Download Atrial Fibrillation: Manual of Clinical Guidelines

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
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 (http://www.acc.org/clinical/guidelines/atrial_fib/).
Published in 2002. 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.
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.
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)
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
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
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)
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
YES
NO
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
Is patient a candidate for beta blocker?
Avoid use in:
•
SBP < 90
•
Uncompensated CHF
•
Active bronchospasm
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
•
•
•
Esmolol drip
Titrate to pulse of < 120
Maintain SBP >90
Up-titrate frequently (q15-30 min) to max
dose of 300 mcg/kg/min
YES
SUCCESSFUL RATE
CONTROL: Monitor and
convert to oral when and
if appropriate
YES
Successful?
Unsuccessful if no change within 2-4 hours with aggressive
up titration to max dose or unable to tolerate adverse effects
NO
Determine whether pharmacologic or electrical cardioversion conversion is indicated if rate control is inadequate and symptoms
remain more than moderate
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
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.
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 0 - 1.5 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,
150 - 300 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 (150 – 300 mg “bolus”), propafenone (300-600
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
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.
♦ “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: 100-400
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
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
♦
♦
♦
♦
Significant negative inotropy
Do not use in CAD or CHF
Check for proarrhythmia with GXT
Well tolerated in general
♦
♦
♦
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
♦
Flecainide:
♦
♦
100 mg to 400 mg/day (BID divided
doses)
Type IC drug
Disopyramide:
♦
♦
200 mg to 600 mg/day (BID CR divided
doses)
Type IA drug
♦
♦
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
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.
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.
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.
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)
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
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.
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 220-270) 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)
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
AF refractory to transthoracic
cardioversion
Atrial overdrive pacing
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
Implantable pacemakers
Atrial implantable defibrillators
AV junction ablation
Atrial flutter ablation
SVT ablation
Atrial fibrillation ablation
MAZE
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
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
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
♦ 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
YES
SEE
NEXT
PAGE
RATE CONTROL STRATEGY
Emergency Department
HEMODYNAMICALLY STABLE AF
♦
♦
♦
♦
FLUTTER?
See
Common
Elements of
Care: Atrial
Flutter
RATE CONTROL ASSESSMENT
Assess underlying conditions that affect rate
control (CHF, hypoxemia, thyrotoxicosis,
COPD, sepsis, etc)
Flutter vs. fibrillation
Symptomatic?
> 100 or < 100 bpm
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)
ANTITHROMBOTIC AND CARDIOVERSION STRATEGY
Emergency Department
ADMISSION VERSUS DISCHARGE
HEMODYNAMICALLY STABLE AF
CHRONICALLY (AND ADEQUATELY)
ANTICOAGULATED?
NO
YES
♦ May consider expeditious CV (in
DURATION OF
AF < 48 HRS
Additional risk factors?
♦ Prior TIA, CVA
♦ LVEF < 0.40
♦ Significant
valvular heart
disease
NO
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)
DURATION OF
AF > 48 HRS OR
UNKNOWN
RATE CONTROL NOT
ACCOMPLISHED IN
ED; SIGNIFICANT
ONGOING
SYMPTOMS or HIGH
RISK FEATURES
RATE CONTROL
ACCOMPLISHED IN ED;
NO SIGNIFICANT
ONGOING SYMPTOMS
and NO HIGH RISK
FEATURES
YES
ANTICOAGULATE
♦ 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)
CARDIOVERSION
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
♦
GUIDE
Common Elements of Care References: Restoration of
Sinus Rhythm, Anticoagulation, Controlling Ventricular Rate
DISCHARGE CHECKLIST:
Atrial Fibrillation and/or Atrial Flutter
Emergency Department
1.
Rate Control Drug
_____________________________
Not needed
2.
Antiarrhythmic Drug
_____________________________
Not needed
Written information about drug
3.
Antithrombotic Therapy
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 __________________________________
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.
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
•
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
YES
SEE
NEXT
PAGE
ANTITHROMBOTIC AND CARDIOVERSION STRATEGY
Hospital Monitored Unit
HEMODYNAMICALLY STABLE AF
CHRONICALLY (AND ADEQUATELY)
ANTICOAGULATED?
NO
DURATION OF
AF < 48 HRS
YES
DURATION OF
AF > 48 HRS OR
UNKNOWN
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
♦ May consider expeditious
CV
♦ See rate control and
antiarrhythmic strategies
♦ Consider whether to leave
in AF long term
♦ 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
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
RATE CONTROL STRATEGY
Hospital Monitored Unit
HEMODYNAMICALLY STABLE AF
RATE CONTROL ASSESSMENT
FLUTTER?
See
Common
Elements of
Care: Atrial
Flutter
♦ Assess underlying conditions that affect rate
control (CHF, hypoxemia, thyrotoxicosis,
COPD, sepsis, etc)
♦ Flutter vs. fibrillation
♦ Symptomatic?
♦ > 100 or < 100 bpm
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)
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
♦ 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
NO
♦ 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
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
Change drugs
♦ Increasingly frequent
♦
♦
♦
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
♦
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
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. _____________________
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 __________________________________
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 2nd and 4th
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%.
Given the frequency with which cardiac surgery is being performed emergently or
urgently, the logistics of systematically applying effective prophylaxis are
challenging. A high level of collaboration between the cardiologists and the
cardiac surgeons (and primary care physicians in some cases) is necessary to
facilitate the implementation of these protocols and to ensure the patient’s safety.
Beta Blockers
Continuation of beta-blockers immediately after surgery in those patients already
on them preoperatively is absolutely necessary to substantially reduce the risk of
postoperative AF. Preoperative initiation of beta-blockers for 3 – 5 days if
possible is a recommended strategy for those patients not on these agents.
Strategy A: Pre-op Beta Blockers
Drug choices
•
•
•
Metoprolol 25 – 75 mg b.i.d.
Atenolol 25 – 100 mg qd.
Propranolol 10 – 40 mg t.i.d. to q.i.d.
Relative or
•
•
•
•
•
HR < 50
Greater than 1st degree AV block
SBP < 90 mmHg
Active bronchospasm or COPD
Overt CHF
absolute
contraindications
Strategy B: Post-op Beta Blockers (not on pre-op)
Drug choices
•
•
•
Relative or
absolute
contraindications
•
•
•
•
•
I.V. metoprolol 5 – 15 mg 3 –7 hours after surgery and
q8h to q12h until able to take P.O.
I.V. esmolol 0.5 mg/kg bolus (bolus optional if giving
prophylactically) 3 –7 hours after surgery followed by a
continuous infusion between 50 and 200 mcg/kg/min
until able to take P.O.
I.V. atenolol 5 – 10 mg I.V. q12 hr, 3 –7 hours after
surgery until able to take P.O.
HR < 50
Greater than 1st degree AV block
SBP < 90 mmHg
Active bronchospasm or COPD
Overt CHF
Amiodarone
Amiodarone is the agent other than beta-blockers that has been most extensively
evaluated and has demonstrated the most promise in reducing postoperative
atrial tachyarrhythmias. Oral administration of this agent can be initiated as an
inpatient (when already hospitalized) or as an outpatient.
Outpatient administration of amiodarone needs to be accompanied by a
systematic protocol (by either surgeon or cardiologist) to ensure that patient
responses to the agent are appropriate. An ECG should be performed 24 hours
after the first dose and reviewed contemporaneously for idiosyncratic excessive
QT prolongation (QTc of > 0.5) or excessive bradycardia. Empirical reduction of
other agents such as beta blockers, verapamil, diltiazem, or clonidine may be
required dependent upon the resting heart rate prior to the first amiodarone dose.
If the patient is on digoxin, its dose needs to be cut in half when
amiodarone is started. Although not likely relevant to preoperative prophylaxis,
the known interaction between warfarin and amiodarone requires cautious
warfarin dosing and very close INR monitoring after discharge from the hospital.
There is no substantial data to support the use of intravenous amiodarone as
prophylaxis against AF either prior to or after surgery. Its high cost, its
preferential requirement for central venous administration, its somewhat more
significant depression of sinus node function and LV systolic function when given
I.V. argues for the use of oral amiodarone when this agent is being used for
prophylaxis alone.
Strategy C: Pre-op Amiodaron
Dosage regimen
•
200 mg t.i.d. with meals up to 7 days
preoperatively (rough correlation between
effectiveness and duration of prophylaxis)
Relative or
absolute
contraindications
•
•
•
•
HR < 55 bpm
Greater than first degree AV block
QTc > 0.46
Taking other agents that prolong QT
Strategy D: Post-op Amiodarone
Dosage regimen
•
200 – 400 mg t.i.d. immediately upon arrival
to ICU and continued through hospital stay
(through NG and then by mouth)
Relative or
absolute
contraindications
•
•
•
•
HR < 55 bpm
Greater than first degree AV block
QTc > 0.46
Taking other agents that prolong QT
Although other drugs such as procainamide, propafenone and sotalol have been
investigated for use in this setting, they have either been less effective or
associated with higher risks of proarrhythmia. Type IC drugs like propafenone
(or flecainide) are contraindicated in ischemic heart disease or in patients with
significant LV dysfunction.
TREATMENT OF POSTOPERATIVE AF
The treatment of post-operative atrial fibrillation is based on the following tenants:
♦ The treatment regimen depends on the hemodynamic consequence of the
atrial tachyarrhythmia;, the underlying cardiac pathology; the type of surgery;
the timing or the persistence of the arrhythmia and the non-cardiac comorbidities
♦ Post-operative atrial fibrillation and flutter pose a significant (albeit difficult to
quantify) risk of thrombo-embolism
♦ Post-operative atrial arrhythmias, even though persistent, will often terminate
spontaneously prior to discharge or during follow-up after discharge
If the atrial arrhythmia is associated with hemodynamic compromise, immediate
cardioversion is likely warranted. Whether pre-treatment with an antiarrhythmic
drug is advisable depends primarily on the urgency of conversion.
Those surgical patients who develop significant hypotension with AF require the
most immediate attention. Patients with hypertrophic cardiomyopathy, significant
LV systolic dysfunction or pre-operative aortic stenosis are likely to be the most
compromised. Cardioversion is best accomplished electrically though
intravenous ibutilide is an option in less urgent situations (and when relative
contraindications for its use are not present).
Rate Control: See Common Elements of Care: Controlling
Ventricular Rate
Maintenance of Normal Sinus Rhythm: See Common Elements
of Care: Maintenance of Sinus Rhythm
When cardioversion has been required because of persistent hemodynamically
important atrial fibrillation or atrial flutter or when paroxysmal post-operative atrial
fibrillation is significantly symptomatic, antiarrhythmic drug therapy for prevention
of recurrences is recommended.
If the patient is unable to take P.O. medicines or naso-gastric tube
administered drugs, intravenous procainamide and intravenous amiodarone are
useful. Either can be used even if prophylactic antiarrhythmic drugs have been
used pre- or post-operatively.
Intravenous Procainamide:
♦ Advantages include rapid onset of action and more rapid excretion; the
ability to quickly measure meaningful serum levels; and little negative
inotropy
♦ Disadvantages include hypotension during load; accumulation of N-acetyl
procainamide in patients with renal insufficiency; and facilitation of AV
nodal conduction (sometimes resulting in a significant increase in
ventricular rate during atrial fibrillation or especially atrial flutter)
♦ Rate control should be successfully achieved prior to the administration of
intravenous procainamide
Intravenous Amiodarone:
♦ Advantages include effectiveness that exceeds that for procainamide; a
Torsade risk that is lower than procainamide; only occasional hypotension;
and a significant concomitant AV nodal blocking effect that may assist in
rate control if in AF
♦ Disadvantages include a somewhat delayed onset of action and slow
excretion; the necessity for central venous access (to prevent phlebitis);
and it is expensive (see attached guidelines for the use of intravenous
amiodarone)
If there is alimentary access, and an antiarrhythmic drug is indicated for postoperative atrial fibrillation or flutter, oral agents should be used.
Amiodarone
Sotalol
Procainamide
800 mg to 1600 mg/day in divided doses
40 mg b.i.d. to 160 mg b.i.d.
2 to 4 grams/day in divided doses
Propafenone and flecainide are contraindicated in ischemic heart disease and in
patients with significant LV dysfunction. They could, however, be used for AF
occurring after cardiac surgery when these clinical features are absent.
Antiarrhythmic drugs that are begun because of the development of atrial
tachyarrhythmias during the post-operative phase are usually stopped six weeks
to three months after surgery. They would be continued more indefinitely if the
patient had these arrhythmias pre-operatively or if they recurred during late postsurgical follow-up.
THROMBO-EMBOLIC PREVENTION
Though there has been conventional wisdom that atrial fibrillation or atrial flutter
experienced post-operatively imparts a lower risk of stroke than in other settings,
there are no studies to corroborate this contention. In fact, AF is a common
accompaniment to stroke when it occurs soon after cardiac surgery.
If atrial fibrillation or flutter persists for more than 24 hours, heparin is indicated.
This not only prophylaxes against spontaneous thrombo-embolism, it is thought
to be necessary to prevent stroke at the time of either electrical or pharmacologic
cardioversion.
If cardioversion is contemplated and the patient hasn’t been continuously
anticoagulated from at least the 48-hr boundary after the development of AF,
transesophageal echo (TEE) to exclude thrombi should precede the
cardioversion.
The decision to administer anticoagulant therapy in the post-operative period is
always made by assessing the potential benefit balanced by the bleeding risk.
If the patient is in AF at the time of discharge they should be sent home on
warfarin unless contraindicated. In most cases a therapeutic protime/INR will
need to have been achieved prior to discontinuation of heparin unless a low
molecular weight heparin transition is planned.
Note that amiodarone discharge doses should not exceed 600 mg/day (often 400
mg/day) and early clinical follow-up with an ECG should be arranged for patients
being discharged on any antiarrhythmic drug.
ATRIAL FLUTTER: See Common Elements of Care: Atrial Flutter
****
A number of patients who either experience paroxysms of AF or are in
AF persistently after surgery will have few, if any, symptoms if ratecontrolled. These are the patients that might be considered for
discharge without attempts to cardiovert or without antiarrhythmics.
They can remain anticoagulated after discharge and if in the arrhythmia
persistently during follow-up can undergo elective, outpatient
cardioversion.
PLANNED CARDIAC SURGERY
AF Prophylaxis Algorithm
Already on Beta Blocker?
NO
YES
Contraindications for beta
blocker?
NO
•
•
Assure adequate dose
Continue beta blocker postop
YES
Institute
STRATEGY A: Pre-Op
Beta Blockers
•
•
•
•
•
•
•
•
Any of the Following: ?
Age > 60 yrs
Hypertension
Preoperative history of atrial
fibrillation
Valvular heart disease
COPD
Previous cardiac surgery
Need for an intra-aortic balloon
pump or pressors pre-operatively
Diabetes Mellitus
YES
Institute
STRATEGY C:
Pre-Op
Amiodarone
(see text for
cautions)
NO
O.R.
Continue
prophylaxis
post-op
Assuming No Pre-Op AF Prophylaxis
POST-OP CARDIAC SURGERY:
AF Prophylaxis Algorithm
Already on Beta Blocker?
NO
YES
Contraindications for beta
blocker?
NO
•
•
Assure adequate dose
Continue beta blocker postop
YES
Institute
STRATEGY B: PostOp Beta Blockers
•
•
•
•
•
•
•
•
•
Any of the Following: ?
Age > 60 yrs
Hypertension
Preoperative history of atrial
fibrillation
Valvular heart disease
COPD
Previous cardiac surgery
Need for an intra-aortic balloon
pump or pressors pre- or postoperatively
Diabetes Mellitus
Artificially ventilated more than 24
hrs
YES
Institute
STRATEGY D:
Post-Op
Amiodarone
(see text for
cautions)
NO
Continue
prophylaxis
Atrial Fibrillation Clinical Algorithms
Physician Office
Patients presenting to a physician’s office in atrial fibrillation are managed
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
♦ Whether the AF is chronic and persistent, of new onset or whether the AF is
merely newly recognized
♦ Presence or absence of chronic and adequate anticoagulation
♦ Past or current antiarrhythmic drug therapy
A patient with atrial fibrillation (or flutter) in the office setting is not likely to be
hemodynamically unstable or markedly symptomatic. If the patient is unstable,
however, normal office emergency procedures should be invoked and, if
appropriate, the patient should be transported by ambulance to an emergency
department.
The more common decisions to be made for the office arrhythmia patient are
whether the patient needs the addition of AV nodal blocking drugs, the institution
or modification of anticoagulation, consideration for elective admission to a
hospital monitored unit, plan for elective cardioversion or referral to Cardiology or
the scheduling of further diagnostic testing. The following algorithm assumes a
Primary Care Physician perspective and is likely to be most useful for the patient
with newly recognized atrial fibrillation (or flutter).
Atrial Fibrillation Clinical Algorithms
Physician Office (Primary Care Perspective)
ATRIAL FIBRILLATION
Initial Assessment
♦
♦
♦
♦
♦
H/P
ECG
CBC, lytes, BUN, creatinine, PT
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?
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)
CHRONICALLY (AND ADEQUATELY)
ANTICOAGULATED?
NO
DURATION OF
AF < 48 HRS
YES
DURATION OF
AF > 48 HRS OR
UNKNOWN
♦ Assess, institute rate control strategy (see COMMON
ELEMENTS OF CARE: Controlling Ventricular Rate)
♦ Assess thromboembolic risk and institute anticoagulation
strategy if appropriate (see COMMON ELEMENTS OF
CARE: Anticoagulation)
♦ If expeditious restoration of sinus is desirable (usually
determined by symptoms) prompt referral to ED or
Cardiology
See
next
page
♦ Expeditious cardioversion cannot
be performed (unless TEE-guided)
♦ Assess, institute rate control
strategy(see COMMON
ELEMENTS OF CARE: Controlling
Ventricular Rate)
♦ Assess thromboembolic risk and
institute anticoagulation strategy
if appropriate (see COMMON
ELEMENTS OF CARE:
Anticoagulation)
♦ Complete outpatient work-up
(labs, echo, possible Cardiology
referral) unless symptoms
warrant inpatient evaluation
Atrial Fibrillation Clinical Algorithms
Physician Office (Primary Care Perspective)
page2
CHRONICALLY (AND ADEQUATELY)
ANTICOAGULATED?
YES
♦ May consider expeditious CV (in ED or diagnostic
unit or short-stay unit)
♦ If symptoms not severe, institute or maintain
current rate control strategy
♦ Complete outpatient work-up (labs, echo, possible
Cardiology referral) unless symptoms warrant
inpatient evaluation
♦ Decision: either plan to not convert (leave in AF) or
to restore sinus rhythm
♦ See Common Elements of Care: Controlling
Ventricular Rate and Maintenance of Sinus Rhythm
(either may require admission to hospital)
APPENDIX:
Data Elements and Quality Indicators
Atrial fibrillation clinical registry
♦
♦
♦
♦
♦
♦
♦
♦
♦
♦
♦
♦
Patient demographics
Type of arrhythmia
Co-morbidities
Cardioversions
Non-pharmacologic therapy
Antiarrhythmic drugs
Anticoagulant drugs and efficacy
Adverse drug events
Thromboembolic complications
Mortality
Readmission
Longitudinal follow up
Quality indicators
1. Entire patient population
•
•
•
•
•
•
•
Length of stay
Cost per case
Readmission
QOL
Match presentation, risk factors and discharge anticoagulation regimen for
appropriateness
Mortality
Stroke
2. Outpatient antiarrhythmic institution
•
Adverse events
3. Drug-specific tracking for efficacy, ADE
4. Electrical cardioversion
•
•
•
•
•
•
Absence of pharmacologic proarrhythmia
Successful cardioversion
Absence of significant skin burns
Absence of bradyarrhythmia requiring therapy
Absence of complications of conscious sedation
Complete amnesia for shock (goal: 100%)
Intravenous Amiodarone
Introduction: Amiodarone is a unique and highly effective drug loosely classified as a
Type III antiarrhythmic. Besides the Type III effects (prolonged action potential), it has
important beta-adrenergic effects, calcium blocking and antithyroid effects and is a
potent sodium channel blocker.
The clinical manifestations of its electrophysiologic effects include sinus slowing, AV
nodal blockade, a slightly prolonged ORS and prolongation of the QT interval. The
electrophysiologic effects of oral amiodarone are different from intravenous amiodarone
for three reasons:
•
•
•
The oral agent results in eventual greater tissue saturation of amiodarone
After oral amiodarone, the active metabolite N-desethyl-amiodarone also
accumulates in tissue.
Only the oral agent has an antithyroid effect (which may have secondary
antiarrhythmic effects)
Intravenous amiodarone is between 75 and 100% bioavailable. Oral amiodarone is 3050% bioavailable. This only impacts the dosing schemes. Dosing need not be altered in
either renal or hepatic dysfunction. It is not dialyzable.
Very few trials have compared oral versus I.V. amiodarone. I.V. amiodarone is
effective (and likely superior to oral) in improving survival from refractory or
recurrent ventricular fibrillation and hemodynamically catastrophic ventricular
tachycardia.
I.V. amiodarone is only modestly effective in converting atrial fibrillation (AF) to sinus
rhythm. It has been shown to be either equivalent or less effective than propafenone,
flecainide, procainamide, quinidine or oral amiodarone. Intravenous ibutilide has the
highest efficacy in conversion of AF to sinus rhythm. No drug is as efficacious as direct
current cardioversion.
Intravenous amiodarone given after cardiac surgery as prophylaxis against AF has not
been convincingly effective. A number of oral amiodarone regimens on the other hand
have been effective in reducing AF incidence after cardiothoracic surgery (See
Postoperative Atrial Fibrillation)
Intravenous amiodarone has the following additional disadvantages not shared by oral:
•
•
•
•
A very high cost
The requirement for a central line (high incidence of phlebitis)
Hypotension (15-25%)
Modest negative inotropy
Intravenous Amiodarone
Clinical Guidelines
(Relevancy to AF Emphasized)
I.
Intravenous amiodarone is indicated in the following clinical
situations:
• Acute treatment of recurrent ventricular fibrillation or ventricular
tachycardia refractory to lidocaine
•
Subacute treatment for recurrent ventricular tachycardia in a patient
who has no alimentary access or is believed to have compromised
gastrointestinal absorption
•
Initial loading for recurrent, hemodynamically significant atrial
fibrillation or atrial flutter in a patient who has no alimentary access or
is believed to have compromised gastrointestinal absorption
II.
Intravenous amiodarone is not indicated in the following clinical
situations
Pre-operative or peri-operative prophylaxis against atrial fibrillation
• Treatment of chronic, persistent or paroxysmal atrial fibrillation
• Treatment of any arrhythmia which is not immediately life-threatening
when patient can take P.O. amiodarone
NOTE: If patient is taking amiodarone chronically and the patient must be
NPO < 7 days, there is typically no need for I.V. amiodarone as replacement
given its long half-life.
III.
Administration
Preferred route for I.V. amiodarone is by central vein
• Initial bolus is 150 – 300 mg, but up to 5 mg/kg can be given (dose
related antiarrhythmic response)
• Initial recommended infusion: 1 mg/min for 12 hours, with a reduction
to 0.5 mg/min for 12 hours
• If more than one day is required approximately one gram of I.V.
amiodarone per day is given by constant infusion
• If oral amiodarone is to be given chronically, the loading dose (8001600 mg/day) is begun as soon as there is alimentary access. If the
I.V. drug has been given for at least 24 hours, it should be stopped
after the first “P.O.” dose.
Relative Stroke Risk Table
RISK FACTORS FOR STROKE IN PATIENTS WITH
NONVALVULAR ATRIAL FIBRILLATION
Risk Factors
Previous stroke or TIA
Hypertension
CHF
Advanced Age (continuous,
per decade)
Diabetes Mellitus
CAD
Relative Risk
2.5
1.6
1.4
1.4
1.7
1.5