Palpation of the precordium

Technique
• Place fingertips over apex (1) to assess for
position and character
• Place heel of hand over left sternal edge (2) for a
• parasternal heave or ‘lift’
• Assess for thrills in all areas, including the aortic
and pulmonary areas (3)
Normal position is the 5th or 6th intercostal space,
at the mid-clavicular line.
Common abnormalities of the apex beat
• Volume overload, such as mitral or aortic
regurgitation: displaced,thrusting
• Pressure overload, such as aortic stenosis,
hypertension: discrete,heaving
• Dyskinetic, such as left ventricular aneurysm:
displaced, incoordinate
Other abnormalities
• Palpable S1 (tapping apex beat: mitral
stenosis)
• Palpable P2 (severe pulmonary hypertension)
• Left parasternal heave or ‘lift’ felt by heel of
hand (right ventricular hypertrophy)
• Palpable thrill (aortic stenosis)
 Auscultation of the heart
• Use the diaphragm to examine at the apex,
lower left sternal edge (tricuspid area) and
upper left (pulmonary area) and right (aortic
area) sternal edges
• Use the bell to examine low-pitched noises,
particularly at the apex for the mid-diastolic
murmur of mitral stenosis
• Time the sounds and murmurs by feeling the
carotid pulse; the first heart sound (S1) just
precedes the upstroke of the pulse and the
second heart sound (S2) is out of step with it
• Systolic murmurs are synchronous with the
pulse
• Listen for radiation of systolic murmurs, over
the base of the neck (aortic stenosis) and in
the axilla (mitral incompetence)
• Listen over the left sternal border with the
patient sitting forward (aortic incompetence),
then at the apex with the patient rolled on to
the left side (mitral stenosis)
• Myocardial cells constitute 75% of the heart
mass but only about 25% of the cell number

• They are designed to perform two

fundamental functions: initiation and
conduction of electrical impulses and
contraction
• Although most myocardial cells are able to
perform both these functions, the vast
majority are predominantly contractile cells
(myocytes) and a small number are specifically
designed as electrical cells
• The latter, collectively known as the
conducting system of the heart, are not
nervous tissue but modified myocytes
• They have the ability to generate electrical
impulses, which are then conducted to the
myocytes, leading to contraction by a process
known as excitation–contraction coupling
• The rate of electrical impulse generation and
the force of myocardial contraction are
modified by numerous factors, including
autonomic input and stretch
• Three epicardial coronary arteries supply blood to
the myocardium, and a more complex network of
veins is responsible for drainage
• As there is continuous arterial pressure
fluctuations, blood vessels, especially in the
cerebral circulation, maintain constant tissue
perfusion by a process known as
‘autoregulation’; blood vessel control is,
however, complex, involving additional local and
central mechanisms
 The conduction system of the heart
The sinus node (sinoatrial node)
• a complex, spindle-shaped structure that lies in
the lateral and epicardial aspects of the junction
between the superior vena cava and the right
atrium
• Physiologically, it generates impulses
automatically by spontaneous depolarization of
its membrane at a rate quicker than any other
cardiac cell type
• It is therefore the naturalpacemaker of the heart.
• During normal (sinus) rhythm, this
depolarisation wave propagates through both
atria via sheets of atrial myocytes
• The annulus fibrosus forms a conduction
barrier between atria and ventricles, and the
only pathway through it is the AV node
• This is a midline structure, extending from the
right side of the interatrial septum,
penetrating the annulus fibrosus anteriorly
• The AV node conducts relatively slowly, producing a
necessary time delay between atrial and ventricular
contraction
• The His–Purkinje system is composed of the bundle of His
extending from the AV node into the interventricular
septum, the right and left bundle branches passing along
the ventricular septum and into the respective ventricles,
the anterior and posterior fascicles of the left bundle
branch, and the smaller Purkinje fibers that ramify through
the ventricular myocardium
• The tissues of the His–Purkinje system conduct very rapidly
and allow near-simultaneous depolarisation of the entire
ventricular myocardium
 Cardiac arrhythmia
• Defined as a disturbance of the electrical
rhythm of the heart often a manifestation of
structural heart disease but may also occur
because of abnormal conduction or
depolarisation in an otherwise healthy heart
• Tachycardia: heart rate of more than 100/min
• Bradycardia: heart rate of less than 60/min
 Clinical features
• Many arrhythmias are asymptomatic but
sustained tachycardias typically present with
rapid palpitation, dizziness, chest discomfort or
breathlessness
• Extreme tachycardias can also cause syncope
because the heart is unable to contract or relax
properly at extreme rates
• Bradycardias cause fatigue, lightheadedness and
syncope
• Extreme bradycardias or tachycardias can
precipitate sudden death or cardiac arrest
• The first-line investigation is a standard 12-
lead ECG, which can be diagnostic in many
cases
• If arrhythmias are intermittent and the resting
ECG is normal, an attempt should be made to
capture the abnormal rhythm using an
ambulatory ECG or a patient-activated ECG
Management
 Sinus arrhythmia
• This is defined as a cyclical alteration of the heart
rate during respiration, with an increase during
inspiration and a decrease during expiration
• A normal phenomenon and can be quite
pronounced in children
• Absence of this normal variation in heart rate
with breathing or with changes in posture may
due to diabetic neuropathy, diseases of
peripheral nerves
• Sinus arrhythmia does not require treatment
 Sinus bradycardia
• This may occur in healthy people at rest and is a
common finding in athletes
• If asymptomatic, then no treatment is required
• Symptomatic sinus bradycardia may occur acutely
during an MI and can be treated with intravenous
atropine
• Patients with recurrent or persistent symptomatic
sinus bradycardia should be considered for
pacemaker implantation
 Sinus tachycardia
• Sinus tachycardia is usually due to exercise,
emotion and pregnancy
• Healthy young adults can produce a rapid
sinus rate, up to 200/min during intense
exercise
• Sinus tachycardia does not require treatment
but sometimes may reflect an underlying
disease
 Sick sinus syndrome
• can occur at any age but is most common in
older people
• Caused by fibrosis, degenerative changes or
ischaemia of the SA node
• Causes palpitation, dizzy spells or syncope,
due to intermittent tachycardia, bradycardia,
or pauses with no atrial or ventricular activity
(SA block or sinus arrest)
 Treatment
• Permanent pacemaker may benefit patients with
troublesome symptoms due to spontaneous
bradycardias, or those with symptomatic
bradycardias induced by drugs required to
prevent tachyarrhythmias
• Atrial pacing may prevent episodes of atrial
• Fibrillation
• Pacing improves symptoms but not prognosis,
and is not indicated in patients who are
asymptomatic
 Heart block
• Heart block or conduction block may occur at
any level in the conducting system
• Block in either the AV node or the His bundle
results in AV block, whereas block lower in the
conduction system produces bundle branch
block
Atrioventricular(AV) block
• There are three forms
• First, Second, Third(complete) degree
 Atrial tachyarrhythmias

• Includes: atrial fibrillation, atrial flutter, atrial

tachycardia and atrial ectopic beats, all arise from
the atrial myocardium
• They share similar aetiologies: increasing age,
myocardial infarction, hypertension, obesity,
diabetes mellitus, hypertrophic cardiomyopathy,
heart failure, valvular heart disease, myocarditis,
pericarditis, cardiothoracic surgery, electrolyte
imbalance, alcohol use, obstructive airway
disease, chest infections and hyperthyroidism
 Atrial flutter
• Atrial flutter is characterised by re-entry
circuit, usually within the right atrium
encircling the tricuspid annulus.
• The atrial rate is approximately 300/min
• ECG shows saw-tooth flutter waves
 Management
• Medical management with digoxin, β-blockers or
verapamil
• Restore sinus rhythm by direct current (DC)
cardioversion
• After cardioversion, β-blockers or amiodarone
can be used to prevent recurrent episodes
• Catheter ablation is a highly effective
treatment,offering a greater than 90% chance of
complete cure, Anticoagulant management in
patients with atrial flutter
 Ventricular fibrillation
• This involves very rapid and irregular ventricular
activation with no mechanical effect
• The patient is pulseless and becomes rapidly
unconscious
• Respiration ceases (cardiac arrest)
• The ECG shows shapeless, rapid oscillations and there
is no hint of organized complexes
• usually provoked by a ventricular ectopic beat
• Ventricular fibrillation rarely reverses spontaneously
• Only effective treatment is electrical defibrillation
• Basic and advanced cardiac life support is needed
• If the attack of ventricular fibrillation occurs
during the first day or two of an acute myocardial
infarction, it is probable that prophylactic therapy
will be unnecessary
• If the ventricular fibrillation was not related to an
acute infarction, the long-term risk of recurrent
cardiac arrest and sudden death is high
• Implantable cardioverter–defibrillators are first-
line therapy in the management of these patients
Congenital Heart Disease
• A congenital cardiac malformation occurs in
about 1% of live births
• There is an overall male predominance, although
some e.g. atrial septal defect and persistent
ductus arteriosus) occur more commonly in
females
• As a result of improved medical and surgical
management, more children with congenital
cardiac disease are surviving into adolescence
and adulthood
 Fetal circulation
• In the developing fetus, oxygenated blood and
nutrients are supplied to the fetus via the
placenta and the umbilical vein
 Congenital
cardiac malformations
• Ventricular septal defect 30
• Atrial septal defect 10
• Persistent ductus arteriosus 10
• Pulmonary stenosis 7
• Coarctation of aorta 7
• Aortic stenosis 6
• Tetralogy of Fallot 6
• Complete transposition of great arteries 4
• Others 20
 Presentation of congenital heart
disease
throughout
Birth and neonatal period
life
Adolescence and adulthood
• Cyanosis • Heart failure
• Heart failure • Murmur
• Arrhythmia
Infancy and childhood • Eisenmenger’s syndrome
• Cyanosis • Hypertension
• Heart failure (coarctation)
• Arrhythmia • Complications of previous
• Murmur cardiac surgery:
• Failure to thrive Arrhythmia related to
scarring
Heart failure secondary to
scarring
 Aetiology
Often unknown but recognized associations include:
• maternal prenatal rubella infection (persistent ductus
arteriosus, and pulmonary valvular and arterial stenosis)
• maternal alcohol misuse (septal defects)
• maternal drug treatment and radiation
• genetic abnormalities (e.g. the familial form of atrial septal
defect and congenital heart block)
• chromosomal abnormalities (e.g. septal defects and mitral
and tricuspid valve defects, which are associated with Down
syndrome (trisomy 21), or coarctation of the aorta in Turner
syndrome (45, XO)
 Ventricular septal defect
• Most common congenital cardiac
malformation (1 : 500 live births)
• The haemo dynamic consequences are
dependent on the shunt size
• Left ventricular pressure is higher than right;
blood therefore moves from left to right and
pulmonary blood flow increases
 Investigations and treatment
• A small VSD produces no abnormal X-ray or ECG
findings
• In larger defects, the chest X-ray prominent pulmonary
arteries
• Pulmonary hypertension may be ‘pruned’ pulmonary
arteries on x-ray
• Cardiomegaly occurs when a moderate or large VSD is
present
• ECG may show both left and right ventricular
hypertrophy
• Echocardiography can assess the size and location
• Interventional options are either surgical
patch repair or device closure
• Patients who have had a successful closure
have an excellent long-term outcome
 Atrial septal defect
Often first diagnosed in adulthood and represents one-
third of congenital heart disease
It is 2–3 times more common in women than in men
There are three main types of ASD
• Sinus venosus defects – located in the superior part of
the septum near the superior vena cava or the inferior
part of the septum near the IVC entry point
• Ostium secundum defects (75%) – located in the mid-
septum
• Ostium primum (atrioventricular septal) defects (15%)
located in the lower part of atrial septum
Symptoms: Dyspnoea and exercise intolerance, and may develop
atrial arrhythmias

• The chest X-ray may demonstrate prominent pulmonary

arteries
• Right bundle branch block and right axis deviation may be
present on the ECG
• Ostium primum defects may have left axis deviation on the
ECG
• Echocardiography may demonstrate hypertrophy and
dilatation of the right heart and pulmonary arteries
• The options for intervention include device closure using a
transcatheter clamshell device
• Surgical closure for all other ASD