominojugular reflux test. 5. Etchells E, Bell C, Robb K. Does this patient
have an abnormal systolic murmur? JAMA 1997;
8. Loosen the patient’s gown further and inspect 277:564–571. The most useful positive predictive
the chest for scars (previous valve surgery). features for aortic stenosis appear to be a slow rate of
9. Look for the apex beat; feel carefully for the apex rise of the carotid pulse, a mid-to-late peak intensity
beat, thrills and parasternal impulse. of the murmur and a decreased second heart sound;
absence of radiation to the right carotid helps rule
10. Listen for gallop rhythm and valvular disease
it out.
(mitral regurgitation may occur as a result of,
or be the cause of, heart failure).
6. Aronow WS. Prevalence and severity of
valvular aortic stenosis determined by Doppler
11. Listen to the lung bases (medium inspiratory echocardiography, and its association with
crackles—not specific); look for sacral oedema. echocardiographic and electrocardiographic left
12. Look at the legs for oedema (not specific). ventricular hypertrophy and physical signs of aortic
stenosis in elderly patients. Am J Cardiol 1991;
13. Collect your thoughts while washing your hands. 67:776–777. Analysis of the signs of severity of aortic
14. Present the positive and negative findings stenosis in elderly patients shows that they are less
associated with heart failure. reliable than in younger patients.

7. Choudhry NK, Etchells EE. Does this patient have
aortic regurgitation? JAMA 1999; 281:2231–2238
OSCE revision topics (Rational Clinical Examination Series). It is easy if
you listen carefully: the presence of an early diastolic
CARDIOVASCULAR EXAMINATION murmur at the left sternal edge best rules in AR;
Use these topics, which commonly occur in the the absence of an early diastolic murmur essentially
OSCE, to help with revision. rules out AR.
8. Aronow WS, Kronzon I. Correlation of prevalence
1. Please examine this man who has previous and severity of aortic regurgitation detected by pulsed
cardiac valve surgery. (page 108) Doppler echocardiography with the murmur of aortic
2. This man has aortic regurgitation. Please regurgitation in elderly patients in a long-term health
examine him and estimate the severity of the care facility. Am J Cardiol 1989; 63:128–129.
condition. (page 104)
3. This woman has had a diagnosis of pulmonary
hypertension. Please examine her. (page 98)
CHAPTER
A summary of the
cardiovascular examination
and extending the cardiovascular
examination
8
TEXT BOX 8.1 The cardiovascular examination: a suggested method continued
Figure 8.1 Cardiovascular system

Patient lying at 45°
1. General inspection Palate (high arched—Marfan’s)

Marfan’s, Turner’s, Down syndrome Dentition
Rheumatological disorders, e.g. ankylosing 5. Neck
spondylitis (aortic regurgitation) Jugular venous pressure
Dyspnoea Central venous pressure height
2. Hands Wave form (especially large n waves)
Radial pulses—right and left Carotids—pulse character
Radiofemoral delay 6. Praecordium
Clubbing Inspect
Signs of infective endocarditis—splinter Scars—whole chest, back
haemorrhages etc Deformity
Peripheral cyanosis Apex beat—position, character
Xanthomata Abnormal pulsations
3. Blood pressure Palpate
4. Face Apex beat—position, character
Eyes Thrills
Sclerae—pallor, jaundice Abnormal impulses
Pupils—Argyll Robertson (aortic regurgitation) Note: beware of dextrocardia
Xanthelasmata 7. Auscultate
Malar flush (mitral stenosis, pulmonary Heart sounds
stenosis) Murmurs
Mouth Position patient
Cyanosis Left lateral position
continues
115
Sitting forwards (forced expiratory apnoea) Percuss for ascites (right heart failure)
NB: Palpate for thrills again after positioning Femoral arteries—palpate, auscultate
Dynamic auscultation 10. Legs
Respiratory phases Peripheral pulses
Valsalva Cyanosis, cold limbs, trophic changes, ulceration
Exercise (isometric, e.g. hand grip) (peripheral vascular disease)
Carotids Oedema
8. Back (sitting forwards) Xanthomata
Scars, deformity Calf tenderness
Sacral oedema 11. Other
Pleural effusion (percuss) Urine analysis (infective endocarditis)
Left ventricular failure (auscultate) Fundi (endocarditis)
9. Abdomen (lying flat—1 pillow only) Temperature chart (endocarditis)
Palpate liver (pulsatile etc.), spleen, aorta
Position the patient at 45° and make sure his or her not displaced (e.g. aortic stenosis, hypertension).
chest and neck are fully exposed. Cover the breasts of A volume-loaded (hyperkinetic, diastolic overloaded)
a female patient with a towel or loose garment. apex beat is a forceful but unsustained impulse that is
Inspect while standing back for the appearance of displaced down and laterally (e.g. aortic regurgitation,
Marfan’s, Turner’s or Down syndromes. Also look for mitral regurgitation). A dyskinetic apex beat (cardiac
dyspnoea, cyanosis, jaundice and cachexia. failure) is palpable over a larger area than normal and
Pick up the patient’s hand. Feel the radial pulse. moves in an uncoordinated way under the examiner’s
At the same time inspect the hands for clubbing. Also hand. Do not miss the tapping apex beat of mitral
look for the peripheral stigmata of infective stenosis (a palpable first heart sound). The double or
endocarditis: splinter haemorrhages are common (and triple apical impulse of hypertrophic cardiomyopathy is
are also caused by trauma), while Osler’s nodes and very important too. Feel also for an apical thrill, and
Janeway lesions are rare. Look quickly, but carefully, at time it.
each nail bed, otherwise it is easy to miss these signs. Then palpate with the heel of your hand for a left
Note any tendon xanthoma (type II hyperlipidaemia). parasternal impulse (which indicates right ventricular
The pulse at the wrist should be timed for rate and enlargement or left atrial enlargement) and for thrills.
rhythm. Feel for radiofemoral delay (which occurs in Now feel at the base of the heart for a palpable
coarctation of the aorta) and radial–radial inequality. pulmonary component of the second heart sound (P2)
Pulse character is best assessed at the carotids. and aortic thrills. Percussion may be helpful if there is
Take the blood pressure (lying and standing or uncertainty about cardiac enlargement.
sitting—postural hypotension). Auscultation begins in the mitral area with both
Next inspect the face. Look at the eyes briefly for the bell and the diaphragm. Listen for each component
jaundice (e.g. valve haemolysis) or xanthelasmata of the cardiac cycle separately. Identify the first and
(type II or type III hyperlipidaemia*). You may also notice second heart sounds, and decide whether they are of
the classical mitral facies. Then inspect the mouth using normal intensity and whether the second heart sound
a torch for a high arched palate (Marfan’s syndrome), is normally split. Now listen for extra heart sounds and
petechiae and the state of dentition (endocarditis). Look murmurs. Do not be satisfied at having identified one
at the tongue or lips for central cyanosis. abnormality.
The neck is very important. The jugular venous Repeat the approach at the left sternal edge and
pressure (JVP) must be assessed for height and then the base of the heart (aortic and pulmonary
character. Use the right internal jugular vein for this areas). Time each part of the cycle with the carotid
assessment. Look for a change with inspiration pulse. Listen over the carotids.
(Kussmaul’s sign). Now feel each carotid pulse It is now time to reposition the patient. First put
separately. Assess the pulse character. him or her in the left lateral position. Again feel the
Proceed to the praecordium. Always begin by apex beat for character (particularly tapping) and
inspecting for scars, deformity, the site of the apex auscultate. Sit the patient up and palpate for thrills
beat and visible pulsations. Do not forget about (with the patient in full expiration) at the left sternal
pacemaker boxes. Mitral valvotomy scars (usually edge and base. Then listen in those areas, particularly
under the left breast) can be quite lateral and very for aortic regurgitation or a pericardial rub.
easily missed. Dynamic auscultation should be done if there is any
Palpate for the position of the apex beat. Count doubt about a systolic murmur. The Valsalva
down the correct number of interspaces. The normal manoeuvre should be performed whenever there is a
position is the fifth left intercostal space, 1 cm medial pure systolic murmur. Hypertrophic cardiomyopathy is
to the midclavicular line. The character of the apex easily missed otherwise.
beat is important. There are a number of types. The patient is now sitting up. Percuss the back
A pressure-loaded (hyperdynamic, systolic overloaded) quickly to exclude a pleural effusion (e.g. due to left
apex beat is a forceful and sustained impulse that is ventricular failure) and auscultate for inspiratory
CHAPTER 8 A summary of the cardiovascular examination 117
crackles (left ventricular failure). If there is a Move on to the legs. Palpate both femoral arteries and
radiofemoral delay, listen for a coarctation murmur over auscultate here for bruits. Go on and examine all the
the back. Feel for sacral oedema and note any back peripheral pulses. Look for signs of peripheral vascular
deformity (e.g. ankylosing spondylitis with aortic disease, peripheral oedema, clubbing of the toes,
regurgitation). Achilles tendon xanthomata and stigmata of infective
Next have the patient lie flat and examine the endocarditis.
abdomen properly for hepatomegaly (right ventricular Finally, examine the fundi (for hypertensive
failure) and a pulsatile liver (tricuspid regurgitation). Test changes, and Roth’s spots in endocarditis) and the
for the abdomino-jugular reflux sign if relevant. Feel for urine (haematuria in endocarditis). Take the
splenomegaly (endocarditis) and an aortic aneurysm. temperature.
*In type III, which is rare, chylomicrons and intermediate density lipoproteins (IDL) are elevated.
Extending the cardiovascular THE CHEST X-RAY: A SYSTEMATIC

physical examination APPROACH
Just as analysis of the chest X-ray has long been Interpretation of the chest X-ray is not easy. It requires
considered an extension of the patient’s physical knowledge of anatomy and pathology, appreciation of
examination, electrocardiography (see online the whole range of normal appearances (see Figure 8.2)
resources) and echocardiography are now essential and knowledge of the likely X-ray changes occurring
and basic parts of cardiac assessment. It is not possible with pathological processes. The clinician should
to order even basic tests without knowing how a test feel personally responsible for viewing a patient’s
might be helpful and what it is able to detect. radiographs.
Most medical students faced with giving their
interpretation of a chest X-ray either opt for a ‘spot
diagnosis’ (usually wrong) or raise their eyes to
a b
Figure 8.2 Normal chest X-ray

(a) The posteroanterior view shows: (1) aortic knuckle; (2) left heart border formed by the lateral border of the left ventricle;
(3) left hilum, formed mostly by the left main pulmonary artery and partly by the left upper pulmonary veins; (4) right heart
border formed by the right atrium; (5) inferior angle of the scapula; (6) right basal pulmonary artery; (7) medial aspect of the
left clavicle; (8) spine of the scapula; (9) right cardiophrenic angle; and (10) superimposition of the right lateral margins of
the superior vena cava and the ascending aorta.
(b) The lateral view shows: (11) anterior border of the trachea; (12) pulmonary vein, entering the left atrium; (13) oblique
fissure; (14) left hemidiaphragm; and (15) right hemidiaphragm.
heaven, hoping for divine inspiration. However, a Hila

systematic approach is generally more useful! More The hila are mostly formed by the pulmonary arteries
is missed by not looking than by not knowing. with the upper lobe veins superimposed. The left
hilum is higher than the right. The left has a squarish
Frontal film shape whereas the right has a V shape.
Name, date and projection A hilum can be more prominent if the patient
First, it is important to check the name and date, to is rotated. Lymphadenopathy or a large pulmonary
be sure that it is the correct patient’s film. The film artery will cause hilar enlargement.
markings also indicate the projection and patient Heart
position. The standard frontal film is taken by a The heart shape is ovoid with the apex pointing to the
posteroanterior (PA; back to front) projection of left. Characteristically, about two-thirds of the heart
an erect patient. Anteroposterior (AP) and supine projects to the left of the spine.
films are only second-best. On a supine film there The right heart border is formed by the outer
is distension of all the posterior (gravity-dependent) border of the right atrium, and the left heart border by
vessels and thus the lung fields appear more plethoric. the left ventricle. The left margin of the right ventricle
A small pleural effusion may not be visible if it is lies about a thumb’s breadth in from the left heart
lying posteriorly, and the heart often appears large border. (On the surface of the heart, this is marked by
on a supine film. the left anterior descending coronary artery.)
Centring The cardiothoracic diameter is a rather approxi-
The medial ends of the clavicles should be equidistant mate way of determining whether the heart is
from the midline spinous processes. If the patient is enlarged. If the heart size is more than 50% of the
rotated, this will accentuate the hilum that is turned transthoracic diameter, enlargement may be present.
forwards. Apparent slight cardiac enlargement can occur
Exposure because of a relatively small AP diameter of the chest.
The quality of the film is important. There should be A cardiothoracic ratio at the upper limit of normal
enough X-ray penetration for the spine to be just seen should not cause alarm if the patient has no reason to
have cardiac failure and no symptoms of it.
through the mediastinum, otherwise the film will be
Valve calcification, if present, is better seen on the
too white. With good radiographic technique, the
lateral view. On the frontal view, valve calcification
scapulae are projected outside the lung fields.
cannot be visualised over the spine.
The film needs to be exposed on full inspiration
Diaphragm
so that there is no basal crowding of the pulmonary
vessels and so that estimation of the cardiothoracic The hemidiaphragms visualised on the frontal films
ratio is accurate. On full inspiration, the diaphragm are the top of the domes seen tangentially. Much lung
lies at the level of the tenth or eleventh rib posteriorly in the posterior costophrenic angles is not seen on
or at the level of the sixth costal cartilage anteriorly. the frontal film.
The right hemidiaphragm usually lies about 2 cm If the hemidiaphragms are low and flat, emphy-
higher than the left. sema may be present. A critical look must be
made beneath the diaphragm to see if there is free
Correct orientation
peritoneal gas.
Do not miss dextrocardia—the heart apex will be to Lung fields
the right and the stomach gas to the left. Do not be
On the frontal field, it is convenient to divide the
misled by left or right markers wrongly placed by a
lung fields into zones. It is easy then to compare
radiographer.
one zone with another for density differences and
Systematic film interpretation the distribution of the vascular ‘markings’.
Mediastinum The apices lie above the level of the clavicles. The
The trachea should lie in the midline. It may be upper zones include the apices and pass down to
deviated by a goitre or mediastinal mass. It is the level of the second costal cartilages. The mid-
normally deviated a little to the left as it passes the zones lie between the second and fourth costal
aortic knuckle. (The aortic arch becomes wider and cartilage levels. The lower zones lie between the
unfolded with age because of loss of elasticity.) fourth and sixth costal cartilages.
The mediastinum, including the trachea, can The radiolucency of the lung fields is due to the
be deviated by a large pleural effusion, a tension air filling the lung. The ‘greyness’ is due to blood in
pneumothorax or pulmonary collapse. the pulmonary vessels.
Rotation of the patient may make the medias- The upper zones of the lungs are normally less
tinum appear distorted. well perfused, resulting in smaller blood vessels. With
raised left atrial pressure, there is upper zone blood The retrocardiac region should be looked at
diversion and the vessels are congested. again. A collapsed left lower lobe will reveal itself as
An increase in lung radiolucency occurs a triangular opacity behind the heart shadow.
with pulmonary vessel loss, as also happens with Both apices should be rechecked for lesions,
emphysema. Lung radiolucency is lost with an especially Pancoast’s tumours or tuberculosis.
effusion or consolidation. Has the patient a pneumothorax? There will be a
Terms such as ‘opacity’, ‘consolidation’ and ‘patchy difference between the translucency of the two lungs.
shadowing’ are used to describe the lung fields. It
is usually unwise to attempt to make too precise a Lateral film
diagnosis of the underlying pathology. The lateral view is used largely for localisation of an
The lungs are divided into lobes by reflections of already visible lesion on the frontal film. Examine it
the visceral pleura. The right lung is composed of the just as carefully. Sometimes a lesion is seen only on
upper, middle and lower lobes. On the left, there are the lateral view. If there is clinical evidence of heart or
only the upper and lower lobes. lung disease, frontal and lateral views should always
The right upper lobe has three segments: anterior, be obtained.
posterior and apical. The right middle lobe has a Points to remember: (1) the retrosternal and
lateral and medial segment. Apical, medial basal, retrocardiac triangles are normally of a similar
lateral basal, anterior basal and posterior basal radiodensity; (2) the thoracic vertebrae become
segments compose the lower lobe. less opaque lower down the spine, unless there is
There are three differences in the segmental pulmonary or pleural disease; and (3) the posterior
anatomy of the left lung (see Figure 12.3, page 165). costophrenic angle is sharp unless there is fluid or
The left upper lobe has four segments: an apico- adjacent consolidation.
posterior, an anterior and two lingular segments. The hemidiaphragms are well defined unless
The superior and inferior lingular segments are the there is pleural or pulmonary disease.
equivalent of the right middle lobe. The left lower The oblique fissure placement is ‘4 to 4’. It passes
lobe has four segments: it does not contain a medial from approximately 4 cm behind the anterior
basal segment. costophrenic angle through the hilum to the T4
The fissures are seen as hairline shadows. The vertebral body level.
horizontal fissure is at the level of the right fourth Heart
costal cartilage. The oblique fissures are not seen on The right ventricle forms the anterior heart border
the frontal view. on the lateral film. The left atrium forms the upper
Bones and soft tissue posterior border.
Nipple shadows are often seen over the lower zones Mitral valve calcification is seen below an
and are about 5 mm in diameter. They can be confused imaginary line drawn from the anterior costophrenic
with a ‘coin’ lesion. In such a case, nipple markers may angle to the hilum, whereas aortic valve calcification
be helpful. lies above this line.

Look carefully for a missing breast shadow in
Examples of chest X-rays in cardiac disease
a female patient. A mastectomy may provide a
The radiological changes seen in pulmonary venous
diagnostic clue to explain bony or pulmonary
congestion, interstitial pulmonary oedema and
metastases, or upper zone post-radiation fibrosis.
alveolar pulmonary oedema are shown in Figures 8.3
Soft-tissue gas may accompany a pneumothorax
to 8.5, respectively. Mitral valve disease is shown in
or be present after a thoracotomy.
Figure 8.6 , while a ventricular aneurysm is seen
Calcified tuberculous glands in the neck should be
in Figure 8.7 . The characteristic notching of the
looked for in patients with lung scarring or calcified
inferior aspects of the ribs, due to hypertrophy
hilar lymph nodes.
of the intercostal arteries, appears in Figure 8.8 ,
Check that there are no rib fractures or space-
while the pulmonary plethora that is characteristic
occupying lesions. Look for rib notching, due to of a left-to-right shunt is obvious in Figure 8.9 .
increased blood flow through intercostal vessels Marfan’s syndrome is illustrated in Figure 8.10 ;
(e.g. coarctation of the aorta). Cervical ribs or and a pacemaker and defibrillators are shown in
thoracic scoliosis should be noted. Erosions or Figure 8.11.
arthritis around the shoulder joints should be
looked for.
Review THE ECHOCARDIOGRAM
Certain parts of the film should be double-checked if Echocardiography is now an essential and basic part
the radiograph appears normal. of cardiac assessment and can be performed at the
Figure 8.3 Pulmonary venous congestion

The heart is enlarged due to failure. This failure is
not severe enough to cause pulmonary oedema.
However, the increased pulmonary venous pressure
has caused upper zone blood diversion so that the
vessels above the hilum appear wider than those
below. (The mechanism of the blood diversion is not
fully understood.) These changes are seen when the
pulmonary venous pressure is about 15 to 20 mmHg.
The cardiothoracic ratio A + B is a useful indicator
of cardiac enlargement if it is greater than 50%. The
thoracic measurement (T) is the widest diameter above
the costophrenic angles, usually at the level of the right
hemidiaphragm. The cardiac diameter is the addition
of the two widths A and B.
Figure 8.4 Interstitial pulmonary oedema

The heart is moderately enlarged. The interstitial
oedema causes fine, diffuse shadowing in the lung
fields with blurring of the vessel margins. The escape
of fluid into the interstitial tissue occurs when the
capillary pressure exceeds the plasma osmotic
pressure of 25 mmHg.
The interstitial oedema is characterised by Kerley ‘B’
lines, which are oedematous interlobular septa. They
are best seen peripherally in the right costophrenic
angle (arrow), where they lie horizontally, and are about
1 cm long. They contain the engorged lymphatics,
which were originally thought by Kerley to be the sole
cause of the ‘B’ lines.
Sternal sutures are present from previous cardiac
surgery.
Figure 8.5 Alveolar pulmonary oedema

When the pulmonary venous pressure reaches
30 mmHg, oedema fluid will pass into the alveoli. This
causes shadowing (patchy to confluent depending on
the extent) in the lung fields. This usually occurs first
around the hila and gives a bat’s wing appearance.
These changes are usually superimposed on the
interstitial oedema.
A lamellar pleural effusion (arrow) is seen at the right
costophrenic angle where Kerley ‘B’ lines are also
evident.
a b
Figure 8.6 Mitral valve disease

The left atrium enlarges because of the pressure and volume load. It bulges posteriorly and to both sides (arrows). The atrial
appendage bulges out below the left hilum. The prominent right border of the atrium causes the ‘double right heart border’
appearance.
To distinguish the valves if calcification is present, draw imaginary lines. On the PA view (a) the line passes from the right
cardiophrenic angle to the inferior aspect of the left hilum. The line on the lateral view (b) passes from the antero-inferior
angle through the midpoint of the hilum. The aortic valve lies above this line whereas the mitral valve lies below it.
Figure 8.7 Ventricular aneurysm

There is a bulge of the left cardiac border (arrow), which indicates
an aneurysm of the left ventricular wall. The most common cause
is weakness following myocardial infarction.
Figure 8.8 Aortic coarctation

The classical sign in aortic coarctation is notching of the inferior
aspects of the ribs (arrow on left). This is due to hypertrophy of
the intercostal arteries in which retrograde flow from the axillary
collaterals is taking blood back to the descending aorta.
Because of the increased resistance to the left heart flow,
left ventricular hypertrophy and then failure can occur. Failure
causing cardiac enlargement has not yet occurred in this
patient. The arrow on the right indicates a smaller than normal
aortic knuckle.
Figure 8.9 Atrial septal defect (ASD)

The most important thing to recognise is that there is
pulmonary plethora indicating a left-to-right shunt. Left-to-right
shunts occur in ASD, ventricular septal defect (VSD) and patent
ductus arteriosus (PDA).
The shunted flow causes enlargement of the main pulmonary
artery and its branches. The right hilum is enlarged because of
the very dilated right pulmonary artery. The left hilum is hidden
by the very dilated main pulmonary artery (arrow).
The ascending aorta is small (in contrast to its enlargement in
PDA). The left atrium and ventricle are not enlarged, as they are
in VSD and PDA.
Figure 8.10 Marfan’s syndrome

The mediastinum is widened by uniform dilation of the
ascending aorta, the aortic arch and the descending aorta.
This patient had Marfan’s syndrome. Dissecting aneurysms
can also occur and have a similar appearance.
Figure 8.11 Pacemaker and defibrillators

(From Baker T, Nikolić G, O’Connor S, Practical cardiology, 2nd edn. © 2008, Sydney: Elsevier Australia.)
bedside. It does not expose the patient to radiation.

Small hand-held models are available that can be
used almost as readily as a stethoscope. Although
these devices will result in the temptation not to
bother listening to the heart, any test used without
an adequate history and examination is likely to be
misleading.
Most echocardiographic studies involve four
modalities:
● In M mode, detailed information is
provided from a single line of ultrasound.
It is used to study motion in detail and to
make measurements of chamber sizes (see
Figures 8.12, 8.13 and 8.14).
● In two-dimensional or sector scanning, Figure 8.13 M mode echo from a 34-year-old man with
ultrasound information is assembled into a two months of increasing dyspnoea, diagnosed initially as
moving picture that shows the relationship asthma. The left ventricle is very dilated. The end-diastolic
between different areas of the heart in a series dimension is 70 mm (<57). The fractional shortening is only
of two-dimensional slices (see Figures 8.15 and 14% (>25–27). Contraction of the septum and posterior
wall are equally reduced, typical of dilated cardiomyopathy
8.16 below). This gives information about valve (page 110).
appearance, cardiac function and the presence of (From Baker T, Nikolić G, O’Connor S, Practical cardiology,
congenital abnormalities. 2nd edn. © 2008, Sydney: Elsevier Australia.)
● In continuous and pulsed wave Doppler,
interrogation of the returning ultrasound
signal enables calculation of the Doppler shift
caused by reflection of the beam from moving
columns of blood. This means that the velocity
and direction of blood flow from different parts
of the heart can be measured. The Doppler
signal can be displayed as a velocity wave.
By superimposing the Doppler callipers on the
two-dimensional image, the echocardiographer
is able to measure the velocity of jets of blood
from a particular area (e.g. in the ascending
Figure 8.14 M-mode measurements in a patient with

hypertension. There is symmetrical thickening of the left
ventricular wall.
(From Baker T, Nikolić G, O’Connor S, Practical cardiology,
2nd edn. © 2008, Sydney: Elsevier Australia.)
aorta just beyond the aortic valve cusps; see

Figure 8.17).
● In colour flow mapping, it is possible for echo
machines to solve the Doppler equations for
sectors of the two-dimensional scan in real time,
assign a colour code depending on the direction
Figure 8.12 Normal long-axis M mode measurements and velocity of flow and superimpose this on the
Both the fractional shortening (change in the dimensions
between systole and diastole; normally >27%) and the
two-dimensional image. In this way, flow within
ejection fraction have been calculated. the heart is visible in relation to the anatomy
(From Baker T, Nikolić G, O’Connor S, Practical cardiology, and abnormal jets of blood can be more easily
2nd edn. © 2008, Sydney: Elsevier Australia.) detected (see Figure 8.18).
Figure 8.15 Normal long-axis view of the heart

The mitral valve leaflets can be seen wide open in this
diastolic frame. The apex of the heart is on the left and the
right ventricle is at the top of the picture.
Figure 8.17 (a) Four-chamber view of a patient with

prolapse of both mitral valve leaflets. This systolic frame
shows the closed mitral leaflets (anterior on the left) bowing
back into the left atrium as they face the full force of left
ventricular systole.
(b) Four-chamber view of a 50-year-old woman with a
middle and late systolic murmur. A brightly coloured (high-
velocity) jet is seen in this systolic frame, extending from the
Figure 8.16 Normal four-chamber view of the heart. The
centre of the mitral valve well back into the left atrium.
left atrium and ventricle are on the right side of the picture.
The AV (mitral and tricuspid) valves are closed in this (From Baker T, Nikolić G, O’Connor S, Practical cardiology,
systolic frame.
Information commonly available from an

echocardiogram
1. Structural and functional measurements.
Assessment of left ventricular function by echo
involves measurement of the left ventricular
end-diastolic dimension (normally less than
about 57 mm) and the end-systolic dimension.
Figure 8.12 shows echo views of the heart in the
long axis. It shows some of the measurements
and structures that can be assessed in this
standard view.
The echo also allows the left ventricle to be Figure 8.18 Colour Doppler showing a jet of mitral
examined for areas of segmental hypokinesis regurgitation extending from the valve back into the left
(reduced wall motion) the presence of which atrium.
suggests previous infarction as the cause of the

cardiac failure. Figure 8.16 shows the structures
seen in the four-chamber view of the heart. Here
the echo transducer scans the heart from the
position of the apex beat.
2. Blood flow measurements.
Sector scanning and M mode pictures can
provide information about valve morphology,
for example thickening or prolapse of the
leaflets (see Figure 8.17). Doppler echo can
reveal abnormal jets of blood, for example
regurgitant jets, and measure flow velocity
across valves. This measurement can be used
to estimate the valve gradient (the difference in
pressure across the valve). Figure 8.20 Aortic regurgitation
3. Mitral regurgitation and mitral valve (From Baker T, Nikolić G, O’Connor S, Practical cardiology,
2nd edn. Sydney: Churchill Livingstone, 2008, with permission.)
prolapse. Here the mitral valve may appear
abnormal and abnormal coaptation of the
leaflets may be visible (see Figure 8.17). ventricle may be used as an indication of
4. Aortic stenosis. Thickening and calcification severity. Doppler interrogation will show the
(bright echoes) of the aortic valve are usually regurgitant jet for a variable distance into the
visible (see Figure 8.19). The movement of the left ventricle.
valve cusps may appear reduced. The anatomy 6. Tricuspid regurgitation. This is more often
of the valve may be apparent. Doppler secondary to abnormalities of right ventricular
interrogation of the jet of blood in the ascending function or to raised RV pressure than to
aorta will enable its velocity to be measured. primary tricuspid valve disease. The valve will
A simple formula enables estimation of the appear normal. Doppler interrogation will show
pressure gradient to be made from this a jet of blood in the right atrium.
measurement. 7. Hypertrophic cardiomyopathy. Certain
5. Aortic regurgitation. The valve may look anatomical abnormalities are characteristic of
thickened or occasionally a cusp may be seen to this condition (see Figure 8.21). There is
prolapse (see Figure 8.20). The aortic root size asymmetrical septal hypertrophy (ASH). The
may be increased, especially if this is the cause normal interventricular septum measures up to
of the aortic regurgitation. Left ventricular 11 mm in thickness. This may be considerably
dilation is often present and the size of the increased to 40 mm or even more. Doppler
interrogation may reveal a gradient in the left
ventricular outflow tract or mitral

regurgitation, or both.
8. Ventricular septal defect. The defect may be
visible in the muscular or membranous septum.
The diameter of the opening can be measured.
Indirect measurements of the effect of the defect
include signs of RV dilation caused by left to
right shunting.
Doppler interrogation, especially with colour
mapping, will usually show left-to-right
shunting across the septum, even if the defect
itself is not visible. Measurement of the velocity
of this jet gives an indication of right ventricular
pressures. If the gradient across the defect is
large, RV pressure must be much lower than LV
pressure, as is normal. A large ventricular septal
Figure 8.19 Short-axis view of the aortic valve in a
patient with severe aortic stenosis. The valve cusps are
defect may cause pulmonary hypertension and
heavily calcified. elevation of RV pressures.
(From Baker T, Nikolić G, O’Connor S, Practical cardiology, 9. Atrial septal defect. The atrial septum can often
2nd edn. Sydney: Churchill Livingstone, 2008, with permission.) be seen well enough to reveal a defect, although
this is sometimes difficult. There may be

indirect indications of left-to-right shunting at
the atrial level, including enlargement of the
right ventricle and abnormal motion of the
interventricular septum.
Doppler interrogation may show shunting
across the defect. If there is doubt, a
transoesophageal echo may be needed for
accurate definition of the anatomy of the atrial
septum.
10. Patent ductus arteriosus. The main
pulmonary artery will appear large. The ductus
a itself may be visible. Doppler interrogation
reveals continuous flow in the main
pulmonary artery at the point where the duct
empties.
T&O’C essentials
1. Chest X-ray, ECG and echocardiography are

extensions of the cardiovascular examination.
2. ECGs and echocardiograms lead to no radiation
exposure and can be repeated as required.
3. Students need to have an approach to
interpreting chest X-rays and ECGs and an
understanding of the information that can be
obtained from an echocardiogram.
b 4. The initial diagnosis of myocardial infarction
should be based on the history, physical
Figure 8.21 (a) and (b) Hypertrophic cardiomyopathy examination and ECG and should not be delayed
(From Baker T, Nikolić G, O’Connor S, Practical cardiology, until blood test results are to hand.
2nd edn. Sydney: Churchill Livingstone, 2008, with permission.)
SECTION
3
The respiratory
system
Chapter 9 The respiratory history
Chapter 10 The respiratory

examination
Chapter 11 Correlation of physical

signs and respiratory

disease
Chapter 12 A summary of the

respiratory examination
and extending the
respiratory examination
This page intentionally left blank
CHAPTER
The respiratory history
9
A medical chest specialist is long winded Questions box 9.1
about the short winded.
Questions to ask the patient with a cough
Kenneth T Bird (b.1917)
! denotes symptoms for the possible diagnosis of
an urgent or dangerous problem.
1. How long have you had the cough?
2. Do you cough up anything? What? How much?
Presenting symptoms 3. Have you had sinus problems?
(see List 9.1) ! 4. Is the sputum clear or discoloured? Is there any
blood in the sputum?
5. Have you had high temperatures?
LIST 9.1 Presenting symptoms 6. Does coughing occur particularly at night (acid
reflux)?
Major symptoms
7. Have you become short of breath?
Cough
8. Have you had lung problems in the past?
Sputum
9. Have you been a smoker? Do you still smoke?
Haemoptysis
10. Have you noticed wheezing? (Asthma, chronic
Dyspnoea (acute, progressive or paroxysmal)
obstructive pulmonary disease [COPD])?
Wheeze
11. Do you take any tablets? (e.g. ACE inhibitors)
Chest pain
Fever
Hoarseness
Night sweats A differential diagnosis of cough based on its
character is shown in Table 9.1 and on its duration is
shown in List 9.2.
A cough associated with a postnasal drip or sinus

COUGH AND SPUTUM congestion or headaches may be due to the upper
Cough is a common presenting respiratory symptom. airway cough syndrome, which is the single most
It occurs when deep inspiration is followed by common cause of chronic cough. Although patients
explosive expiration. Flow rates of air in the trachea with this problem often complain of a cough, when
approach the speed of sound during a forceful asked to demonstrate their cough they do not cough
cough. Coughing enables the airways to be cleared
but clear the throat. This annoys chest doctors (who
of secretions and foreign bodies.
feel their time is valuable) intensely.
The duration of a cough is important (see
Questions box 9.1). Find out when the cough An irritating, chronic dry cough can result from
first became a problem. A cough of recent origin, oesophageal reflux and acid irritation of the lungs.
particularly if associated with fever and other There is some controversy about these as causes of
symptoms of respiratory tract infection, may be true cough. A similar dry cough may be a feature
due to acute bronchitis or pneumonia. A chronic of late interstitial lung disease or associated with
cough (of more than 8 weeks duration) associated the use of the angiotensin-converting enzyme
with wheezing may be due to asthma; sometimes (ACE) inhibitors—drugs used in the treatment of
asthma can present with just cough alone. A change hypertension and cardiac failure. Cough that wakes
in the character of a chronic cough may indicate a patient from sleep may be a symptom of cardiac
the development of a new and serious underlying failure or of the reflux of acid from the oesophagus
problem (e.g. infection or lung cancer). into the lungs that can occur when a person lies down.
129
130 SECTION 3 The respiratory system
TABLE 9.1 Differential diagnosis of cough based on its character

Origin Character Causes
Nasopharynx/larynx Throat clearing, chronic Postnasal drip, acid reflux
Larynx Barking, painful, acute or persistent Laryngitis, pertussis (whooping cough), croup
Trachea Acute, painful Tracheitis
Bronchi Intermittent, sometimes productive, worse Asthma
at night
Worse in morning Chronic obstructive pulmonary disease
(COPD)
With blood Bronchial malignancy
Lung parenchyma Dry then productive Pneumonia
Chronic, very productive Bronchiectasis
Productive, with blood Tuberculosis
Irritating and dry, persistent Interstitial lung disease
Worse on lying down, sometimes with frothy Pulmonary oedema
sputum
ACE inhibitors Dry, scratchy, persistent Medication-induced
LIST 9.2 Differential diagnosis of cough based

of the epiglottis may have a muffled quality and
on its duration cough related to viral croup is often described as
‘barking’. Cough caused by tracheal compression by
Acute cough (<3 weeks duration): differential a tumour may be loud and brassy. Cough associated
diagnosis with recurrent laryngeal nerve palsy has a hollow
Upper respiratory tract infection
• Common cold, sinusitis sound because the vocal cords are unable to close
Lower respiratory tract infection completely; this has been described as a bovine
• Pneumonia, bronchitis, exacerbation of COPD cough. A cough that is worse at night is suggestive of
• Irritation—inhalation of bronchial irritant asthma or heart failure, while coughing that comes
(e.g. smoke or fumes) on immediately after eating or drinking may be due
Chronic cough: differential diagnosis and clues to incoordinate swallowing or oesophageal reflux or,
COPD—smoking history rarely, a tracheo-oesophageal fistula.
Asthma—wheeze, relief with bronchodilators It is an important (though perhaps a somewhat
Gastro-oesophageal reflux—occurs when lying unpleasant task) to enquire about the type of sputum
down, burning central chest pain
Upper airway cough syndrome—history of rhinitis,
produced and then to look at it, if it is available. Be
postnasal drip, sinus headache and congestion warned that some patients have more interest in their
Bronchiectasis—chronic, very productive sputum than others and may go into more detail
ACE inhibitor medication—drug history than you really want. A large volume of purulent
Carcinoma of the lung—smoking, haemoptysis (yellow or green) sputum suggests the diagnosis of
Cardiac failure—dyspnoea, PND
Psychogenic—variable, prolonged symptoms,
bronchiectasis or lobar pneumonia. Foul-smelling
usually mild dark-coloured sputum may indicate the presence
of a lung abscess with anaerobic organisms. Pink
ACE = angiotensin-converting enzyme; COPD = chronic obstructive frothy secretions from the trachea, which occur in
pulmonary disease; PND = paroxysmal nocturnal dyspnoea.
pulmonary oedema, should not be confused with
sputum. It is best to rely on the patient’s assessment
of the taste of the sputum, which, not unexpectedly, is
A chronic cough that is productive of large volumes
of purulent sputum may be due to bronchiectasis. foul in conditions like bronchiectasis or lung abscess.
Some patients feel the need to cough after an
ectopic heartbeat. There may be an associated HAEMOPTYSIS
sensation of a missed heartbeat. Haemoptysis (coughing up of blood) can be a
Patients’ descriptions of their cough may be helpful. sinister sign of lung disease (see Table 9.2) and must
In children, a cough associated with inflammation always be investigated. It must be distinguished
CHAPTER 9 The respiratory history 131
TABLE 9.2Causes (differential diagnosis) of TABLE 9.3 Features distinguishing

haemoptysis and typical histories haemoptysis from haematemesis and
nasopharyngeal bleeding
Respiratory
Bronchitis Small amounts of blood with Favours
sputum Favours Favours nasopharyngeal
haemoptysis haematemesis bleeding
Bronchial carcinoma Frank blood, history of
smoking, hoarseness Mixed with Follows nausea Blood appears
sputum in mouth
Bronchiectasis Large amounts of sputum
with blood Occurs Mixed with
immediately vomitus;
Pneumonia Fever, recent onset of after coughing follows dry
symptoms, dyspnoea retching
(The above four account for about 80% of cases)
Pulmonary infarction Pleuritic chest pain, dyspnoea be due to respiratory or cardiac disease, or lack
Cystic fibrosis Recurrent infections of physical fitness or sometimes to anxiety (see
List 9.3). Careful questioning about the timing of
Lung abscess Fever, purulent sputum
onset, severity and pattern of dyspnoea is helpful
Tuberculosis (TB) Previous TB, contact with TB, in making the diagnosis (see Questions box 9.2 and
HIV-positive status
List 9.4).1 The patient may be aware of this only on
Foreign body History of inhalation, cough, heavy exertion or have much more limited exercise
stridor tolerance. Dyspnoea can be graded from I to IV based
Goodpasture’s* Pulmonary haemorrhage, on the New York Heart Association classification:
syndrome glomerulonephritis, antibody Class I Disease present but no dyspnoea or
to basement membrane dyspnoea only on heavy exertion.
antigens
Class II Dyspnoea on moderate exertion.
Wegener’s History of sinusitis, saddle- Class III Dyspnoea on minimal exertion.
granulomatosis nose deformity
Class IV Dyspnoea at rest.
Systemic lupus Pulmonary haemorrhage, It is more useful, however, to determine the amount
erythematosus multisystem involvement of exertion that actually causes dyspnoea—that is, the
Rupture of a mucosal History of severe cough distance walked or the number of steps climbed.
blood vessel after preceding haemoptysis The association of dyspnoea with wheeze suggests
vigorous coughing
airways disease, which may be due to asthma or
Cardiovascular chronic obstructive pulmonary disease (COPD; see
Mitral stenosis (severe) List 9.5). The duration and variability of the dyspnoea
are important. Dyspnoea that worsens progressively
Acute left ventricular failure

over a period of weeks, months or years may be due
Bleeding diatheses to interstitial lung disease (ILD). Dyspnoea of more
Note: Exclude spurious causes, such as nasal bleeding or rapid onset may be due to an acute respiratory infection
haematemesis.
*Ernest W Goodpasture (1886–1960), pathologist at Johns
(including bronchopneumonia or lobar pneumonia)
Hopkins, Baltimore. He described this syndrome in 1919. or to pneumonitis (which may be infective or
secondary to a hypersensitivity reaction). Dyspnoea
that varies from day to day or even from hour to
from haematemesis (vomiting of blood) and from hour suggests a diagnosis of asthma. Dyspnoea of
nasopharyngeal bleeding (see Table 9.3). very rapid onset associated with sharp chest pain
Ask how much blood has been produced. Mild suggests a pneumothorax (see List 9.6). Dyspnoea
haemoptysis usually means less than 20 mL in that is described by the patient as inability to take a
24 hours. It appears as streaks of blood discolouring breath big enough to fill the lungs and associated with
sputum. Massive haemoptysis is more than 250 mL sighing suggests anxiety. Dyspnoea that occurs on
of blood in 24 hours and represents a medical moderate exertion may be due to the combination of
emergency. Its most common causes are carcinoma, obesity and a lack of physical fitness (‘deconditioning’;
cystic fibrosis, bronchiectasis and tuberculosis. a not uncommon occurrence).
BREATHLESSNESS (DYSPNOEA) WHEEZE

The awareness that an abnormal amount of effort A number of conditions can cause a continuous
is required for breathing is called dyspnoea. It can whistling noise that comes from the chest (rather
LIST 9.3 Causes of dyspnoea Questions box 9.2
Respiratory Questions to ask the breathless patient

1. Airways disease ! denotes symptoms for the possible diagnosis of
Chronic bronchitis and emphysema (chronic an urgent or dangerous problem.
obstructive pulmonary disease [COPD]) 1. How long have you been short of breath? Has it
Asthma come on quickly?
Bronchiectasis 2. How much exercise can you do before your
Cystic fibrosis shortness of breath stops you or slows you
Laryngeal or pharyngeal tumour down? Can you walk up a flight of stairs?
Bilateral cord palsy ! 3. Have you been woken at night by breathlessness
Tracheal obstruction or stenosis or had to sleep sitting up? (Paroxysmal nocturnal
Tracheomalacia dyspnoea [PND], orthopnoea)
Cricoarytenoid rheumatoid arthritis 4. Have you had heart or lung problems in the
2. Parenchymal disease past?
Interstitial lung diseases (diffuse parenchymal lung ! 5. Have you had a temperature?
diseases, e.g. idiopathic pulmonary fibrosis, 6. Do you smoke?
sarcoidosis, connective tissue disease, inorganic or ! 7. Is there a feeling of tightness in the chest when
organic dusts) you feel breathless? (Angina)
Diffuse infections 8. Do you get wheezy in the chest? Cough?
Acute respiratory distress syndrome (ARDS) 9. Is the feeling really one of difficulty getting a
Infiltrative and metastatic tumour satisfying breath? (Anxiety)
Pneumothorax 10. Is it painful to take a big breath? (Pleurisy or
Pneumoconiosis pericarditis)
3. Pulmonary circulation !11. Did the shortness of breath come on very quickly
Pulmonary embolism or instantaneously? (Pulmonary embolus [very
Chronic thromboembolic pulmonary hypertension quick onset] or pneumothorax [instantaneous
Pulmonary arteriovenous malformation onset])
Pulmonary arteritis 12. Are you often short of breath when you are
4. Chest wall and pleura anxious? Do you feel numbness and tingling
Effusion or massive ascites around your lips when you are breathless?
Pleural tumour (Hyperventilation associated with anxiety)
Fractured ribs
Ankylosing spondylitis
Kyphoscoliosis
Neuromuscular diseases
Bilateral diaphragmatic paralysis
Cardiac LIST 9.4 Differential diagnosis of dyspnoea

based on time course of onset
Left ventricular failure
Mitral valve disease Seconds to minutes—favours:

Cardiomyopathy Asthma
Pericardial effusion or constrictive pericarditis Pulmonary embolism
Intra-cardiac shunt Pneumothorax
Pulmonary oedema
Anaemia
Anaphylaxis
Non-cardiorespiratory Foreign body causing airway obstruction
Psychogenic
Hours or days—favours:
Acidosis (compensatory respiratory alkalosis)
Exacerbation of chronic obstructive pulmonary
Hypothalamic lesions
disease (COPD)
Cardiac failure
Asthma
Respiratory infection
Pleural effusion
than the throat) during breathing. These include Metabolic acidosis
asthma or COPD, infections such as bronchiolitis
and airways obstruction by a foreign body or tumour. Weeks or longer—favours:
Wheeze is usually maximal during expiration and is Pulmonary fibrosis
accompanied by prolonged expiration. This must be COPD
differentiated from stridor (see below), which can Interstitial lung disease
Pleural effusion
have a similar sound, but is loudest over the trachea Anaemia
and occurs during inspiration.
LIST 9.5 Characteristics of chronic obstructive pain and dyspnoea begin. Viral pneumonia is often
pulmonary disease (COPD) preceded by a longer (days) prodromal illness.
Patients may occasionally present with episodes of
History fever at night. Tuberculosis, pneumonia and lymph-
History of smoking oma should always be considered in these cases.
Breathlessness and wheeze
Occasionally, patients with tuberculosis present with
Examination episodes of drenching sweating at night.
Increased respiratory rate Hoarseness or dysphonia (an abnormality of the
Pursed-lips breathing voice) may sometimes be considered a respiratory
Cyanosis system symptom. It can be due to transient inflam-
Leaning forwards—arms on knees mation of the vocal cords (laryngitis), vocal cord
Intercostal and supraclavicular in-drawing
tumour or recurrent laryngeal nerve palsy.
Hoover’s sign
Tracheal tug Sleep apnoea is an abnormal increase in the
periodic cessation of breathing during sleep. Patients
with obstructive sleep apnoea (OSA, where airflow
LIST 9.6 Differential diagnosis of dyspnoea of stops during sleep for periods of at least 10 seconds
sudden onset based on other features and sometimes for more than 2 minutes, despite
persistent respiratory efforts) typically present with
Presence of pleuritic chest pain—favours: daytime somnolence, chronic fatigue, morning head-
Pneumothorax, pleurisy/pneumonia aches and personality disturbances. Very loud snoring
Pulmonary embolism
may be reported by anyone within earshot. These
Trauma
patients are often obese and hypertensive. The Epworth
Absence of chest pain—favours: sleepiness scale is a way of quantifying the severity of
Pulmonary oedema sleep apnoea (see List 9.7). Patients with central sleep
Metabolic acidosis apnoea (where there is cessation of inspiratory muscle
Pulmonary embolism activity) may also present with somnolence but do not
Presence of central chest pain—favours: snore excessively (see Table 9.4).
Myocardial infarction and cardiac failure Some patients respond to anxiety by increasing
Large pulmonary embolism the rate and depth of their breathing. This is called
hyperventilation. The result is an increase in CO2
Presence of cough and wheeze—favours: excretion and the development of alkalosis—a rise in
Asthma the pH of the blood. These patients may complain of
Bronchial irritant inhalation
Chronic obstructive pulmonary disease (COPD) variable dyspnoea; they have more difficulty breathing
in than out. The alkalosis results in paraesthesias of
the fingers and around the mouth, light-headedness,
CHEST PAIN chest pain and a feeling of impending collapse.
Chest pain due to respiratory disease is usually

different from that associated with myocardial
ischaemia (page 95). The pleura and central airways LIST 9.7 The Epworth sleepiness scale
have pain fibres and may be the source of respiratory ‘How easily would you fall asleep in the following
pain. Pleural pain is characteristically pleuritic in circumstances?’*
nature: sharp and made worse by deep inspiration 0 = never
and coughing. It is typically localised to one area 1 = slight chance
of the chest. It may be of sudden onset in patients 2 = moderate chance
with lobar pneumonia, pulmonary embolism and 3 = high chance
• Sitting reading
infarction or pneumothorax, and is often associated • Watching television
with dyspnoea. The sudden onset of pleuritic • At a meeting or at the theatre
chest pain and dyspnoea is an urgent diagnostic • As a passenger in a car on a drive of more than
problem, as all three of these conditions may be an hour
life-threatening if not treated promptly. • Lying down in the afternoon to rest
• Sitting talking to someone
• Sitting quietly after lunch (no alcohol)
Other presenting symptoms • When driving and stopped at traffic lights
Bacterial pneumonia is an acute illness in which
*A normal score is between 0 and 9. Severe sleep apnoea scores
prodromal symptoms (fever, malaise and myalgia) from 11 to 20.
occur for a short period (hours) before pleuritic
TABLE 9.4 Abnormal patterns of breathing

Type of breathing Cause(s)
1. Sleep apnoea—cessation of airflow for more than 10 seconds more than Obstructive (e.g. obesity with upper
10 times a night during sleep airway narrowing, enlarged tonsils,
pharyngeal soft-tissue changes in
acromegaly or hypothyroidism)
2. Cheyne-Stokes* breathing—periods of apnoea (associated with reduced Left ventricular failure
level of consciousness) alternate with periods of hyperpnoea (lasts 30 s Brain damage (e.g. trauma, cerebral
on average and is associated with agitation); this is due to a delay in the haemorrhage)
medullary chemoreceptor response to blood gas changes High altitude
3. Kussmaul’s breathing (air hunger)—deep, rapid respiration due to Metabolic acidosis (e.g. diabetes
stimulation of the respiratory centre mellitus, chronic renal failure)
4. Hyperventilation, which results in alkalosis and tetany and peri-oral Anxiety
paraesthesias
5. Ataxic (Biot†) breathing—irregular in timing and depth Brainstem damage
6. Apneustic breathing—a post-inspiratory pause in breathing Brain (pontine) damage
7. Paradoxical respiration—the abdomen sucks inwards with inspiration Diaphragmatic paralysis
(it normally pouches outwards due to diaphragmatic descent)
*John Cheyne (1777–1836), Scottish physician who worked in Dublin, described this in 1818. William Stokes (1804–1878), Irish
physician, described it in 1854.
†
Camille Biot (1878–1936), French physician.
LIST 9.8 Drugs and the lungs

Treatment
It is important to find out what drugs the patient Cough
ACE inhibitors
is using (see List 9.8), how often they are taken Beta-blockers
and whether they are inhaled or swallowed. The
patient’s previous and current medications may give Wheeze
a clue to the current diagnosis. Bronchodilators Beta-blockers
and inhaled steroids are prescribed for COPD and Aspirin (aspirin sensitivity)
Other non-steroidal anti-inflammatory drugs
asthma. A patient’s increased use of bronchodilators
(NSAIDs)
suggests poor control of asthma and the need for Tamoxifen, dipyridamole (idiosyncratic)
review of treatment. Chronic respiratory disease, Morphine sulfate
including sarcoidosis, hypersensitivity pneumonias
Succinylcholine
and asthma, may have been treated with oral steroids.
Oral steroid use may predispose to tuberculosis or Interstitial lung disease (pulmonary fibrosis)
Amiodarone
pneumocystis pneumonia. Patients with chronic lung Hydralazine
conditions like cystic fibrosis or bronchiectasis will Gold salts
often be very knowledgeable about their treatment Bleomycin
and can describe the various forms of physiotherapy Nitrofurantoin
that are essential for keeping their airways clear. Methotrexate
Find out whether home oxygen has been pre- Pulmonary embolism
scribed. An oxygen concentrator or oxygen cylinder Oestrogens
may be used and the oxygen administered by a Tamoxifen
mask or with nasal prongs. The flow rate is usually Raloxifene
2 L/minute or more and oxygen may be prescribed
Non-cardiogenic pulmonary oedema
for 24 hours a day in some cases. Portable oxygen Hydrochlorothiazide
cylinders and rechargeable concentrators are avail-
able. Home oxygen is expensive and the rules for its Pleural disease/effusion
prescription are quite strict. Usually arterial blood gas Nitrofurantoin
measurements that show low oxygen concentrations Phenytoin, hydralazine (induction of systemic lupus
are required before oxygen can be prescribed. For erythematosus)
Methotrexate
safety reasons patients must have given up smoking Methysergide
before home oxygen can be allowed.
Pulmonary rehabilitation courses are now or pneumoconioses cause interstitial lung disease by
commonly prescribed for patients with chronic lung damaging the alveoli and small airways. Prolonged
disease. They involve graded exercise programs and exposure to substances whose use is now heavily
information about ways of dealing with chronic restricted is usually required. Cigarette smoking
respiratory symptoms. Find out if this has been has an additive effect for these patients. These
recommended and whether it has been helpful. occupational conditions are now rare, and the most
Almost every class of drug can produce lung common occupational lung disease is asthma.
toxicity. Examples include pulmonary embolism Ask about exposure to dusts in mining industries
from use of the oral contraceptive pill, interstitial and factories (e.g. asbestos, coal, silica, iron oxide,
lung disease from cytotoxic agents (e.g. methotrexate, tin oxide, cotton, beryllium, titanium oxide, silver,
cyclophosphamide, bleomycin), bronchospasm from nitrogen dioxide, anhydrides). Heavy exposure to
beta-blockers or non-steroidal anti-inflammatory asbestos can lead to asbestosis (see List 9.9), but
drugs (NSAIDs), and cough from ACE inhibitors. even trivial exposure can result in pleural plaques or
Some medications known to cause lung disease mesothelioma (malignant disease of the pleura). The
may not be mentioned by the patient because they patient may be unaware that his or her occupation
are illegal (e.g. cocaine), are used sporadically (e.g. involved exposure to dangerous substances; for
hydrochlorothiazide), can be obtained over the example, factories making insulating cables and
counter (e.g. tryptophan) or are not taken orally boards very often used asbestos until 25 years ago.
(e.g. timolol; beta-blocker eye drops for glaucoma). Asbestos exposure can result in the development
The clinician therefore needs to ask about these types of asbestosis, pleural plaques, mesothelioma or
of drug specifically. carcinoma of the lung up to 30 years later. Relatives of
people working with asbestos may be exposed when
Past history handling work clothes. Only very minor exposure
is required for patients to develop the disease and
Always ask about previous respiratory illness, sometimes considerable detective work is needed to
including pneumonia, tuberculosis or chronic work out the source of exposure. Finding the source
bronchitis, or abnormalities of the chest X-ray that of exposure can be important as a public health
have previously been reported to the patient. Many matter.
previous respiratory investigations may have been Work or household exposure to animals, includ-
memorable, such as bronchoscopy, lung biopsy and ing birds, is also relevant (e.g. Q fever or psittacosis,
video-assisted thoracoscopy. Spirometry, with or which are infectious diseases caught from animals).
without challenge testing for asthma, may have been Exposure to organic dusts can cause a local
performed. Many severe asthmatics perform their immune response to organic antigens and result
own regular peak flow testing (page 163). Ask about in extensive allergic alveolitis. Within a few hours
the results of any of these investigations. Patients of exposure, patients develop flu-like symptoms.
with the acquired immunodeficiency syndrome These often include fever, headache, muscle pains,
(AIDS) have a high risk of developing Pneumocystis dyspnoea without wheeze and dry cough. The culprit
jiroveci (carinii) pneumonia and indeed other chest antigens may come from mouldy hay, humidifiers or
infections, including tuberculosis. air conditioners, among others (see Table 9.6).
It is most important to find out what the patient
Occupational history actually does when at work, the duration of any
In no other body system assessment are the
patient’s present and previous occupations of more LIST 9.9 Possible occupational exposure to
importance (see Table 9.5).2 A detailed occupational asbestos
history is essential. The occupational lung diseases
Asbestos mining, including relatives of miners
Naval dockyard workers and sailors—lagging of
TABLE 9.5Occupational lung disease pipes
Builders—asbestos in fibreboard (particles are
(pneumoconioses)
released during cutting or drilling)
Substance Disease Factory workers—manufacture of fibro-sheets, brake
linings, some textiles
Coal Coal worker’s pneumoconiosis
Building maintenance workers—asbestos insulation
Silica Silicosis Building demolition workers
Home renovation
Asbestos Asbestosis
Emergency workers—cleaning up after floods and
Talc Talcosis fires
TABLE 9.6 Allergic alveolitis: sources intravenous drug use may be related to an increased
risk of HIV infection and susceptibility to infection.
Disorder Source
Such information may influence the decision about
Bird fancier’s lung Bird feathers and excreta whether to advise treatment at home or in hospital.
Farmer’s lung Mouldy hay or straw (Aspergillus
fumigatus)
Family history
Byssinosis Cotton or hemp dust
A family history of asthma or other atopic diseases,
Cheese worker’s Mouldy cheese (Aspergillus cystic fibrosis, lung cancer or emphysema should be
lung clavatus)
sought. Alpha1-antitrypsin deficiency, for example, is
Malt worker’s lung Mouldy malt (Aspergillus clavatus) an inherited disease, and those affected are extremely
Humidifier fever Air-conditioning (thermophilic susceptible to the development of emphysema.
Actinomycetes) A family history of infection with tuberculosis is also
important. A number of pulmonary diseases may
have a familial or genetic association. These include
exposure, use of protective devices and whether carcinoma of the lung and pulmonary hypertension.
other workers have become ill. An improvement in
symptoms over the weekend is a valuable clue to the T&O’C essentials
presence of occupational lung disease, particularly
occupational asthma. This can occur as a result of 1. A careful history will often help in deciding if
exposure to spray paints or plastic or soldering fumes. dyspnoea is due to cardiac or respiratory causes.
2. The diagnosis of COPD can be made based on
the smoking history.
Social history 3. A careful occupational history is more important
A smoking history must be routine, as it is the for the respiratory system assessment than for
major cause of COPD3 and lung cancer (see List 1.2, any other body system assessment.
4. Consider deconditioning and anxiety as possible
page 11). It also increases the risk of spontaneous causes of dyspnoea where no other cause is
pneumothorax and of Goodpasture’s syndrome. It apparent.
is necessary to ask how many packets of cigarettes 5. Anxious patients who complain of breathlessness
per day the patient has smoked and how many years often describe an inability to take a satisfying
the patient has smoked. An estimate should be breath.
made of the number of packet-years of smoking (see
Chapter 1). Occupation may further affect cigarette
smokers; for example, asbestos workers who smoke OSCE revision topics
are at an especially high risk of lung cancer. Passive
THE RESPIRATORY HISTORY
smoking is now regarded as a significant risk for
lung disease and the patient should be asked about Use these topics, which commonly occur in the
exposure to other people’s cigarette smoke at home OSCE, to help with revision.
and at work. 1. This man has been found on X-ray to have
Many respiratory conditions are chronic and pleural plaques. Please take a respiratory and
may interfere with the ability to work and exercise as occupational history from him. (page 135)
well as interfering with normal family life. In some 2. This man has been troubled by asthma. Please
take a history from him. (page 132)
cases involving occupational lung disease there 3. Find out if this woman’s history is consistent with
may be compensation matters affecting the patient. COPD. (page 133)
Ask about these problems and whether the patient 4. This woman has a cough. Ask her about it and
has been involved in a pulmonary rehabilitation take a respiratory history. (page 129)
program. Housing conditions may be inappropriate 5. Assess this man for possible sleep apnoea.
for a person with a limited exercise tolerance or an (page 133)
infectious disease.
An enquiry about the patient’s alcohol consump-
tion is important. Drinking large amounts of References
alcohol in binges can sometimes result in aspiration 1. Schmitt BP, Kushner MS, Wiener SL. The diagnostic
pneumonia, and alcoholics are more likely to develop usefulness of the history of the patient with dyspnea.
pneumococcal or Klebsiella pneumonia. Intravenous J Gen Intern Med 1986; 1:386–393. History alone
drug users are at risk of lung abscess and drug-related was correct three out of four times when deciding
pulmonary oedema. Sexual orientation or history of the cause of dyspnoea in defined circumstances.
2. Anonymous. Obtaining an exposure history. Agency COPD in suspected or known cases: a systematic
for Toxic Substances and Disease Registry. United review. Fam Pract 2009; 26(4):260–268. Items of
States Department of Health and Human Services, diagnostic value for COPD included a history of
Public Health Service, Atlanta, Georgia. Am Fam dyspnoea, wheezing and smoking. Items of value
Phys 1993; 48:483–491. on examination included audible wheezing and
3. Broekhuizen BD, Sachs AP, Oostvogels R, forced expiratory time. However, the data were
Hoes AW, Verheij TJ, Moons KG. The diagnostic heterogeneous.
value of history and physical examination for
CHAPTER
10 The respiratory examination
More would I, but my lungs are wasted so, to elevate the ribs. Intrathoracic pressure falls as
That strength of speech is utterly air is forced under atmospheric pressure into the
denied me. lungs. Expiration is a passive process resulting
from elastic recoil of the muscles. Abnormalities of
William Shakespeare, Henry IV, Part 2
lung function or structure may change the normal
anatomy and physiology of respiration, for example
as a result of over-inflation of the lungs (chronic
Examination anatomy obstructive pulmonary disease [COPD]. Muscle
The lungs are paired asymmetrical organs protected and neurological diseases can also affect muscle
by the cylinder composed of the ribs, vertebrae and function adversely, and abnormalities of the control
diaphragm. The surface of the lungs is covered by the of breathing in the respiratory centres of the brain
visceral pleura, a thin membrane, and a similar outer in the pons and medulla can interfere with normal
layer (the parietal pleura) lines the rib cage. These breathing patterns.
membranes are separated by a thin layer of fluid and During the respiratory examination, keep in mind
enable the lungs to move freely during breathing. the surface anatomy (see Figure 10.2) of the lungs and
Various diseases of the lungs and of the pleura try to decide which lobes are affected.
themselves, including infection and malignancy, can
cause accumulation of fluid within the pleural cavity Positioning the patient
(a pleural effusion). The patient should be undressed to the waist. 1
The heart, trachea, oesophagus and the great blood Women should wear a gown or have a towel or
vessels and nerves sit between the lungs and make up some clothing to cover their breasts when the front
the structure called the mediastinum. The left and of the chest is not being examined. If the patient is
right pulmonary arteries supply their respective lung. not acutely ill, the examination is easiest to perform
Gas exchange occurs in the pulmonary capillaries with him or her sitting over the edge of the bed or
that surround the alveoli, the tiny air sacs which lie on a chair.
beyond the terminal bronchioles. Oxygenated blood
is returned via the pulmonary veins to the left atrium.
Abnormalities of the pulmonary circulation such as
General appearance
raised pulmonary venous pressure resulting from If the patient is an inpatient in hospital, look around
heart failure or pulmonary hypertension can interfere the bed for oxygen masks, metered dose inhalers
with gas exchange. (puffers) and other medications, and the presence
The position of the heart, whose apex points to the of a sputum mug. Then make a deliberate point of
left, means that the left lung is smaller than the right looking for the following signs before beginning the
and has only two lobes, which are separated by the detailed examination.
oblique fissure. The right lung has both horizontal
(upper) and oblique (lower) fissures dividing it into DYSPNOEA
three lobes (see Figure 10.1). Watch the patient for signs of dyspnoea at rest. Count
The muscles of respiration are the diaphragm the respiratory rate; the normal rate at rest should
upon which the bases of the lungs rest and the not exceed 25 breaths per minute (range 16–25).
intercostal muscles. During inspiration, the dia- The frequently quoted normal value of 14 breaths
phragm flattens and the intercostal muscles contract per minute is probably too low; normal people can
138
CHAPTER 10 The respiratory examination 139
Upper Upper
lobe lobe
Middle Upper Upper
lobe lobe lobe
Lower Lower
lobe lobe
a b
T2 Upper Upper
lobe lobe
Oblique Middle
fissure lobe
Lower
Lower
lobe
lobe
T11
c d
Figure 10.1 Lobes of the lung

(a) Anterior; (b) posterior; (c) lobes of the right lung; (d) lobes of the left lung. Refer to Figure 12.4, page 165, for a list of the
segments in each lobe.
have a respiratory rate of up to 25, and the average increase in the work of breathing, and COPDa is
is 20 breaths per minute. It is traditional to count an important cause. These muscles include the
the respiratory rate surreptitiously while affecting sternocleidomastoids, the platysma and the strap
to count the pulse. The respiratory rate is the only muscles of the neck. Characteristically, the accessory
vital sign that is under direct voluntary control. muscles cause elevation of the shoulders with
Tachypnoea refers to a rapid respiratory rate of greater inspiration, and aid respiration by increasing chest
than 25. Bradypnoea is defined as a rate below 8, a expansion. Contraction of the abdominal muscles
level associated with sedation and adverse prognosis.
In normal relaxed breathing, the diaphragm is the a
This condition has undergone many changes in nomenclature,
only active muscle and is active only in inspiration; and it is pleasing to think that chest doctors have something to
expiration is a passive process. keep them occupied. The term COPD encompasses emphysema,
chronic bronchitis, chronic obstructive lung disease (COLD) and
chronic airflow limitation (CAL). This term seems quite firmly
CHARACTERISTIC SIGNS OF COPD established (at least for now). The diagnosis of COPD depends
on clinical, radiographic and lung function assessment. There may
Look to see whether the accessory muscles of be components of what used to be called chronic bronchitis and
respiration are being used. This is a sign of an emphysema.
Carotid artery
Trachea
Clavicle Subclavian artery
Upper lobe
First rib
Second rib
(first palpable rib)
Upper lobe Left lung
Third rib
Fourth rib
Middle lobe
Fifth rib
Sixth rib
Lower lobe
Seventh rib
Lower lobe
Eighth rib
Ninth rib
Tenth rib
Right lung
Sternum
Xiphisternum
Figure 10.2 Basic anatomy of the lungs

may occur in expiration in patients with obstructed may cause downward displacement of the trachea
airways. Patients with severe COPD often have during inspiration—tracheal tug (this is also a sign
in-drawing of the intercostal and supraclavicular of severe asthma, especially in children).b
spaces during inspiration. This is due to a delayed
increase in lung volume despite the generation of CYANOSIS
large negative pleural pressures. Central cyanosis is best detected by inspecting the
In some cases, the pattern of breathing is diag- tongue. Examination of the tongue differentiates
nostically helpful (see Table 9.4, page 134). Look central from peripheral cyanosis. Lung disease
for pursed-lips breathing, which is characteristic of severe enough to result in significant ventilation–
patients with severe COPD. This manoeuvre reduces perfusion imbalance (such as pneumonia, COPD
the patient’s breathlessness, possibly by providing and pulmonary embolism), may cause reduced
continuous positive airways pressure and helping to arterial oxygen saturation and central cyanosis.
prevent airways collapse during expiration. Patients Cyanosis becomes evident when the absolute
with severe COPD may feel more comfortable concentration of deoxygenated haemoglobin is
leaning forwards with their arms on their knees. This
position compresses the abdomen and pushes the
b
diaphragm upwards. This partly restores its normal When the trachea moves in time with the pulse, the sign suggests
an aneurysm of the thoracic aorta—this is the original meaning of
domed shape and improves its effectiveness during tracheal tug. Its appropriation by the chest doctors annoys those
inspiration. Increased diaphragmatic movements aware of its original meaning.
50 g/L of capillary blood. Cyanosis is usually obvious LIST 10.1 Important causes of stridor in
when the arterial oxygen saturation falls below 90% adults
in a person with a normal haemoglobin level. Central
cyanosis is therefore a sign of severe hypoxaemia. In Sudden onset (minutes)
patients with anaemia, cyanosis does not occur until Anaphylaxis
Toxic gas inhalation
even greater levels of arterial desaturation are reached.
Acute epiglottitis
The absence of obvious cyanosis does not exclude Inhaled foreign body
hypoxia. The detection of cyanosis is much easier
in good (especially fluorescent) lighting conditions Gradual onset (days, weeks)
and is said to be more difficult if the patient’s bed is Laryngeal or pharyngeal tumours
surrounded by cheerful pink curtains. Cricoarytenoid rheumatoid arthritis
Bilateral vocal cord palsy
Tracheal carcinoma
CHARACTER OF THE COUGH Paratracheal compression by lymph nodes
Coughing is a protective response to irritation of Post-tracheostomy or intubation granulomata
sensory receptors in the submucosa of the upper
airways or bronchi. Ask the patient to cough several
times. Lack of the usual explosive beginning may Hands
indicate vocal cord paralysis (the ‘bovine’ cough). As usual, examination in detail begins with the hands.
A muffled, wheezy, ineffective cough suggests
obstructive pulmonary disease. A very loose productive CLUBBING
cough suggests excessive bronchial secretions due to
chronic bronchitis, pneumonia or bronchiectasis. Look for clubbing, which is due to respiratory
A dry, irritating cough may occur with chest infection, disease in up to 80% of cases (see Figure 10.3 and
asthma or carcinoma of the bronchus and sometimes List 5.1 on page 62). An uncommon but important
with left ventricular failure or interstitial lung disease association with clubbing is hypertrophic pulmonary
(ILD). It is also typical of the cough produced by osteoarthropathy (HPO). HPO is characterised by
ACE inhibitor drugs. A barking or croupy cough the presence of periosteal inflammation at the distal
may suggest a problem with the upper airway—the ends of long bones, the wrists, the ankles and the
pharynx and larynx, or pertussis infection. metacarpal and the metatarsal bones. There is swelling
and tenderness over the wrists and other involved
SPUTUM areas. Rarely HPO may occur without clubbing. The
causes of HPO include primary lung carcinoma and
Sputum should be inspected. Careful study of the pleural fibromas. It is important to note that clubbing
sputum is an essential part of the physical examination. does not occur as a result of COPD.
The colour, volume and type (purulent, mucoid
or mucopurulent), and the presence or absence of STAINING
blood, should be recorded.

Look for staining of the fingers (actually caused
STRIDOR by tar, as nicotine is colourless); a sign of cigarette
smoking (see Figure 3.12 on page 36). The density of
Obstruction of the larynx or trachea (the extra- staining does not indicate the number of cigarettes
thoracic airways) may cause stridor, a rasping or
croaking noise loudest on inspiration. This can
be due to a foreign body, a tumour, infection (e.g.
epiglottitis) or inflammation (see List 10.1). It is a sign
that requires urgent attention.
HOARSENESS
Listen to the patient’s voice for hoarseness (dysphonia),
as this may indicate recurrent laryngeal nerve palsy
associated with carcinoma of the lung (usually left-
sided), or laryngeal carcinoma. However, the most
common cause is laryngitis and the use of inhaled
corticosteroids for asthma. Non-respiratory causes
include hypothyroidism.
Figure 10.3 Finger clubbing

smoked, but depends rather on the way the cigarette the maxilla and mandible appear retracted (receding
is held in the hand. chin).
Sinusitis is suggested by tenderness over the
WASTING AND WEAKNESS sinuses on palpation. If acute sinusitis is suspected,
Compression and infiltration by a peripheral lung a torch can be used to transilluminate the frontal
tumour of a lower trunk of the T1 nerve root results and maxillary sinuses. 3 Place the torch in the
in wasting of the small muscles of the hand and patient’s mouth and examine the sinuses in a dark
weakness of finger abduction. room. Normal transillumination generally excludes
sinusitis. Complete opacification suggests sinusitis
PULSE RATE but partial opacification is less helpful. The torch
should then be used to look for purulent discharge
Tachycardia and pulsus paradoxus are important
in the pharynx.
signs of severe asthma. Tachycardia is a common
Look at the patient’s face for the red, leathery,
side effect of the treatment of asthma with β-agonist
wrinkled skin of the smoker. 4 There may be facial
drugs, and accompanies dyspnoea or hypoxia of any
plethora or cyanosis if superior vena caval obstruction
cause.
is present. Look for the characteristics of obstructive
sleep apnoea (see above).
FLAPPING TREMOR (ASTERIXIS) Inspect the eyes for evidence of the rare Horner’sd
Ask the patient to dorsiflex the wrists with the arms syndrome (a constricted pupil, partial ptosis and
outstretched and to spread out the fingers. A flapping loss of sweating), which can be due to an apical lung
tremor with a 2- to 3-second cycle may occur with carcinoma (Pancoast’se tumour) compressing the
severe CO2 retention, usually due to severe COPD.2 sympathetic nerves in the neck. There may be skin
The problem is an inability to maintain a posture. changes on the face that suggest scleroderma or
Asterixisc can also be demonstrated by asking the connective tissue disease.
patient to protrude the tongue or lift the leg and
keep the foot dorsiflexed. However, this is a late
and unreliable sign and can also occur in patients Trachea
with liver or renal failure. Patients with severe CO2 The position of the trachea is most important, and
retention may be confused, and typically have warm time should be spent establishing it accurately. This
peripheries and a bounding pulse. examination is uncomfortable for the patient, so you
must be gentle. From in front of the patient push
the forefinger of your right hand up and backwards
Face from the suprasternal notch until the trachea is felt
The nose is sited conveniently in the centre of the face. (see Figure 10.4). If the trachea is displaced to one
In this position it may readily be inspected inside and side, its edge rather than its middle will be felt and a
out. Ask the patient to tilt the head back. It may be larger space will be present on one side than the other.
necessary to use a nasal speculum to open the nostrils, Slight displacement to the right is fairly common
and a torch. Look for polyps (associated with asthma), in normal people. Significant displacement of the
engorged turbinates (various allergic conditions) and trachea suggests, but is not specific for, disease of the
a deviated septum (nasal obstruction). upper lobes of the lung (see List 10.2).
As already discussed, look at the tongue for A tracheal tug is demonstrated when the finger
central cyanosis. Look in the mouth for evidence resting on the trachea feels it move inferiorly with
of an upper respiratory tract infection (a reddened each inspiration. This is a sign of gross overexpansion
pharynx and tonsillar enlargement, with or without of the chest because of airflow obstruction. This
a coating of pus). A broken tooth or a rotten tooth movement of the trachea may be visible, and it is
stump may predispose to lung abscess or pneumonia. worth spending time inspecting the trachea when
Patients with sleep apnoea may have ‘crowding’ of the COPD is suspected.
pharynx. This means a reduction in the size of the If the patient appears dyspnoeic and use of the
velopharyngeal lumen, which is the space between accessory muscles of respiration is suspected, place
the soft palate, the tonsils and the back of the tongue. your fingers in the supraclavicular fossae. When the
Those who use a sleep apnoea mask at night often scalene muscles are recruited, they can be felt to
have marks from the mask on the face and puffiness contract under the fingers. Even more severe dyspnoea
around the eyes. They tend to be obese and have a
short thick neck and a small pharynx; sometimes d
Johann Horner (1831–1886), professor of ophthalmology in Zurich,
described this syndrome in 1869.
c e
The word is derived from the Greek word sterigma, which means to Henry Khunrath Pancoast (1875–1939), professor of roentgenology,
support, and refers to a flapping tremor. University of Pennsylvania, described this in 1932.
a b
Figure 10.4 Feeling for the position of the trachea—a similar gap should be palpable on each side
LIST 10.2 Causes of tracheal displacement

INSPECTION
Shape and symmetry of chest
1. Towards the side of the lung lesion When the anteroposterior (AP) diameter is increased
Upper lobe collapse
Upper lobe fibrosis
compared with the lateral diameter, the chest is
Pneumonectomy described as barrel-shaped (see Figure 10.5). An
increase in the AP diameter compared with the lateral
2. Away from the side of the lung lesion diameter (the thoracic ratio) beyond 0.9 is abnormal
(uncommon) and is often seen in patients with severe asthma or
Massive pleural effusion emphysema. It is not always a reliable guide to the
Tension pneumothorax
severity of the underlying lung disease and may be
3. Upper mediastinal masses, such as present in normal elderly people. It is sometimes
retrosternal goitre an illusion when the abdomen is relatively small
in thin people. Severe kyphoscoliosis is a cause of
asymmetrical chest deformity.
A pigeon chest (pectus carinatum) is a localised
will result in use of the sternomastoid muscles. Their prominence (an outward bowing of the sternum
contraction is also easily felt with inspiration. Use of and costal cartilages; see Figure 10.6(b)). It may be
these muscles for long periods is exhausting and a a manifestation of chronic childhood respiratory
sign of impending respiratory failure. illness, in which case it is thought to result from
repeated strong contractions of the diaphragm while
the thorax is still pliable. It also occurs in rickets.f
Chest A funnel chest (pectus excavatum) is a develop-
The chest should be examined anteriorly and pos- mental defect involving a localised depression of the
teriorly by inspection, palpation, percussion and lower end of the sternum (see Figure 10.6(a)). The
auscultation.1 Compare the right and left sides during
each part of the examination. f
Bone disease caused by vitamin D deficiency in childhood.
Figure 10.5 Barrel chest

(From McDonald FS, ed. Mayo Clinic images in internal medicine, a
with permission. © Mayo Clinic Scientific Press and CRC Press.)
problem is usually an aesthetic one, but in severe

cases lung capacity may be restricted.
Harrison’sg sulcus is a linear depression of the
lower ribs just above the costal margins at the site
of attachment of the diaphragm. It can result from
severe asthma in childhood, or rickets.
Kyphosis refers to an exaggerated forward
curvature of the spine, while scoliosis is lateral
bowing. Kyphoscoliosis may be idiopathic (80%),

secondary to poliomyelitis or associated with
Marfan’s syndrome. Severe thoracic kyphoscoliosis
may reduce the lung capacity and increase the work
of breathing.
Lesions of the chest wall may be obvious. Look
for scars from previous thoracic operations or from
chest drains for a previous pneumothorax or pleural
effusion. Surgical removal of a lung (pneumonectomy)
or of the lobe of a lung (lobectomy) leaves a long
diagonal posterior scar on the thorax. The presence
of three 2–3 centimetre scars suggests previous
video-assisted thoracoscopic surgery, which can be
performed to biopsy lymph nodes or carry out lung
reduction surgery or pleurodesis. Thoracoplasty
causes severe chest deformity; this operation was b
g
Edward Harrison (1766–1838), British general practitioner in
Figure 10.6 (a) Funnel chest (pectus excavatum);
Lincolnshire, described this deformity in rickets in 1798. The sign (b) Pigeon chest (pectus carinatum)
has also been ascribed to Edwin Harrison (1779–1847), a London (From Mir MA. Atlas of clinical diagnosis, 2nd edn. Edinburgh:
physician. Saunders, 2003, with permission.)
performed for tuberculosis and involved removal

of a large number of ribs on one side of the chest to
achieve permanent collapse of the affected lung. It is
no longer performed because of the availability of
effective anti-tuberculous chemotherapy.
Radiotherapy may cause erythema and thickening
of the skin over the irradiated area. There is sharp
demarcation between abnormal and normal skin.
There may be small tattoo marks indicating the
limits of the irradiated area. Signs of radiotherapy
usually indicate that the patient has been treated
for carcinoma of the lung or breast or, less often, for
a
lymphoma.
Subcutaneous emphysema is a crackling sensation
felt on palpating the skin of the chest or neck.
On inspection, there is often diffuse swelling of the
chest wall and neck. It is caused by air tracking from
the lungs and is usually due to a pneumothorax; less
commonly it can follow rupture of the oesophagus or
a pneumomediastinum (air in the mediastinal space).
Prominent veins may be seen in patients with
superior vena caval obstruction. It is important to
determine the direction of blood flow (page 158).
Movement of the chest wall should be noted.
Look for asymmetry of chest wall movement
anteriorly and posteriorly. Assessment of expansion b
of the upper lobes is best achieved by inspection
from behind the patient, looking down at the clavi- Figure 10.7 Inspecting upper lobe expansion:
cles during moderate respiration (see Figure 10.7). (a) expiration; (b) inspiration—note symmetrical elevation
of the clavicles
Diminished movement indicates underlying lung
disease. The affected side will show delayed or
decreased movement. For assessment of lower lobe
expansion, the chest should be inspected posteriorly. at least 5 centimetres. Reduced expansion on one
Reduced chest wall movement on one side may be side indicates a lesion on that side. The causes have
due to localised lung fibrosis, consolidation, collapse, already been discussed.
If COPD is suspected, Hoover’sh sign may be
pleural effusion or pneumothorax.

Bilateral reduction of chest wall movement sought (see Figure 10.9). Place your hands along
indicates a diffuse abnormality such as COPD or the costal margins with your thumbs close to the
diffuse interstitial lung disease. Unilateral reduced xiphisternum. Normally inspiration causes them to
chest excursion or splinting may be present when separate, but the overinflated chest of the COPD
patients have pleuritic chest pain or injuries such as patient cannot expand in this way and the diaphragm
rib fractures. pulls the ribs and your thumbs closer together 5
Look for paradoxical inward motion of the (LR+ 4.2).6
abdomen during inspiration when the patient is Lower lobe expansion is assessed from the back
supine (indicating diaphragmatic paralysis). in this way. Some idea of upper and middle lobe
expansion is possible when the manoeuvre is repeated
PALPATION on the front of the chest, but this is better gauged by
inspection.
Chest expansion
Place your hands firmly on the patient’s chest Apex beat
wall with your fingers extending around the sides When the patient is lying down, establishing
of the chest. Your thumbs should almost meet in the position of the apex beat may be helpful, as
the middle line and should be lifted slightly off the displacement towards the side of the lesion can be
chest so that they are free to move with respiration h
Charles Hoover (1865–1927), professor of medicine in Cleveland
(see Figure 10.8). As the patient takes a big breath from 1907. He also described Hoover’s test for non-organic limb
in, your thumbs should move symmetrically apart weakness.
Thumbs not in contact

with chest wall
Greater than 5 cm
a b
Figure 10.8 Palpation for lower lobe expansion: (a) expiration; (b) inspiration
a b
c d
Figure 10.9 (a) Normal inspiration; (b) normal expiration; (c) Hoover’s inspiration; Hoover’s expiration (d).
caused by collapse of the lower lobe or by localised that the note generated is not dampened (this may be
interstitial lung disease. Movement of the apex less important if the pleximeter finger is held firmly
beat away from the side of the lung lesion can be on the chest wall, as it should be). The percussing
caused by pleural effusion or tension pneumothorax. finger must be held partly flexed and a loose swinging
The apex beat is often impalpable in a chest that is movement should come from the wrist and not from
hyperexpanded secondary to COPD. the forearm. Medical students soon learn to keep the
right middle fingernail short.
Vocal (tactile) fremitus Percussion of symmetrical areas of the anterior,
This is a palpable vibration felt by the examiner’s posterior and axillary regions is necessary (see
hands on a patient’s chest wall when the patient is Figure 10.10). Percussion in the supraclavicular fossa
speaking (or singingi). Palpate the chest wall with over the apex of the lung and direct percussion of the
the palm of the hand while the patient repeats clavicle with the percussing finger are a traditional
‘ninety-nine’. The front and back of the chest are part of the examination. For percussion posteriorly,
each palpated in two comparable positions, with the the scapulae should be moved out of the way by asking
palm of one hand on each side of the chest. In this the patient to move the elbows forwards across the
way differences in vibration on the chest wall can front of the chest; this rotates the scapulae anteriorly.
be detected. This can be a difficult sign to interpret, The feel of the percussion note is as important
with considerable inter-observer variability, and it as its sound. The note is affected by the thickness of
is no longer a routine part of the examination. It the chest wall, as well as by underlying structures.
depends on the recognition of changes in vibration Percussion over a solid structure, such as the liver
conducted to the examiner’s hands while the patient or a consolidated or collapsed area of lung, produces
speaks. Practice is needed to appreciate the difference a dull note. Percussion over a fluid-filled area, such
between normal and abnormal. Vocal fremitus is as a pleural effusion, produces an extremely dull
more obvious in men because of their lower-pitched (stony dull) note. Percussion over the normal lung
voices. It may be absent in normal people (high- produces a resonant note and percussion over hollow
pitched voice or thick chest wall). It is only abnormal structures, such as the bowel or a pneumothorax,
if different on one side from the other. The causes of produces a hyperresonant note.
change in vocal fremitus are the same as those for Considerable practice is required before expert
vocal resonance (page 150). percussion can be performed, particularly in front
Ribs of an audience. The ability to percuss well is usually
Gently compress the chest wall anteroposteriorly and obvious in clinical examinations and counts in a
laterally. Localised pain suggests a rib fracture, which student’s favour, as it indicates a reasonable amount
may be secondary to trauma or may be spontaneous of experience in the wards.
as a result of tumour deposition, bone disease or Liver dullness
sometimes the result of severe and prolonged cough-
The upper level of liver dullness is determined by
ing. Tenderness over the costochondral junctions

percussing down the anterior chest in the mid-
suggests the diagnosis of costochondritis as the
clavicular line. Normally, the upper level of liver
cause of chest pain.
dullness is the sixth intercostal space in the right
Regional lymph nodes midclavicular line. If the chest is resonant below
The axillary and cervical and supraclavicular nodes this level, it is a sign of hyperinflation, usually
must be examined (Chapter 21); they may be enlarged due to emphysema or asthma. This is a sign with
in lung malignancies and some infections. considerable inter-observer variability.
Cardiac dullness
PERCUSSION The area of cardiac dullness usually present on the
With your left hand on the patient’s chest wall left side of the chest may be decreased in emphysema
and fingers slightly separated and aligned with or asthma.
the patient’s ribs, press your middle finger firmly
against the patient’s chest. Use the pad of your right AUSCULTATION
middle finger (the plexor) to strike firmly the middle
phalanx of the middle finger of your left hand (the Breath sounds
pleximeter).j Remove the percussing finger quickly so Using the diaphragm of the stethoscope, listen front
and back (Figure 10.11).7–9 It is important to compare
i
each side with the other. Remember to listen high up
Probably not to be encouraged during an OSCE exam.
j
This was often a piece of wood, ivory or a coin in the 19th century but into the axillae and, using the bell of the stethoscope
is now always the examiner’s finger. applied above the clavicles, to listen to the lung apices.
A number of observations must be made while

auscultating and, as with auscultation of the heart,
different parts of the cycle must be considered. Listen
for the quality of the breath sounds, the intensity of
the breath sounds and the presence of additional
(adventitious) sounds.
Quality of breath sounds
Normal breath sounds are heard with the stethoscope
over nearly all parts of the chest. The patient should
be asked to breathe in and out through the mouth so
that added sounds from the nasopharynx do not inter-
fere.k During expiration these sounds are produced in
the large airways rather than in the alveoli. However,
inspiratory sounds are probably produced close to
where they are heard, in the peripheral parts of the
lungs. Since both sounds were once thought to arise
in the alveoli, or vesicles of the lungs, they are called
vesicular sounds. They have rather fancifully been
compared by Laënnec to the sound of wind rustling
in leaves. Their intensity is related to total airflow at
the mouth and to regional airflow. Normal (vesicular)
breath sounds are louder and longer on inspiration
than on expiration and there is no gap between the
inspiratory and expiratory sounds.
a Bronchial breath sounds are present when
turbulence in the large airways is heard without being
filtered by the alveoli. Bronchial breath sounds have a
hollow, blowing quality. They are audible throughout
expiration and there is often a gap between inspira-
tion and expiration. The expiratory sound has a
higher intensity and pitch than the inspiratory sound.
Bronchial breath sounds are more easily remembered
than described. They are audible in normal people,
posteriorly over the right upper chest where the
trachea is contiguous with the right upper bronchus.
They are heard over areas of consolidation, as solid

lung conducts the sound of turbulence in main
airways to peripheral areas without filtering. Causes
of bronchial breath sounds are shown in List 10.3.
Occasionally, breath sounds over a large cavity
have an exaggerated bronchial quality. This very
hollow or amphoric l sound has been likened to that
heard when air passes over the top of a hollow jar.
Intensity of the breath sounds
It is better to describe breath sounds as being of
normal or reduced intensity than to speak about
air entry. The entry of air into parts of the lung
cannot be directly gauged from the breath sounds.
Asymmetrical reduction of breath sounds is a sign of
b bronchial obstruction, for example by carcinoma or
Figure 10.10 Percussion of the chest

k
(a) Percussing (plexor) finger poised. Inset: plexor finger Many people when asked to take big breaths, breathe in, and then,
for some reason, stop. Although it is tempting to amuse oneself by
strikes pleximeter finger. (b) Direct percussion of the clavicle
waiting patiently for the patient to realise that expiration is also a part
for upper lobe resonance. of breathing, this tends to waste time.
l
(Courtesy of Glenn McCulloch) From the Greek amphiphoreus meaning a ‘vase with a narrow neck’.
Bronchial
Normal bronchial Apex
breath sounds
breathing 2 1
4 3
6 5
10 9 End of inspiration
8 7 Figure 10.11 Normal and bronchial breath

sounds
Auscultate in each area shown (the numbers
represent a suggested order). Distinguish
normal breath sounds from bronchial
Normal
breathing.
breath sounds
LIST 10.3 Causes of bronchial breath sounds Wheezes are usually the result of acute or chronic
airflow obstruction due to asthma (often high-
Common pitched) or COPD (often low-pitched), secondary to
Lung consolidation (lobar pneumonia) a combination of bronchial muscle spasm, mucosal
oedema and excessive secretions. Wheezes are a poor
Uncommon
Localised pulmonary fibrosis
guide to the severity of airflow obstruction. In severe
Pleural effusion (above the fluid) airway obstruction, wheeze can be absent because
Collapsed lung (e.g. adjacent to a pleural effusion) ventilation is so reduced that the velocity of the air jet
is reduced below a critical level necessary to produce
Note: The large airways must be patent. the sound.
A fixed bronchial obstruction, usually due to a
carcinoma of the lung, tends to cause a localised
wheeze, which has a single musical note (monophonic)
a foreign body on the side where breath sounds are and does not clear with coughing.
reduced. Causes of reduced breath sounds include Wheezes must be distinguished from stridor
COPD (especially emphysema), pleural effusion, (page 141), which sounds very similar to wheeze but
pneumothorax, pneumonia, a large neoplasm and is louder over the trachea and is always inspiratory
pulmonary collapse. Breath sounds are generally (wheezes usually occur in expiration but can occur
louder if a patient breathes more deeply, for example in both inspiration and expiration).
after exercise. Interrupted non-musical sounds are best called
Added (adventitious) sounds crackles.10,11 There is a lot of confusion about the

There are two types of added sounds: continuous naming of these sounds, perhaps as a result of
(wheezes) and interrupted (crackles). mistranslations of Laënnec. Some authors describe
Continuous sounds are called wheezes. They are low-pitched crackles as râles and high-pitched ones as
abnormal findings and have a musical quality. The crepitations, but others do not make this distinction.
wheezes must be timed in relation to the respiratory The simplest approach is to call all these sounds
cycle. They may be heard in expiration or inspiration, crackles, but also to describe their timing and pitch.
or both. Wheezes are due to continuous oscillation of Crackles are sometimes present in normal people but
opposing airway walls and imply significant airway these crackles will always clear with coughing.
narrowing. Wheezes tend to be louder on expiration. Crackles are probably the result of loss of stability
This is because the airways normally dilate during of peripheral airways that collapse on expiration. With
inspiration and are narrower during expiration. An high inspiratory pressures, there is rapid air entry into
inspiratory wheeze implies severe airway narrowing. the distal airways. This causes the abrupt opening
The pitch (frequency) of wheezes varies. It is of alveoli and of small- or medium-sized bronchi
determined only by the velocity of the air jet and containing secretions in regions of the lung deflated to
is not related to the length of the airway. High- residual volume. More compliant (distensible) areas
pitched wheezes are produced in the smaller bronchi open up first, followed by the increasingly stiff areas.
and have a whistling quality, whereas low-pitched Fine- and medium-pitched crackles are not caused by
wheezes (sometimes called rhonchi) arise from the air moving through secretions as was once thought,
larger bronchi. but by the opening and closing of small airways.
The timing of crackles is of great importance. consolidated lung the numbers will become clearly
Early inspiratory crackles (which cease before the audible, while over normal lung the sound is muffled.
middle of inspiration) suggest disease of the small If vocal resonance is present, bronchial breathing
airways and are characteristic of COPD. 10 The is likely to be heard (see List 10.3). Sometimes
crackles are heard only in early inspiration and are vocal resonance is increased to such an extent that
of medium coarseness. They are different from those whispered speech is distinctly heard; this is called
heard in left ventricular failure, which occur later in whispering pectoriloquy.
the respiratory cycle. If a very localised abnormality is found at
Late or pan-inspiratory crackles suggest disease auscultation, try to determine the lobe and approxi-
confined to the alveoli. They may be fine, medium or mately which segment or segments are involved (see
coarse in quality. Fine crackles have been likened to Figure 10.1).
the sound of hair rubbed between the fingers, or to
the sound Velcro makes when pulled apart. They are The heart
typically caused by interstitial lung disease (pulmon-
ary fibrosis). Characteristically, more crackles are Cardiac examination is an essential part of the
heard in each inspiration when they are due to respiratory assessment and vice versa. These two
fibrosis—up to 14 compared with 1 to 4 for COPD and systems are intimately related.
4 to 9 for cardiac failure. As interstitial lung disease Lay the patient down at 45° and measure the jugular
becomes more severe the crackles extend earlier venous pressure (JVP) for evidence of right heart
into inspiration and are heard further up the chest.m failure (page 94). Next examine the praecordium. It
Medium crackles are usually due to left ventricular is important to pay close attention to the pulmonary
failure. Here the presence of alveolar fluid disrupts component of the second heart sound (P2). This is
the function of the normally secreted surfactant. best heard at the second intercostal space on the left.
Coarse crackles are characteristic of pools of retained It should not be louder than the aortic component,
secretions and have an unpleasant gurgling quality. best heard at the right second intercostal space. If
They tend to change with coughing, which also has the P2 is louder (and especially if it is palpable),
an unpleasant gurgling quality. Bronchiectasis is a pulmonary hypertension should be strongly
common cause, but any disease that leads to retention suspected. There may be signs of right ventricular
of secretions may produce these features. failure or hypertension. Pulmonary hypertensive
Pleural friction rub: when thickened, roughened heart disease (cor pulmonale) may be due to COPD,
pleural surfaces rub together as the lungs expand and ILD, pulmonary thromboembolism, marked obesity,
contract, a continuous or intermittent grating sound sleep apnoea or severe kyphoscoliosis.
may be audible. A pleural rub indicates pleurisy,
which may be secondary to pulmonary infarction The abdomen
or pneumonia. Rarely, malignant involvement of the Palpate the liver for ptosis,o due to emphysema, or for
pleura, a spontaneous pneumothorax or pleurodynia
enlargement from secondary deposits of tumour in

may cause a rub. cases of lung carcinoma.
Vocal resonance
Auscultation over the chest while a patient speaks Other
gives further information about the lungs’ ability PEMBERTON’Sp SIGN
to transmit sounds. Over normal lung, the low-
pitched com ponents of speech are heard with Ask the patient to lift the arms over the head and
a booming quality and high-pitched components wait for one minute.13 Note the development of facial
are attenuated. Consolidated lung, however, tends plethora, cyanosis, inspiratory stridor and non-
to transmit high frequencies so that speech heard pulsatile elevation of the JVP. This occurs in superior
through the stethoscope takes on a bleating quality vena caval obstruction.
(called aegophonyn by Laënnec12). When a patient with
aegophony says ‘e’ as in ‘bee’ it sounds like ‘a’ as in ‘bay’. LEGS
Increased vocal resonance is a helpful sign in Inspect the patient’s legs for swelling (oedema) or
confirming consolidation but may not be necessary cyanosis, which may be clues to cor pulmonale, and
as a routine. Ask the patient to say ‘ninety-nine’ look for evidence of deep venous thrombosis.
while you listen over each part of the chest. Over
o
From the Greek word for falling, this was once mostly applied to the
eyelid but now seems accepted as a description of the displacement
m
Expiratory crackles may also occur with lung fibrosis. of any organ.
n p
From the Greek aix meaning ‘goat’ and phone meaning ‘voice’. Hugh Pemberton (1891–1956), physician, Liverpool, UK.

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CHAPTER 7 Correlation of physical signs and cardiovascular disease 101

S1 A2 P2 S1 Chordae often thickened

Loud (S2) Opening snap

Left atrium often

dyspnoea and exertional syncope.

Systole Diastole High velocity flow

Left atrium often

Posterior leaflet prolapse

Ascending aorta may

Valve cusps often

GOOD SIGNS GUIDE 7.2

where there is narrowing of the ascending aorta

or if the stenosis is not at the valve level but course).

pulse. However, the harsher and louder the

TABLE 7.2 Eponymous signs of aortic regurgitation

TRICUSPID REGURGITATION ● Auscultation: there may be a pansystolic

Diastolic murmur begins

Figure 7.11 Aortic regurgitation: (a) murmur, at the

to dance in time with the heart beat; ascites,

ejection systolic murmur, heard best in the

for pulmonary stenosis or surgery for

PROSTHETIC HEART VALVES

TABLE 7.3 Prosthetic heart valves: physical signs

left ventricular or right ventricular outflow tract, or

ventricle early in systole is followed by Acyanotic congenital heart

● Causes of dilated cardiomyopathy: pulmonary systolic ejection murmur—these are

High velocity jet

S1 A2 P2 S1 Tricuspid valve Mitral valve

● Palpation: often there is a hyperkinetic apex

COARCTATION OF THE AORTA

LIST 7.2 Classification of congenital heart

This is a very rare lesion. The abnormality is a A RIGHT-TO-LEFT SHUNT)

of the right ventricular outflow obstruction and

OSCE example References

associated with heart failure. reliable than in younger patients.

Figure 8.1 Cardiovascular system

1. General inspection Palate (high arched—Marfan’s)

TEXT BOX 8.1 The cardiovascular examination: a suggested method continued

TEXT BOX 8.1 The cardiovascular examination: a suggested method continued

Extending the cardiovascular THE CHEST X-RAY: A SYSTEMATIC

Figure 8.2 Normal chest X-ray

heaven, hoping for divine inspiration. However, a Hila

be helpful. lies above this line.

Figure 8.3 Pulmonary venous congestion

Figure 8.4 Interstitial pulmonary oedema

Figure 8.5 Alveolar pulmonary oedema

Figure 8.6 Mitral valve disease

Figure 8.7 Ventricular aneurysm

Figure 8.8 Aortic coarctation

Figure 8.9 Atrial septal defect (ASD)

Figure 8.10 Marfan’s syndrome

Figure 8.11 Pacemaker and deﬁbrillators

bedside. It does not expose the patient to radiation.

Figure 8.14 M-mode measurements in a patient with

aorta just beyond the aortic valve cusps; see

Figure 8.15 Normal long-axis view of the heart

Figure 8.17 (a) Four-chamber view of a patient with

Information commonly available from an

suggests previous infarction as the cause of the