2. OUTLINES
DEFINITION
THE HEART’S ELECTRICAL SYSTEM
TYPES OF ARRHYTHMIA
CAUSES OF ARRHYTHMIA
SIGNS AND SYMPTOMS
DIAGNOSES
TREATMENT
SIDE EFFECTS OF ANTIARRHYTHMIC AGENTS
THE ROLE OF PHARMACISTS IN THE MANAGEMENT OF
ARRHYTHMIAS
CONCLUSION
3. CARDIAC ARRHYTHMIA (CA)
• CA also known as dysrhythmia or irregular heartbeats is any of a large and
heterogeneous group of conditions in which there is abnormal electrical
activities in the heart. The heartbeat maybe too fast or too slow and maybe
regular or irregular. A heartbeat the is too fast is called tachycardia and a
heartbeat that is too slow is called bradycardia.
4. DEFINITION……….
• Although many arrhythmias are not life threatening, some can cause cardiac
arrest. During arrhythmia, the heart may not be able to pump enough blood
to the vital organs including the brain. Arrhythmia can occur in the upper
chambers of the heart (ATRIA) or in the lower chambers of the heart
(VENTRICLES).
•
To understand arrhythmia, it helps to understand the heart's electrical
system because this electrical system controls the rate and rhythm of the
heartbeat.
5. THE HEART’S ELECTRICAL SYSTEM
• With each heartbeat, an electrical signal spreads from the top of the heart to
the bottom and as the signal travels, it causes the heart to contract and
pump blood.
6. THE PROCESS OF HEARTBEAT
•
Each electrical signal begins in a group of cells called the sinus node or
Sinoatria node (SA NODE). The SA node is located in the heart's upper
right chamber (the right atrium). In a healthy adult heart at rest, the SA
node fires off an electrical signal to begin a new heartbeat 60-100
times/min. from the SA node, the electrical signal travels through special
pathways in the right and left atria, this causes the atria to contract and pump
blood into the heart’s lower chambers, the ventricles. This signal moving
through the atria is recorded as the P-WAVE on the EKG/ECG.
•
The electrical signal then moves down to a group of cells called the
atriaventricular (AV) node located between the atria and the ventricles.
Here the signal slows down just a little as it passes through the AV
node, allowing the ventricles time to finish filling with blood (ventricular
filling). On the EKG, this part of the process is the flat line between the end
of the P-waves and the beginning of the Q-waves.
7. ELECTRICAL SYSTEM……….
•
The electrical signal then leaves the AV nodes and travels along a pathway called
the BUNDLE OF HIS (PURKINJE FIBERS). This pathway divides into the right
bundle branch (going to the right ventricle) and the left bundle branch (going to the
left ventricle). This signal goes down this branches to the ventricles causing the
ventricles to contract and pump blood to the lungs and the rest of the body. This
process is recorded As the QRS-waves on the EKG. The ventricles then recovers
their normal electrical state showing as the T-wave on the EKG, the muscles stops
contracting to allow the heart refill with blood . A problem with any part of this process
can cause an ARRHYTHMIA.
8. TYPES OF ARRHYTHMIA
•
The four main types of arrhythmia are;
•
Premature (extra) beats
•
Supraventricular arrhythmia
•
Ventricular arrhythmia
•
Bradycardia
PREMATURE (EXTRA) BEATS (PB)
This is the most common type of arrhythmia, they are harmless most of the time and does not
cause any symptom, but when symptoms do occur, they usually feel like fluttering in the chest
or a feeling of a skipped heartbeat. Most of the time it does not need treatment especially in
healthy people. It can occur in the atria (premature atrial contraction) PACs, or in the
ventricles (premature ventricular contraction) PVCs.
PACs
PVCs
Causes; heart diseases, stress, too much exercise, too much caffeine and nicotine. It can
also happen naturally.
9. SUPRAVENTRICULAR ARRHYTHMIA (SVA)
These are tachycardia's (fast heart rates) that starts in the atria or AV node.
Types;
•
atrial fibrillation (AF)
•
atrial flutter
•
paroxysmal supraventricular tachycardia (PSVT)
•
wolf-parkinson-white syndrome (WPW)
ATRIAL FIBRILLATION (AF)
AF is the most common type of serious arrhythmia. It involves a very fast and irregular
contraction of the atria. In AF, the heart’s electrical signal do not begin in the SA
node, instead, they begin in another part of the atria or in the nearby pulmonary veins.
The signals may spread throughout the atria in a rapid, disorganized way. This causes
the walls of the atria to quiver very fast (fibrillate) and as a result the atria is not able to
pump blood into the ventricles the way it should. In AF, electrical signals can travel
through the atria at a rate more than 300 times/min. Some of these AF can travel to the
ventricles, causing them to beat too fast and with an irregular rhythm. AF isn't usually life
threatening, but it can be dangerous if it causes the ventricles to beat too fast.
10. COMPLICATIONS OF AF
• Stroke; this is due to blood pool in the atria causing clot to form which can
break away and travel to the brain. (Blood thinning medicines are therefore
important part of treatment for people with AF.)
• Heart failure; due to the ventricles beating very fast and can’t completely fill
with blood, thus may not be able to pump blood enough to the lungs and the rest
of the body.
CAUSES OF AF
Damage to the heart’s electrical system which can be as a result of ;
•
High blood pressure
•
Coronary heart disease
•
Rheumatic heart disease.
All of which affects the health of the heart.
Also; over reactive thyroid gland and heavy alcohol use is a risk factor. The risk of
AF increases wit age.
11. TYPES OF SVA…….
ATRIAL FLUTTER;
Similar to AF but here, the electrical signals spreads through the atria in a fast and
regular, instead of irregular rhythm (in AF). Atrial flutter is much less common than AF but
with similar symptoms and complications.
PAROXYSMAL SUPRAVENTRICAL TACHYCARDIA (PSVT)
PSVT is a very fast heart rate that begins and ends suddenly. It occurs because of
problem with electrical connections between the atria and ventricles. In PSVT, electrical
signal that begins in the atria and travels to the ventricles can reenter the atria causing
extra heartbeats. This type of arrhythmia occurs more in young people and can happen
during vigorous physical activity.
A special type of PSVT is called WOLF-PARKINSON-WHITE SYNDROME (WPW). It is a
condition in which the heart’s electrical signal travels along an extra pathway from the
atria to the ventricles. This extra pathway disrupts the timing of the electrical signal and
can cause the ventricles to beat very fast. This type of arrhythmia can life threatening.
12. VENTRICULAR ARRHYTHMIA (VA)
This arrhythmia starts in the heart’s lower chambers (the ventricles). They can be very
dangerous and usually requires medical care right away.
TYPES OF VA:
•
Ventricular tachycardia
•
Ventricular fibrillation.
CAUSES;
•
Coronary heart disease
•
Heart attack
•
Weakened heart muscles
13. • VENTRICULAR TACHYCARDIA
It is a fast, regular beating of the ventricles that may last for only a few seconds or more. A
few beats of the ventricular tachycardia often do not cause problems but episodes that lasts
for more than a few seconds can be dangerous and can turn into ventricular fibrillation .
• VENTRICULAR FIBRILLATION (VF)
This makes the ventricles quiver instead of pump normally, these can lead to cardiac arrest
and death can occur within a few minutes. To prevent death, the condition must be treated
right away with an electric shock to the heart called DEFIBRILLATION.
VF may occur during or after heart attack or in someone whose heart is already weak because
of another condition.
14. BRADYARRHYTHMIA
It occurs if the heart rate is slower than normal. If the heart rate is too slow, not enough
blood reaches the brain and this can cause the person to pass out. In adult, a heart rate
slower than 60beats/sec is considered a bradyarrhythmia. Although, some people
normally have slow heart rates, especially people who are very physically fit and this is
not dangerous in them.
Causes;
•
Heart attack
•
Underactive thyroid gland
•
Ageing (people older than 60yrs)
•
Imbalance in chemicals or other substances in the blood e.g. potassium
•
Medicines e.g. B-blockers, calcium channel blockers.
•
Some antiarrhythmic agents and digoxin
15. GENERAL CAUSES OF ARRHYTHMIAS
• Smoking,
• Heavy alcohol
• Drugs e.g. cocaine, amphetamines, too much caffeine or nicotine
• Strong emotional stress or anger
• Heart attack or other conditions that damages the heart’s electrical system
e.g. HBP, coronary heart disease, heart failure, over reactive or under
reactive thyroid gland and rheumatic heart disease.
• Congenital heart defects can cause arrhythmia such as wolf- Parkinsonwhite syndrome.
•
Causes of arrhythmias can sometimes be unknown.
16. SIGNS AND SYMPTOMS OF ARRHYTHMIA
Many arrhythmias can cause no sign and symptoms , but when there are signs and
symptoms, the most common ones are;
•
Palpitation
•
A slow heart beat
•
Feeling pauses between heartbeats
More serious signs and symptoms are;
•
Anxiety
•
Weakness, dizziness, light-headedness
•
Fainting or nearly fainting
•
Sweating
•
Shortness of b reath
•
Chest pain
17. DIAGNOSES
Because a number of tests are available for the diagnoses of cardiac arrhythmia, it is
important to proceed with a stepwise approach. The goal is to obtain a correlation between
symptoms and the underlying arrhythmia and initiation of appropriate therapy. Additional
testing is usually advocated to identify patients wit arrhythmias due to ischemia or who are at
risk of sudden cardiac death.
ASSESSMENT OF STRUCTURAL HEART DISEASE.
This begins with history and physical examination. Careful attention to CAD or MI, family
history of sudden cardiac death are important.
•
ECG/EKG (Electrocardiography ): is a transthoracic interpretation of the electrical
•
CARDIAC AUSCULTATION: it may detect irregular heart rhythm or premature beats.
•
ECHOCARDIOGRAPHY: it is a test that uses sound waves to create a moving picture
•
EVENT RECORDING / LOOP RECORDERS: for patients that has symptoms occurring on
a weekly or monthly basis. This can be worn for months and can record infrequent
arrhythmia episodes.
activities of the heart over a period of time as detected by electrodes. It is used to detect
conduction system delay, QRS widening, previous MI or PVC.
of the heart. This test can detect the presence of CAD, LV dysfunctions or valvular heart
disease.
18. TREATMENT OF CARDIAC ARRHYTHMIAS
Treatment can be pharmacological (drugs) or non-pharmacological:
Pharmacological approach:
The CAST ( cardiac arrhythmia suppression trial) study published in 1989, radically changed
the use of antiarrhythmic medications. CAST was designed to test the hypothesis that
antiarrhythmic medication suppression of PVCs and non-sustained VT would improve
mortality in patients following myocardial infarction (MI) due to left ventricular dysfunction. The
medications used moricizine, flecanaide and encanaide were known to have potent ventricular
arrhythmia suppression properties. However, CAST demonstrated an increase in mortality in
patients treated with medications compared with placebo……..why?
It was suspected that this is because of the pro-arrhythmic effects (more frequent
occurrence of pre-existing arrhythmia) of these medications especially in the presence of
ischemia and LV dysfunction. Therefore, the type 1C drugs are contraindicated in
patients with CAD and ischemia . Quinidine was subsequently shown to increase
mortality in patients with atrial fibrillation.
Two major classification of antiarrhythmic agents:
•
The Vaughan William classification
•
The Sicilian Gambit classification
19. THE VAUGHAN WILLIAM CLASSIFICATION
.
CLASS
ACTION
EXAMPLES
1
Sodium channel blockers
1A
Depress phase 0 of action potential
(AP), delay conduction , prolong
repolarization.
Quinidine, procainamide,
disopyramide
1B
Little effect on phase 0 of AP in normal
tissues, depress phase 0 in abnormal
tissue, shortens or have little effects
on repolarization
Lidocaine, tocanamide,
mexilitine, diphenyl hydantoin
1C
Depress phase 0 of AP, markedly slow
conduction in normal tissues
Fecanamide, propafenone,
moricizine,
II
B-adrenergic blockers
Acebutalol, atenolol,
bisoprolol,carvedilol,metoprolo
l, pindolol, propranolol
III
Prolong AP duration by increasing
repolarization and refractoriness by
blocking K-channels
Amiodarone, sotalol,
dofetilide, bretylium, ibutilide.
IV
Calcium channel blockers
Diltiazem, verapamil.
others
Digoxin, adenosine
20. LIMITATIONS OF VW CLASSIFICATIONS
The VW scheme classifies drugs based on the primary mechanism of action which is
one the limitations of this classification e.g. Amiodarone has effects consistent with all of
the four classes, another limitation is lack of consideration for the effects of the
metabolites e.g. procainamide (class 1A) has a metabolite N-acetyl procainamide
(NAPA) which has class III action. Yet another limitation is that drugs like digoxin and
adenosine (important antiarrhythmic agents) had no place at all in this classification.
With regards to the management of atrial fibrillation, class 1 and III are used in rhythm
control, while class II and IV are used as rate control agents. Type 1C agents are
relatively safe when used in normal hearts.
Amiodarone due to its long half life (43days-months) and also low incidence of
proarrhythmia can be used at low doses in an outpatient setting with absence of sever
LV dysfunction or bradycardia.
The Sicilian Gambit classifications not regarded as a true classification because it does
not aggregate drugs into categories but has them on X and Y axis.
X-axis: listed drugs as in VW classification
Y-axis: chemicals, receptors, trials and clinical effects.
21. MAJOR SIDE EFFECTS OF ANTIARRHYTHMIC AGENTS
CLASS 1
•
Disopyramide: anticholinergic effects; dry mouth, urinary hesitancy, constipation
cardiac toxicity; due to its negative ionotropic effects.
proarrhythmic effects and hypoglycemia
•
Procainamide: lupus-like syndrome, blood dyscrasias, cardiac toxicity, proarrhythmia
•
Lidocaine: neurological toxicity, cardiovascular toxicity, GI toxicity
CLASS II: bradycardia, heart failure, hypotension, AV-node block. They should not be co-
administered with cardiac selective CCB e.g. verapamil because of their additive
effects in producing electrical and mechanical depression.
CLASS III: by prolonging action potential duration, they can lead to long QT syndrome
and this can trigger a type of ventricular arrhythmia known as TORSADE DE POINTES,
sotalol: bradycardia, hypotension, exacerbation of heart failure
CLASS IV: (cardiac selective non-dihydropyridines); excessive bradycardia, impaired
electrical conduction (AV-nodal block) and depressed contractility.
22. NON- DRUG TREATMENT OF CA
Other methods of treating arrhythmia are:
• Defibrillation: it is a common treatment for life threatening CAs.
This involves delivering a therapeutic dose of electrical energy
to the affected heart with a device called defibrillators.
• Radiofrequency ablation
• Surgery
• Artificial cardiac pacemakers
23. THE ROLE OF PHARMACISTS IN THE MANAGEMENT
OF CARDIAC ARRHYTHMIAS
•
Pharmacists have an important role to play in the treatment of patients with
arrhythmias. Arrhythmic medications are associated with many adverse effects as
well as numerous drug interactions. Pharmacists must closely monitor patients to
ensure they recieve effective therapy with minimal side effects.
•
Patients should receive extensive education to be able to recognize symptoms
associated with arrhythmias and toxic effects of individual antiarrhythmic agents or a
combination of these agents. Patients should be encouraged to check with their
pharmacists and physicians before selecting any OTC medication and encouraged to
avoid alternative treatments and herbal drugs.
•
Lastly, pharmacists in all practice settings should be familiar with automated
defibrillators as this is a life saving device.
24. CONCLUSION
• Management of CA has changed drastically in the last decades due to the
success of procedures such as radiofrequency ablation, surgery, and ICD
(implantable cardioverter defibrillators). Antiarrhythmic drugs has many
limitations including adverse effects, drug interaction and proarrhythmic
potentials. However many patients still rely on these drugs to control
symptoms and increase quality of life, it is therefore important for
pharmacists to have full understanding of arrhythmia as well as preventions
and treatments.
• Antiarrhythmic drug therapy in patients at low risk for serious arrhythmia
should be discouraged .
