Atrial Fibrillation

 

Welcome to PT 635 Pathophysiology of Complex Patient Problems This is a wiki created by and for the students in the School of Physical Therapy at Bellarmine University in Louisville KY. Please do not edit unless you are involved in this project, but please come back in the near future to check out new information!!

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 heart arrhythmia. During atrial fibrillation 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 known as the atria to fibrillate.  The term "fibrillate" means that a muscle uscle is not performing 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.¹

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. ²

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^.3

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, 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.³

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.³

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.³

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.⁴

"An estimated 2.7–6.1 million people in the United States have AFib. With the aging of the U.S. population, this number is expected to increase.⁵"

"Approximately 2% of people younger than age 65 have AFib, while about 9% of people aged 65 years or older have AFib.⁵"

"African Americans are less likely than those of European descent to have AFib.⁵"

Characteristics/Clinical Presentation

Symptoms vary on the functional state of the heart, the location of the fibrillation, and may exist without symptoms.^1,5 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} Therefore AF can increase the risk of stroke.¹

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.⁹
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.³
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).⁸

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. ⁷

Diagnostic Tests/Lab Tests/Lab Values

12 lead EKG⁶
Several characteristic electrocardiogram (ECG) changes define AF: 1. 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. ⁸
Holter monitor⁷
Event recorder⁷
Blood test⁷
Stress tests⁷
Chest X-ray⁷
LV Hypertrophy³
6 minute walk test³
Physical Exam: Irregular pulse, irregular jugular venous pulsations, variation in intensity of first heart sound.⁴

Etiology/Causes

AF is a common early postoperative complication of cardiac and thoracic surgery. (other sources (Surgery (intrathoracic) - common as an early post op complication of thoracic surgery including cardiac surgery. )
Alcohol use (Holiday syndrome)
Caffeine*
High fevers*severe infection/ pneumonia
Presence of helicobacter pylori in stomach is associated with persistent AF*
Emotional stress* BOOK

MI
Pericarditis/pericardial disease/myocarditis
Pulmonary Embolism
Electrocution
Hyperthyroidism (up to 15% of hyperthyroidism pts)
Kidney dis/ electrolyte abnormalities/Other metabolic
Increasing age
Male > Female (source 8 also)
mitral valve disease,
conduction system disorders, Wolff-Parkinson-White syndrome,
Conditions associated with AF:
thyrotoxicosis, hypothermia, hypoxia,
Digoxin toxicity
Lone AF applies to AF in individuals younger than 60 years of age without clinical or echocardiographic evidence of cardiopulmonary disease (including hypertension), Lone AF is favorable in regard to statistics of thromboembolism and mortality.^3,6,7,8,9

Systemic Involvement

High concentrations of CRP, which confirm the presence of systemic inflammation are present in people with AF. A potential non-cardiovascular disease that predisposes individuals to AF may be chronic gastritis caused by chronic H. pylori infection.³ 

Medical Management (current best evidence)

Rate control and rhythm control through medications
Catheter ablation
Atrioventricular node ablation
Surgical maze procedure
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. add text here
Thromboembolism Prevention^3,6,7

Physical Therapy Management (current best evidence)

Limited research on the effect of traditional physical therapy and Atrial Fibrillation
Conflicting information on the use of exercise to reduce the risk of AF

Differential Diagnosis

Atrial tachycardia

Atrial flutter with variable AV block
Frequent atrial ectopiesPulmonary Embolism

Hyperthyroidism

Pericarditis

 MI
Antegrade atrioventricular nodal conduction

Case Reports/ Case Studies

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Resources

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Recent Related Research (from Pubmed)

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References

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