Download Atrial fibrillation

Welcome to the
Medical Risk Webinar:
Cardiology
4 October 2013
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The heart (beat)
The primary function of the heart is to supply
blood and nutrients to the body
This is accomplished by regular beating
[contraction] of the heart
Each heart beat is controlled by electrical
impulses travelling through the heart at regular
intervals
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Interior of heart
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The heart consists of 4 cavities filled with blood
Right & left atria (RA/LA)
Right & left ventricles (RV/LV)
Atria form curved top - apex
Ventricles meet at bottom
to form pointed base
• Atria & ventricles separated
by valves
• Left ventricle largest
Systemic & pulmonary circulation
The human heart is placed in the
middle of a circle shaped like the
figure ‘8’
It is structurally and functionally
compartmentalised to create a
double pump
The left half pumps oxygenated
blood to the general circulation
-the systemic circulation
The right half pumps deoxygenated
blood to the lungs
- the pulmonary circulation
Conducting system
Conduction pathways & the heartbeat
• The rhythmic contraction of the heart is
called the heart beat
• The impulse to contract is generated
intrinsically in specialised tissue in the
wall of the right atrium (SA node) and
modified when necessary extrinsically by
the autonomic nervous system
(particularly the vagus nerve)
Anatomy – conducting system
Electrical impulses from the conducting
system cause the heart to beat - contract
The electrical signal begins at
sinoatrial [SA] node and
causes the atria to contract
SA node = ‘pacemaker’
The signal then passes through
Atrio-ventricular [AV] node
which checks the signal and
sends it through the muscle
fibres of the ventricles,
causing them to contract
Arrhythmias
A heart beating regularly, albeit varying with breathing, at
60-100 (120 USA) bmp is said arbitrarily to be in normal
sinus rhythm - any variation from this is, by definition, is
an arrhythmia
determining an arrhythmia usually requires an electrocardiogram
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Arrhythmias
• The most common arrhythmia is an extrasystole
• A few people will suffer from recurrent arrhythmias but it is difficult to
obtain any precise figures about prevalence as many arrhythmias
are asymptomatic and go unreported
• The range of arrhythmias varies from innocent extrasystoles to
immediate life-threatening conditions such as asystole or ventricular
fibrillation
• Arrhythmias may be present in the absence of cardiac disease, but
are more commonly associated with structural heart disease or
external provoking factors
• Transient arrhythmias, such as extrasystoles, are very common
and do not usually indicate heart disease
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The heartbeat
A heartbeat is a two-part pumping action that
takes about a second.
Part 1
As blood collects in the right and left atria, the SA
node sends out an electrical signal that causes
the atria to contract.
This contraction pushes blood through the tricuspid
and mitral valves into the resting right and left ventricles.
This is the longer part of the two-part pumping phase
and is called diastole
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The heartbeat
Part 2 of the pumping phase begins when the ventricles
are full of blood.
The electrical signals from the SA node travel through
the AV node along a pathway of cells to the ventricles
causing them to contract. This is called systole.
The pulmonary and aortic valves are
pushed open.
Blood is squeezed from the ventricles to the lungs, via
the pulmonary artery and to the coronary arteries and
other parts of the body through the aorta.
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Diagramtic representation
Atrial depolarisation
Atria
SA node
AV node
Ventricles
Ventricular depolarisation
His-Purkinge system
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The Sinus (SA) Node
The onset of depolarisation in the healthy heart begins
within a focus of pacemaker cells found at the upper
right border of the heart.
These cells which give the initial activation are collectively
known as the sinus (or sinoatrial) node
Healthy rhythms are classified by heart rate as follows:
Sinus rhythm — a heart rate between 50 and 100 (120) bpm.
Sinus tachycardia — a heart rate over 120 bpm.
Sinus bradycardia — a heart rate below 50 bpm.
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Sinus Rhythm
Sinus rhythm occurs when the sinus node depolarises
spontaneously, and the consequent wave of depolarisation
follows the natural pathways through the heart.
When this electrical impulse is released from the SA node
it causes the atria to contract
The following ECG trace shows sinus rhythm at a rate of 77 bpm.
Each QRS complex (shaded) is preceded by a P wave (arrowed) of
regular shape
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Reminder of ECG nomenclature
P wave = activation (depolarization) of atria.
QRS complex = depolarization of ventricles,
T wave = ventricular repolarisation
PR interval = time interval between onset of atrial depolarization and
onset of ventricular depolarization
QT interval = time interval between onset of ventricular depolarization
and end of ventricular repolarisation
R-R interval = time interval between 2 QRS complexes
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The Atrioventricular (AV) Node
The atrioventricular node introduces a delay in
conduction which allows atrial contraction to fill the
relaxed ventricles before ventricular contraction
pushes blood around the body
It also acts as a gate to prevent the ventricles from
contracting too rapidly in response to atrial arrhythmias
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Abnormal rhythms
• Abnormal heart rhythms (arrhythmias)
result from disorders of the normal
conducting system
They fall into two general types:
• excessively slow heart rates, known as
bradyarrhythmias or bradycardias, and
• excessively fast [rapid] heart rates,
known as tachyarrhythmias or
tachycardias
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Arrhythmias
Fast – tachycardias
Slow - bradycardiaas
Classified where they begin
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Supraventricular [atria]
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SVT
AF
etc
Ventricular [ventricles]
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Ventricular ectopics
Ventricular tachycardias
VF
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Atrioventricular node & heart block
Atrioventricular block describes a
partial or total interruption of the
conduction of electrical impulses from
the atria to the ventricles
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Atrioventricular block
AV block is classified as follows:
First degree — all heart beats are conducted
from the atria to the ventricles. The conduction,
however, is delayed
Second degree — some, but not all, heart
beats are conducted from the atria to the
ventricles
Third degree — no heart beats are conducted
from the atria to the ventricles
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Supraventricular tachycardia [SVT]
• The atrial arrhythmias vary considerably in their rate and
regularity, their clinical manifestations and the setting in
which they occur.
• SVT is a common clinical condition
• The pulse has a regular, rapid rhythm and occurs in
people of all age groups
• SVT is a general term that describes tachycardias
arising from within the atria or the atrioventricular node
• It is the preferred term as the exact cause of the
tachycardia is not always obvious from reviewing the
ECG
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Atrial fibrillation
• Atrial fibrillation (AF) is a common arrhythmia
• It is a significant public health problem affecting almost
5% of the population in people over 70 years of age
• The prevalence of AF increases with advancing age
• Data from the Framingham heart study show that AF is
associated with a 1.5- to 2.0 - fold higher risk of death,
because of a 5 fold increase in thrombo-embolic stroke
• About 1/3 of people with AF have no symptoms
• However, many experience a wide variety of symptoms,
including palpitations, dyspnoea, fatigue, dizziness and
angina
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Types of Atrial Fibrillation
Paroxysmal AF recurrent fibrillation that
terminates spontaneously within 7 days
Persistent AF lasts longer than 7 days or
doesn’t stop without treatment
Permanent (longstanding) AF persisting
for more than a year, and possibly
Acute-onset AF sudden onset (NICE 2006)
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Aetiology of AF
Known risk factors include:
• male sex,
• valvular heart disease (rheumatic valvular disease),
• congestive heart failure,
• hypertension, and
• diabetes
• hyperthyroidism
Additional risk factors, such as
– advanced age
– prior history of stroke
– diabetes, and
– hypertension,
place patients with pre-existing AF at even higher risk for further
co-morbidities such as stroke
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Atrial fibrillation
Atrial fibrillation is usually due to constant conduction within
the atria caused by multiple circuits.
Certain parts of the atria are depolarising whilst other parts
are repolarising.
This causes a loss of atrial contraction due to the ineffective
quiver of the muscle
P waves are absent from the ECG and the baseline consists of irregular
waveforms that continuously change in shape, duration, amplitude, and
direction.
The resulting ventricular response (seen as QRS complexes) is completely
irregular
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Atrial fibrillation
In this ECG tracing the QRS complexes (arrowed) form an irregular rhythm
with an average rate of 78 bpm. The ECG baseline (shaded) shows
Irregular waveforms
Patients are categorised clinically based on whether their atrial fibrillation
is paroxysmal (self-terminating), persistent (can be converted to sinus rhythm),
or permanent (unable to convert or maintain sinus rhythm)
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Atrial fibrillation
Investigations
• A thorough history, physical examination, and an ECG
are key to making an accurate diagnosis
Blood tests include:
• A thyroid function study to exclude hyperthyroidism.
• Blood count.
• Kidney and liver function
• Digoxin level if taken
Other tests include a chest X-ray, echocardiogram and 24
rhythm tape and where chest pain is a symptom catheter
studies [coronary angiogram]
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Atrial fibrillation
Treatment
• Generally the initial aim of treatment is to control the
rhythm, however
• In some patients with longstanding disease the
focus is on rate control – these are usually patients
with permanent AF (BMJ Sept 2013)
• Two randomised controlled trials have demonstrated
that a strategy aimed at restoring (and maintaining)
sinus rhythm (rather than rate) neither improves the
survival rate nor reduces the risk of stroke
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Treatment of AF
• Rhythm control
– Flecanide and Amiodarone are used but in many patients
(43-67% meta-analysis) they are not effective and, have
significant side effects
• Rate control
– Beta-blockers and calcium channel blockers are the drugs
of choice for rate control. They are effective at rest and
with exertion
– Digoxin can be used in the acute setting but does little to
control the ventricular rate in active patients
• Anticoagulation
– AF is recognized as a powerful risk factor for stroke
– One of the most important concerns in treating patients is
the need for anticoagulation
– Effective anticoagulation in patients with AF reduces the
risk of stroke 3-fold
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Treatment of AF
Cardioversion
• Pharmacological
– in the absence of structural heart disease, a drug such as
flecainide or propafenone is the drug of choice
– in the presence of structural heart disease, amiodarone
should be the drug of choice
• Electrical
– External and internal
Catheter ablation
– Suitable for patients with no underlying structural or
valvular disease (about 2% patients with AF under 60
years) and paroxysmal disease (BMJ Sept 2013)
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Atrial fibrillation
Elective conversion to sinus rhythm
• The longer patients are in AF, the more likely they are to develop
atrial thrombus
• In general, if the arrhythmia is present for less than 48 hours,
cardioversion can be accomplished safely without further need for
anticoagulation
• In patients with AF longer than 48 hours in duration or of unknown
duration, cardioversion is not recommended until sufficient
anticoagulation is achieved
• Because embolic events can occur following cardioversion as atrial
mechanical function returns, continued anticoagulation for an
additional 4-6 weeks is usually required
• Pacing devices are available to prevent AF from recurring in
susceptible individuals
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AF
Atrial fibrillation carries a particularly poor
prognosis if associated with:
• Mitral valve disease
• Enlargement of the left atrium
• Hypertension
• Old age
• Diabetes
• History of embolism
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Ventricular arrhythmias
The term ventricular arrhythmia refers to any cardiac
rhythm in which both the pacemaker site and conduction
path are confined to the ventricles
Arrhythmias arising from the ventricles are less
common than SVTs and are more likely to be found
in people with heart disease
Conduction irregularities that bypass the atrioventricular node will cause the
ventricles to be stimulated early and not through the standard pathways
This is referred to as ventricular pre-excitation
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Ventricular arrhythmias
Ventricular ectopic beats
• The most common type of ventricular ectopic
beat is premature, causing ventricular
contraction before the underlying rhythm would
normally depolarise the ventricles
• The resultant heartbeat morphology on the ECG
often appears wider and taller than that seen
with the underlying rhythm
• Ventricular ectopic beats may indicate heart
disease, be induced by stimulation (e.g., stress,
alcohol, caffeine, medication, cocaine, or
amphetamines) or occur naturally - innocently
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Ventricular ectopic beats
Ventricular ectopic beats may occur in patterns, such as:
•bigeminy (every other beat),
•trigeminy (every third beat), or
•quadrigeminy (every forurth beat).
They may also occur in sequences, such as couplets,
triplets, salvos (four to seven), or episodes (eight or more)
This ECG tracing shows ventricular bigeminy, in which every other beat is
a ventricular ectopic beat. These beats are premature, wider,
and larger than the sinus beats
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Ventricular tachycardias
Ventricular tachycardia occurs when a rapid and
repetitive conduction path exists entirely within the
ventricles
Usually a re-entrant arrhythmia, it is often caused as
a result of scarred heart tissue. Once the conduction
circuit is initiated, the rhythm may stabilise, extinguish
and revert to sinus rhythm, or degenerate into
ventricular fibrillation.
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Ventricular fibrillation [VF]
• VF arises when there is uncoordinated
contraction of the cardiac muscle of the
ventricles in the heart.
• As a result the heart fails to adequately
pump blood and hypoxia (shortage of
oxygen) will occur followed by
unconsciousness within 20 - 30 seconds.
• Ventricular fibrillation is a medical
emergency
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Ventricular fibrillation [VF]
Ventricular fibrillation is a cause of cardiac arrest and sudden cardiac
death
The ventricular muscle twitches randomly, rather than contracting in unison,
and so the ventricles fail to pump blood into the arteries and into
systemic/pulmonary circulation
Ventricular fibrillation is a sudden lethal arrhythmia responsible for
many deaths in the Western world, mostly brought on by ischaemic
heart disease
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Arrhythmias
Prognosis
• Prognosis depends on the type of
arrhythmia. There may be no excess
mortality (e.g. with extra systoles), or a
very high mortality (e.g. ventricular
fibrillation).
• A worsening prognosis occurs if the
arrhythmia is associated with other
aggravating factors such as cardiac
ischaemia
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