ATRIAL F IBRILLATION PBL I

Electrocardiogram (ECG):

AF is mainly diagnosed on ECG, performed routinely when irregular heart beat

suspected
Findings = absence of P waves, irregular R-R intervals and conduction of impulses

Echocardiogram:

Performed generally in newly diagnosed AF

Ultrasound-based, usually Transesophageal (TEE) where a probe is placed in the
oesophagus
Help identify valvular heart disease (which increase stroke risk) + left and right
atrial size

Chest X-ray:

Used not necessary in most pt with AF, only when a reversible cause is suggested
or more evaluation needed to determine path of treatment
If pulmonary cause of AF suggested or other cardiac conditions suspected
reveal problem in lungs or blood vessel e.g. pneumonia

Holter monitor:

Ambulatory heart monitor that monitors heart rate for short duration of time of
24hours

Blood tests:

Thyroid gland activity usually measured as over-activity provokes AF

If suffered chest pain, troponin; marker of cadiac muscle damage is measured.
detect abnormalities in blood oxygen and carbon dioxide levels, electrolytes as
well

Introduction to the ECG [Vanessa]

Electrocardiogram (ECG) is a recording of the electrical activity of the heart.

As heart is excited the area surrounding the heart will have a current flow. This is
detected at the body surface using electrodes.

Detects disturbances in cardiac rhythm and conduction and extent and location of
the damage.

Fluctuations in potential differences create the P-QRS-T pattern.

P wave: atrial depolarisation

QRS complex: ventricular depolarization

T wave: slow, low-amplitude deflection from ventricular repolarisation

Depolarisation towards the positive electrode produces an upward deflection on

an ECG, as does repolarisation away from the positive electrode.

ECG records 12 projections called leads

o

6 leads are obtained by recording voltages from the limbs (I, II, III, AVR,
AVL, AVF)

Other 6 leads record potential between points on the chest surface and an
average of the 3 limbs (V1-6)

ECG reading looks different depending

position of the lead in relation to the heart.

Atrial fibrillation is often detected on an ECG as fine oscillations of the baseline

with no clear P waves. The QRS rhythm is rapid and irregular.

o
Causes

Coronary artery disease

Heart attack

Illicit drugs (specifically cocaine)

on the

Certain medications

Undergoing heart surgery

Congenital heart defects

Abnormal heart valves

Viral infections

Overactive thyroid

Metabolic imbalance

Sick sinus syndrome (dysfunction of the hearts natural pacemaker)

AF can be classified based on whether it:

1) Occurs without identifiable cause in patients with a structurally normal heart
(about 15%)
In this case it could be due to rapid activity often extending from the left atrium
(SA node) into the proximal parts of pulmonary veins leading to initiation of AF
linked to imbalance of parasympathetic/sympathetic activity or prolongation of
the sinus node recovery time suggesting that dysfunction of the SA. Inefficient
and irregular firing SA compromises the overall activity of the heart. It results in
an increased heartbeat rate. This type is common with paroxysmal AF.
2) It complicates hypertension, valvar diseases such as stenosis, causing a rise in the
intra-cardiac pressure, mitral regurgitation, and tricuspid regurgitation, genetic
causes and inflammation. Structural damage may lead to loss of atrial contraction,
accompanying rapidity and irregularity of ventricular contraction.
Acute atrial fibrillation due to:

Alcohol toxicity
Chest infection
Hyperthyroidism

Strategies for acute management:

Ventricular rate control

o Achieved by drugs which block the AV node
Digoxin, calcium-channel blockers, -adrenergic blockers and
amiodarone
Cardioversion ( anticoagulation)
o Achieved either
Electrically by DC shock
If atrial fibrillation has been present for more than a few
days, it is necessary to anticoagulate the patient with
warfarin adequately for 3 weeks before elective
cardioversion to reduce the risk of embolization and for at
least 4 weeks afterwards
Medically either by
Antiarrhythmic drug such as a class Ic (sodium-channel
blocker decreases amplitude of action potential) or a class
III agent (prolongs action potential)

Complications of Atrial Fibrillation [Wei Chong]

CONGESTIVE CARDIAC FAILURE
Congestive cardiac failure, commonly known as heart failure, is one of the 2 major
complications which can arise from atrial fibrillation. It is a condition whereby the heart is
unable to pump enough blood to support the bodys metabolic needs. The fibrillating
atrium is unable to pump blood efficiently into the ventricles, and correspondingly, the
ventricles may be unable to maintain a stroke volume necessary to supply the bodys
metabolic needs, in accordance with Frank Starlings law of intrinsic regulation. However,
since 80% of ventricular filling occurs passively without atrial contraction, the ventricles
can usually still sustain a stroke volume sufficient to perfuse the body. Despite this, heart
failure is still a possibility, especially during periods of exertion, or when there are
problems associated with ventricular output in addition to atrial fibrillation
In addition, since the atria are unable to empty blood into the ventricles efficiently, it is
also thus unable to act as an efficient collector of blood from systemic and pulmonary

circulation. This results in the tissues retaining fluid, causing oedema. Of particular
concern are patients with left atrial fibrillation, which can result in pulmonary oedema.
Retention of fluid in the lungs in pulmonary oedema impedes the process of gaseous
exchange in the lungs. Levels of oxygen in the blood can drop, causing the body to
become hypoxic, further exacerbating the problem of inadequate perfusion already
brought on by heart failure. Patients might thus go into a state of shock due to
inadequate perfusion of the body.
EMBOLIC DISORDERS
The fibrillating atria are unable to pump out blood efficiently into the ventricles, causing
blood to stagnate. There is thus a higher risk of blood clot formation in the atria in atrial
fibrillation, as compared to in a normal heart. The blood clots can dislodge, and,
particularly if in the left atrium, can enter the systemic circulation through the left
ventricle. Patients with atrial fibrillation are thus at significantly increased risk of embolic
disorders such as stroke, and will usually have to be given anticoagulants such as
warfarin as a preventive measure. Other complications relating to emboli may include
ischaemia and subsequent necrosis and gangrene of tissues at the extremities, such as in
the digits, due to the fine network of blood vessels there which easily causes the lodging
of emboli. If emboli form in the fibrillating right atrium, it might go into pulmonary
circulation, lodging in the lungs and causing a pulmonary embolism.

Long Term Management of Cardiac Tachyarrhythmias [Dan]

The three primary methods of managing chronic arrhythmias are Antiarrhythmic drugs,
Catheter Ablation and Implantable Cardioverter Defibrillators (ICDs).
Antiarrhythmic Drugs
These drugs affect the rhythm and conduction of the heart, and so can be used to treat
arrhythmias. They are generally used for symptomatic relief in patients whose
tachyarrhythmias are not life threatening, or patients who have an ICD (see below).
These drugs can, however, have a proarrhythmic effect or reduce ventricular
contractility, so the use of the correct class of drug is very important. Generally, class Ic
agents are used for structurally normal hearts and class III agents in cases of structural
heart disease. In brief, the different classes are;
Class 1 drugs act as membrane depressants, reducing the entry rate of Sodium. Class 1a
drugs also lengthen the action potential, class 1b shortens and class 1c does not affect
the action potential. These drugs should not be prescribed to patients with structural
heart disease. Class 2 drugs are beta blockers, which act to suppress AV node
conduction. They have proven benefits post myocardial infarction and in patients with
congestive heart failure. These drugs should be considered when treating symptomatic
arrhythmias, particularly when coronary heart disease is present. Class 3 drugs prolong
the action potential. They have several possible severe complications, but they are used
in patients with structural defects as they do not affect the rate of Sodium transportation.
Catheter Ablation
Ablation is an invasive procedure used for the treatment of chronic arrhythmias. It
involves placing electrical stimulators and recorders in locations within the heart, and
triggering the arrhythmia to pinpoint its location. The abnormal tissue causing the
incorrect electric signaling is the ablated. It has a very high success rate amongst young
sufferers, however myocardial remodeling, due to long term chronic arrhythmias, reduces
the success rate.
Implantable Cadioverter Defibrillator

The ICD is a device, only slightly larger than a pacemaker, which is inserted pectorally in
patients whose chronic arrhythmias are life threatening. They are also occasionally
implanted in patients who are extremely high risk for an arrhythmia. The ICD can
recognize fibrillation or tachycardia and deliver a defibrillating shock or act as a
pacemaker, whichever is appropriate. The ICD is currently the most successful treatment
option, with several large multicentre studies showing that it reduces mortality over time
more successfully than drug treatment. The ICD has reduced deaths from arrhythmias in
chronic sufferers to less than 2% (patients are still at a higher risk for other cardiac
complications, however.