OUTLINE FOR PRESENTATIONS

1. INTRODUCTION
2. EPIDEMIOLOGY
Atrial fibrillation, the commonest and most persistent form of cardiac arrhythmia was
shown to affect 33.5 million people worldwide (20.9 million males and 12.6 million
females) in the year 2010
Approximately 5.2 million Americans have AF, and as many as 8.8 million in the
European Union.
Prevalence and incidence of AF increase with advancing age; roughly 8% of patients
between 80 and 89 years old have AF. AF occurs more commonly in men than
women

A report by Noubiap and Nyaga (2019) states that the community-based prevalence of
AF was 4.3% and 0.7% in individuals aged ≥40 years and aged ≥70 years,
respectively.
The prevalence of AF ranged between 6.7% and 34.8% in patients with ischemic
stroke, between 9.5% and 46.8% in those with rheumatic heart disease (RHD),
between 5% and 31.5% in patients with dilated cardiomyopathy. The main risk factors
for AF were hypertension, affecting at least one-third of patients with AF, and
valvular heart disease (12.3%-44.4%) and cardiomyopathy (~20%).
3. PATHOPHYSIOLOGY

AF may be caused by both abnormal impulse formation and abnormal impulse

conduction.
In most patients AF is triggered by electrical impulses generated within the
pulmonary veins
These impulses initiate the reentry process within the atria
AF leads to electrical remodeling of the atria
AF is associated with chaotic, disorganized atrial electrical activity, resulting in no
atrial contraction.
AF occurs due to structural and/or electrophysiological abnormalities that promote
abnormal atrial and/or pulmonary vein automaticity and/or atrial reentry.
Atrial structural abnormalities include fibrosis, dilation, ischemia, infiltration, and
hypertrophy.
Other contributing factors include inflammation, oxidative stress, activation of the
renin-angiotensinaldosterone system, autonomic nervous system activation, and
genetic variants in myocardial ion channels and those leading to
cardiomyopathy.
AF is associated with substantial morbidity and mortality,
including risk of ischemic stroke of approximately 5% per year.
Stroke risk is increased two- to sevenfold in patients with AF
compared to patients without this arrhythmia.6
AF is the cause
of roughly one of every six strokes. During AF, atrial contraction
is absent. Because atrial contraction is responsible for approximately 30% of LV
filling, blood that is not ejected from the left
atrium to the LV pools in the atrium, particularly in the left atrial
appendage. Blood pooling facilitates thrombus formation, which
subsequently may travel across the mitral valve into the LV and
be ejected during ventricular contraction. The thrombus then
may travel through a carotid artery into the brain, resulting in
an ischemic stroke. Patients with AF are also at increased risk for
systemic thromboembolism
AF is associated with a threefold increase in risk of HF as a
result of tachycardia-induced cardiomyopath

4. CLASSIFICATION/TYPES IF ANY
5. SIGNS AND SYMPTOMS

6. COMPLICATIONS
Stroke
Heart failure

7. . LABORATORY INVESTIGATIONS
 lead ECG
 Serum electrolytes, calcium, magnesium assay (LOE C)
 Chest Xray
 Full blood count
 ECG
 ESR/CRP
 Echocardiography to detect valvular and other structural abnormalities
 Holter monitoring (ambulatory ECG)
 Exercise stress test
 Coronary angiogram
 Thyroid function test, particularly, thyroxin stimulating hormone (TSH)
 Serum cardiac enzyme levels particularly troponins and CK-MB during acute episodes
 Arterial blood gases (ABG) if available

8. TREATMENT
a. Aims of therapy
b. Non pharmacological management
c. Pharmacological management
d. Monitoring (Toxicity and Efficacy of medications)
e. Counselling (disease and medications)
9. ROLE OF A PHARMACIST
10. REFERENCES

11. CASE STUDY

CARDIAC CONDUCTION PATHWAY

The cardiac cycle is a sequence of mechanical events
that is regulated by the electrical activity of the myocardium
The natural pacemaker of the heart is the sinoatrial (SA) node, a specialized group of
cardiac muscle cells located in the wall of the right atrium just below the opening of
the superior vena cava
In adults at rest, normal intrinsic depolarization rate of the sinus node is 60 to 100 per
minute
From the SA node, impulses for contraction travel to the atrioventricular (AV) node,
located in the lower interatrial septum
normal depolarization rate of the atrioventricular (AV) node and ventricular tissue is
40 to 60 per minute and 30 to 40 per minute, respectively
. The transmission of impulses from the SA node to the AV node and to the rest of the
atrial myocardium brings about atrial systole.
atrioventricular bundle (AV bundle), also called the bundle of His,receives impulses
from the AV node and transmits
them to the right and left bundle branches
From the bundle branches, impulses travel along Purkinje fibers to the rest of the
ventricular myocardium and bring about ventricular systole.

A typical ECG consists of three distinguishable waves or deflections: the P wave, the
QRS complex, and the T wave. Each represents a specific electrical even
The P wave represents depolarization of the atria, that is, the transmission of electrical
impulses from the SA node throughout the atrial myocardium. The QRS complex
represents depolarization of the ventricles as the electrical impulses spread throughout
the ventricular myocardium. The T wave represents repolarization of the ventricles
(atrial repolarization does not appear as a separate wave because it is masked by the
QRS complex)

Mechanisms of Cardiac Arrhythmias

Abnormal Impulse Initiation
Due to abnormal automaticity(increased or decreased)
A decrease in sinus node automaticity results in a reduced rate of impulse generation
and a slow heart rate (sinus bradycardia)
an increase in sinus node automaticity results in an increased rate of impulse
generation and a rapid heart rate (sinus tachycardia)

Abnormal automaticity of other cardiac fibres such as atrial tissue, the AV node, the
Purkinje fibers, and ventricular muscle

Cardiac fiber automaticity is controlled in part by sympathetic and parasympathetic

nervous system activity

Other factors include

hypoxia,
atrial or ventricular stretch (uncontrolled hypertension or during and after
development of heart failure [HF]),
electrolyte abnormalities such as hypokalemia or hypomagnesemia,
certain drugs including digoxin and adrenergic agonists.

Abnormal Impulse Conduction

The mechanism of abnormal impulse conduction is termed reentry
For reentry to occur, three conditions must be present:
(a) at least two pathways down which an electrical impulse may travel; (b) a
“unidirectional block” in one of the conduction pathways
(b) slowed impulse conduction velocity down the other conduction pathway

Arrhythmias are abnormal heart rate or rhythm.

an increase in the rate of occurrence of impulses (tachyarrhythmias), a decrease in the
rate of occurrence of electrical impulses (bradyarrhythmias)
change in the normal rhythm of impulses. The commonest form of arrhythmia
worldwide is atrial fibrillation

Arrhythmias are classified into two broad categories: supraventricular (those

occurring above the ventricles)
ventricular (those occurring in the ventricles)
ATRIAL FIBRILLATION
AF is characterized as an extremely rapid (400 to 600 atrial beats/min) and
disorganized atrial activation.
There isa loss of atrial contraction (atrial kick), and supraventricular impulses
penetrate the atrioventricular (AV) conduction system in variable degrees, resulting in
irregular ventricular activation and irregularly irregular pulse (120 to 180 beats/min).

CLINICAL PRESENTATION
Palpation of the pulse as a basic screening tool may help detect AF
The pulse is characteristically described as being “irregularly irregular” (in both
volume and rhythm)
A definitive diagnosis of AF requires rhythm documentation using an ECG showing
a typical pattern of no discernible, distinct P waves and irregular RR interval

AF may be classiied as:

Paroxysmal: self-limiting episodes of AF lasting no more than 7 days;
Persistent: AF lasting more than 7 days or requiring cardioversion;
Longstanding persistent: continuous AF for more than 1 year; or
Permanent: where a decision has been made not to attempt cure
of persistent AF
REFERENCES
Potpara, T., Dagres, N., Arbelo, E., Bax, J. J., & Blomstrom-Lundqvist, C. (2021). 2020 ESC guidelines for
the diagnosis and management of atrial fibrillation developed in collaboration with the european Association
of Cardio-Thoracic Surgery (EACTS). Eur. Heart J., 42, 373-498.

Bookstaver, P. B., Chisholm-Burns, M. A., Kolesar, J. M., Lee, K. C., Malone, P. M., & Schwinghammer, T.
L. (Eds.). (2019). Pharmacotherapy Principles & Practice. McGraw-Hill Education.

National Guidelines for the Management of Cardiovascular Diseases. (2019). Ministry of Health, Ghana

Koda-Kimble, M. A. (2012). Koda-Kimble and Young's applied therapeutics: the clinical use of drugs.
Lippincott Williams & Wilkins.
DiPiro, J. T., DiPiro, C. V., Schwinghammer, T. L., & Wells, B. G. (2015). Pharmacotherapy handbook.
McGraw-hill.

Noubiap, J. J., & Nyaga, U. F. (2019). A review of the epidemiology of atrial fibrillation in sub‐Saharan
Africa. Journal of Cardiovascular Electrophysiology, 30(12), 3006-3016.

DRUGS-MOA,SIDE EFFECTS, CONTRAINDICATIONS

AMIODARONE-HOW IT CAUSES HYPER/HYPO
Amiodarone markedly prolongs the action potential duration (and the QT interval on
the ECG) by blockade of potassium channels
Amiodarone also significantly blocks inactivated sodium channels.
Amiodarone also has weak adrenergic and calcium channel-blocking actions.
Consequences of these actions include slowing of the heart rate and AV node conduction.
The broad spectrum of actions may account for its relatively high efficacy and its low incidence of torsades
de pointes despite significant QT-interval prolongation.
The drug accumulates in many tissues, including the heart (10–50
times more so than in plasma), lung, liver, and skin, and is
concentrated in tears.

Toxicity
symptomatic bradycardia and heart block in patients with preexisting
sinus or AV node disease
Abnormal liver function tests and hypersensitivity hepatitis
fatal pulmonary fibrosis
photodermatitis and a gray-blue skin discoloration in sun-exposed
areas,
Asymptomatic corneal microdeposits(After a few weeks of treatment)
Amiodarone blocks the peripheral conversion of thyroxine (T 4 )
to triiodothyronine (T 3 ). It is also a potential source of large
amounts of inorganic iodine. Amiodarone may result in hypothyroidism
or hyperthyroidism
CCBS
Verapamil and diltiazem also have antiarrhythmic effects. The dihydropyridines (eg, nifedipine) do not share
antiarrhythmic efficacy and may precipitate arrhythm
blocks both activated and inactivated L-type calcium channels
AV nodal conduction time and effective refractory period are
prolonged
ADENOSINE
a nucleoside that occurs naturally throughout the body.
Its half-life in the blood is less than 10 seconds.
Its mechanism of action involves activation of an inward rectifier K
+ current and inhibition of calcium current
Adenosine directly inhibits AV nodal conduction and increases the AV
nodal refractory period
the drug of choice for prompt conversion of paroxysmal
supraventricular tachycardia to sinus rhythm
Side effects
headache, hypotension, nausea, paresthesias, flushing, shortness of
breath or chest burning
CARDIAC GLYCOSIDES- DIGOXIN TOXICITY MANAGEMENT
WHY DIGITALIS OVER DIGOXIN
WARFARIN-THERAPEUTIC RANGE, MOA