The heart is a vital human organ that is comprised of four chambers. Atrial fibrillation and ventricular fibrillation are both conditions that occur in different parts of the heart. Contextually, fibrillation is the irregular contraction of the heart muscles. Despite the fact that the two conditions are characterized by the same phenomenon, atrial fibrillation occurs in the the atria, while ventricular fibrillation occurs in the ventricles. Principally, both conditions are classified as types of arrhythmia. The clinical diagnostic procedures for the two conditions have proven futile in some instances due to the rampancy of cases in which atrial fibrillation mimics ventricular fibrillation (Pappone et al., 2015). In this regard, this critical analysis report seeks to explore the similarities and differences of the pathophysiology, workup, complications, laboratory, and diagnostic studies of atrial fibrillation and ventricular fibrillation.
Pathophysiology
Atrial fibrillation is characterized by high-frequency excitation that results in dyssnychronous atrial contractions coupled with episodes of irregular ventricular excitations. According to Staerk, Sherer, Ko, Benjamin, and Helm (2017), the prevailing hypothesis on the pathophysiology of atrial fibrillation is that rapid triggering initiates reentrant waves in atrial substrates that are vulnerable. The eminence of initiating trigger decreases as the atrial fibrillation progresses, and the atrial fibrillation becomes somewhat stabilized. Other studies in the area have determined that pulmonary veins have unique electric properties and a complicated fiber architecture that promotes ectopic initiation of atrial fibrillation (Staerk et al., 2017). Autopsy studies seeking to explore the molecular basis of the pulmonary vein have determined that the section contains transitional cells, Purkinje cells, and pacemaker cells.
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The molecular composition of the cells initiates triggers because of abnormal handling of calcium ions. Staerk et al. (2017) hypothesize that a diastolic leak of calcium ions at the sarcoplasmic reticulum tends to initiate an inward sodium ion current that occurs as a result of the calcium ion-sodium ion exchange. The exchange contributes to spontaneous myocyte depolarization. The instability of the sarcoplasmic reticulum, which results in the overload and leakage of calcium ions occurs as a result of the phosphorylation of calmodium kinase II, kinase A, 2 the ryanodione receptor type 2, and phospholamban.
The second aspect of the pathophysiology of atrial fibrillation is the perpetuation of the condition. Although triggers are essential for the onset of atrial fibrillation, a vulnerable substrate is integral in promoting reentry of the disorder The reentry and the perpetuation of atrial fibrillation is dependent on the architecture, electrophysiology, and structure of atrial abnormalities. Staerk et al. (2017) posit that there is no consensus in the scientific community on the mechanisms of reentry in atrial fibrillation. However, two hypotheses have been advanced, and they include the multiple independent wavelengths and the reentrant rotors. The underlying principle of the multiple independent wavelengths is that a propagating wavefront must complete one circuit movement in a period that will allow muscles of the atria to recover their excitability (Xu, Luc, & Phan, 2016). Atrial substrates that have been noted to propagate reentry are synonymous with numerous abnormalities in the atrial cardiomyocyte, alterations in the intestinal matrix, and fibrotic changes (Staerk et al., 2017). The molecular and histological changes impair normal atrial rhythm. For instance, in the case of familial atrial fibrillation, the condition is propagated by a congenital abnormality that results in potassium ion gain.
On the other hand, ventricular fibrillation occurs in a myriad of clinical situations, such as in cases of coronary artery disease, ischemia, acute myocardial infection, and myocardial scarring stemming from old infarcts. Also, when ventricular tachycardia is not managed in time, it is likely to degenerate into ventricular fibrillation. Moreover, intracellular calcium accumulation, the presence of free radicals, metabolic alteration, and autonomic modulation also elevate the risk of developing ventricular fibrillation. The most well-understood manner in which ventricular fibrillation develops is the stimulation of the myocardium by a ventricular premature complex (Spartalis et al., 2018). It is imperative that a clear-cut difference between atrial fibrillation and ventricular fibrillation is determined as a means to improve treatment regimes .
Atrial and Ventricular fibrillation Workup
The presence of arrhythmia on the ventricles (ventricular fibrillation) can only be confirmed using electrocardiography (ECG). ECG output indicated in patients that were diagnosed with ventricular fibrillation as a means to determine the risk factors that resulted in the occurrence of the episode. Similarly, an electrocardiogram is used in cases of suspected atrial fibrillation. Since atrial fibrillation is caused by irregular activation of the atrial muscles at 350-600 beats per minute, the response of the atrial muscles will be evidenced on an ECG as irregular, but narrow tachycardia (Mulder & Gelder, 2015). In the workup of both cases, it is imperative to pay attention to ECG signs of associated cardiovascular conditions.
Laboratory and Diagnostic Studies
Laboratory and diagnostic procedures are used to determine the condition and eliminate other disorders that may have similar manifestations to ventricular fibrillation and atrial fibrillation. In the laboratory, blood tests are used to rule out the possibility of thyroid problems in the diagnosis of atrial fibrillation. Moreover, a chest x-ray is used to produce a comprehensive overview of the patient’s heart and lung anatomy (Dewar & Lip, 2007). The approach can be used to explain the symptoms manifested by the patient and detect anatomical abnormalities. Finally, an electrocardiogram and Holter monitor are used to detect the abnormality in rhythm. Dewar and Lip (2007) suggest that an echocardiograph, particularly, a transthoracic echocardiograph (TTE), should be used because it provides vital insight that could be integral in improving a patient’s chances of prognosis.
The diagnosis for ventricular fibrillation is undertaken using heart monitoring and pulse check. To warrant efficacious management of the condition, additional tests are done to determine the cause of the ventricular fibrillation. The tests include ECG, blood test, chest x-ray, echocardiogram, and cardiac computerized tomography.
Complications
The aforementioned conditions are associated with a myriad of complications. According to Wren (2011), ventricular fibrillation is the leading cause of sudden cardiac death globally. The correlation between cardiac death and ventricular fibrillation is the rapidity of the heartbeats associated with the condition that often results in episodes of heart failure (Wren, 2011). When the heart fails, all body organs are deprived of blood; hence, escalating the risk of damage to body organs such as the brain. When episodes of heart failure occur, treatment should be started immediately because death can occur within minutes. The episode of ventricular fibrillation can be treated with defibrillation, which is undertaken by delivering electrical shock to the heart with the aim of restoring normal heart rhythm (Wren, 2011). The rate of development of severe long-term complications and death is directly proportional to the promptness with which a patient receives defibrillation treatment.
When atrial fibrillation is left untreated, complications such as stroke and heart failure are bound to occur. If the upper chamber of the heart fails to pump blood, blood clots are likely to form. The blood clots may move to the ventricles and get pumped to the lungs or the rest of the body. If the clot is pumped to the brain and it blocks the arteries, a patient may experience an episode of stroke (Wren, 2011). Typically, atrial fibrillation increases the risks of suffering a stroke by four to five times as opposed to individuals that are not diagnosed with the condition (Wren, 2011). Moreover, persistent cases of atrial fibrillation could weaken the capacity of the heart to pump blood to all parts of the body. The situation may degenerate to episodes of heart failure.
Medical and Surgical Treatment
The treatment of atrial fibrillation aims to reset the rhythm, control the heartbeat, and prevent the formation of blood clots. Hearth rhythm resetting procedures are electrical cardioversion, which entails administration of electrical shock and the administration of a class of drugs called anti-arrhythmic, and anti-arrhythmic medications such as Dofetilide, Flecainide, and Sotalol may be administered. Also, Digoxin may be prescribed to control the patient’s heart rate at rest (Amin et al., 2016). Alternatively, catheter ablation can be used to destroy heart tissues that are causing recurrent episodes of arrhythmia. Other surgical procedures may include the maze procedure and atrioventricular node ablation. Moreover, the formation of cloths can be prevented by administering anticoagulants such as Warfarin, Dabigatran, apixaban, and edoxaban.
Treatment regimens for ventricular fibrillation are aimed at restoring blood flow immediately to reduce the severity of damage to the brain and other body organs. The first line of treatment is cardiopulmonary resuscitation (CPR) and defibrillation. Future episodes of ventricular fibrillation can be prevented by the use of anti-arrhythmic drugs, implantable cardioverter-defibrillator, stent placement, and coronary angioplasty (Wren, 2011). Alternatively, coronary bypass surgery can be used to improve coronary blood flow beyond narrowed or blocked arteries.
In conclusion, the different types of arrhythmia discussed in this research paper follow different pathophysiologies and are treated using different treatment regimens, but are all caused by irregular excitation of the heart muscles. Furthermore, the site of the excitability differentiates atrial fibrillation from ventricular fibrillation. The other notable difference is that while ventricular fibrillation predisposes a patient to recurrent episodes of heart attack, atrial fibrillation is associated with complications such as stroke and heart failure. In this regard, it is crucial that medical practitioners identify the exact type of arrhythmia that the patient is suffering from as a means of informing the choice of treatment regimen .
References
Amin, A., Houmsse, A., Ishola, A., Tyler, J., & Houmsse, M. (2016). The current approach of atrial fibrillation management. Avicenna journal of medicine , 6 (1), 8– 16. doi:10.4103/2231-0770.173580.
Dewar, R. I., Lip, G. Y., & Guidelines Development Group for the NICE clinical guideline for the management of atrial fibrillation (2007). Identification, diagnosis and assessment of atrial fibrillation. Heart (British Cardiac Society) , 93 (1), 25–28. doi:10.1136/hrt.2006.099861.
Mulder, B. A., & Gelder, I.S.V. (2015). Workup for patients with atrial fibrillation. DOI : 10.1093/med/9780199686315.003.0003.
Pappone, C., Vicedomini, G., Petretta, A., Giannelli, L., Cuko, A., & Santinelli, V. (2015). Ventricular fibrillation in lone atrial fibrillation as clinical manifestation of latent Brugada syndrome: Usefulness of flecainide testing. HeartRhythm case reports , 1 (5), 285–289. doi:10.1016/j.hrcr.2015.02.013.
Staerk, L., Sherer, J. A., Ko, D., Benjamin, E. J., & Helm, R. H. (2017). Atrial fibrillation: epidemiology, pathophysiology, and clinical outcomes. Circulation research , 120 (9), 1501-1517.
Wren, C. (2011). Concise guide to pediatric arrhythmias . John Wiley & Sons.
Xu, J., Luc, J. G., & Phan, K. (2016). Atrial fibrillation: review of current treatment strategies. Journal of thoracic disease , 8 (9), E886–E900. doi:10.21037/jtd.2016.09.13.
