Atrial fibrillation is the most common type of heart arrhythmia. It is due to abnormal electrical activity within the atria of the heart causing them to fibrillate. Is characterized as a tachyarrhythmia, which means that the heart rate is often fast. This arrhythmia may be paroxysmal (less than 7 days) or persistent (more than 7 days). Due to its rhythm irregularity, blood flow through the heart becomes turbulent and has a high chance of forming a thrombus (blood clot) which can ultimately dislodge and cause a stroke. Atrial fibrillation is the leading cardiac cause of stroke. Risk factors for atrial fibrillation include advanced age, high blood pressure, underlying heart and lung disease, congenital heart disease, and increased alcohol consumption. Symptoms vary from asymptomatic to symptoms such as chest pain, palpitations, fast heart rate, shortness of breath, nausea, dizziness, diaphoresis (severe sweating), and generalized fatigue. Although atrial fibrillation may be a permanent disease, various treatments have been developed, and risk modifying strategies to help reduce the risk of stroke in patients that remain in atrial fibrillation exist. Treatments include anticoagulation, rate control medication, rhythm control medication, cardioversion, ablation, and other interventional cardiac procedures. 
There are many causes of atrial fibrillation. Advanced age, congenital heart disease, underlying heart disease (valvular disease, coronary artery disease, structural heart disease), increased alcohol consumption, hypertension, and obstructive sleep apnea are all common causes of atrial fibrillation. Any process that causes inflammation, stress, damage, and ischemia to the structure and electrical system of the heart can lead to the development of atrial fibrillation. In some cases, the cause is iatrogenic.
The prevalence of atrial fibrillation has been increasing worldwide. It is known that the prevalence of atrial fibrillation generally increases with age. It has been estimated that the number of individuals with atrial fibrillation will double or triple by the year 2050. Although the world white prevalence of atrial fibrillation is approximately 1%, it is found in approximately 9% in individuals over the age of 75. At the age of 80, the lifetime risk of developing atrial fibrillation jumps to 22%. In addition, atrial fibrillation has more commonly been associated with males and seen more often in whites as compared to black.
There are a wide variety of pathophysiology mechanisms that play a role in the development of atrial fibrillation. Most commonly, hypertension, structural, valvular, and ischemic heart disease illicit the paroxysmal and persistent forms of atrial fibrillation but the underlying pathophysiology is not well understood. Some research has shown evidence of genetic causes of atrial fibrillation involving chromosome 10 (10q22-q24) that involves a mutation in the gene, alpha-subunit of the cardiac Ik5, which encodes pore formation protein. This mutation increases the function of this protein allowing for more pores, and thus, activity within the ion channels of the heart, therefore affecting the stability of the membranes and reducing its refractory time. 
Most cases of atrial fibrillation are non-genetic and relate to underlying cardiovascular disease. Typically, an initiating trigger excites an ectopic focus in the atria, most commonly around the area of the pulmonary veins, and allows for an unsynchronized firing of impulses and electricity leading to fibrillation of the atria. These impulses are irregular, and pulse rates can vary tremendously. Overall, atrial fibrillation leads to a turbulent and abnormal flow of blood through the heart chamber decreasing the heart effectiveness to pump blood while increasing the likelihood of thrombus formation within the atria, most commonly the left atrial appendage.
History and physical exam are crucial for diagnosing and risk stratifying patients with atrial fibrillation. A complete history should focus on symptoms such as palpitations, chest pain, shortness of breath, increased lower extremity swelling, dyspnea with exertion, dizziness, among others. In addition, history is imperative in identifying risk factors such as hypertension, history of valvular, structure, or ischemic heart disease, obstructive sleep apnea, obesity hypoventilation syndrome, smoking, alcohol intake, illicit drug use, history of rheumatic fever/heart disease, history of pericarditis, hyperlipidemia, among others. A physical exam should include the patient's overall appearance (obese), examine the patient neck for signs of JVD, carotid bruits, circumference. A cardiovascular exam should consist of carefully auscultating all 4 cardiac posts and palpating for apical impulse. A pulmonary exam should consist of auscultation, percussion, and specialized tests, if needed, to assess pulmonary status. Extremities should be evaluated for edema, peripheral pulses in both upper and lower extremities, and integumentary signs of PVD such as hair loss and skin breakdown. An abdominal exam should consist of palpating the aorta and listening for abdominal bruits. Depending on the severity of the atrial fibrillation, signs, and symptoms can range from none to evidence of acute heart failure.
Aside from a detailed history and examine, the ECG is critical in making the diagnosis of atrial fibrillation. On ECG, atrial fibrillation presents with the typical narrow complex "irregularly irregular" pattern with no distinguishable p-waves. Laboratory work is required to evaluate for the causes of atrial fibrillation, for example, a complete blood count (CBC) for infection, basic metabolic panel (BMP) for electrolyte abnormalities, thyroid function tests to evaluate for hyperthyroidism, and a chest x-ray to evaluate the thorax for any abnormality. It is imperative to evaluate the patient for pulmonary embolism (for example with d-dimer, CT scan) because right heart strain can lead to atrial malfunctioning and result in atrial fibrillation. The patient should be risk stratified for pulmonary embolism using the PERC and/or Wells criteria. In addition, a transesophageal echocardiogram should be done for these patients to evaluate for atrial thrombus secondary to atrial fibrillation and heart structure. It is important to note that Transesophageal echocardiogram (TEE) should always be done prior to cardioversion for these patients to minimize the risk of stroke.
The management of atrial fibrillation in the acute setting relies on patient hemodynamic stability and risk stratification. If the patient is hemodynamically unstable, immediate cardioversion with anticoagulant therapy is indicated. TEE is recommended prior to any cardioversion; however, if the patient is in hemodynamic stability due to atrial fibrillation with a rapid ventricular response, cardioversion may be performed without prior TEE. If the patient has evidence of rapid ventricular response, rate control should be initiated using a beta-blocker or calcium-channel blocker. These medications can be used as intravenous (IV) pushes or drips. Typically, the patient is given a bolus then started on a drip if symptoms do not resolve. Digoxin can be considered as a rate control agent but is not recommended as a first-line agent due to its side-effects and tolerance. Amiodarone can also be considered for a rhythm controlling agent but is also not first-line therapy in the acute setting. Amiodarone is also considered as a rhythm control, but cardiology should be consulted prior to use.
In the chronic setting of atrial fibrillation, the patient should be risk stratified using the CHADs-2-Vasc score which is helpful in estimate risk of CVA per year. If the patient receives a 0 score, they will be considered "low-risk" and anticoagulation is not recommended. If the patient receives a score of 1, they are "low-moderate" risk; the physician should consider anticoagulant or antiplatelet therapy. If the patient receives a score of greater than 2, they are in the "moderate-high" risk, and anticoagulation therapy is indicated. Rate or rhythm control should also be given to the patient, medications such as beta-blockers, calcium channel blockers, amiodarone, dronedarone, and digoxin. HAS-BLED is also a scoring system that can be used to asses the risk of bleeding for the patient. This is a good indicator of bleeding risk for a patient that is considering starting anticoagulation.
Differential diagnosis includes atrial flutter; however atrial fibrillation has the distinctive irregularly irregular rhythm with absent P-waves whereas atrial flutter has a regularly irregular rhythm with absent P-waves.
Classification of atrial fibrillation
The major side effect of atrial fibrillation is a stroke. Cerebral vascular accident (CVA) can lead to severe morbidity and mortality. CVA risk can be reduced significantly by anticoagulation with adjunct rate/rhythm therapy. Other complications include heart disease and heart failure secondary.
Cardiology consultation is recommended for a patient with atrial fibrillation.
Atrial fibrillation is a common disease that affects many individuals. The prevalence of this disease increases with age with the most severe complication being acute CVA. Due to the irregularly of the atria, blood blow through this chamber becomes turbulent leading to a blood clot (thrombus). This thrombus is commonly found in the atrial appendage. The thrombus can dislodge and embolize to the brain and other parts of the body. It is important for the patient to seek medical care immediately if they are experiencing chest pain, palpitations, shortness of breath, severe sweating, or extreme dizziness.
Atrial fibrillation is a chronic disorder that can seriously affect the quality of life and costs the healthcare billions of dollars each year. While cardiologists treat the disorder, the role of the pharmacist is critical. Many of these patients are on multiple medications including antiarrhythmic agents and anticoagulants. In addition, there is some evidence indicating that use of Angiotensin receptor blockers and statins may lower the frequency of atrial fibrillation and increase the probability of successful cardioversion. Thus, the pharmacist has to make sure that the patient' medication doses are therapeutic, there are no drug interactions and that the patient has therapeutic anticoagulation to prevent a stroke. The nurse has to educate the patient on medication compliance for hypertension, coronary disease and ensure follow-up at regular intervals. Finally, the patient should be educated about the symptoms of a stroke and when to return to the emergency department. (Level V)
Atrial fibrillation prevalence has been on the rise. The risk of stroke is 5-times higher in a patient with known atrial fibrillation compared to the general public. It is estimated that 19.6% of patients over the age of 65, will have apparent atrial fibrillation by 2030. The most feared side effect of atrial fibrillation is acute stroke which can lead to severe morbidity and mortality. It has been shown though that 60% of strokes secondary to atrial fibrillation can be avoided with the use of anticoagulants. Using the CHADs-2-VASc score to evaluate patients with atrial fibrillation is a helpful guide for management of these patients with the ultimate goal of preventing stroke. Proper risk factor stratification and medical/surgical therapy can decrease the risk of stroke and heart failure significantly.
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