Atrial Fibrillation

Original Editors - Students from Bellarmine University's Pathophysiology of Complex Patient Problems project.
Top Contributors - Paul McDermott, James Moore, Lucinda hampton, Kim Jackson, Adam Vallely Farrell, Vidya Acharya, Elaine Lonnemann, George Prudden, WikiSysop and Karen Wilson  

Introduction

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  

Atrial Fibrillation (A Fib)

Nesheiwat Z, Goyal A, Jagtap M.

Publication Details

Introduction

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. [1][2][3]

Etiology

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.[4]

The 3 patterns of atrial fibrillation include:

Paroxysmal AF: Here the episodes terminate spontaneously within 7 days.

Persistent AF: The episodes last more than 7 days and often require electrical or pharmacological interventions to terminate the rhythm

Long-standing persistent AD: rhythm that has persisted for more than 12 months, either because a pharmacological intervention has not been tried or cardioversion has failed.

Permanent AF where a decision has been made to abort all therapies because the rhythm is unresponsive.

Epidemiology

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.[5][6]

Pathophysiology

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. [1]

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.

Triggers for aF

• Atrial ischemia
• Inflammation
• Alcohol and illicit drug use
• Hemodynamic stress
• Neurological and endocrine disorders
• Advanced age
• Genetic factors

History and Physical

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.

Evaluation

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.[7][8]

Treatment / Management

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.[2] 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.

Non-pharmacological therapy includes ablation therapy. Pacemaker placement is considered in severe causes resulting in heart failure in atrial fibrillation.[9][10][11]

Current guidelines

1. Patients with AF and elevated CHA2DS2-VASc score of 2 or more, oral anticoagulation is recommended.
2. Female sex with absence of AF risk factors and CHA2DS2-VASc of 1 or 0 in males have alow stroke risk.
3. Non-vitamin K oral anticoagulants (apixaban, dabigatran, edoxaban, and rivaroxaban) are recommended over warfarin, except in those patients with moderate to severe MS with a mechanical heart valve
4. In all patients with AF, the CHA2DS2-VASc score is recommended to assess stroke risk.
5. Obtain renal and liver function before initiating non-vitamin K oral anticoagulants
6. Aspirin is not recommended in patients with low CHA2DS2-VASc scores
7. Idarucizumab is recommended for dabigatran reversal if there is an urgent procedure or bleeding. Andexanet alfa is recommended for reversal of rivaroxaban and apixaban associated bleeding.
8. Percutaneous left atrial appendage occlusion is recommended in AF patients with a risk of stroke who have contraindications to long term anticoagulation.
9. If AF less than 48 hours or if time unknown, start anticoagulation and maintain INR 2-3 or a factor Xa inhibitor for at least 3 weeks before and at least 4 weeks after cardioversion
10. Catheter ablation is an option in patients with a low ejection fraction
11. Recommend weight  loss in obese patients with AF

Differential Diagnosis

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.

Staging

Classification of atrial fibrillation

1. Paroxysmal AF is when the episodes terminate spontaneously or with treatment within 7 days. But they may recur with an unpredictable frequency
2. Persistent AF is when the AF is continuous and lasts for more than 7 days, and fails to terminate spontaneously.
3. Long-standing AF is when the continuous AF lasts more than 12 months
4. Permanent is when AF is accepted and no further treatments are attempted to restore or maintain normal sinus rhythm
5. Non-valvular AF occurs in the absence of rheumatic mitral valve disease, mitral valve repair or a prosthetic heart valve.

CHA2DS2-VASc score

• Heart failure               1
• Hypertension             1
• Age More than 75      2
• Diabetes                   1
• Stroke, TIA               2
• PVD                         1
• Age 65-74                1
• Female sex               1

Prognosis

AF is associated with a high risk of thromboembolism and death. Evidence shows that rhythm control does not offer a survival advantage over rate control. Patients with AF have multiple admissions and anti-coagulation related complications over their lifetime. The risk of stroke is ever present and the overall quality of life of patients is poor.  Finally, the management of atrial fibrillation is prohibitively expensive with most of the financial burden beared by the patient.

Complications

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.

Consultations

Cardiology consultation is recommended for a patient with atrial fibrillation.

Pearls and Other Issues

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 (A Fib)

Nesheiwat Z, Goyal A, Jagtap M.

Publication Details

Introduction

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. [1][2][3]

Etiology

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.[4]

The 3 patterns of atrial fibrillation include:

Paroxysmal AF: Here the episodes terminate spontaneously within 7 days.

Persistent AF: The episodes last more than 7 days and often require electrical or pharmacological interventions to terminate the rhythm

Long-standing persistent AD: rhythm that has persisted for more than 12 months, either because a pharmacological intervention has not been tried or cardioversion has failed.

Permanent AF where a decision has been made to abort all therapies because the rhythm is unresponsive.

Epidemiology

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.[5][6]

Pathophysiology

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. [1]

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.

Triggers for aF

• Atrial ischemia
• Inflammation
• Alcohol and illicit drug use
• Hemodynamic stress
• Neurological and endocrine disorders
• Advanced age
• Genetic factors

History and Physical

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.

Evaluation

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.[7][8]

Treatment / Management

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.[2] 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.

Non-pharmacological therapy includes ablation therapy. Pacemaker placement is considered in severe causes resulting in heart failure in atrial fibrillation.[9][10][11]

Current guidelines

1. Patients with AF and elevated CHA2DS2-VASc score of 2 or more, oral anticoagulation is recommended.
2. Female sex with absence of AF risk factors and CHA2DS2-VASc of 1 or 0 in males have alow stroke risk.
3. Non-vitamin K oral anticoagulants (apixaban, dabigatran, edoxaban, and rivaroxaban) are recommended over warfarin, except in those patients with moderate to severe MS with a mechanical heart valve
4. In all patients with AF, the CHA2DS2-VASc score is recommended to assess stroke risk.
5. Obtain renal and liver function before initiating non-vitamin K oral anticoagulants
6. Aspirin is not recommended in patients with low CHA2DS2-VASc scores
7. Idarucizumab is recommended for dabigatran reversal if there is an urgent procedure or bleeding. Andexanet alfa is recommended for reversal of rivaroxaban and apixaban associated bleeding.
8. Percutaneous left atrial appendage occlusion is recommended in AF patients with a risk of stroke who have contraindications to long term anticoagulation.
9. If AF less than 48 hours or if time unknown, start anticoagulation and maintain INR 2-3 or a factor Xa inhibitor for at least 3 weeks before and at least 4 weeks after cardioversion
10. Catheter ablation is an option in patients with a low ejection fraction
11. Recommend weight  loss in obese patients with AF

Differential Diagnosis

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.

Staging

Classification of atrial fibrillation

1. Paroxysmal AF is when the episodes terminate spontaneously or with treatment within 7 days. But they may recur with an unpredictable frequency
2. Persistent AF is when the AF is continuous and lasts for more than 7 days, and fails to terminate spontaneously.
3. Long-standing AF is when the continuous AF lasts more than 12 months
4. Permanent is when AF is accepted and no further treatments are attempted to restore or maintain normal sinus rhythm
5. Non-valvular AF occurs in the absence of rheumatic mitral valve disease, mitral valve repair or a prosthetic heart valve.

CHA2DS2-VASc score

• Heart failure               1
• Hypertension             1
• Age More than 75      2
• Diabetes                   1
• Stroke, TIA               2
• PVD                         1
• Age 65-74                1
• Female sex               1

Prognosis

AF is associated with a high risk of thromboembolism and death. Evidence shows that rhythm control does not offer a survival advantage over rate control. Patients with AF have multiple admissions and anti-coagulation related complications over their lifetime. The risk of stroke is ever present and the overall quality of life of patients is poor.  Finally, the management of atrial fibrillation is prohibitively expensive with most of the financial burden beared by the patient.

Complications

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.

Consultations

Cardiology consultation is recommended for a patient with atrial fibrillation.

Pearls and Other Issues

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 (A Fib)

Nesheiwat Z, Goyal A, Jagtap M.

Publication Details

Introduction

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. [1][2][3]

Etiology

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.[4]

The 3 patterns of atrial fibrillation include:

Paroxysmal AF: Here the episodes terminate spontaneously within 7 days.

Persistent AF: The episodes last more than 7 days and often require electrical or pharmacological interventions to terminate the rhythm

Long-standing persistent AD: rhythm that has persisted for more than 12 months, either because a pharmacological intervention has not been tried or cardioversion has failed.

Permanent AF where a decision has been made to abort all therapies because the rhythm is unresponsive.

Epidemiology

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.[5][6]

Pathophysiology

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. [1]

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.

Triggers for aF

• Atrial ischemia
• Inflammation
• Alcohol and illicit drug use
• Hemodynamic stress
• Neurological and endocrine disorders
• Advanced age
• Genetic factors

History and Physical

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.

Evaluation

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.[7][8]

Treatment / Management

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.[2] 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.

Non-pharmacological therapy includes ablation therapy. Pacemaker placement is considered in severe causes resulting in heart failure in atrial fibrillation.[9][10][11]

Current guidelines

1. Patients with AF and elevated CHA2DS2-VASc score of 2 or more, oral anticoagulation is recommended.
2. Female sex with absence of AF risk factors and CHA2DS2-VASc of 1 or 0 in males have alow stroke risk.
3. Non-vitamin K oral anticoagulants (apixaban, dabigatran, edoxaban, and rivaroxaban) are recommended over warfarin, except in those patients with moderate to severe MS with a mechanical heart valve
4. In all patients with AF, the CHA2DS2-VASc score is recommended to assess stroke risk.
5. Obtain renal and liver function before initiating non-vitamin K oral anticoagulants
6. Aspirin is not recommended in patients with low CHA2DS2-VASc scores
7. Idarucizumab is recommended for dabigatran reversal if there is an urgent procedure or bleeding. Andexanet alfa is recommended for reversal of rivaroxaban and apixaban associated bleeding.
8. Percutaneous left atrial appendage occlusion is recommended in AF patients with a risk of stroke who have contraindications to long term anticoagulation.
9. If AF less than 48 hours or if time unknown, start anticoagulation and maintain INR 2-3 or a factor Xa inhibitor for at least 3 weeks before and at least 4 weeks after cardioversion
10. Catheter ablation is an option in patients with a low ejection fraction
11. Recommend weight  loss in obese patients with AF

Differential Diagnosis

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.

Staging

Classification of atrial fibrillation

1. Paroxysmal AF is when the episodes terminate spontaneously or with treatment within 7 days. But they may recur with an unpredictable frequency
2. Persistent AF is when the AF is continuous and lasts for more than 7 days, and fails to terminate spontaneously.
3. Long-standing AF is when the continuous AF lasts more than 12 months
4. Permanent is when AF is accepted and no further treatments are attempted to restore or maintain normal sinus rhythm
5. Non-valvular AF occurs in the absence of rheumatic mitral valve disease, mitral valve repair or a prosthetic heart valve.

CHA2DS2-VASc score

• Heart failure               1
• Hypertension             1
• Age More than 75      2
• Diabetes                   1
• Stroke, TIA               2
• PVD                         1
• Age 65-74                1
• Female sex               1

Prognosis

AF is associated with a high risk of thromboembolism and death. Evidence shows that rhythm control does not offer a survival advantage over rate control. Patients with AF have multiple admissions and anti-coagulation related complications over their lifetime. The risk of stroke is ever present and the overall quality of life of patients is poor.  Finally, the management of atrial fibrillation is prohibitively expensive with most of the financial burden beared by the patient.

Complications

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.

Consultations

Cardiology consultation is recommended for a patient with atrial fibrillation.

Pearls and Other Issues

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 (A Fib)

Nesheiwat Z, Goyal A, Jagtap M.

Publication Details

Introduction

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. [1][2][3]

Etiology

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.[4]

The 3 patterns of atrial fibrillation include:

Paroxysmal AF: Here the episodes terminate spontaneously within 7 days.

Persistent AF: The episodes last more than 7 days and often require electrical or pharmacological interventions to terminate the rhythm

Long-standing persistent AD: rhythm that has persisted for more than 12 months, either because a pharmacological intervention has not been tried or cardioversion has failed.

Permanent AF where a decision has been made to abort all therapies because the rhythm is unresponsive.

Epidemiology

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.[5][6]

Pathophysiology

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. [1]

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.

Triggers for aF

• Atrial ischemia
• Inflammation
• Alcohol and illicit drug use
• Hemodynamic stress
• Neurological and endocrine disorders
• Advanced age
• Genetic factors

History and Physical

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.

Evaluation

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.[7][8]

Treatment / Management

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.[2] 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.

Non-pharmacological therapy includes ablation therapy. Pacemaker placement is considered in severe causes resulting in heart failure in atrial fibrillation.[9][10][11]

Current guidelines

1. Patients with AF and elevated CHA2DS2-VASc score of 2 or more, oral anticoagulation is recommended.
2. Female sex with absence of AF risk factors and CHA2DS2-VASc of 1 or 0 in males have alow stroke risk.
3. Non-vitamin K oral anticoagulants (apixaban, dabigatran, edoxaban, and rivaroxaban) are recommended over warfarin, except in those patients with moderate to severe MS with a mechanical heart valve
4. In all patients with AF, the CHA2DS2-VASc score is recommended to assess stroke risk.
5. Obtain renal and liver function before initiating non-vitamin K oral anticoagulants
6. Aspirin is not recommended in patients with low CHA2DS2-VASc scores
7. Idarucizumab is recommended for dabigatran reversal if there is an urgent procedure or bleeding. Andexanet alfa is recommended for reversal of rivaroxaban and apixaban associated bleeding.
8. Percutaneous left atrial appendage occlusion is recommended in AF patients with a risk of stroke who have contraindications to long term anticoagulation.
9. If AF less than 48 hours or if time unknown, start anticoagulation and maintain INR 2-3 or a factor Xa inhibitor for at least 3 weeks before and at least 4 weeks after cardioversion
10. Catheter ablation is an option in patients with a low ejection fraction
11. Recommend weight  loss in obese patients with AF

Differential Diagnosis

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.

Staging

Classification of atrial fibrillation

1. Paroxysmal AF is when the episodes terminate spontaneously or with treatment within 7 days. But they may recur with an unpredictable frequency
2. Persistent AF is when the AF is continuous and lasts for more than 7 days, and fails to terminate spontaneously.
3. Long-standing AF is when the continuous AF lasts more than 12 months
4. Permanent is when AF is accepted and no further treatments are attempted to restore or maintain normal sinus rhythm
5. Non-valvular AF occurs in the absence of rheumatic mitral valve disease, mitral valve repair or a prosthetic heart valve.

CHA2DS2-VASc score

• Heart failure               1
• Hypertension             1
• Age More than 75      2
• Diabetes                   1
• Stroke, TIA               2
• PVD                         1
• Age 65-74                1
• Female sex               1

Prognosis

AF is associated with a high risk of thromboembolism and death. Evidence shows that rhythm control does not offer a survival advantage over rate control. Patients with AF have multiple admissions and anti-coagulation related complications over their lifetime. The risk of stroke is ever present and the overall quality of life of patients is poor.  Finally, the management of atrial fibrillation is prohibitively expensive with most of the financial burden beared by the patient.

Complications

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.

Consultations

Cardiology consultation is recommended for a patient with atrial fibrillation.

Pearls and Other Issues

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 (A Fib)

Nesheiwat Z, Goyal A, Jagtap M.

Publication Details

Introduction

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. [1][2][3]

Etiology

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.[4]

The 3 patterns of atrial fibrillation include:

Paroxysmal AF: Here the episodes terminate spontaneously within 7 days.

Persistent AF: The episodes last more than 7 days and often require electrical or pharmacological interventions to terminate the rhythm

Long-standing persistent AD: rhythm that has persisted for more than 12 months, either because a pharmacological intervention has not been tried or cardioversion has failed.

Permanent AF where a decision has been made to abort all therapies because the rhythm is unresponsive.

Epidemiology

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.[5][6]

Pathophysiology

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. [1]

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.

Triggers for aF

• Atrial ischemia
• Inflammation
• Alcohol and illicit drug use
• Hemodynamic stress
• Neurological and endocrine disorders
• Advanced age
• Genetic factors

History and Physical

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.

Evaluation

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.[7][8]

Treatment / Management

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.[2] 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.

Non-pharmacological therapy includes ablation therapy. Pacemaker placement is considered in severe causes resulting in heart failure in atrial fibrillation.[9][10][11]

Current guidelines

1. Patients with AF and elevated CHA2DS2-VASc score of 2 or more, oral anticoagulation is recommended.
2. Female sex with absence of AF risk factors and CHA2DS2-VASc of 1 or 0 in males have alow stroke risk.
3. Non-vitamin K oral anticoagulants (apixaban, dabigatran, edoxaban, and rivaroxaban) are recommended over warfarin, except in those patients with moderate to severe MS with a mechanical heart valve
4. In all patients with AF, the CHA2DS2-VASc score is recommended to assess stroke risk.
5. Obtain renal and liver function before initiating non-vitamin K oral anticoagulants
6. Aspirin is not recommended in patients with low CHA2DS2-VASc scores
7. Idarucizumab is recommended for dabigatran reversal if there is an urgent procedure or bleeding. Andexanet alfa is recommended for reversal of rivaroxaban and apixaban associated bleeding.
8. Percutaneous left atrial appendage occlusion is recommended in AF patients with a risk of stroke who have contraindications to long term anticoagulation.
9. If AF less than 48 hours or if time unknown, start anticoagulation and maintain INR 2-3 or a factor Xa inhibitor for at least 3 weeks before and at least 4 weeks after cardioversion
10. Catheter ablation is an option in patients with a low ejection fraction
11. Recommend weight  loss in obese patients with AF

Differential Diagnosis

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.

Staging

Classification of atrial fibrillation

1. Paroxysmal AF is when the episodes terminate spontaneously or with treatment within 7 days. But they may recur with an unpredictable frequency
2. Persistent AF is when the AF is continuous and lasts for more than 7 days, and fails to terminate spontaneously.
3. Long-standing AF is when the continuous AF lasts more than 12 months
4. Permanent is when AF is accepted and no further treatments are attempted to restore or maintain normal sinus rhythm
5. Non-valvular AF occurs in the absence of rheumatic mitral valve disease, mitral valve repair or a prosthetic heart valve.

CHA2DS2-VASc score

• Heart failure               1
• Hypertension             1
• Age More than 75      2
• Diabetes                   1
• Stroke, TIA               2
• PVD                         1
• Age 65-74                1
• Female sex               1

Prognosis

AF is associated with a high risk of thromboembolism and death. Evidence shows that rhythm control does not offer a survival advantage over rate control. Patients with AF have multiple admissions and anti-coagulation related complications over their lifetime. The risk of stroke is ever present and the overall quality of life of patients is poor.  Finally, the management of atrial fibrillation is prohibitively expensive with most of the financial burden beared by the patient.

Complications

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.

Consultations

Cardiology consultation is recommended for a patient with atrial fibrillation.

Pearls and Other Issues

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 (A Fib)

Nesheiwat Z, Goyal A, Jagtap M.

Publication Details

Introduction

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. [1][2][3]

Etiology

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.[4]

The 3 patterns of atrial fibrillation include:

Paroxysmal AF: Here the episodes terminate spontaneously within 7 days.

Persistent AF: The episodes last more than 7 days and often require electrical or pharmacological interventions to terminate the rhythm

Long-standing persistent AD: rhythm that has persisted for more than 12 months, either because a pharmacological intervention has not been tried or cardioversion has failed.

Permanent AF where a decision has been made to abort all therapies because the rhythm is unresponsive.

Epidemiology

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.[5][6]

Pathophysiology

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. [1]

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.

Triggers for aF

• Atrial ischemia
• Inflammation
• Alcohol and illicit drug use
• Hemodynamic stress
• Neurological and endocrine disorders
• Advanced age
• Genetic factors

History and Physical

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.

Evaluation

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.[7][8]

Treatment / Management

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.[2] 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.

Non-pharmacological therapy includes ablation therapy. Pacemaker placement is considered in severe causes resulting in heart failure in atrial fibrillation.[9][10][11]

Current guidelines

1. Patients with AF and elevated CHA2DS2-VASc score of 2 or more, oral anticoagulation is recommended.
2. Female sex with absence of AF risk factors and CHA2DS2-VASc of 1 or 0 in males have alow stroke risk.
3. Non-vitamin K oral anticoagulants (apixaban, dabigatran, edoxaban, and rivaroxaban) are recommended over warfarin, except in those patients with moderate to severe MS with a mechanical heart valve
4. In all patients with AF, the CHA2DS2-VASc score is recommended to assess stroke risk.
5. Obtain renal and liver function before initiating non-vitamin K oral anticoagulants
6. Aspirin is not recommended in patients with low CHA2DS2-VASc scores
7. Idarucizumab is recommended for dabigatran reversal if there is an urgent procedure or bleeding. Andexanet alfa is recommended for reversal of rivaroxaban and apixaban associated bleeding.
8. Percutaneous left atrial appendage occlusion is recommended in AF patients with a risk of stroke who have contraindications to long term anticoagulation.
9. If AF less than 48 hours or if time unknown, start anticoagulation and maintain INR 2-3 or a factor Xa inhibitor for at least 3 weeks before and at least 4 weeks after cardioversion
10. Catheter ablation is an option in patients with a low ejection fraction
11. Recommend weight  loss in obese patients with AF

Differential Diagnosis

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.

Staging

Classification of atrial fibrillation

1. Paroxysmal AF is when the episodes terminate spontaneously or with treatment within 7 days. But they may recur with an unpredictable frequency
2. Persistent AF is when the AF is continuous and lasts for more than 7 days, and fails to terminate spontaneously.
3. Long-standing AF is when the continuous AF lasts more than 12 months
4. Permanent is when AF is accepted and no further treatments are attempted to restore or maintain normal sinus rhythm
5. Non-valvular AF occurs in the absence of rheumatic mitral valve disease, mitral valve repair or a prosthetic heart valve.

CHA2DS2-VASc score

• Heart failure               1
• Hypertension             1
• Age More than 75      2
• Diabetes                   1
• Stroke, TIA               2
• PVD                         1
• Age 65-74                1
• Female sex               1

Prognosis

AF is associated with a high risk of thromboembolism and death. Evidence shows that rhythm control does not offer a survival advantage over rate control. Patients with AF have multiple admissions and anti-coagulation related complications over their lifetime. The risk of stroke is ever present and the overall quality of life of patients is poor.  Finally, the management of atrial fibrillation is prohibitively expensive with most of the financial burden beared by the patient.

Complications

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.

Consultations

Cardiology consultation is recommended for a patient with atrial fibrillation.

Pearls and Other Issues

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 

Definition/Description

Atrial fibrillation (AF) is the most common type of heart arrhythmia. During atrial fibrillation the heart can beat too fast, too slow, or with an irregular rhythm.
AF occurs when rapid, disorganised electrical signals cause the heart's two upper chambers known as the atria to fibrillate.  The term "fibrillate" means that a muscle is not performing full contractions. Instead, the cardiac muscle in the atria is quivering at a rapid and irregular pace.  This ultimately leads to blood pooling in the atria as it is not completely pumped out of the atria into the two lower chambers known as the ventricles.
Atrial Fibrillations can occur independently or may be associated with underlying causes. AF not associated with an underlying cause is known as "lone AF". AF can manifest itself suddenly as in "paroxysmal AF" which terminates spontaneously or with intervention within 7 days of onset. If sustained longer than seven days it is known as "persistent AF". When it occurs continuously for longer than twelve months it is known as "long-standing persistent AF". The term "permanent AF" is used when the patient and clinician make a joint decision to stop further attempts to restore or maintain sinus rhythm. Acceptance of permanent AF represents a therapeutic attitude on the part of the patient and clinician rather than an inherent pathophysiological attribute of AF. Acceptance of AF may change as symptoms, efficacy of therapeutic interventions, and patient and clinician preferences evolve.  Further, the term "nonvalvular AF" is a term used to describe when there is the absence of rheumatic mitral stenosis, a mechanical or bioprosthetic heart valve, or mitral valve repair.

AF may occur in the elderly without underlying heart disease as well. Changes in cardiac structure and function that accompany the aging process, such as increased myocardial stiffness, may be associated with AF^.

AF with associated heart disease: specific cardiovascular conditions associated with AF include valvular heart disease (most often mitral valve disease), heart failure (HF), coronary artery disease, and hypertension, particularly when LV hypertrophy is present.  In addition, heart disease leading to thicker ventricular walls (HCM), dilated cardiomyopathy, and congenital heart disease, especially atrial septal defect in adults are associated with AF. Potential etiologies also include restrictive cardiomyopathies (e.g., amyloidosis, hemochromatosis, and endomyocardial fibrosis), cardiac tumours, and constrictive pericarditis. Further, other heart diseases such as mitral valve prolapse with or without mitral regurgitation, calcification of the mitral annulus, cor pulmonale, and idiopathic dilation of the right atrium, have been associated with a high incidence of atrial fibrillation.

Familial associated AF: familial AF, defined as lone AF running in a family, is more common than previously recognized but should be distinguished from AF secondary to other genetic diseases like familial cardiomyopathies. The likelihood of developing AF is increased among the offspring of parents with AF, suggesting a familial link to AF but the mechanisms associated with transmission are not necessarily electrical, because the relationship has also been seen in patients with a family history of hypertension, diabetes, or heart failure.

Autonomic Influence in AF: in general, vagally mediated AF occurs at night or after meals, while adrenergically induced AF typically occurs during the daytime. Beta blockers are initial drug of choice for adrenergic dominated AF.

Prevalence

Atrial fibrillation (AF) is associated with significant morbidity and mortality, affecting more than 3 million people in the United States and 1-2% of the population worldwide. Its estimated prevalence is expected to double within the next 50 years.

AF without associated heart disease: Approximately 30% to 45% of cases of paroxysmal AF and 20% to 25% of cases of persistent AF occur in young patients without demonstrable underlying disease. This is considered lone AF although, over the course of time, an underlying disease that may be causing the atrial fibrillation may appear.

"An estimated 2.7–6.1 million people in the United States have AF. With the aging of the U.S. population, this number is expected to increase.

"Approximately 2% of people younger than age 65 have AF, while about 9% of people aged 65 years or older have AF.

"African Americans are less likely than those of European descent to have AF.

Characteristics/Clinical Presentation

Atrial Fibrillation (AF) symptoms vary on the functional state of the heart, the location of the fibrillation, and may exist without symptoms.^,6 Individuals are usually aware of the irregular heart action and may report feeling palpitations or sensations of fluttering, skipping and pounding. Other symptoms experienced can be inadequate blood flow which can cause feelings of dizziness, chest pain, fainting, dyspnea, pallor, fatigue, nervousness, and cyanosis. More than six palpitations occurring in a minute or prolonged repeated palpitations should be reported to the physician.  Over time, palpitations may disappear as the arrhythmia becomes permanent; it may become asymptomatic. This is common in the elderly. Some patients experience symptoms only during paroxysmal AF, or only intermittently during sustained AF. An initial appearance of AF may be caused by an embolic complication or an exacerbation of heart failure. Most patients complain of palpitations, chest pain, dyspnea, fatigue, lightheadedness, or syncope. Further, frequent urination (Polyuria) may be associated with the release of atrial natriuretic peptide, particularly as episodes of AF begin or terminate.

An irregular pulse should raise the suspicion of AF. Patients may present initially with a transient ischemic attack (TIA) or ischemic stroke. Most patients experience asymptomatic episodes of arrhythmias before being diagnosed. Patients with mitral valve disease and heart failure often have higher incidence of AF. Intermittent episodes of AF may progress in duration and frequency.  Over time many patients may develop sustained AF. For a newly diagnosed patient of AF, reversible causes such as pulmonary embolism, hyperthyroidism, pericarditis and MI should be investigated.

Pathophysiology
Atrial factors: Any kind of structural heart disease may trigger remodeling of the heart. Structural remodeling such as atrial fibrosis and loss of muscle mass are the most frequent histopathological changes in AF which facilitates initiation and perpetuation of AF. Electrical remodeling occurs, which results in changes in the action potential and contributes to the maintenance of AF.  In other words, when structural and electical changes occur in conjunction with AF, this perpetuates fibrillations. Ultimately AF causes delayed emptying from atria. This can increase the risk of stroke. Prolonged AF makes restoration and maintenance of sinus rhythm more difficult.

Associated Co-morbidities

• Stroke
• Obesity
• Obstructive sleep apnea
• Diabetes
• Congestive Heart Failure
• Mitral valve disease
• Heart failure
• Coronary artery disease
• Hypertension associated with left ventricular hypertrophy
• Hypertrophic obstructive cardiomyopathy
• Dilated cardiomyopathy
• Atrial septal defect
  

Medications

Rate control (The typical approach to treating Atrial Fibrillation)

Beta Blockers

• Metoprolol CR/XL(Toprol XL)
• Bisoprolol (Zebeta)
• Atenolol (Tenormin)
• Esmolol (Brevibloc)
• Propranolol (Inderal)
• Carvedilol (Coreg)

Antihypertensive and calcium channel blocker

• Verapamil (Calan)
• Diltiazem (Cardizem)

Antiarrhythmic and blood pressure support

• Digoxin (Lanoxin)
• Antiarrhythmic
• Amiodarone (Cordarone)
• Dronedarone (Multaq)

Rhythm control

Antiarrhythmic

• Amiodarone(Cordarone)
• Flecainide (Tambocor)
• Propafenone(Rythmol)
• Sotalol(Betapace)

Meds such as anticoagulants (commonly used along side these medications due to AF causing stroke) can cause brain hemorrhage. Benefits must be closely monitored.

Diagnostic Tests/Lab Tests/Lab Values

• 12 lead EKG
  • Presence of low-amplitude fibrillatory waves on ECG without defined P-waves 2. Irregularly irregular ventricular rhythm 3. Fibrillatory waves typically have a rate of > 300 beats per minute 4. Ventricular rate is typically between 100 and 160 beats per minute. 

• Holter monitor
• Event recorder
• Blood test
• Stress tests
• Chest X-ray
• LV Hypertrophy
• 6 minute walk test
• Physical Exam: Irregular pulse, irregular jugular venous pulsations, variation in intensity of first heart sound.

Aetiology/Causes

Atrial Fibrillation is a common early postoperative complication of cardiac and thoracic surgery. 

• Alcohol use (Holiday syndrome)
• Caffeine
• High fevers
• Severe infection
• Pneumonia
• Chronic gastritis caused by chronic H. pylori infection
• Emotional stress
• Myocardial Infarction
• Pericarditis
• Pericardial disease
• Myocarditis
• Pulmonary Embolism
• Electrocution
• Hyperthyroidism (up to 15%)
• Thyrotoxicosis
• Kidney disease
• Electrolyte abnormalities
• Increasing age
• Mitral valve disease
• Conduction system disorders
• Wolff-Parkinson-White syndrome
• Hypothermia
• Hypoxia
• Digoxin toxicity

Systemic Involvement

High concentrations of CRP, which confirm the presence of systemic inflammation are present in people with Atrial Fibrillation (AF).

Changes in an individual's health such as a newly diagnosed complication may have psychological impact. Patients may experience depression and other psycho-social challenges as a result of changes in their health status, treatment, frequent visits to the physicians office, and fear of the unknown that may accompany a diagnosis of atrial fibrillation.

Medical Management (current best evidence)

• Rate control and rhythm control through medications
  • Studies have demonstrated that a rate control strategy, with a target resting heart rate between 80 and 100 beats/minute, is recommended over rhythm control in the vast majority of patients.

• Catheter ablation
• Atrioventricular node ablation
• Surgical maze procedure
• Thromboembolism Prevention

Physical Therapy Management (current best evidence)

There is limited research on the effect of traditional physical therapy and Atrial Fibrillation. 
There is also conflicting information on the use of exercise to reduce the risk of AF.  Since obesity is an important risk factor, management of weight through exercise and education is a crucial, proactive measure that may reduce the incidence of AF. However there is conflicting evidence in regard to the optimal prescription of exercise. 

Differential Diagnosis

• Atrial tachycardia
• Atrial flutter with variable AV block
• Frequent atrial ectopies
• Pulmonary Embolism
• Hyperthyroidism
• Pericarditis
• Myocardial Infarction 
  

Case Reports/ Case Studies

1. Hwang KO. Case Study: Acute and Long-term Management of Atrial Fibrillation. MedPage Today. 2015. Available from: MedPage Today.

http://www.medpagetoday.com/resource-center/atrial-fibrillation/Case-Study/a/51000
2. Ezekowitz MD, Aikens TH, Nagarakanti R, Shapiro T. Atrial fibrillation: outpatient presentation and management. Circulation. 2011; 124: 95–99. Available from: American Heart Association.

http://circ.ahajournals.org/content/124/1/95.full#cited-by
3. Peake ST, Mehta PA, Dubrey SW. Atrial fibrillation-related cardiomyopathy: a case report. Journal of Medical Case Reports. 2007;1:111. Available from: National Center for Biotechnology Information.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2100064/

Resources

AFIB matters: Atrial Fibrilation

• http://www.afibmatters.org/Living-with-atrial-fibrillation

American Heart Association: Atrial Fibrillation Resources For Patients & Professionals

• http://www.heart.org/HEARTORG/Conditions/Arrhythmia/AboutArrhythmia/AFib-Resources-For-Patients-Professionals_UCM_423786_Article.jsp#.Vww-X4S9jzI

Cleveland Clinic: Advanced Treatment for Atrial Fibrillation

• http://www.clevelandclinic.org/lp/atrial_fibrillation/index.html?searchdef=21076362156527&002=2107636&006=89400250002&007=Search&008=&009=b&012=a%20fib&021=26286861794902&025=c&026=&utm_campaign=CS+-+Heart+-+DR+-+Afib+Local&utm_medium=cpc&utm_source=google_ppc&utm_term=a+fib&utm_content=89400250002&k_clickid=d4933b79-9aaf-4351-b2b0-eab57ffb625b&gclid=CjwKEAjw86e4BRCnzuWGlpjLoUcSJACaHG55gPkgoyxTsODA4sc2FaTx-j9dd0P8TON9Rr-8A1OWBRoCCr3w_wcB&k_clickid=d4933b79-9aaf-4351-b2b0-eab57ffb625b

Mayo Clinic: Atrial Fibrillation

• http://www.mayoclinic.org/diseases-conditions/atrial-fibrillation/atrial-fibrillation-care-at-mayo-clinic/ovc-20164979

StopAfib.org: Atrial Fibrillation Resources

• http://www.stopafib.org/resources.cfm