Atrial Fibrillation

 

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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, Elaine Lonnemann, George Prudden, WikiSysop, Karen Wilson and Vidya Acharya  

Definition/Description

Atrial fibrillation (AF), is the most common type of arrhythmia During an arrhythmia, the heart can beat too fast, too slow, or with an irregular rhythm.

AF occurs when rapid disorganized electrical signals cause the heart's two upper chambers- the atria to fibrillate. “Fibrillate" means that the heart muscle is not making full contractions. Instead, the cardiac muscle in the atria is quivering at a rapid and irregular pace.

Due to the atrial fibrillations, blood pools in the atria as it is not completely pumped out of the atria into the two lower chambers known as the ventricles.

People who have AF may not feel symptoms. In some individuals AF can cause chest pain,(MORE SYMPTOMS FOR THE LAY PERSON HERE)*** heart failure, and can increase the risk of stroke.¹

Atrial Fibrillations can occur independently or may be associated with underlying causes. It can manifest itself suddenly as in paroxysmal AF which terminates spontaneously or with intervention within 7 days of onset. AF not associated with an underlying cause is known as lone AF.

AF sustained longer than seven days 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 and/or maintain sinus rhythm. Acceptance of 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

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. ²

Prevalence

Atrial fibrillation (AF) is a cardiac arrhythmia 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, causal disease may appear.³

AF may occur in the elderly without underlying heart disease as well. However changes in cardiac structure and function that accompany the aging process, such as increased myocardial stiffness, may be associated with AF.⁴

AF with associated heart disease: Specific cardiovascular conditions associated with AF include valvular heart disease (most often mitral valve disease), HF, coronary artery disease (CAD), and hypertension, particularly when LV hypertrophy (LVH) is present. In addition, AF may be associated with HCM, dilated cardiomyopathy, or congenital heart disease, especially atrial septal defect in adults. Potential etiologies also include restrictive cardiomyopathies (e.g., amyloidosis, hemochromatosis, and endomyocardial fibrosis), cardiac tumors, and constrictive pericarditis. 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.⁴

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 susceptibility to the arrhythmia, 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 HF.⁴

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.⁴

Characteristics/Clinical Presentation

Symptoms vary on the functional state of the heart, the location of the fibrillation, and may exist without symptoms. The affected individual is usually aware of the irregular heart action and reports 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.⁵

Over time, palpitation may disappear as the arrhythmia becomes permanent, it may become asymptomatic- this is particularly common among 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 HF. 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. AF associated with a sustained, rapid ventricular response can lead to tachycardia-mediated cardiomyopathy, especially in patients unaware of the arrhythmia. Syncope is an uncommon complication that can occur upon conversion in patients with sinus node dysfunction or because of rapid ventricular rates in patients with HCM, valvular aortic stenosis, or an accessory pathway.⁴

Patient may or may not have symptoms with AF. Commonly associated symptoms include palpitations, shortness of breath, fatigue, decreasing exercise tolerance, or chest discomfort. An irregular pulse should raise the suspicion for AF. Patients may present initially with 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 and over time many patients will develop sustained AF. For a newly diagnosed patient of AF, reversible causes such as pulmonary embolism, hyperthyroidism, pericarditis and MI should be investigated.⁶

Pathophysiology
Atrial factors: Any kind of structural heart disease may trigger remodeling of both the atria and ventricles. Structural remodeling such as atrial fibrosis and loss of atrial muscle mass are the most frequent histopathological changes in AF which facilitates initiation and perpetuation of AF. Electrical remodeling occurs, resulting in multiple reentry circuits or rapidly firing atrial foci and shortening of atrial refractoriness and action potential, thus contributing to the maintenance of AF. Electrophysiological mechanisms: Focal mechanisms of triggered activity and re-entry have attracted much attention recently. Wavelet Hypothesis suggests several independent wavelets propagating AF rather than a single focus.Familial component should be investigated with early onset AF. AF reduces left atrial flow velocities and causes delayed emptying from atrial appendage and are implicated in thrombus formation.^{6, 7}
Prolonged AF makes restoration and maintenance of sinus rhythm more difficult.⁷

Associated Co-morbidities

Obesity - Obesity and the magnitude of nocturnal oxygen desaturation, which is an important pathophysiological consequence of OSA, are independent risk factors for incident AF in individuals <65 years of age.⁸
Obesity is an important risk factor for the development of AF (103). After adjustment for clinical risk factors, the excess risk of AF appears related to LA dilation. There is a graded increase in LA size as body mass index increases from normal to the overweight and obese categories, and weight has been linked to regression of LA enlargement (104). These findings suggest a physiological link between obesity, AF, and stroke and raise the intriguing possibility that weight reduction may decrease the risk associated with AF.⁴
Diabetes
May cause CHF
Mitral valve disease
Heart failure
Coronary artery disease
Hypertension associated with left ventricular hypertrophy
Hypertrophic obstructive cardiomyopathy
Dilated cardiomyopathy
Atrial septal defect
A persistently elevated ventricular rate during AF (usually > 120 beats/min) for prolonged time periods may also result in increased mitral regurgitation, eventually leading to a dilated ventricular cardiomyopathy (tachycardia-induced cardiomyopathy).⁷

Medications

Rate control*
Beta Blocker
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 (Antiarrhythmics)
Amiodarone(Cordarone)
Flecainide (Tambocor)
Propafenone(Rythmol)
Sotalol(Betapace)

Meds such as anticoagulants can cause brain hemorrhage. Benefits must be closely monitored. ⁶

Diagnostic Tests/Lab Tests/Lab Values

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Etiology/Causes

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Systemic Involvement

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Medical Management (current best evidence)

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Physical Therapy Management (current best evidence)

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Differential Diagnosis

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Resources

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Recent Related Research (from Pubmed)

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