Atrial fibrillation or flutter

I. What every physician needs to know.

Atrial fibrillation (AF) is an abnormal heart rhythm distinguished by rapid (usually greater than 300 beats per minute) irregularly irregular heart beat with no distinct P-wave on an electrocardiogram (EKG). AF can cause reduction in cardiac output and atrial thrombus leading to stroke risk and therefore affected patients may be at increased risk of mortality. Atrial flutter is characterized by rapid and regular atrial depolarizations.

II. Diagnosis:

The diagnosis of atrial fibrillation is made using the 12-lead EKG.

AF can be challenging to diagnose due to its paroxysmal and minimally symptomatic nature. However, many individuals with AF experience symptoms which may include palpitations, lightheadedness, near syncope, shortness of breath, fatigue, exercise intolerance, and chest discomfort (including chest pressure).

Atrial fibrillation is a common heart rhythm disorder encountered in clinical practice, affecting the elderly. The prevalence of AF continues to increase with the aging of the United States population.

D. Physical Examination Findings.

Physical findings consistent with AF include:

An irregular pulse
A rapid pulse

Physical findings sometimes present in patients with AF include:

Elevated neck veins (heart failure)
Pulmonary rales (heart failure)
Lower extremity edema (heart failure)
Cardiac murmur (valvular disease)
Inferolateral displacement of the point of maximal impulse (cardiac enlargement)
Thyroid enlargement (hyperthyroidism)

E. What diagnostic tests should be performed?

History and physical examination (as above)
12-lead EKG
Thyroid function testing
Chemistry panel (particularly to evaluate potassium and magnesium levels)

If AF is suspected but not present on the EKG, longer-term monitoring with 24-48 hour Holter monitors, or 30-day event monitors.

2. What imaging studies (if any) should be ordered to help establish the diagnosis? How should the results be interpreted?

A transthoracic echocardiogram should be performed to evaluate for the presence of the left atrial size, a predictor of AF recurrence and risk for heart failure as well as the left ventricular function and valvular abnormalities.

III. Management.

Multiple factors play a role in the management of atrial fibrillation. These include symptoms, hemodynamic stability, evidence of preexcitation (wolff-parkinson-white syndrome), or evidence of myocardial ischemia/infarction. Hall-mark of treatment revolves around rate control and the decision of cardioversion.

The use of anticoagulant and antiplatelet agents in AF has been shown to reduce risk for stroke and improve overall longevity. The choice of using an anticoagulant therapy is based on a systematic assessment of stroke risk. The most commonly used stroke risk prediction tool is the CHADS2, but the CHADS2-VASC is a newer and alternative stroke risk prediction algorithm that can be used to estimate stroke risk from AF. See Table I. Scores of < 1 on either scale are considered low risk for stroke and do not need anticoagulation.

Table I.n

CHADS2-VASC stroke risk prediction algorithm

Although AF is typically well tolerated in the short-term, in patients with concomitant medical illnesses such as heart failure or an acute coronary syndrome, development of AF can precipitate hemodynamic collapse. In such settings, urgent or emergent cardioversion is recommended.

In patients who are relatively asymptomatic and clinically stable, the acute treatment of AF typically consists of the use of atrioventricular (AV) nodal blocking drugs to slow the ventricular response rate; for patients who have signs or symptoms of hypoperfusion rate control rate control or cardioversion may be needed urgently. Next determine the need for anticoagulation therapy based on the assessment of stroke and bleeding risks. Consult a cardiologist or electrophysiologist if needed.

Test such as thyroid stimulating hormone (TSH), serum electrolytes, complete blood count (CBC), cardiac biomarkers, brain natriuretic peptide (BNP), echocardiogram should be performed.

Oral (or intravenous) beta blocker or calcium channel blocker (verapamil and diltiazem) can be used to achieve rate control. Digoxin is also used for rate control though less effective and generally used in patients with heart failure. Another option for rate control is amiodarone, however, there is a risk for cardioversion with this medication which can result in stroke in patients that are not adequately anticoagulated. In patients with preexcitation, AV blocking agents should be avoided as preferential AV nodal blockade with these drugs may lead to more rapid accessory pathway conduction which can lead to ventricular fibrillation.

Next, patients who are stable and rate-controlled need a decision regarding rhythm control. Most patients with new onset AF should have an attempt at cardioversion. If cardioverted some patients will never have a second episode or will have infrequent episodes. It can also improve functional status. The longer the patient has been in atrial fibrillation the less likelihood of achieving sinus rhythm with cardioversion.

It is important that the patient with AF of unknown duration or an AF episode lasting greater than 48 hours undergo treatment with an anticoagulant with therapeutic levels for at least 3 weeks prior to cardioversion. Alternatively, patients with AF who cannot, or who choose not to, wait for 3 weeks can undergo a transesophageal echocardiogram prior to cardioversion to rule out the presence of an atrial thrombus and reduce stroke risk from cardioversion.

All patients undergoing electrical cardioversion must be anticoagulated for 4 weeks following their procedure.

Cardioversion can be performed by using either electrical or pharmacologic method. Choices for pharmacologic cardioversion includes flecainide, dofetilide, propafenone, ibutilide and amiodarone. Generally speaking, in first time atrial fibrillation an attempt should be made to convert with electrical cardioversion. Antiarrhythmic drugs can be administered prior to cardioversion to increase the chance of reversion and to prevent recurrence of AF. For patients with paroxysmal atrial fibrillation, rhythm control drug therapy is preferred if they will have sinus rhythm maintained with long-term antiarrhythmic drug therapy.

Management of atrial flutter is similar to the management of atrial fibrillation. Major issues to address would be controlling the ventricular rate, reversion to normal sinus rhythm, maintenance of normal sinus rhythm, prevention of embolism. In patient with atrial flutter, radiofrequency catheter ablation is generally preferable to long-term pharmacologic therapy in patient with type I (typical) atrial flutter.

C. Laboratory Tests to Monitor Response To, and Adjustments in, Management.

If anticoagulation with warfarin is used, monitoring of prothrombin time/international normalized ratio (PT/INR) is necessary to gauge drug response. The target INR for AF/Flutter is 2.0 to 3.0. Use of dabigatran does not require checking the PT/INR. If heparin is instituted, a target partial thromblastin time (PTT) of 50-70 seconds is recommended. A hemoglobin level and renal function evaluation are also recommended for patients initiated on anticoagulation.

D. Long-term management.

Patients with minimally or asymptomatic AF who are appropriately anti-coagulated and easily rate-controlled can be managed by a primary care physician or general practitioner. Referral to a cardiologist is recommended for patients whom primary care physician is having difficulty managing. Long-term management of anticoagulants, antiarrhythmic drugs, and the scheduling of elective operations such as catheter-based ablation are based on factors such as patient symptomatology, medication side effects, or drug-drug interactions.

E. Common Pitfalls and Side-Effects of Management

Use of anticoagulants predisposes to bleeding, including major bleeding (e.g., intracranial bleeding). Use of dabigatran can precipitate bleeding and is a frequent cause of gastrointestinal symptoms, including nausea, heartburn, and bloating.

Coumadin – bleeding risk, drug-drug interactions
Dabigatran – bleeding risk, gastrointestinal side-effects (bloating, gastroesophageal reflux disease)
Anti-arrhythmic drugs – QRS or QT prolongation, ventricular arrhythmias including Torsades de Pointes
Rate-controlling agents – bradycardia

IV. Management with Co-Morbidities

The typical management of AF is affected by the presence of significant cardiovascular comorbidities, including hypertension, stroke, heart failure, vascular disease, and chronic kidney disease.

A. Renal Insufficiency.

Anti-arrhythmic drug dosing may be affected and/or the use contraindicated (e.g., sotalol, dofetilide). Bleeding risk from the use of anticoagulants is higher among patients with end-stage renal disease and the overall thromboembolic risk from AF is higher among patients with chronic kidney disease and proteinuria.

B. Liver Insufficiency.

The use of anticoagulants, particularly warfarin (hepatic clearance), is associated with a high rate of side effects, including major bleeding. The use of amiodarone is contraindicated in patients with severe hepatic failure.

C. Systolic and Diastolic Heart Failure

Heart failure and AF commonly occur together, and the concomitant presence of AF and heart failure is associated with a poorer prognosis than either disease alone. AF can result in a non-ischemic cardiomyopathy (a so-called tachycardia-mediated cardiomyopathy) and thus when heart failure has developed after AF and there has been a chronic and persistent rapid ventricular response associated with AF, aggressive rate or rhythm-control efforts must be pursued.

V. Transitions of Care

A. Sign-out considerations While Hospitalized.

Hemodynamic stability should be assessed and communicated as should the use of any anti-arrhythmic medications, anticoagulants, and planned procedures (e.g., cardioversion, AF ablation, pacemaker implantation).

D. Arranging for Clinic Follow-up

Follow-up is generally scheduled with a primary medical doctor or cardiologist 2-4 weeks after discharge.

VII. What's the Evidence?

**The original source for this chapter was Dr. David McManus. The chapter was revised for this program by Dr. Maharshi Bhakta.

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