Atrial Fibrillation: Manual of Clinical Guidelines

Transcription

1 Atrial Fibrillation: Manual of Clinical Guidelines Table of Contents Table of Contents...1 Introduction...2 How to Use this Manual...3 Atrial Fibrillation: COMMON ELEMENTS OF CARE...4 Definitions...4 Controlling Ventricular Rate...5 Restoration of Sinus Rhythm...9 Maintenance of Sinus Rhythm...12 Transesophageal Echocardiography...16 Anticoagulation...17 Atrial Flutter...21 Advanced Electrophysiology Techniques...22 Atrial Fibrillation: GUIDELINES AND ALGORITHMS...23 Emergency Department...23 Hospital Monitored Unit...28 Postoperative Atrial Fibrillation...35 Physician Office...43 APPENDIX:...46 Data Elements and Quality Indicators...46 Intravenous Amiodarone...47 Relative Stroke Risk Table...49

2 Introduction Atrial fibrillation is the most common sustained cardiac arrhythmia. Though it can occur in patients whose heart is otherwise normal, it is more commonly associated with cardiovascular disease and can result in substantial morbidity. It becomes increasingly common as one ages and is destined to be one of the largest clinical problems in cardiology as the population's median age rises. It is already responsible for a huge consumption of health care resources, as patients often require hospitalizations, expensive medications and a variety of procedures. The ongoing monitoring of these patients is complicated and labor-intensive. The purpose of this manual is to provide clinical guidelines for the evaluation and treatment of patients with atrial fibrillation or atrial flutter for the various ways with which they present. As the patient characteristics and their clinical presentations vary widely, the development of succinct guidelines is challenging. Recommendations made in this document are based on a review of the pertinent literature and are intended to be guidelines, not necessarily mandates. As is always the case with clinical guidelines, the specific course of therapy continues to be at the discretion of the clinician and determined by the individual patients' circumstance. Clinical guidelines for patients with atrial fibrillation are also available from the American College of Cardiology ( Published in The St. Joseph Mercy Atrial Fibrillation Manual is intended to provide a practical, algorithmic approach to the most common clinical presentations of this arrhythmia, but the user is encouraged to use the ACC guidelines as a supportive reference.

3 How to Use this Manual The specific method and timing of evaluation and treatment for the patient with atrial fibrillation or flutter (AF) depends upon an individual patient's clinical characteristics. Symptoms, concomitant co-morbidities and the venue in which they present dictate therapy. Appropriate goals of therapy for AF include: The prevention or reduction of symptoms The prevention of thromboembolic complications The prevention of long term atrial "conditioning" The reduction of unnecessary hospitalizations (and) The minimization of adverse effects associated with therapy. In accomplishing these goals, the clinician will rely on certain Common Elements of the evaluation and therapy for atrial tachyarrhythmias. Thus, guidelines for ventricular rate control, restoration and maintenance of sinus rhythm, the appropriate use of transesophageal echocardiography and anticoagulation therapy are delineated first. There is also a brief description of advanced electrophysiologic techniques. Each of the venue-specific AF guidelines and/or critical paths that follow will then refer to these Common Elements. This part of the manual describes appropriate care of patients presenting with AF in the Emergency Department; for patients admitted to the hospital with AF; for patients developing AF after cardiac surgery and for patients presenting with AF in the physician office. Except when specified, atrial fibrillation and atrial flutter will be considered identically and referred to as simply atrial fibrillation or AF. The sections of this manual that refer to specific drugs, their dosages and important adverse effects are not meant to be exhaustive. The clinician is urged to consult other references for more detailed pharmacology.

4 Atrial Fibrillation: COMMON ELEMENTS OF CARE Definitions For the purposes of this manual, the following definitions will be used: Acute (or new onset) atrial fibrillation: AF whose onset is observed electrocardiographically or by history clearly began no longer than 48 hours prior to presentation Newly recognized atrial fibrillation: AF that is newly discovered but whose onset is unknown. Persistent atrial fibrillation: An episode of acute AF or newly recognized AF that is then persistent for greater than 48 hours. Paroxysmal atrial fibrillation: Intermittent episodes of self-terminating AF Chronic, persistent atrial fibrillation: AF that has been present at least one month Chronic, permanent atrial fibrillation: AF that has been present at least one month and which has either been shown to be unconvertible or has been deemed best to be left unconverted. Idiopathic (or lone ) atrial fibrillation: AF in a patient under the age of 65 years in the absence of any cardiovascular disease (including hypertension) or non-cardiovascular condition that is known to cause AF (e.g., hyperthyroidism)

5 Controlling Ventricular Rate General Considerations One of the principal causes of symptoms during AF is the rapid and chaotic ventricular rates that can occur. When symptoms are present, especially if they are accompanied by hemodynamic compromise, rate control is paramount. It is accomplished by giving drugs that decrease or delay AV nodal conduction. Drugs that block AV nodal conduction during atrial fibrillation or atrial flutter include: beta-blockers certain calcium channel blockers (only verapamil and diltiazem) digoxin antiarrhythmic drugs (in varying degrees) These drugs can be used alone or in combination with other agents for acute or chronic rate control. Acute Rate Control: Because digoxin has a delayed and less predictable effect on rate during atrial fib or atrial flutter, beta blockers or calcium channel blockers are preferred as initial therapy. Diltiazem: O.25 mg/kg I.V. bolus Can repeat 0.25 to 0.35 mg/kg boluses Continuous infusion: 5-15 mg/min; titrated to rate (and BP) Variable, but at most modest, negative inotropic effect usually Antihypertensive Antiischemic Can depress sinus node function and result in exaggerated post-conversion pauses Esmolol: O.5 mg/kg I.V. bolus Can repeat 0.25 to 0.5 mg/kg boluses Continuous infusion is 0.05 mg/kg/min to start; titrated to rate (and BP) Shortest half-life Anti-ischemic Antihypertensive Modest negative inotropic effects Can cause bronchospasm Can depress sinus node function and result in exaggerated post-conversion pauses

6 Digoxin: O.25 mg I.V. boluses Q3-4 hours to a usual total dose of 1 mg Delayed onset of action Additive bradycardic side effects to esmolol and diltiazem Positive inotrope Other agents: Metoprolol, atenolol, and verapamil are other commonly used effective AV nodal blocking drugs that can be given intravenously, though usually in just bolus doses. The antiarrhythmic drugs that also have variably predictable AV nodal blocking properties include amiodarone, sotalol and propafenone. Especially when given I.V., procainamide and quinidine enhance AV nodal conduction and can aggravate attempts to control rate. Chronic Rate Control: Digoxin is often used for chronic rate control, especially in patients with LV systolic dysfunction. It is often effective in controlling ventricular rates during atrial fib at rest. However, digoxin is often ineffective in controlling rates during exercise or other stresses, and therefore, the majority of patients in chronic persistent atrial fibrillation who require drugs for rate control are best treated with either beta or calcium blocking drugs (not uncommonly in combination with digoxin). Holter monitoring or exercise testing is recommended to assess the degree of rate control in this patient population. Asymptomatic pauses of < 3 seconds during ambulatory monitoring (especially during sleep) should be considered a normal finding. A number of other caveats about ventricular rate control are important: Negative inotropic effects of calcium channel blockers can limit their utility in patients with severe LV dysfunction. Beta blockers can be difficult to administer to these patients but are now considered important adjuncts to the therapy of chronic CHF Catheter ablation of the AV junction is sometimes indicated when rate control during chronic persistent atrial fibrillation is not achievable Poor rate control over the long term can contribute to progressive LV dysfunction in some patients A number of patients will have well-controlled ventricular rates in the absence of AV nodal blocking drugs (for example, with high vagal tone). There is no indication for these drugs if rates are slow or well controlled (either in the acute or chronic setting) It is often unnecessary or inappropriate to continue AV nodal blocking drugs in the patient who has had sinus rhythm restored. Ventricular rates are difficult to control in most patients with typical ATRIAL FLUTTER because of fixed ratio block (2:1, 3:1, etc.) The continued titration of I.V. AV nodal blocking drugs to control rates is often futile and more expeditious cardioversion is often the more appropriate choice. Adequate AV nodal blockade is paramount in advance of the institution of antiarrhythmic drugs which either enhance AV nodal conduction (e.g.: quinidine and procainamide) or which can significantly slow the atrial rate

7 during atrial flutter (e.g., flecainide, propafenone, etc.) These two effects can precipitate 1:1 AV conduction during atrial flutter or an undesired increase in ventricular rate during atrial fibrillation. Rate control may also be especially challenging in special circumstances such as sepsis, anemia, thyrotoxicosis, CHF, WPW or when the patient is receiving sympathomimetics or intravenous catecholamines NOTE: ON THE FOLLOWING PAGE IS A SAMPLE ALGORITHM FOR ACUTE RATE CONTROL (emphasis on frequent up-titration of intravenous AV nodal blocking drugs)

8 Hemodynamically stable AF HR > 100 Symptomatic patient Correct underlying conditions that affect rate control: CHF, hypoxemia, thyrotoxicosis, COPD, sepsis, etc Use oral AV nodal blocking agents for patients with mild symptoms who can tolerate oral NO Moderate to Severe Symptoms? YES Is patient a candidate for IV diltiazem? Avoid in the following situations: SBP < 90 WPW Caution in the following situations: History of significant sinus node dysfunction MI CHF NO Is patient a candidate for beta blocker? Avoid use in: SBP < 90 Uncompensated CHF Active bronchospasm YES IV diltiazem at 10 mg/hr and titrate to pulse of < 120 Up-titrate frequently (q15-30 min) to max rate of 15 mg/min Maintain SBP >90 Successful? If no change within 2-4 hours and with aggressive up-titration to max dose - add another agent If adverse effects intolerable - dc diltiazem and switch to another agent NO NO NO Esmolol drip Titrate to pulse of < 120 Maintain SBP >90 Up-titrate frequently (q15-30 min) to max dose of 300 mcg/kg/min Successful? Unsuccessful if no change within 2-4 hours with aggressive up titration to max dose or unable to tolerate adverse effects YES SUCCESSFUL RATE CONTROL: Monitor and convert to oral when and if appropriate YES Determine whether pharmacologic or electrical cardioversion conversion is indicated if rate control is inadequate and symptoms remain more than moderate

9 Restoration of Sinus Rhythm General Considerations The decision to restore sinus rhythm or cardiovert is highly dependent upon the duration of atrial fibrillation, the symptoms associated with the arrhythmia, prior history of cardioversion and the underlying cardiovascular pathology. Many of these factors will be addressed specifically later. Recent studies confirm the clinical experience that rate control and an appropriate anti-thrombotic strategy is not uncommonly the appropriate choice over aggressive attempts to restore and maintain sinus rhythm. The following description of methods of cardioversion assumes that these issues have been appropriately assessed. Electrical (D.C.) Cardioversion Electrical cardioversion is by far the most efficacious technique to restore sinus rhythm in patients with AF. In properly selected patient populations, sinus rhythm is at least temporarily achieved in > 90% of patients. Effective energy levels generally range from 100 to 360 joules (monophasic shocks) for atrial fibrillation, and lower energies are frequently effective in converting atrial flutter. Failure to cardiovert can be a manifestation of the duration of the arrhythmia, the underlying cardiac pathology or because of large body habitus. When adhesive (passively attached) patch electrodes are used and do not result in successful cardioversion, success can sometimes be instead achieved using the more traditional handheld paddles in the sternal-apical positions. This may be because of decreased transthoracic impedance created by more forceful application of the paddles or by improved geometry. Patients who fail electrical cardioversion with maximal energy are sometimes able to be cardioverted acutely after the administration of I.V. ibutilide or I.V. procainamide. Successful electrical cardioversion can also be rendered successful by pretreatment with a number of oral antiarrhythmic drugs; for example, amiodarone. Newer technology using external biphasic (rather than monophasic) shocks can improve efficacy in challenging cases. Biphasic defibrillators are now being routinely used in the electrophysiology laboratory with increased efficacy and a lower mean required energy. For patients who are deemed to require sinus rhythm for maximal clinical benefit

10 and for whom transthoracic cardioversion is unsuccessful, intraatrial defibrillation can result in successful cardioversion. This procedure should only be performed by qualified cardiac electrophysiologists. Atrial flutter can be converted in many cases with atrial overdrive pacing instead of transthoracic cardioversion. This can be accomplished using either transvenous or epicardial atrial electrodes. ELECTRICAL CARDIOVERSION Location: monitored procedure area or patient's room. Equipment: Defibrillator with synchronization Transcutaneous pacing capability Gel or gelpads Suction capability, oxygen delivery Continuous ECG monitoring Non-invasive BP monitoring Oximetry monitoring Airway management equipment Appropriate cardiac medicines (e.g., atropine) Operator: physician with appropriate credentials and experience (per Departmental DOP) Ancillary personnel: dependent on venue and Departmental conscious sedation policies Sedation/anesthesia/recovery: dependent on venue and Departmental conscious sedation policies Methodology: Anteroposterior (AP) or sternal-apical placement of paddles/patches with gel or gelpad medium Appropriate QRS synchronization documented prior to delivery of DC countershock Pharmacologic Cardioversion Pharmacologic cardioversion may be preferable to electrical cardioversion in some clinical situations. If the clinician has decided that the patient with AF should be pre-treated with an antiarrhythmic drug to maintain sinus rhythm once converted, then an antiarrhythmic might be given at an appropriate dose with the intention to also convert AF. If the means to provide conscious sedation or general anesthesia for electrical cardioversion are not immediately available, pharmacologic cardioversion might be considered preferable. It also might be considered for the rare patient where deep sedation or general anesthesia is considered to be undesirable. There is no firm data as yet to suggest that spontaneous or pharmacologic cardioversion result in a more expeditious return of atrial mechanical function or a reduced risk of thromboembolic complications when compared to electrical cardioversion.

11 Possible drug regimens for pharmacologic conversion of AF: Ibutilide: 1 mg I.V. over 10 min 10 min observation Repeat 1 mg over 10 min (if not converted (If patient is < 60 kg; each dose should be 0.01 mg/kg) Contraindicated when the QTc > 0.46 or when the patient is on other agents that prolong the QT Check Mg++, Ca++ and K+ Peak Torsade VT risk is hours after initiation Procainamide: 8-10 mg/kg I.V. (</= 50 mg/min) followed by a 2-5 mg/min infusion Can significantly enhance AV node function during AF; ventricular rate control is paramount before starting drug Significantly less efficacious than ibutilide Hypotension not uncommon Amiodarone: If unable to take P.O. or unstable, mg I.V.; followed initially by 1mg/min infusion If able to take P.O., 400 mg TID Has unknown but finite efficacy for conversion I.V. amio may be an appropriate means of loading the drug for eventual maintenance of NSR only if unable to take P.O. Has AV nodal blocking effects Other agents for pharmacologic conversion: Oral agents have been used successfully to intentionally convert AF to sinus rhythm. They include flecainide ( mg bolus ), propafenone ( mg bolus ), but both are contraindicated in patients with ischemic heart disease or significant LV dysfunction. These doses have been shown to increase cardioversion efficacy when compared to maintenance dosage regimens. Dofetilide appears to have a somewhat higher efficacy than other oral agents in

12 converting AF (using usual initial doses). Any of the other antiarrhythmic drugs can result in conversion during their initial administration. There is no data to support a role of digoxin in converting AF to sinus rhythm. If AF converts while a patient is being digitalized, the conversion should be considered spontaneous. All attempts to pharmacologic convert AF should be done in a monitored setting (ED, progressive care, intensive care or electrophysiologic laboratory) with sufficient staff to carefully review the response to therapy. Comment: During atrial fibrillation and atrial flutter, there is always some degree of sinus node suppression. This is physiologic. It is not uncommon for these patients to also have sinus node dysfunction resulting in even higher degrees of suppression. The drugs used to slow ventricular rates and some of the antiarrhythmic drugs have additional sinus node depressing actions. At the moment of conversion from AF to sinus rhythm, whether it is spontaneous or a result of either electrical or pharmacologic cardioversion, there can be significant sinus pauses, prolonged sinus bradycardia or junctional rhythms. See Appendix regarding I.V. Amiodarone Indications Maintenance of Sinus Rhythm General Considerations The decision to attempt pharmacologic maintenance of sinus rhythm once it has been restored with cardioversion is a complicated one. The factors that are important to consider include the symptoms caused by AF, the age of the patient, the situation in which AF occurred, the likelihood of recurrence, the risk factors for proarrhythmia and the underlying cardiac pathology. When deciding to prophylax with antiarrhythmic drug therapy, the following caveats should be remembered: There is no data to support the popular notion that control of AF with an antiarrhythmic drug reduces the incidence of thromboembolic events. In fact, recent studies confirm that there is at least as high or higher incidence of stroke in cohorts who underwent concerted efforts to maintain sinus rhythm. No more than 60% of patients on any antiarrhythmic drug regimen for AF will be arrhythmia-free two years after initiation.

13 Successful control of paroxysmal AF (PAF) might be a significant reduction of either the frequency or duration of AF rather than complete control. The incidence of significant proarrhythmia due to antiarrhythmic drugs is between 2 and 12%. Atrial fibrillation begets atrial fibrillation and a younger person who has PAF may experience an ever-shortening inter-event period if preventative therapy isn t entertained. Special populations of patients may tolerate AF less well hemodynamically; e.g., those with HOCM, MS, AS, or dilated cardiomyopathy and their presentation with AF may result in compelling reasons to try to prevent recurrences. Beta blockers (with rare exceptions), digoxin and calcium channel blockers cannot generally be expected to prevent (or convert) AF Possible drugs for the maintenance of sinus rhythm: Amiodarone: Oral load from 600 mg to 1200 mg daily in divided doses Eventual goal for maintenance: mg/day Type III drug with some beta and calcium channel blockade No significant negative inotropy Difficult pharmacokinetics Can be used in CAD, CHF Significant sinus node dysfunction occasionally Torsade risk relatively low Sotalol: 80 mg to 480 mg/day (BID divided doses) Type III drug with significant beta blockade Significant bradycardia not uncommon Torsade risk Caution with severe LV dysfunction, diuretics (hypokalemia) or renal insufficiency Can be used in CAD Dofetilide: 250 microgms to 1000 microgms/day (BID divided doses) Type III drug FDA mandate for inpatient 72 hour initiation Torsade risk Can be used in CAD, CHF Caution with diuretics (hypokalemia) and renal insufficiency

14 Propafenone: 150 mg to 900 mg/day (in TID divided doses) Type IC drug with mild to moderate beta blockade Moderate negative inotropy Do not use in CAD or CHF or significant asthma Post-conversion pauses significantly accentuated Check for proarrhythmia with GXT Well tolerated in general Flecainide: 100 mg to 400 mg/day (BID divided doses) Type IC drug Significant negative inotropy Do not use in CAD or CHF Check for proarrhythmia with GXT Well tolerated in general Disopyramide: 200 mg to 600 mg/day (BID CR divided doses) Type IA drug Significant anticholinergic side effects Significant negative inotropy May have special utility in vagallymediated AF and HOCM Do not use in CHF Can be used in CAD Procainamide: 1000 mg to 4000 mg/day (QID SR or BID divided doses) Type IA drug Can be used in CHF Torsade risk between disopyramide and quinidine Caution in renal insufficiency (increased NAPA) Can be used in CAD and CHF

15 Quinidine: 648 mg to 1396 mg/day (BID gluconate divided doses) Type IA drug Diarrhea in 25% Torsade risk Can be used in CAD and CHF Monitoring antiarrhythmic drugs In general, most antiarrhythmic drugs are initiated in a monitored setting with attention to potential excessive bradycardia, AV block, ventricular proarrhythmia, QRS and QT interval prolongation. A highly select group of patients may safely have certain of these drugs begun as outpatients. This should only be done with agents considered to have a low incidence of proarrhythmia, in patients at low risk for proarrhythmia, by experienced practitioners and with close follow-up. Specific protocols have been developed. Once initiated, outpatient follow up assessment should, in general, include a history (to detect drug adverse effects, concomitant medication use and arrhythmia recurrence), physical exam (to detect CHF or bronchospasm, for example), an ECG for bradyarrhythmias, QRS or QT prolongation or proarrhythmia. Certain antiarrhythmic drugs require special laboratory tests in follow up, including in some cases drug levels or to detect specific toxicities. Normal levels of all of the electrolytes should be periodically confirmed.

16 Transesophageal Echocardiography General Considerations Transesophageal echocardiography (TEE) can identify intracardiac thrombus that by its presence indicate an increased risk of thromboembolic events in patients with atrial fibrillation or atrial flutter. In particular, LA appendage thrombus can be identified with TEE when transthoracic echo has failed to show clot. Other related findings can include spontaneous echo contrast (SEC) or abnormal LA appendage flow velocities. The finding of thrombus is considered to be a contraindication to either pharmacologic or DC cardioversion. It is less certain whether SEC or abnormal LA appendage flow affects risk if patients are adequately anticoagulated at the time of the cardioversion. Indications for TEE-guided cardioversion Atrial fibrillation or atrial flutter of > than 48 hours duration when cardioversion is indicated but a protracted period of anticoagulation prior to cardioversion is not desirable or is contraindicated History of prior thromboembolic event Atrial fibrillation or atrial flutter of < 48 hours duration in patients with LV dysfunction (LVEF < 0.4), in patients with significant valvular heart disease (if patient has not been chronically anticoagulated) Caveats: Whether routine use of a TEE-guided approach will eventually be proven to be superior to the more conventional approach using 3 to 6 weeks of anticoagulation therapy for patients presenting with AF without being chronically anticoagulated remains to be determined. Full dose anticoagulation is indicated before, during and after TEEguided cardioversion (see anticoagulation protocol). If thrombus is found on TEE, the plan to cardiovert is abandoned, chronic warfarin therapy instituted and then continued for 4 to 6 weeks. A repeat TEE is performed prior to cardioversion.

17 Anticoagulation General Considerations The most important guidelines for the treatment of patients who are experiencing or have experienced AF in both the acute and chronic settings are those that are designed to prevent thromboembolic complications, especially stroke. Recommendations can be divided by AF duration. For the purposes of these guidelines, AF of unknown duration shall be considered to be persistent AF, that is, of greater than 48 hours duration. Acute (new onset) AF (< 48 hours duration): Although not well studied, conventional recommendations suggest it is safe to electrically or pharmacologically cardiovert AF of < 48 hrs duration in an unanticoagulated patient. However, it is recommended that even in this group of patients that cardioversion be performed under TEE guidance with the patient acutely, parentally (and then continuously) anticoagulated if they: Have LV dysfunction (LVEF < 0.40) Have had a history of TIA or CVA, or Have significant valvular heart disease If the low risk patient with acute AF is successfully cardioverted in the unanticoagulated state and they do not have an indication for chronic anticoagulation, they can be discharged without anticoagulants once converted. See chronic risk factor discussion below. If a low risk patient is anticoagulated using heparin within the first 48 hours of new onset atrial fibrillation or atrial flutter, cardioversion may be able to be safely delayed beyond 48 hours without having to then resort to TEE (e.g., during titration of antiarrhythmic drugs). This presumption has not yet been prospectively studied but accumulated clinical experience supports its relative safety.

18 Persistent AF (> 48 hours duration): There are two approaches: 1. Conventional recommendations mandate 3 to 6 weeks of oral anticoagulation with warfarin prior to electrical or pharmacologic cardioversion when the patient presents with AF of either > 48 hrs or unknown duration. Rate control measures are instituted in the interim. 2. TEE-guided cardioversion can be performed in this group if delay in cardioversion is deemed to be inappropriate (e.g., in patients with poor rate control or with ongoing symptoms). Given the known rate control challenges of atrial flutter, this arrhythmia is often better approached with TEE-guided cardioversion. This involves full dose anticoagulation before, during and after cardioversion in this patient group. Heparin is continued while warfarin is instituted (for long term use) until the INR > 2.0. Continuous, effective anticoagulation through the cardioversion event and prior to discharge is paramount. Post-cardioversion stunning can facilitate thrombus formation (even if the pre-cv TEE was negative). Chronic warfarin therapy (INR 2-3) indications: For at least one month after cardioversion for ALL patients (without a contraindication) who were cardioverted after presenting with persistent AF Chronic warfarin therapy: All patients with either chronic, persistent AF or a history of paroxysmal AF (not due to a reversible cause) with any one of the following: Age > 65 yrs Hypertension (controlled) TIA or CVA thought to be thromboembolic LV dysfunction (LVEF < 0.40) Rheumatic valvular heart disease Other valvular heart disease (e.g: significant MR or TR, or prosthetic valve) Hypertrophic obstructive cardiomyopathy (HOCM) Hyperthyroidism (while active) Diabetes mellitus Clinically significant CAD Mobile, significant plaque or thrombus in aorta (by TEE)

19 Caveats and further guidelines: The immediate period after cardioversion (minutes later to 2 weeks postconversion) is accompanied by increased risk for new atrial thrombus formation in susceptible patients. This is likely to be due to what can be thought of as atrial stunning. Mechanical and endothelial function of the atria gradually recovers. The transition from parenteral anticoagulation to warfarin after cardioversion must result in continuous effective anticoagulant effect. The efficacy and safety of low molecular weight (LMW) heparin in this patient population is being studied. If these studies support its use, it may provide another therapeutic option for transitioning to warfarin and thereby be helpful in reducing the patients hospital length of stay. Most neurologic consultants advise against heparinization during an evolving CVA because of the concern of hemorrhagic transformation (see Department of Medicine Neurology Guidelines). Higher INR goals are recommended for some patients (e.g., patients with mechanical valve prostheses, or patients with a history of thromboembolic events associated with lower INR) Reasonable or excellent control of atrial fibrillation or atrial flutter with antiarrhythmic drugs has not been shown to lower the thromboembolic risk. Both chronic persistent and paroxysmal atrial fibrillation impart thromboembolic risk. Relative contraindications to long term warfarin use include (but are not limited to) : - significant difficulty in ambulation (marked increased risk for falls) - previous bleeding episodes - poor compliance - significant liver disease or dysfunction - pregnancy For those patients who undergo TEE-guided cardioversion but who are felt to be poor candidates for long-term anticoagulation, heparin should be continued after cardioversion. The appropriate duration of heparin administration before discontinuation and hospital discharge is unknown. The degree of atrial stunning after restoration of sinus rhythm is likely to vary from patient to patient. All patients regardless of their thromboembolic risk who present after 48 hours with AF, and are subsequently cardioverted should be continuously anticoagulation for one month as atrial mechanical function returns to normal. Chronic, long term warfarin decisions dependent upon the risks outlined above are made after one month. The mere persistence of sinus rhythm is not an indication for warfarin withdrawal if the patient is in the higher risk stratum defined above. Outpatient warfarin therapy should be monitored by a single physician or anticoagulation clinic. A system should be in place such that patients receive notification of their INR results, dosing recommendations, and timing of next

20 protime draw within 24 hours of each protime draw. Once stabilized, protimes should be checked on a schedule appropriate for each patient (but not less often than once a month). Formal warfarin education should be provided verbally and in written form to all patients. Many drugs affect warfarin metabolism. Patients and health care providers need to be kept appraised of any changes in all prescribed, OTC medicines or supplements.

21 Atrial Flutter For the purposes of this manual, atrial fibrillation and atrial flutter are treated identically. This is particularly important as it applies to anticoagulation recommendations. However, as has been highlighted above, there are some features of flutter that mandate or allow slightly different strategies than with atrial fibrillation. Atrial flutter is a regular (macrorentry) atrial rhythm that results in fixed ratio AV block : that is, 2:1, 3:1, etc. The usual, untreated ventricular rate is 150 bpm Rate control with AV nodal blocking drugs is often challenging. Though 4:1 AV ratios (ventricular rate ~70 bpm) might be able to be achieved temporarily, a small amount of patient activity often results in 2:1 conduction and therefore fast rates can result despite high doses of AV nodal blocking drugs For this reason, more expeditious cardioversion is often warranted for flutter even if persistent (i.e., > 48 hrs on presentation) Atrial flutter, as opposed to atrial fibrillation, can be pace-terminated in many cases. This can be accomplished with some indwelling pacemakers of ICD s or with temporary pacemaker electrodes (e.g., with the epicardial atrial wires sometimes present after open heart surgery). Patients with flutter are uniquely susceptible to the development of 1:1 AV conduction (e.g., at ventricular rates of ) when an antiarrhythmic drug is given that slows the atrial rate from 300 to a rate that the AV node can better handle (if inadequately blocked). This phenomenon is most commonly observed with flecainide, propafenone and procainamide. Typical atrial flutter is often approached with a high degree of success with percutaneous RF ablation (see Advanced EP Techniques)

22 Advanced Electrophysiology Techniques There are a number of non-pharmacologic approaches to the treatment of atrial fibrillation and atrial flutter that are provided by cardiac electrophysiologists (or surgeons). Each will be listed with a brief list of indications. Intraatrial cardioversion Atrial overdrive pacing Implantable pacemakers Atrial implantable defibrillators AV junction ablation Atrial flutter ablation SVT ablation Atrial fibrillation ablation MAZE AF refractory to transthoracic cardioversion Conversion of atrial tachycardia or flutter using transvenous or epicardial atrial electrodes In tachy-brady syndrome, DDD pacing may decrease AF Prevents symptomatic post-conversion pauses May allow appropriate drugs to be given for AF AF suppression pacing algorithm may be helpful For treatment of AF in patients who also need ICD Limited indication for merely atrial therapy Refractory, chronic persistent AF (and occasionally PAF) with fast, poorly controlled ventricular rates or intolerance to AV nodal blocking drugs Refractory typical atrial flutter May sometimes be offered as initial therapy When SVT (or WPW) is the cause of AF Ablation of specific focal sites of AF generation; e.g., pulmonary veins For refractory patients (especially lone fibrillators) Open heart operation to dissect both atria to eliminate AF

23 Atrial Fibrillation: GUIDELINES AND ALGORITHMS Atrial Fibrillation Clinical Algorithms Emergency Department Patients presenting to the Emergency Department in atrial fibrillation are treated dependent upon a number of features of their clinical history and presenting symptoms. The factors determining the approach include amongst other things the following: Hemodynamic status Ventricular rate Presence or absence of myocardial ischemia or heart failure Whether the arrhythmia is chronic, persistent AF, new onset AF or newly recognized AF Presence or absence of chronic anticoagulation Past or current antiarrhythmic drug therapy The physician needs to decide what therapy in the ED setting is appropriate: whether to immediately convert the AF to sinus; whether to admit the patient to a monitored setting; whether to manage the patient in the ED in preparation for discharge or whether the patient is a candidate for an observation status (rather than admission) after acute care has stabilized the patient. After initial assessment and the patient is deemed to be hemodynamically stable, the patient is stratified into low risk or higher risk based on certain clinical characteristics. The clinical features outlined in the tables below are used in the algorithms that follow. HIGHER RISK AF FEATURES Angina Definite evidence of ischemia Significant heart failure Known significant LV dysfunction, AS, HOCM, RHD Severe symptoms WPW Prior CVA, TIA LOW RISK AF FEATURES Absence of higher risk features Recurrent AF in patient on antiarrhythmic agents and/or chronic anticoagulants

24 Atrial Fibrillation Clinical Algorithms Emergency Department ATRIAL FIBRILLATION Initial Assessment H/P ECG CBC, lytes, BUN, creatinine, PT TO BE DETERMINED Atrial fibrillation or atrial flutter? Recurrent, paroxysmal? Chronic AF with new rate problem? Duration (< 48 hrs; > 48 hrs; or undetermined) Chronically aniticoagulated (adequately?) On antiarrhythmic therapy? Recent symptoms of TIA or CVA? Underlying condition (CAD, CHF, HTN, etc) HEMODYNAMICALLY STABLE? NO YES Consider urgent cardioversion if AF is thought to be cause or likely contributor to instability Risk/benefit assessment required as it applies to thromboembolism complication SEE NEXT PAGE

25 RATE CONTROL STRATEGY Emergency Department HEMODYNAMICALLY STABLE AF RATE CONTROL ASSESSMENT Assess underlying conditions that affect rate control (CHF, hypoxemia, thyrotoxicosis, COPD, sepsis, etc) Flutter vs. fibrillation Symptomatic? > 100 or < 100 bpm FLUTTER? See Common Elements of Care: Atrial Flutter Symptomatic Rate > 100 Asymptomatic Rate > 100 Rate < 100 Consider I.V. diltiazem or esmolol (especially if rate > 120) P.O. AV nodal blocking agents still a choice (especially if rate < 120) P.O. AV nodal blocking drugs (beta blockers, diltiazem, verapamil, digoxin) I.V. drugs only if unable to take P.O. Likely to not need AV nodal blocking drugs if rate is consistently controlled (at rest and with exertion) GUIDE Common Elements of Care References: Controlling Ventricular Rate Patient Education: Categories of medicines Note: digoxin has slower onset of action and is less effective at controlling ventricular rates with exertion than other agents; may be used as an adjunct (or on occasion as sole agent)

26 ANTITHROMBOTIC AND CARDIOVERSION STRATEGY Emergency Department ADMISSION VERSUS DISCHARGE HEMODYNAMICALLY STABLE AF CHRONICALLY (AND ADEQUATELY) ANTICOAGULATED? NO YES DURATION OF AF < 48 HRS Additional risk factors? Prior TIA, CVA LVEF < 0.40 Significant valvular heart disease NO YES DURATION OF AF > 48 HRS OR UNKNOWN ANTICOAGULATE RATE CONTROL NOT ACCOMPLISHED IN ED; SIGNIFICANT ONGOING SYMPTOMS or HIGH RISK FEATURES May consider expeditious CV (in ED or diagnostic unit or shortstay unit) See Common Elements of Care: Controlling Ventricular Rate and Maintenance of Sinus Rhythm (either may require admission to hospital) RATE CONTROL ACCOMPLISHED IN ED; NO SIGNIFICANT ONGOING SYMPTOMS and NO HIGH RISK FEATURES May consider observation for spontaneous conversion or expeditious CV without anticoagulation or TEE (in ED or diagnostic unit or short-stay unit) Long term anticoagulation decision dependent upon chronic thromboembolic risk factors See Common Elements of Care: Anticoagulation See Common Elements of Care: Controlling Ventricular Rate and Maintenance of Sinus Rhythm (the latter may require admission to hospital for antiarrhythmic drugs) ADMIT TO MONITORED UNIT for further evaluation and possible TEE guided cardioversion with or without antiarrhythmic drugs ADMIT One of 2 OUTPATIENT strategies: Warfarin for 4 weeks as outpatient, then CV Leave in AF (PCP and/or cardiology decision) with long term anticoagulation decision dependent upon chronic thromboembolic risk factors See Common Elements of Care: Anticoagulation OUTPATIENT FOLLOW-UP CARDIOVERSION GUIDE Common Elements of Care References: Restoration of Sinus Rhythm, Anticoagulation, Controlling Ventricular Rate

27 DISCHARGE CHECKLIST: Atrial Fibrillation and/or Atrial Flutter Emergency Department 1. Rate Control Drug Not needed 2. Antiarrhythmic Drug 3. Antithrombotic Therapy Not needed Written information about drug Risk factors for stroke: Age > 65 yrs, HTN, DM, CAD, LVEF < 0.40, significant valvular heart disease, previous TIA/CVA, hyperthyroidism Warfarin Discharge dose: CURRENT INR: Outpatient INR monitoring Dr. Phone: INR goal: Next P.T.: Warfarin education No warfarin Reason: Lone atrial fibrillation Contraindicated Other LMW Heparin Discharge dose: LMW Heparin Education/instruction Aspirin Clopidogrel Dose: Dose: Other

28 Atrial Fibrillation Clinical Algorithms Hospital Monitored Unit It is perhaps the hospital-monitored unit that presents the most hetereogeneous group of patients with atrial fibrillation. Patients there may have primary diagnoses of acute myocardial infarction, unstable angina, congestive heart failure, pericarditis, respiratory failure, pneumonia or pulmonary embolus, amongst others. AF in this group can result from their temporarily acute condition and can be an important complication of their illness or it can be incidentally observed and transient. AF might be chronic, persistent (permanent) or paroxysmal. It could be associated with no symptoms or even result in precipitous hemodynamic compromise. AF patients admitted to monitored units often have AF as their primary diagnosis, but again can represent a diverse group. The patient may have been electively admitted for the administration of an antiarrhythmic drug for AF. They may be in AF at the time and the goal is to convert them to sinus rhythm or they may be in sinus rhythm and merely have had a history of paroxysms of AF. Patients with pacemakers or an automatic defibrillator (ICD) can develop AF that complicates their device function and be admitted for intervention. Patients with AF can be admitted to a monitored bed having presented to the Emergency Department or physician s office or they may be transferred from another unit having developed AF or may be post-operative patients with AF. And finally, patients may be admitted to these units specifically to prepare for a more advanced electrophysiologic approach to their arrhythmia or arrive there after such a procedure has been performed. Despite the challenge of this heterogeneous group, their management is guided by the Common Elements of Care outlined in this manual. Rate controlling drugs to control symptoms, antithrombotic therapy to address their individualized risk for stroke, prevention of adverse effects of antiarrhythmic agents and in many cases restoration of sinus rhythm remain the primary goals. This setting is also ideal to begin or continue patient education specific to AF and its treatment. On the following pages an algorithm for the hospital-monitored patient is provided to organize the clinical approach to the patient with AF as their primary clinical problem. It is divided into Initial Assessment, Antithrombotic and Cardioversion Strategy, Rate Control Strategy, Antiarrhythmic Strategy and Discharge Checklist.

29 Atrial Fibrillation Clinical Algorithms Hospital Monitored Unit ATRIAL FIBRILLATION Initial Assessment H/P ECG CBC, lytes, BUN, creatinine, PT, (PTT if on heparin) Free T4, TSH (if not in last 3 months) TRANSTHORACIC ECHO (if not done in last 6 mos. and if TEE is not planned) TO BE DETERMINED Atrial fibrillation or atrial flutter (or sinus rhythm) Recurrent, paroxysmal? Chronic AF with new rate problem? Duration (< 48 hrs; > 48 hrs; or undetermined) Chronically aniticoagulated (adequately?) On antiarrhythmic therapy? Recent symptoms of TIA or CVA? Underlying condition (CAD, CHF, HTN, etc) HEMODYNAMICALLY STABLE? NO YES Consider urgent cardioversion if AF is thought to be cause or likely contributor to instability Risk/benefit assessment required as it applies to thromboembolism complication SEE NEXT PAGE

30 ANTITHROMBOTIC AND CARDIOVERSION STRATEGY Hospital Monitored Unit HEMODYNAMICALLY STABLE AF CHRONICALLY (AND ADEQUATELY) ANTICOAGULATED? NO YES DURATION OF AF < 48 HRS Additional risk factors? Prior TIA, CVA LVEF < 0.40 Significant valvular heart disease NO YES May consider expeditious CV without anticoagulation or TEE, or Initiate warfarin and CV in 4 weeks if still in AF Long term anticoagulation dependent upon chronic thromboembolic risk factors See Common Elements of Care: Anticoagulation See rate control and antiarrhythmic strategies Consider whether to leave in AF long term DURATION OF AF > 48 HRS OR UNKNOWN Acutely anticoagulate and plan expeditious TEE-guided CV if: Sinus rhythm is deemed necessary in near term, or Rate control is too challenging (e.g., flutter) If not planning CV during hospitalization and not planning invasive procedure, initiate heparin to warfarin transition See rate control and antiarrhythmic strategies Consider whether to leave in AF long term May consider expeditious CV See rate control and antiarrhythmic strategies Consider whether to leave in AF long term GUIDE Common Elements of Care References: Restoration of Sinus Rhythm, Transesophageal Echocardiography, Anticoagulation When heparin to warfarin transition is indicated, this means continuous effective anticoagulation Patient Education: Nature of AF condition, cardioversion, categories of medicines and stroke prevention

31 RATE CONTROL STRATEGY Hospital Monitored Unit HEMODYNAMICALLY STABLE AF RATE CONTROL ASSESSMENT Assess underlying conditions that affect rate control (CHF, hypoxemia, thyrotoxicosis, COPD, sepsis, etc) Flutter vs. fibrillation Symptomatic? > 100 or < 100 bpm FLUTTER? See Common Elements of Care: Atrial Flutter Symptomatic Rate > 100 Asymptomatic Rate > 100 Rate < 100 Consider I.V. diltiazem or esmolol (especially if rate > 120) P.O. AV nodal blocking agents still a choice (especially if rate < 120) P.O. AV nodal blocking drugs (beta blockers, diltiazem, verapamil, digoxin) I.V. drugs only if unable to take P.O. Likely to not need AV nodal blocking drugs if rate is consistently controlled (at rest and with exertion) GUIDE Common Elements of Care References: Controlling Ventricular Rate Patient Education: Categories of medicines Note: digoxin has slower onset of action and is less effective at controlling ventricular rates with exertion than other agents; may be used as an adjunct (or on occasion as sole agent)

32 ANTIARRHYTHMIC STRATEGY (PART 1) Hospital Monitored Unit HEMODYNAMICALLY STABLE AF DECISIONS/CONSIDERATIONS Whether to commit to Type I or Type III antiarrhythmic (AA) drugs: Factors: Duration and frequency of AF episodes Severity of symptoms with AF episodes Concomitant heart disease and likelihood of recurrence Perceived association of AF episodes with either an acute or reversible cause (e.g., P.E., pericarditis, electrolyte disturbance, etc) Assessed risk for proarrhythmia Already on AA drugs? SEE NEXT PAGE COMMIT TO AA DRUGS? YES NO Drug-specific monitoring protocol (ECG measurements, baseline labs and drug levels if appropriate for given drug) Continuous ECG monitoring Most drugs and most patients require inpatient (rather than outpatient) monitoring-- see Common Elements of Care: Maintenance of Sinus Rhythm Duration of therapy is either indefinitely or temporary, the latter appropriate if AF likely to be caused by an acute or reversible cause (e.g., MI or postoperative) See rate control strategy Leave patient in AF permanently or temporarily to assess permanence (e.g., while acute causative illness is being treated) If AF has already been cardioverted or has spontaneously converted, withhold AA therapy until or unless episodes are more frequent or associated with more severe symptoms See rate control and antithrombotic strategies GUIDE Common Elements of Care References: Maintenance of Sinus Rhythm, Controlling Ventricular Rate, Anticoagulation Patient Education: Nature of AF condition,categories of medicines, specific AA drug information and stroke prevention

33 ANTIARRHYTHMIC STRATEGY (PART 2) Hospital Monitored Unit HEMODYNAMICALLY STABLE AF ALREADY ON A TYPE I OR TYPE III AA DRUG Leave on same drug at same dose Widely spaced AF episodes Tolerating drug Non-compliance suspected Check blood level if appropriate for drug Titrate same drug to higher dose Increasingly frequent symptomatic episodes Tolerating present drug No clinical, ECG or laboratory evidence of drug excess Drug-specific monitoring protocol (ECG measurements, baseline labs and drug levels if appropriate for given drug) Inpatient continuous ECG monitoring if proarrhythmia or bradycardia is significant risk Change drugs Increasingly frequent symptomatic episodes Not tolerating present drug Present dose perceived as maximum safe or tolerated dose Drug-specific monitoring protocol (ECG measurements, baseline labs and drug levels if appropriate for given drug) Most drugs and most patients require inpatient (rather than outpatient) monitoring-- see Common Elements of Care: Maintenance of Sinus Rhythm GUIDE Common Elements of Care References: Maintenance of Sinus Rhythm Patient Education: Categories of medicines, specific AA drug information Note: 100% control and prevention of AF with an AA drug is usually an unrealistic expectation

34 DISCHARGE CHECKLIST: Atrial Fibrillation and/or Atrial Flutter Hospital Monitored Unit 1. Rate Control Drug (s) Not needed 2. Antiarrhythmic Drug Written information about drug Antiarrhythmic drug not needed 3. Antithrombotic Therapy Risk factors for stroke. CHECK if any of the following are present: age > 65 yrs, HTN, DM, CAD, LVEF < 0.40, significant valvular heart disease, previous TIA/CVA, hyperthyroidism Warfarin Discharge dose: CURRENT INR: Outpatient INR monitoring Dr. INR goal: Phone: Next P.T.: Warfarin education No warfarin Reason: Lone atrial fibrillation Contraindicated Other LMW Heparin Discharge dose: LMW Heparin Education/instruction Aspirin Clopidogrel Dose: Dose: Other

35 Atrial Fibrillation Clinical Algorithms Postoperative Atrial Fibrillation Atrial fibrillation or flutter occurs in from 25 to 40% of patients having undergone cardiac (or thoracic) surgery, with the usual onset between the 2 nd and 4 th postoperative day. For patients who had not had AF preoperatively, nearly 90% will be free of the arrhythmia at two months. A major cause of morbidity, including stroke, there appears to be little resultant mortality. AF and its treatment commonly prolong postoperative hospital stays and can result in substantial excess financial costs. The secondary morbidity from AF is primarily attributable to the thromboembolic complications of AF, congestive heart failure, occasionally hemodynamic compromise and generalized weakness, the latter retarding recovery. Definite and Possible Predictors and of Post Operative AF Increasing age Hypertension Preoperative history of atrial fibrillation Valvular heart disease COPD Previous cardiac surgery Need for an intra-aortic balloon pump or pressors post-operatively Artificial mechanical ventilation > 24 hours Diabetes Mellitus Postoperative withdrawal of beta blockers if used preoperatively PROPHYLAXIS It is abundantly clear that there are a number of measures that can be implemented that can reduce the incidence of postoperative atrial fibrillation and flutter. Of the multitude that has been evaluated, the following regimens are the least disputable and have the potential to reduce postoperative AF rates by 30 50%.