Atrial Fibrillation


The human heart is a pump that delivers blood and nutrients to other organs. Myocardial
cells are striated, uninucleate with myofibrils and intercalated. The heart has the capacity of
creating its own intrinsic electrical impulses through specialized conducting pathways. This
conduction pathway comprises five elements namely; the purkinje fibres, left and right bundle
branches, the bundle of His, AVN and SAN. Initiation of heart conductivity begins at the right
atrial wall where SAN is located as a natural pacemaker. The stimuli is released in such a fashion
that is regular and is dictated by tissue requirements. When the electrical stimuli from SAN
passes through the AVN, it is briefly delayed so as to enable the atria contract adequately and
pump the remaining end diastolic blood to the ventricles during atrial systole. Once this is done,
the electrical impulses pass to the bundle of His then into the right and left bundle branches and
Purkinje fibers. The cardiac output varies proportionally in relation to the demands of the body.
Therefore, in a single heat beat, the heart undergoes three stages of contractility and relaxation.
These are; ventricular repolarization, ventricular depolarization and atrial depolarization, Atrial
fibrillation is a subtype of dysrhythmia. The normal rate ranges are between 60 to 100 beats per
minute and should be regular and consistent.
Physical and Psychological impact of A-fib
Atrial fibrillation has both serious physical and psychological ramifications. Anxiety,
panic attack and depression are the major psychiatric conditions related to atrial fibrillation. Aliot
et al., (2014) state that when first diagnosed, many patients despair, have decreased self-esteem


and have reduced energy with a feeling of total lethargy and anhedonia. The uncertain and
irregular nature of AF episodes can make people feel out of control and unable to plan their life
with confidence. Some patients have an adamant feeling that they do not want AF as their
diagnosis (Lim et al., 2015). Most patients find the unpredictability and lack of control very
unnerving and feel anxious that their AF would take over eventually. Living in fear of having an
episode of AF makes the patient feel as if he is in trap. Normal people with sinus rhythm may
say that AF is a benign condition but the affected populations feel it as a great concern that is
life-threatening. Some patients speak of how they had become afraid to go too far from home
and from their local A&E department. To try to improve the quality of their lives, some people
tried antidepressants or cognitive behavioral therapies. Most people, however, resolved to be
positive, not worry about AF too much, and just get on with life (January et al., 2014). For some
it was a ‘wake-up call’ to reassess their lives. AF is tied to a wide range of physical symptoms
that differ inter-individually. Some individuals have no awareness about the aura of AF while
others have a clear cut difference between the between the period of normal sinus rhythm and the
onset of AF. Frequent and irregular rapid heart pulsations or occasionally an uncomfortable chest
sensation of flutter are also common symptoms. This is then accompanied by chest discomfort,
breathlessness, sweating, dizziness and passing out. A small percentage of patients may
experience exercise intolerance and extreme fatigue. There may be a progression of the
symptoms to an extent that many patients feel incapable to carry out normal daily activities. AF
is unpredictable in character. Therefore, patients often avoid absolute commitment towards
social engagements and become too reluctant to travel away from home. The frequent trips to the
health facility for repeated incidences of atrial fibrillation can completely disrupt one’s life to
cause significant physical and emotional and physical distress.


Classes of Afib
Classification of AF is based on etiology, whether it’s a complication of valvar,
hypertension or a structural abnormality of the heart and if whether it occurs with or without
identifiable risk factor (Frangogiannis, 2014). The temporal pattern of the arrhythmia can be
used as a main mode of classification. In paroxysmal AF, arrhythmias begin suddenly and then
stop spontaneously on their own within a week.
Persistent AF is a condition in which cardiac arrhythmias persist for more than a week. It
may stop following treatment or spontaneously on its own. Medications are used to return the
heart to a normal rhythm. If no treatment is given, the heart will stay out of rhythm. A type of in
which normal heart rhythm cannot be restored even with treatment is called permanent AF. If
previous arrhythmic episodes have been documented, then this will be recurrent arrhythmia
(Saxena, Russo & Frangogiannis, 2016).
Objectives in A-fib management
The primary objectives in A-fib management are prevention of strokes, cardiac
remodeling and cardiomyopathy and amelioration of symptoms that reduce quality of life.
Reduction of frequency, severity and duration of recurrence is another goal that may lead to
improved quality of life and enhanced reduction in development of psychosocial conditions.
Cardiac remodeling in A-fib as a risk factor for cardiac failure
Cardiac remodeling in AF is defined as any structural or functional changes in the atria
that promote atrial arrhythmias. Remodeling can be as a result of the underlying AF, systemic
processes and aging. There are four pathophysiological elements of cardiac remodeling. These
are electrical remodeling, structural transformations, and sympathetic and parasympathetic


nervous system remodeling and physiological abnormalities of calcium handling (Turner, 2014).
The heart is vulnerable to Afib-induced remodeling and if the A-fib is maintained long enough to
warrant atrial changes and adaptability. This is an auto-reinforcement property of localized
ectopic trigger that maintains a re-entrant AF via a re-entry-maintaining substrate. The major
elements of electrical remodeling consist of decreased rectifier K + current, type L Ca 2+ current
pathways, and acetylcholine-regulated K + current and a decrease in distribution of the gap
junction connexin hemichannels that connect cardiomyocytes electrically (Stewart et al., 2015).
Structural remodeling is characterized by atrial enlargement and fibrosis. Bundle
continuity is interrupted by fibrosis and thus causes disturbances in the local conduction. The
interaction between fibroblast and cardiomyocytes may cause arrhythmogenic changes in the
electrical flow of cardiomyocyte. Furthermore, atrial fibrosis has a large contribution to
therapeutic resistance among patients who have had long-standing dysrhythmias.
Thromboembolism in A-fib and involved organs
Thromboembolism is the most common complication of AF and the most clinically
evident thromboembolic event is ischemic stroke. This phenomenon is ascribed to hemostasis
within the functionally compromised left atrium. Atrial endothelial damage leads to activation of
the coagulation cascade and subsequent thrombogenesis (Gladstone et al., 2014). These thrombi
may dislodge to the lungs, kidney and peripheral tissues thus compromising the physiological
function of the involved organ.
Pathophysiology associated with hemorrhagic and ischemic CVA and the aggravating


Swirski & Nahrendorf, (2013) define hemorrhagic stroke as a condition in which there is
intracranial blood spill that compromises brain function. This creates pressure effect on the brain.
There is a midline shift, reduced ventricular space, blocked CSF flow.
Ischemic stroke are caused by thrombosis, embolism and systemic hypoperfusion. This is
usually acute and it compromises oxygen and nutrient supply to the brain.
1 st line drugs for rate control and rhythm management work by decreasing the
automaticity of ectopic pacemakers. They also reduce conduction and excitability by increasing
the refractory period in depolarized tissue. These are sodium channel blockers which include;
procainamide, mexiletine, flecainamide and propafenone. Beta adrenoceptor blockers are in class
two and include esmolol and sotalol. Amiodarone is in third class and prolongs the action
potential. Calcium channel blockers like diltiazem and verapamil are in the fourth class.
1 st line medication for thromboemboelic prophylaxis are indirect thrombin inhibitors like
heparin, direct thrombin inhibitors such as argatroban and factor Xa inhibitors such as
rivaroxiban and apixaban.
Vitamin K antagonists such as warfarin can easily cross the placenta and cause fetal
defects and hemorrhagic phenomena in the fetus (Simons et al., 2016). There is 8-12 hour delay
in action of warfarin thus cannot be used where an immediate effect is preferred. Novel
anticoagulants like factor X inhibitors have a short time of onset, better safety profile and have
fewer tendencies to cause tissue hemorrhage.
Measures to ensure medical compliance and follow-up determine in risk stratification.
Knowledge of the risk of stroke is vital to help the patient better understand AF and its potential


complications. Also, it helps to determine if the patient might benefit from interventions to
prevent thromboembolism.
Education about recognition of warning signs of CVA may help the patient report to a
medical facility on time before serious irreversible damage to brain tissue has occurred. These
signs include; visual disturbance, unilateral numbness, sudden confusion and stupor, dizziness,
loss of coordination and severe headache of unknown cause.
A lifestyle modification in patients with AF decreases mortality. Advise the patient about
weight reduction, low calorie diet, frequent exercise, and smoking and heavy alcohol intake.
Assessment of efficiency of the provided information is very important in improving the
outcome. Check monthly BMI to assess whether there is a reduction.
Atrial fibrillation is a life-changing arrhythmic condition that imparts negatively on all
aspects of quality life. It is a cardiac condition that has several effects on a number of organs and
system ranging from the central nervous system, respiratory system and musculoskeletal. Early
diagnosis and full management is crucial in prevention multiple organ damage and permanent
change in normal anatomy and physiology. Its early diagnosis and management are crucial in
preventing major permanent heart changes that may be severe and debilitating. Prevention of any
complication that may arise as a result of atrial fibrillation or any medical condition triggered by
this cardiac condition is necessary. This is due to the fact that the complications may be fatal and
debilitating than the primary underlying condition. Furthermore, patient education on the
expected outcome the protracted period of recovery should be well explained to achieve
compliance from the patient and avoid any overvalued expectations. Medical care should be
multidisciplinary so as to achieve the intended goal and meet the expected standards. In so


saying, it is thus mandatory to follow frequent check-ups and comply with prescribed drugs for a
better outcome.



Aliot, E., Botto, G. L., Crijns, H. J., & Kirchhof, P. (2014). Quality of life in patients with atrial
fibrillation: how to assess it and how to improve it. Europace, eut369.
Frangogiannis, N. G. (2014). The inflammatory response in myocardial injury, repair, and
remodelling. Nature Reviews Cardiology, 11(5), 255-265.
Gladstone, D. J., Spring, M., Dorian, P., Panzov, V., Thorpe, K. E., Hall, J., … & Sharma, M.
(2014). Atrial fibrillation in patients with cryptogenic stroke. New England Journal of
Medicine, 370(26), 2467-2477.
January, C. T., Wann, L. S., Alpert, J. S., Calkins, H., Cigarroa, J. E., Cleveland, J. C., … &
Murray, K. T. (2014). 2014 AHA/ACC/HRS guideline for the management of patients
with atrial fibrillation. Circulation, 130(23), e199-e267.
Kondalsamy-Chennakesavan, S., Richardson, T., & Gange, N. (2015). Significance of atrial
fibrillation on the outcomes of thrombolysed stroke patients in regional Queensland. In
Australasian Journal On Ageing (Vol. 34, pp. 48-48). Wiley-Blackwell Publishing Asia.
Saxena, A., Russo, I., & Frangogiannis, N. G. (2016). Inflammation as a therapeutic target in
myocardial infarction: learning from past failures to meet future challenges. Translational
Research, 167(1), 152-166.
Simons, L. A., Ortiz, M., Freedman, S. B., Waterhouse, B. J., Colquhoun, D., & Thomas, G.
(2016). Improved persistence with non-vitamin-K oral anticoagulants compared with
warfarin in patients with atrial fibrillation: recent Australian experience. Current Medical
Research and Opinion, 32(11), 1857-1861.
Stewart, S., Ball, J., Horowitz, J. D., Marwick, T. H., Mahadevan, G., Wong, C., … & Scuffham,
P. A. (2015). Standard versus atrial fibrillation-specific management strategy (SAFETY)


to reduce recurrent admission and prolong survival: pragmatic, multicentre, randomised
controlled trial. The Lancet, 385(9970), 775-784.
Swirski, F. K., & Nahrendorf, M. (2013). Leukocyte behavior in atherosclerosis, myocardial
infarction, and heart failure. Science, 339(6116), 161-166.
Turner, N. A. (2014). Effects of interleukin-1 on cardiac fibroblast function: relevance to post-
myocardial infarction remodelling. Vascular pharmacology, 60(1), 1-7.