Article Reviews on Atrial Fibrillation
Atrial fibrillation is a kind of cardiac arrhythmia, which is featured by brief periods of rapid and irregular contractions at the rate of 300 to 400 beats per minute. Such phenomenon results from the circus movements of impulses generated in the SA node. The circus movements are due to the irregularities or loss or disorientation of the normal atrial musculature. The present article will portray a literature review on atrial fibrillation from various scholarly articles.
Arrhythmia refers to the irregularity in heart beat or disturbance in rhythm of the heart. In arrhythmias the heart beat may become faster or slower, or might be supplemented by an extra beat or a missed beat. Most of the time such beats may be prolonged or become constant over time. The common symptoms of atrial fibrillation include palpitations, fainting, and shortness of breath, chest tightness or chest pain (Mischke et al., 2013).
Various types of atrial fibrillation can be noted in clinical situations. Hence, it may be paroxysmal (with recurrent episodes of arrhythmia that ends on its own within 7 days), it may be permanent (with recurrent episodes of arrhythmia that lasts more than 7 days), it may be persistent (permanent arrhythmia over time) or first detected (only one diagnosed episode of arrhythmia) (Munger, Wu & Shen, 2014).
Maintenance of normal rhythmic activity of the heart is extremely important for distributing blood towards various end organs. Atrial fibrillation is caused due to various pathological or physiological conditions. Most cases of atrial fibrillation are asymptomatic and related to hemodynamic changes (Munger, Wu & Shen, 2014).
Atrial fibrillation is often diagnosed by an absence of P wave in the electrocardiogram. The other diagnostic criteria include physical examination, transthoracic echocardiogram, 24-hour ambulatory holter monitoring, complete blood count, exercise stress testing and assay of serum thyroid stimulating hormone levels (Mischke et al., 2013). Peripheral resistance and increased systolic blood pressure may lead to atrial fibrillation. Further, there can be genetic risk factors like production of laminin that may lead to atrial fibrillation (Anumonwo & Kalifa., 2014).
Normally, the regular impulses are generated by the pacemakers, as the SA node. However, in atrial fibrillation such impulses are jeopardized by sudden electrical discharges, which occur in the atrial muscles or at the base of the pulmonary veins. The production of such electrical impulses is from automatic foci and may travel in any directions within the atrial musculature leading to circus movements (Mischke et al., 2013).
Moreover, there can be areas of fibrosis and necrosis in the atrial musculature. Such areas occur due to inflammation and the resultant dilation of the atria leads to a chain of events. The rennin-aldosterone-angiotensin system becomes stimulated, and an increase in matrix metalloproteinase occurs. This leads to remodelling and loss of atrial musculature mass. The fibrosis may be extended to the SA node and AV node. When such incidences occur, arrhythmia or atrial fibrillation tends to become permanent (Mischke et al., 2013).
The main goals of management of atrial fibrillation are to prevent episodes of circulatory instability (altered perfusion) and stroke. Anticoagulants like heparin and rivaroxaban are used to prevent the episodes of circulatory instability (Sharma et al., 2015). Heart rate control is achieved by administering beta-adrenergic blockers, calcium channel blockers and cardiac glycosides. They are administered to prevent episodes of stroke, associated with atrial fibrillation (Oishi & Xing., 2013).
Atrial fibrillation is a disorder of the heart. In this condition the normal rhythm of heart beat increases or becomes irregular. Such phenomenon occurs due to the inappropriate spread of cardiac impulse over the atrial muscle fibres. This situation leads to inefficient contraction of the atrium and leads to a decrease in end-diastolic volume. Owing to a reduced blood volume, ventricles cannot generate an effective force of contraction. The condition is potentiated by increased peripheral resistance. The result of these actions leads to ventricular failure and stroke. Since, ventricular contractions become inappropriate the chances of stroke increases. Moreover, due a decrease in blood flow throughout the body, chances of vascular stasis increase. This may potentiate the formation of clots within the blood vessels. The management of atrial fibrillation is based on the reduction of risk factors for stroke and blood clots.
Anumonwo, J., & Kalifa, J. (2014). “Risk Factors and Genetics of Atrial
Fibrillation.” Cardiology clinics 32 (4): 485–494
Munger, T; Wu, L; & Shen, W. (2014). “Atrial fibrillation.” Journal of biomedical
research 28 (1): 1–17
Mischke, K; Knackstedt, C; Marx, N; & Vollmann, D (2013). “Insights into atrial
fibrillation.”. Minerva medica 104 (2): 119–30.
Oishi, M., &; Xing, S. (2013). “Atrial fibrillation: management strategies in the emergency
department.”. Emergency medicine practice 15 (2): 1–26
Sharma, M; Cornelius, V; Patel, J; Davies, J; & Molokhia, M (2015). “Efficacy and Harms
of Direct Oral Anticoagulants in the Elderly for Stroke Prevention in Atrial
Fibrillation and Secondary Prevention of Venous Thromboembolism: Systematic
Review and Meta-Analysis.”. Circulation 132: 194–204.