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Sudden Cardiac Arrest and Its Potential Etiology Research Paper

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Updated: Aug 10th, 2020


This case report presents sudden cardiac arrest, its potential etiology, the typical progression of the disease in an afflicted individual, clinical manifestation, and treatment for sudden cardiac arrest. Sudden cardiac arrest (SCA) is a critical public health challenge, notwithstanding a striking decline in the age-adjusted risk factor of deaths because the aggregate cases of fatal SCA incidence in the US remain large. It is estimated that there are between 170,000 and 450,000 serious SCA cases every year, but a range of 300,000 to 370,000 is preferred (Patil, Halperin, & Becker, 2015). Additionally, SCA is responsible for about 50% of all deaths related to cardiovascular conditions, and about 50% of the SCAs reflect clinical indicators of a past undetected heart condition. Further, nearly 80% of SCA takes place outside hospitals, mainly in private homes or other living facilities (Patil et al., 2015).

SCA is an abrupt cessation of cardiac functions associated with the collapse of the hemodynamic generally because of continued ventricular fibrillation (Lother, Beyersdorf, Osterhues, Bode, & Wengenmayer, 2016). The sudden cardiac arrest also leads to sudden cardiac death (SCD). These cases are common in patients with existing structural heart conditions, which might not have been earlier detected, especially coronary heart disease (Luong et al., 2016). It is referred to as sudden cardiac arrest or aborted sudden cardiac death if an intervention, such as defibrillation or natural reversion, has successfully restored the circulation. Multiple cardiac conditions that result in the development of the arrhythmia causing cardiac malfunction and sudden death are not clearly understood. It is difficult to identify both patients at risk for SCA and various factors that culminate to a fatal arrhythmia.

Common classifications of electric mechanisms related to SCA are mainly bradyarrhythmia (nontachyarrhythmic) and tachyarrhythmia. Nontachyarrhythmic accounts for other related mechanisms, such as electromechanical dissociation (currently known as pulseless electric activity), asystole, extreme bradycardia, and other mechanisms, in most instances linked to noncardiac factors (Patil et al., 2015).

The precise arrhythmia mechanisms of the cardiac function’s collapse in specific patients are always difficult to determine because, for many patients who experience sudden deaths, cardiac functions are not generally monitored during the period of the collapse. Consequently, the cardiac arrest mechanism may merely be inferred based on data gathered after an analysis has been conducted. Nonetheless, under constant observation in the coronary care unit, patients may present relevant data for analyses of the cardiac activity during the collapse. It has been noted that ventricular tachycardia (VT) or ventricular fibrillation (VF) is responsible for most sudden cardiac arrest cases. Nevertheless, some instances have been attributed to bradyarrhythmia.

A cardiac arrhythmia is an event in which an unusual activity is observed in cardiac rhythm. Bradyarrhythmias consist of sinus bradycardia and heart block. Sinus bradycardia may result from internal or external factors. Extrinsic factors impair the regular sinus node activity, and the drug, such as beta-blockers, initiate most cases. Conversely, intrinsic factors are mainly related to degeneration or diseases of the sinus node. These conditions include sick sinus syndrome and myocarditis, among others. Sinus bradycardia has been associated with a declined heart rate, syncope, and sinus arrest (Joseph & Palatty, 2012).

Any obstruction that affects the conduction of an impulse within the conductive system is an instance of a heart block (Joseph & Palatty, 2012). Two types of heart block have been identified. The atrioventricular block shows a malfunction in the level of the bundle, while the bundle branch block only reflects the impairment of an impulse below the level of the block. Tachyarrhythmias consist of supraventricular tachycardias, atrial tachyarrhythmias, and ventricular tachyarrhythmias.

Asystole is normally the first rhythm noted in patients who collapse in unmonitored environments where the precise time of the inception and the etiologic arrhythmia is unknown. Asystole correlates with the time of the cardiac arrest. It might be the outcome of ventricular fibrillation that has existed for multiple minutes or longer and then results in the loss of all the electrical functions because of acidosis, hypoxia, and myocardial tissue death. In nearly 80% of patients with ventricular tachycardia or ventricular fibrillation, the continued ventricular arrhythmia is led by an elevation in ventricular ectopy and the emergence of constant ventricular arrhythmia. These are mainly impulsive arrhythmias found across different periods before VT or VF (Patil et al., 2015).

Persistent monomorphic VT can steadily develop and degenerate into VF. No clear relationship has been established between SCD and VT. Thus, persistent monomorphic VT could be a part of VF or degenerate rapidly into some conditions involving constant coronary ischemia, leading to VF. Further, persistent polymorphic VT may lead to VF, particularly due to primary ischemia, while VF may also emerge as an underlying event. In some cases (1/3), tachyarrhythmia emanates from an early R on the ventricular premature beat (VPB) while the rest (2/3) of the cases result from a late-cycle of VPB.

A bradyarrhythmia and asystole (pulseless electrical activity) are not common causes of SCD. They account for less than ten percent of the documented deaths. Nonetheless, a bradyarrhythmia is common nonischemic cardiomyopathy, whereas asystole is the most common rhythm for a pulmonary embolism. In some instances, a bradyarrhythmia may progress to a ventricular tachyarrhythmia.

It is also imperative to recognize that the ventricular fibrillation mechanism involves several localized sites of micro reentry that lack any form of structured electrical activity. Thus, rotating spiral waves are considered the possible mechanisms for ventricular fibrillation, particularly in the presence of a primary myocardial condition that is diffused in most cases. A precondition for reentry requires a disparity of the electrophysiologic features, which initiate events to cause the arrhythmia in a susceptible heart.

Case Report

Sudden cardiac arrest results from defects of the electric activity at the heart that abruptly turns abnormal. This case involves a 35-year-old patient who had been complaining of heart palpitations for over ten years. The patient has a medical history of ectopic atrial bradyarrhythmia with multiple PVCs and valvular disorder, did a yearly stress test that was normal, had no accompanying symptoms with heart palpitations. Some aspects discussed include manifestations and symptoms, such as dysthymias associated with the disease, treatment, and the outcome if not treated.

The etiology of the patient reflects an existing valvular heart disease leading to cardiac arrest. The patient has a valvular disorder. This condition is related to constricting or seeping of the valves, which could result in stiffening or enlarging of the heart muscles. The chamber of the heart becomes larger or weaker due to stress resulting from the tight or leaking valve. Consequently, the patient develops an increased risk of arrhythmia. Luong et al. (2016) identified that most cases of SCD, especially in athletes, were associated with “hypertrophic cardiomyopathy and arrhythmogenic right ventricular cardiomyopathy, myocarditis, coronary artery anomalies, valvular disease, aortic dissection, commotion cordis, and electrical disorders, such as Wolff-Parkinson-White syndrome, long QT syndrome, and Brugada syndrome” (p. 138).

Premature ventricular complexes (PVCs) are considered benign (Zipes et al., 2015). Nevertheless, their presence needs a thorough assessment before clearance (Zipes et al., 2015). In the presence of bradycardia, a complete heart block is experienced, followed by acute hypotension, and circulatory collapse (Rumore, 2012).

Pathogenesis of cardiac arrest results in global ischemia with effects at the cellular level that adversely impair functions of organs. It is imperative to recognize that cardiac arrest is sudden, and determining the exact stages of development in the pre-hospital setting is difficult (Reis et al., 2017). Thus, attention should turn to the underlying valvular disease. Based on histopathologic evidence, valvular heart diseases have been linked to the presence of calcified nodules made up of amorphous calcium phosphate, and inflammation is observed in the affected valves (Zeng et al., 2016). The pathogenesis of valvular disease also reveals the accumulation of lipids and subendothelial matrix after the endothelial cell dysfunction (Zeng et al., 2016).

Clinical manifestations of cardiac arrest include no pulse, fatigue, dizziness, chest pain, loss of consciousness, sudden collapse, syncope, palpitations, general cortical dysthymia, or dyspnea (American Academy of Pediatrics, 2012). A cardiac arrest is a sentinel event, and notably, SCA is associated with no warning. Evidence suggests that it is not possible to know the exact stage of the disease the patient is in because of poorly understood etiology and pathogenesis (Patil et al., 2015).

The two major organs affected by cardiac arrest are mainly the brain and the heart. The brain is the first organ that experiences the adverse outcome of cardiac arrest. It lacks a reserve of oxygen-rich blood and completely relies on the uninterrupted supplied oxygen. Thus, a decline in oxygen supply to the brain leads t unconsciousness, and failure to restore normal heart rhythm leads to brain damage and subsequent death of a patient. Beyond eight minutes, survival rates are minimal, while any survivors may display signs associated with brain impairment.

Cardiac lesions are not common following cardiopulmonary resuscitation (CPR). Nonetheless, some complications related to the vessel may be observed. They include vena cave perforation, bubbles, contusion, and aortic hemorrhage.

Cardiac arrest is associated with multiple risk factors that could influence its progression in patients. Notably, the underlying coronary condition could trigger cardiac arrest. Factors related to the patient’s lifestyle, family history of cardiac arrest, and heart diseases important for evaluation. Age is important because instances of cardiac arrest increase with age, and evidence suggests that children may be asymptomatic (West, Beerman, & Arora, 2015). Additionally, it is also imperative to explore gender because men are more likely (two to three times) to experience sudden cardiac arrest than women. Some drugs, including amphetamines and cocaine, influence cardiac arrest events, and poor nutritional diets with low magnesium or potassium levels also affect the development of the condition. Overall, many interacting clinical, environmental, pharmacological, and other interventional factors may influence cardiac arrest in patients (Patil et al., 2015).

Cases of sequelae involving brain damage, dysthymias, and reperfusion injury have been noted following cardiac arrest. Biological processes that influence normal functions and recovery of organs affected following cardiac arrest are not known (Patil et al., 2015). Cells may die during prolonged cardiac arrest and fail to recover or may experience cellular derangements associated with ischemia.

A meaningful patient’s prognosis should demonstrate better neurological stability compared to a simple restoration of natural circulation. Survival rates differ, but favorable cases may include immediate and efficient initiation of CPR in out-of-hospital settings, in-hospital setting monitoring, initial VF/VT restoration, early defibrillation, and post resuscitative management. If most factors are favorable, then most patients should survive to hospital discharge. Nonetheless, survival is unlikely in cases where cases are unwitnessed, experienced in out-of-hospital settings, and patients suffer asystole (Lother et al., 2016). Neurologic dysfunction and prearrest status may occur among patients who survive SCA.

Sudden cardiac arrest therapies vary but must focus on the immediate survival of the patient. Immediate CPR (100-120 compressions per minute) is necessary to sustain the flow of oxygen-rich blood to the brain until more advanced care is provided. Defibrillation is necessary to manage ventricular fibrillation. This procedure shortly stops the heart and its hectic rhythm to allow regular heart rhythm to recommence. The emergency room management involves treatments to steady the heart and potential complications associated with SCA. Long-term interventions focus on preventive treatment options. Anti-arrhythmic drugs, such as beta-blockers, angiotensin-converting enzyme (ACE) inhibitors, or amiodarone, are used for long-term care in emergency cases.

Additionally, implantable cardioverter-defibrillator (ICD), coronary angioplasty, coronary artery bypass grafting, bypass surgery, radiofrequency catheter ablation, and corrective heart surgery are long-term management options for SCA. Self-management focuses on a lifestyle change, the use of the recommended drugs, and living with a care provider with CPR training. Treatment should also focus on the underlying causes of the disease.


Sudden cardiac arrest is the cessation of cardiac activity leading to no blood circulation to body organs. It is associated with a high rate of morbidity and mortality. Besides, its etiology and pathogenesis are poorly understood. Survival rates are low, and treatment options should be immediate and long-term to manage adverse outcomes.


American Academy of Pediatrics. (2012). Pediatric sudden cardiac arrest. Pediatrics, 129(4), e1094-e1102. Web.

Joseph, T., & Palatty, P. L. (2012). The changing facade of anti-arrhythmics. Journal of Clinical and Diagnostic Research, 6(3), 510 – 516.

Lother, A., Beyersdorf, F., Osterhues, H. H., Bode, C., & Wengenmayer, T. (2016). Recurrent pulseless electrical activity in a patient with coronary vasospasm and supravalvular aortic stenosis: A case report. BMC Cardiovascular Disorders, 16, 100. Web.

Luong, M. W., Morrison, B. N., Lithwick, D. J., Isserow, S., Heilbron, B., & Krahn, A. D. (2016). Sudden cardiac death in young competitive athletes. The British Columbia Medical Journal, 58(3), 138-144.

Patil, K. D., Halperin, H. R., & Becker, L. B. (2015). Sudden cardiac death compendium: Cardiac arrest, resuscitation and reperfusion. Circulation Research, 116(12), 2041-2049. Web.

Reis, C., Akyol, O., Araujo, C., Huang, L., Enkhjargal, B., Malaguit, J.,… Zhang, J. H. (2017). Pathophysiology and the monitoring methods for cardiac arrest associated brain injury. International Journal of Molecular Sciences, 18(1), 129-146. Web.

Rumore, M. M. (2012). Cardiovascular adverse effects of metoclopramide: Review of literature. International Journal of Case Reports and Images, 3(5), 1 –1 0. Web.

West, L., Beerman, L., & Arora, G. (2015). Ventricular ectopy in children without known heart disease. The Journal of Pediatrics, 166(2), 338–342. Web.

Zeng, Y., Sun, R., Li, X., Liu, M., Chen, S., & Zhang, P. (2016). Pathophysiology of valvular heart disease. Experimental and Therapeutic Medicine, 11(4), 1184–1188. Web.

Zipes, D. P., Link, M. S., Ackerman, M. J., Kovacs, R. J., Myerburg, R. J., & Estes, M. (2015). Eligibility and disqualification recommendations for competitive athletes with cardiovascular abnormalities. Circulation, 132, e315-e325. Web.

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