National University of Rwanda Family and Community Medicine

Atrial Fibrillation
KABERA Ren,MD PGY IV Resident Family and Community Medicine National University of Rwanda

Background
Classification of atrial fibrillation (AF) 1. Paroxysmal AF Episodes of AF that terminate spontaneously within 7 days (most episodes last less than 24 hours) 2. Persistent AF - Episodes of AF that last more than 7 days and may require either pharmacologic or electrical intervention to terminate 3. Permanent AF - AF that has persisted for more than 1 year, either because cardioversion has failed or because cardioversion has not been attempted.

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Pathophysiology
Atrial fibrillation (AF) shares strong associations with other cardiovascular diseases, such as heart failure, coronary artery disease (CAD), valvular heart disease, diabetes mellitus, and hypertension. The relationship between comorbid cardiovascular disease and AF is incompletely understood and more complex than this terminology implies. Catecholamine excess, hemodynamic stress, atrial ischemia, atrial inflammation, metabolic stress, and neurohumoral cascade activation are all purported to promote AF.

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Physiopathology
Focal pulmonary vein triggers, but alternative and non mutually exclusive mechanisms have also been evaluated. These mechanisms include multiple wavelets, mother waves, fixed or moving rotors, and macro-reentrant circuits. Multiple mechanisms may coexist at any given time. The automatic focus theory and the multiple wavelet hypothesis appear to have the best supporting data.

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Etiology
AF is strongly associated with the following risk factors: Hemodynamic stress Atrial ischemia Inflammation Noncardiovascular respiratory causes Alcohol and drug use Endocrine disorders Neurologic disorders Genetic factors Advancing age
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Etiology
Hemodynamic stress Increased intra-atrial pressure results in atrial electrical and structural remodeling. The most common causes of increased atrial pressure are mitral or tricuspid valve disease and left ventricular dysfunction. Systemic or pulmonary hypertension also commonly predisposes to atrial pressure overload, and intracardiac tumors or thrombi are rare causes. Atrial ischemia Coronary artery disease infrequently leads directly to atrial ischemia and AF. More commonly, severe ventricular ischemia leads to increased intra-atrial pressure and AF.

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Etiology
Inflammation Myocarditis and pericarditis may be idiopathic or may occur in association with collagen vascular diseases; viral or bacterial infections; or cardiac, esophageal, or thoracic surgery. Noncardiovascular respiratory causes Pulmonary embolism, pneumonia, lung cancer, and hypothermia. Drug and alcohol use Stimulants, alcohol, and cocaine can trigger AF.
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Etiology
Endocrine disorders Hyperthyroidism, diabetes, and pheochromocytoma. Neurologic disorders Intracranial processes such as subarachnoid hemorrhage or stroke. Familial AF A history of parental AF (ion channel abnormalities, especially sodium channels). Advancing age 4% of individuals older than 60 years and 8% of persons older than 80 years.
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Epidemiology
Atrial fibrillation affects more than 2.2 million persons in the United States. AF is strongly age-dependent, affecting 4% of individuals older than 60 years and 8% of persons older than 80 years. Approximately 25% of individuals aged 40 years and older will develop AF during their lifetime. AF is uncommon in childhood except after cardiac surgery. Rwanda: No specific data

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Prognosis
AF is associated with increased morbidity and mortality, in part due to the risk of thromboembolic disease, particularly stroke, in AF and in part due to its associated risk factors. Development of AF predicts heart failure and is associated with a worse NYHA Heart Failure classification. The risk of stroke from AF that lasts longer than 24 hours is a major concern Atrial fibrillation in association with acute myocardial infarction

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History
Unstable patients requiring immediate DC cardioversion include the following: Decompensated congestive heart failure (CHF) Hypotension Uncontrolled angina/ischemia Less severe symptoms and patient complaints include the following: Palpitations Fatigue or poor exercise tolerance Presyncope or syncope Generalized weakness, dizziness, fatigue
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History
Documentation of clinical type of AF (paroxysmal, persistent, or permanent) Assessment of type, duration, and frequency of symptoms Assessment of precipitating factors (eg, exertion, sleep, caffeine, alcohol use) Assessment of modes of termination (eg, vagal maneuvers) Documentation of prior use of antiarrhythmics and ratecontrolling agents Assessment of presence of underlying heart disease Documentation of any previous surgical or percutaneous AF ablation procedures
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Physical Examination
Airway , breathing, and circulation (ABCs) . Vital signs: Heart rate, blood pressure, respiratory rate, and oxygen saturation Patients will have an irregularly irregular pulse and will commonly be tachycardic (110-140 rarely over 170) Patients who are hypothermic or who have cardiac drug toxicity may present with bradycardic atrial fibrillation.

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Physical examination
Head and neck Exophthalmos, thyromegaly, elevated jugular venous pressures, or cyanosis. Carotid artery bruits suggest peripheral arterial disease and increase the likelihood of comorbid coronary artery disease. Pulmonary Heart failure (rales, pleural effusion). Wheezes or diminished breath sounds are suggestive of underlying pulmonary disease (chronic obstructive pulmonary disease [COPD], asthma).
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Physical examination
Cardiac The cardiac examination is central to the physical examination of the patient with AF. A displaced point of maximal impulse or S3 suggests ventricular enlargement and elevated left ventricular pressure. A prominent P2 points to the presence of pulmonary hypertension.

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Physical examination
Abdomen 1. The presence of ascites, hepatomegaly, or hepatic capsular tenderness suggests right ventricular failure or intrinsic liver disease. 2. Left upper quadrant pain may suggest splenic infarct from peripheral embolization.

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Physical examination
Lower extremities Examination of the lower extremities may reveal cyanosis, clubbing, or edema. A cool or cold pulseless extremity may suggest peripheral embolization. assessment of peripheral pulses may lead to the diagnosis of peripheral arterial disease or diminished cardiac output.

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Physical examination
Neurologic Signs of a transient ischemic attack or cerebrovascular accident may be discovered. Evidence of prior stroke and increased reflexes is suggestive of hyperthyroidism.

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Diagnostic Considerations
The diagnosis of AF is based on the physical finding of an irregular heart rhythm and is confirmed with an ECG or rhythm strip.

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Diagnostic considerations
Electrocardiography ECG findings usually confirm the diagnosis of atrial fibrillation and include the following: The ventricular rate is typically irregular Discrete P waves are absent, replaced by irregular, chaotic F waves, in the setting of irregular QRS complexes, (as shown in the image below) Look also for aberrantly conducted beats after long-short R-R cycles (ie, Ashman phenomenon) Heart rate (typically in the 110-140 range, but rarely over 160-170) Preexcitation Left ventricular hypertrophy Bundle-branch block Acute or prior MI
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Ventricular rate varies from 130-168 beats per min Ventricular rate varies from 130-168 beats per minute. Rhythm is irregularly irregular. P waves are not discernible.

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Diagnostic considerations
Laboratory studies : CBC count (looking for anemia, infection) Serum electrolytes and BUN/creatinine (looking for electrolyte disturbances or renal failure) Cardiac enzymes - CK and/or troponin level (to investigate myocardial infarction as a primary or secondary event)

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Diagnostic considerations
BNP (to evaluate for CHF) D-dimer (if the patient has risk factors to merit a pulmonary embolism workup) Thyroid function studies (looking for thyrotoxicosis, a rare, but not-to-be-missed, precipitant) Digoxin level (may be obtained when appropriate for subtherapeutic levels and/or toxicity; Toxicology testing or ethanol level

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Diagnostic considerations
Transthoracic echocardiography (TTE) : Evaluate for valvular heart disease Evaluate atrial and ventricular chamber and wall dimensions Estimate ventricular function and evaluate for ventricular thrombi Estimate pulmonary systolic pressure (pulmonary hypertension) Evaluate for pericardial disease

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Diagnostic considerations
Transesophageal echocardiography (TEE) : Evaluate for LA thrombus (particularly in the LA appendage) To guide cardioversion (if thrombus is seen, cardioversion should be delayed) When TEE is planned, the concurrent use of TTE may increase cost without providing significant additional information. CT and MRI In patients with a positive D-dimer result, chest CT angiography may be necessary to rule out pulmonary embolus.
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Diagnostic considerations
CXR Chest radiographic findings are usually normal. Evidence of CHF as well as signs of lung or vascular pathology (embolism, pneumonia).

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Diagnosis consideration
Six-Minute Walk Test or Exercise Test Assess the adequacy of rate control (eg, target heart rate of 110 bpm or less during a 6-minute walk). Exclude ischemia prior to treatment of patients with class Ic antiarrhythmic drugs and can be used to reproduce exerciseinduced AF. Holter Monitoring or Event Recording Electrophysiology Study

Nov 2011-Kabgayi

Differentials
Atrial Flutter Atrial Tachycardia Atrioventricular Nodal Reentry Tachycardia (AVNRT) Multifocal Atrial Tachycardia Paroxysmal Supraventricular Tachycardia Wolff-Parkinson-White Syndrome

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Management
1. Management of New-Onset AF Rate control 1. Beta-blockers and calcium channel blockers 2. Digoxin 3. Amiodarone Anticoagulation 1. Warfarin 2. Heparin 3. Oral direct thrombin 4. Dabigatran (Pradaxa) 5. Rivaroxaban (Xarelto) Cardioversion Restore sinus rhythm within 7 days after AF
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Management
2.Long term management Anticoagulation 1. Warfarin 2. Clopidogrel 3. Aspirin 4. Dabigatran Rate control Adequate rate control was previously defined as a heart rate of 60-80 bpm at rest and 90-115 bpm with moderate exercise 1. Beta-blockers and calcium channel blockers 2. Digoxin 3. Amiodarone
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Management
Rhythm control Flecainide, Propafenone , Dofetilide, Amiodarone Electrical cardioversion Catheter ablation and surgical treatment of AF Disconnect triggers and/or to modify the substrate for AF Compartmentalization of the Atria

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References
o o o o Published guidelines from : American College of Cardiology (ACC) American Heart Association (AHA) European Society of Cardiology (ESC) American Academy of Family Physicians E-medicine :Atrial fibrillation

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END

THANK YOU
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