Classifications for Atrial Fibrillation (AF)

AF is classified according to its etiology, depending on whether it occurs without a known cause in people with physically normal hearts, or it causes problems from vulvar or hypertensive heart disease (Markides & Schilling, 2012). Experts recently recommended a classification scheme based on the historical pattern of arrhythmia. If previous occurrences of AF or recurrent arrhythmia have been noticed, patients may experience a "first detected episode" of AF or recurrent arrhythmia. Paroxysmal episodes are those that vanish rapidly, usually within one week, while persistent episodes are those that require pharmaceutical or electrical cardioversion to disappear. AF is considered to be permanent if longstanding and cardioversion, for more than a year, cannot successfully terminate it – where there are no indications of cardioversion (Wyse, 2012).

The primary objectives when managing patients with AF

There are three therapeutic goals to consider in the management of persons with AF: controlling ventricular rate, restoring and maintaining sinus rhythm, and preventing thromboembolism. It is also imperative to consider the benefits as well as risks of each treatment for each patient. (January, Wann, Alpert, & Calkins, 2014)

Cardiac remodeling with relation to AF

Cardiac remodeling refers to a genome expression that causes interstitial, cellular, and molecular changes and is exhibited clinically through changes in function, shape, and size of the heart arising from cardiac injury or load. The primary factors that influence cardiac remodeling include neurohormonal activation and hemodynamic pressure (Cohn, Sharpe, & Ferrari, 2013).

How Cardiac Remodeling Could Impact on the Risk for Cardiac Failure

Cardiac remodeling is the primary determining factor of the clinical course of heart failure and patients with severe remodeling exhibit continual deterioration of heart function (Cohn, Sharpe, & Ferrari, 2013).

Why Kevin Is at Risk of Thromboembolism

Kevin risks contracting thromboembolism since AF increases chances of thrombus formation thus increasing the risks of thromboembolism. Abnormalities that are associated with AF such as pathologic alteration of blood components and atrial endothelium damages contribute to the prothrombotic state. Besides, atrial endothelial damage resulting from AF triggers coagulation cascade as well as subsequent thrombogenesis (Abrahams, 2012).

Where Thrombus Is most likely to Manifest

Thrombus develops when an imbalance occurs in the blood coagulation system resulting in several health conditions, for instance, cardioembolic stroke and heart attacks. It involves clotting of blood in a blood vessel, hindering blood flow in the circulatory system. Damage to a blood vessel causes the body to use fibrin and thrombocytes for the formation a blood clot to stop loss of blood (Moll & Waldron, 2014).

Pathophysiology Associated with Hemorrhagic and Ischemic CVA

Ischemic CVA causes rapid loss of flow of blood to a section of the brain, leading to a loss of neurologic function and the precipitating factor is embolic or thrombotic occlusion of a cerebral artery. Hemorrhagic CVA causes bleeding right into the parenchyma of the brain, and the precipitating factor is leakage when chronic hypertension damages small intracerebral arteries.

The Likelihood of Cerebrovascular Accident (CVA) in Individuals Who Have Suffered a TIA

Patients who have suffered transient ischemic attack (TIA) are more likely to contract cerebrovascular accident (CVA). TIA is a disturbance in the function of the brain function due to a temporary blockage blood supply to the brain and lasts less than an hour. It is normally the last warning before CVA occurs (Giraldo, 2017).


The First Line Treatments for Controlling Heart Rate and Managing Sinus Rhythm in AF

The primary goal of medicines for AF is the prevention of complications like stroke and to relieve the signs. Drug medications include administering anticoagulants to minimize the risk of contracting stroke and antiarrhythmic drugs to slow heart rate in patients with AF. Non-pharmacological management of AF includes electrical cardioversion that is helpful in “shocking” the heart to its regular rhythm, and surgical ablation or catheter to cause lesions stop abnormal electrical impulses, which result in AF. Pharmacologic management of AF is intended to prevent fibrosis electrical and remodeling of the atria and maintain sinus rhythm. Healthcare professionals usually use the “Vaughn-Williams Class IC” drugs such as propafenone and flecainide for AF patients do not have a significant cardiac disease (WebMD LLC., 2017).

The First Line Medications for Thromboembolic Prophylaxis in AF

Thrombolytic and anticoagulant therapy are helpful to treat thromboembolic prophylaxis. Anticoagulant therapy helps in the prevention of additional deposition of a clot and enables the natural fibrinolytic mechanisms of the patient with AF to lyse the clot. It is important for anticoagulant medications administered during inpatient treatment to include a low-molecular-weight heparin (LMWH). Healthcare professionals should then initiate an oral coumarin-derivative such as warfarin sodium. According to experts, the anticoagulant features of warfarin sodium, LMWH, and unfractionated heparin (UFH) are a result of their impact on the coagulation cascade’s factors and cofactors (De Palo & Gellman, 2016).

Warfarin sodium acts on coagulation cascade by blocking the coagulation factors (X, IX, VII, and II), which are dependent on vitamin K. It is imperative to carboxylate these factors to bind calcium since it is tightly involved in the coagulation cascade. Vitamin K is responsible for carrying out the carboxylation. During this process, it changes to an oxidized state from a reduced state, and then an enzyme referred to as vitamin K epoxide reductase converts it back to the reduced state. Warfarin sodium inhibits that enzyme to prevent vitamin K from carboxylating the coagulation cascade factors thus preventing them from binding calcium, and rendering them ineffective (Arbor, 2014).

LMWH and UFH act on coagulation cascade by attaching to antithrombin III (ATIII), a natural anticoagulant, which acts on various factors on either side of the coagulant cascade though appears to result in a greater impact on coagulation’s intrinsic arm than on the extrinsic arm. These anticoagulants bind to ATIII and effect a conformational alteration, which results in activation of ATIII and potentiation of its action (Arbor, 2014).

The Lifestyle Impact and Side Effects of Novel Oral Anticoagulants and Vitamin K Antagonists

Hemorrhage (excessive bleeding) is one of the most common side effects of taking novel oral anticoagulants since they result in an increase in the time blood takes to clot. The indications of excessive bleeding include passing blood in one’s urine, severe bruising, having a black stool or passing blood when pooping, having bleeding gums, coughing blood, experiencing severe chest and back pains, and vomiting blood. Women who take these medications are likely to experience heavy bleeding during menstruation periods. Indeed, excessive bleeding requires patients to seek medical attention constantly (NHS, 2015). Other side effects of these kinds of anticoagulants vary according to the medication a healthcare practitioner has administered to a patient. These side effects include indigestion, itchy skin, jaundice (having white eyes and yellow skin), constipation, diarrhea, headaches, hair loss, rashes, feeling sick.

Conversely, the side effects of taking vitamin K anticoagulants include varying dose response, need for regular monitoring and adjustment of dosage, interactions with various medications and foods that contain significant amounts of vitamin K, and narrow therapeutic window. Patients could also experience delayed commencement as well as a counterbalance of anticoagulant effect. This limitation is for venous thromboembolism prevention wherein therapy duration is relatively short (WebMD LLC., 2015).

Psychosocial Issues

Important Measures to Make Sure that Kevin Complies with Treatment as well as Follow-Up Healthcare

Kevin can stay compliant with medications for AF if he is engaged in a full discussion of the rationale for AF medication and monitoring care. It is imperative to give him information about the reason why a given kind of drug is administered to him and why other treatment options are not recommended (Thrall, Lip, Carroll, & Lane, 2007). Indeed, giving him information about a particular medication, its benefits, perils, as well as side effects through an encouraging manner is helpful to him to develop expectations that are realistic and support positive adjustment. Such information will prevent him from coming to his conclusions and enable him to take cognizance of the difference between a rhythm-control approach and a rate-control approach and develop realistic expectations regarding the results of the care plan (McCabe, 2011).

Important Measures to Ensure that Kevin Can Recognize the Signs of CVA

It is noteworthy to inform Kevin that CVA refers to a situation when the circulation of blood to certain parts of a human brain has stopped due to a blood vessel’s rupture or blockage and that it is commonly referred to as a stroke. It is important to notify Kevin of the symptoms of CVA and strongly advise him to regularly watch out for them. These symptoms include experiencing difficulties when walking, feeling dizzy every so often, experiencing loss of coordination or balance, darkened or blurred vision, or difficulties understanding what other people say. A sudden headache accompanied by dizziness, vomiting, or nausea is also an indication of CVA, which Kevin should watch out for. Paralysis or numbness in the arm, leg or face, mostly on one of the body is another sign of CVA. Informing Kevin that one can receive treatment when they seek medical attention the moment they think they you might have developed CVA will help him be on the watch out for its symptoms. He should also be aware that if CVA is left untreated for a long time, one can suffer a permanent brain damage (Massachusetts Department of Public Health, 2012).

Important Nursing Measures to Educate Kevin about Necessary Lifestyle Modifications to Lower the Risk of Morbidity and Mortality Associated with AF

It is imperative to counsel Kevin regarding strategies to manage symptoms of AF to promote his quality of life and decrease his risk of morbidity and mortality. It is also important to let him know that shortness of breath and decreased endurance and energy level are the primary symptoms of AF; therefore, modifying his lifestyle to relieve such symptoms is necessary (McCabe, 2009).

Evaluating Kevin’s Cognizance of the Information He Receives

Kevin’s understanding of the information given to him can be evaluated through ascertaining his attitude towards medication and if he has modified his lifestyle to ease the symptoms of AF. Finding out if he is constantly on the watch out for CVA symptoms is also an excellent way of assessing his understanding of the information he has received.


Abrahams, M. (2012). Mechanisms of thrombosis in atrial fibrillation. Retrieved from M

Arbor, A. (2014). ELSO anticoagulation guideline. MI, USA: The Extracorporeal Life Support Organization (ELSO).

Cohn, J. N., Sharpe, N., & Ferrari, R. (2013). Cardiac remodeling—concepts and clinical implications: A consensus paper from an international forum on cardiac remodeling. Journal of the American College of Cardiology, 35(3), 569-582.

De Palo, V. A., & Gellman, H. (2016). Thromboembolism treatment & management. Retrieved from:

Giraldo, E. A. (2017). Transient ischemic attacks. Retrieved from,-spinal-cord,-and-nerve-disorders/stroke-cva/transient-ischemic-attacks.

January, C. T., Wann, S., Alpert, J. S., & Calkins, H. (2014). Guideline for the management of patients with atrial fibrillation. Journal of the American College of Cardiology, 64(21), 1-8.

Markides, V., & Schilling, R. J. (2012). Atrial fibrillation: Classification, pathophysiology, mechanisms and drug treatment. Education in Heart, 89(8), 939–943.

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McCabe, P. J. (2009). Predictors of symptoms and psychological distress in patients with recurrent symptomatic atrial fibrillation. Omaha, NE: University of Nebraska Medical Center.

McCabe, P. J. (2011). What patients want and need to know about atrial fibrillation. Journal of Multidisciplinary Healthcare, 413-419.

Moll, S., & Waldron, B. (2014). Deep vein thrombosis and pulmonary embolism. Chapel Hill, NC: Hemophilia and Thrombosis Center.

NHS. (2015). Anticoagulant medicines - side effects. Retrieved from

Thrall, G., Lip, G. Y., Carroll, D., & Lane, D. (2007). Depression, anxiety, and quality of life in patients with atrial fibrillation. Journal of Multidisciplinary Healthcare, 1259–1264.

WebMD LLC. (2015). Vitamin K side effects. Retrieved from

WebMD LLC. (2017). Pharmacologic strategies: Rate control vs rhythm control. Retrieved from

Wyse, D. G. (2012). The Euro heart survey on atrial fibrillation: A picture and a thousand words. European Heart Journal, 2356-2357.

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