Physical diagnosis

Of
THE HEART

SYMPTOMS
a

good clinical history remains the clinicians

most valuable diagnostic tool.
the diagnosis may be made from the history
alone, and examination and investigations are
confirmatory.
A key objective of history-taking is to establish a
clear de-scription of the presenting symptom, and
to detect any pattern to episodes of the symptom.
the previous medical history, medication and
the social history.
a useful differential diagnosis list

Common cardiac
symptoms
Chest

pain or discomfort
is one of the most common
symptoms encountered in clinical
practice, and is a major cause of
admission to hospital.

Differential diagnosis of acute chest

pain/discomfort

Cardiovascular
CAD
Unstable - stable angina
Myocardial infarction
Variant angina
Syndrome X (microvascular
angina)
NON_CAD
Aortic dissection
Rupture of thoracic aortic
aneurysm
Myopericarditis, pericarditis

Pulmonary
Pulmonary embolism
Pneumonia (usually lobar)

Pleuritis

Gastrointestinal
Oesophagitis
Oesophageal spasm
Hiatus hernia
Peptic ulcer disease
Biliary colic
Pancreatitis
Pneumothorax
Acute asthma
Pneumomediastinum
Others
Chest wall muscle pain
Psychogenic chest pain
Costochondritis
Cervical spondylosis

angina pectoris

The typical description of angina is a tight,

heavy or constricting discomfort in the centre
of the chest. This sometimes radiates to the
neck or jaw, and to one or both shoulders or
arms.
Presentation can vary, however, and some
patients complain of back pain, epigastric pain,
or isolated jaw or arm pain
Other ischaemic pattern :
atypical angina
equivalent angina

Canadian Cardiovascular Society functional

classification

Applies to angina only

Class I
No angina on ordinary activity
Angina on strenuous, rapid, or prolonged exertion
Class II
Slight limitation of ordinary activity
Angina when walking up stairs briskly, or walking on a cold
or windy day
Class III
Marked limitation angina when walking at normal pace up
a flight of stairs, or walking one or two blocks
Class IV
Angina on minimal exertion or at rest

Breathlessness
Almost

all types of cardiac illness can

cause breathlessness. It is most helpful to
consider the following broad categories:

pulmonary oedema
reduced cardiac output
obstruction to cardiac output
arrhythmia
DD :
Central Psychiatric
Respiratory app
Resp app golgi
metabolic

New York Heart Association functional classification

Applies to fatigue, dyspnoea and angina
Class I
No limitations during ordinary activity
Class II
Slight limitation during ordinary activity (e.g.
mild or occasional angina/dyspnoea)
Class III
Marked limitation of normal activities without
symptoms at rest
Class IV
Unable to undertake physical activity without
symptoms
Symptoms may be present at rest

Palpitation
is used by patients to describe various
sensations, some of which are related to
cardiac rhythm.
Dizziness and syncope
Dizziness is a nonspecific symptom that is
common in cardiac patients. It affects about
one-third of patients aged over 65 years.
cardiac syncope caused by arrhythmia or reduced cardiac
output from structural disease
. inappropriate vasodilatation (including vasovagal syncope)
neurogenic syncope (e.g. epilepsy, cerebrovascular
ischaemia)
metabolic syncope (e.g. hypoglycaemia).

The key to Practice points

diagnosis is establishing a clear description of the
nature and pattern of symptom episodes
New chest pain or discomfort requires prompt
assessment it may reflect serious pathology such as
MI, aortic dissection or pulmonary embolism
Dizziness is a common symptom in the elderly and
may be multifactorial; drug treatment may be a
contributing factor
Syncope of cardiac origin is associated with high
mortality; identification of underlying structural and
electrical disease is important in the evaluation of
syncope

Clinical examination of the heart

making an initial anatomical diagnosis

rapidly assessing cardiac function and progress
at the bedside
The skill of examination is best learned at the
bedside from a practitioner already experienced
in it, and is best perfected by practice
the traditional sequence of inspection, palpation
and auscultation is valuable

Jugular

venous pulse

The jugular venous pulse (JVP) gives

important information about right
heart function, and thereby about
left heart function.

Arterial pressure and pulse

Blood pressure
Sphygmomanometry is often performed poorly.
The standard cuff is 5 inches (about 12.5 cm)
wide, but this may not be appropriate for all
patients
Arterial pulse should be examined for rate,
rhythm, amplitude and waveform, and the
character of the arterial wall should be assessed .
Rate heart rate is a simple means of detecting
bradycardia (< 60 beats/minute) or tachycardia
(> 100 beats/minute) arising physiologically (e.g.
exercise, emotion) or as a forewarning of
dysrhythmia.

Rhythm two abnormal rhythms are common and are

sometimes confused:
atrial fibrillation
multiple extrasystoles.
They are characterized by differences in periodicity
and volume, but clinical differentiation may be
difficult.
Volume a low-volume pulse can result from low
blood pressure
Waveform it is best to seek an abnormal waveform in an
artery larger than the radial artery

Palpation

of the cardiac impulse

normal
hyperdynamic
sustained

Heart sounds
A comfortable, practical stethoscope with a diaphragm and
a bell is needed.
Practice in use of the stethoscope and in interpretation of
what is heard are more important
Low-frequency and medium-frequency sounds (e.g. third
and fourth heart sounds, mid-diastolic murmurs) are
more easily heard with the bell applied lightly to the
chest wall.
The diaphragm is more appropriate for high-frequency
sounds (e.g. first and second heart sounds, opening
snap, ejection and some regurgitant murmurs).
Pressing hard with the bell tightens the skin and converts
the bell into a diaphragm.
The traditional method of placing the stethoscope over the
mitral, aortic, pulmonary and tricuspid areas is of
value only in determining which valve is most likely to be
the source of the murmur.

 First

heart sound:
S1 marks the onset of systole.
It is produced mainly by mitral valve
closure and, to a lesser extent, by
tricuspid valve closure.
Timing of the heart sounds is aided
by gently palpating the carotid
pulse with the fingers of the left
hand

Second heart sound:

S2 is produced by closure of the aortic and pulmonary valves,
and marks the end of systole and the beginning of diastole.
The valves close asynchronously; the aortic valve closes first.
The aortic component of S2 is accentuated:
by systemic hypertension
in thin-chested individuals with a forward- projecting
aorta.
The aortic component of S2 is reduced in intensity in patients
with:
poorly mobile cusps (e.g calcification)
aortic root dilatation (e.g. syphilitic aortitis).
Pulmonary hypertension accentuates the pulmonary component.

The intensity of S1 varies with the position of the

valve cusps at the onset of ventricular
contraction.
Their position is determined by the volume and
pressure of blood on either side of the valve;
the wider apart the cusps at the onset of
systole, the louder the sound produced.
Any change in cusp position at the onset of
systole affects the sound produced
it varies with, for example:
PR interval
rate of valve closure
valve mobility
force of ventricular systole.

 Heart

sounds and their relationship

to the first (S1) and second (S2)
sounds
Splitting of S2
Splitting of S1
Fourth, presystolic, heart sound
Third heart sound
Ejection click (preceding aortic or
pulmonary systolic murmur)
Opening snap
Mid-systolic ejection

Splitting physiological splitting becomes greater

with inspiration,because pulmonary vascular
impedance is reduced during inspiration in relation
to systemic impedance, but it becomes fixed in:
atrial septal defect
left-to-right and bidirectional shunts
right heart failure.
In reversed splitting (P2 precedes A2), the splitting is
maximum in expiration.
Common causes are left bundle branch block and
pacing.
Prolonged ejection time in aortic stenosis also causes
reversed splitting

Third and fourth heart sounds:

additional heart sounds may occur in early
diastole (S3) and late diastole (presystole S4).
They result from rapid ventricular filling; S3 when
the atrioventricular pressure gradient is high,
and
S4 as atrial contraction gives a boost to
ventricular filling.
Heart muscle can be viewed as thixotropic; it
can be slowly stretched using little force, but
sudden stretching

 Murmurs
are graded on a four-point or, more commonly a
six-point scale is:
grade 1 audible with difficulty
grade 2 faint but recognizable
grade 3 moderate intensity
grade 4 loud
grade 5 louder, but still needing a stethoscope
grade 6 audible without a stethoscope.It is a
common misconception that the intensity of
the murmur indicates the severity of the valve
defect.

Common heart murmurs

Aortic systolic ejection following an ejection
click
Pansystolic murmur of mitral regurgitation
Early aortic diastolic murmur
Mid-diastolic and pre-systolic murmurs of
mitral stenosis

It

is a common misconception that

the intensity of the murmur indicates
the severity of the valve defect

Auscultation of the heart sounds provides a

helpful clue.
If A2 is clearly audible at the apex, it is likely to
be a systolic ejection murmur.
If A2 is audible at the base but not at the apex, it
is probably a systolic regurgitant murmur.
An ejection systolic murmur is accentuated by a
post-ectopic beat; a regurgitant murmur
remains unchanged.
Sustained handgrip, by increasing blood
pressure, accentuates systolic regurgitant
murmurs but diminishes systolic ejection
murmurs.
Aortic systolic murmurs often radiate to the neck.
Mitral systolic murmurs often radiate to the
axilla.

Innocent murmurs : increased flow through a normal valve in pregnancy,

anaemia or thyrotoxicosis. Young children with a thin chest wall
sometimes have a precordial vibratory murmur of no pathological
significance.
Papillary muscle rupture and dysfunction, or chordal rupture, produces a
loud crescendodecrescendo murmur heard widely over the precordium.
Diastolic murmurs occur early, during mid or late diastole.
Early diastolic murmur, beginning immediately following S2, arises from
aortic or pulmonary regurgitation and rapidly diminishes in a decrescendo
manner.
Mid-diastolic murmurs are produced by rapid LV filling through a
stenosed mitral or tricuspid valve, or when a left atrial myxoma or severe
aortic regurgitation (Austin Flint murmur) impedes LV filling.
Late (presystolic) murmurs arise when atrial systole ejects blood through
a stenosed mitral or tricuspid valve; patients with mitral stenosis and atrial
fibrillation thus do not have a presystolic murmur.