CONSENSUS DOCUMENT

Formacin
acreditada

Atrial fibrillation management in the hospital emergency

department: 2012 update*
ALFONSO MARTN MARTNEZ1, IGNACIO FERNNDEZ LOZANO2, BLANCA COLL-VINENT PUIG1,
LUIS TERCEDOR SNCHEZ2, CARMEN DEL ARCO GALN1, FERNANDO ARRIBAS YNSAURRIAGA2,
CORAL SUERO MNDEZ1, LLUIS MONT GIRBAU2
Grupo de Arritmias Cardiacas. Sociedad Espaola de Medicina de Urgencias y Emergencias, Spain.
Seccin de Electrofisiologa y Arritmias. Sociedad Espaola de Cardiologa, Spain.

1
2

CORRESPONDENCE:
Alfonso Martn Martnez
Servicio de Urgencias Generales
Hospital Universitario
Severo Ochoa
Avda. Orellana, s/n
28911 Legans, Madrid, Spain.
E-mail:
amartin@arritmias-semes.org y
alfonso.martin@salud.madrid.org

RECEIVED:

Atrial fibrillation is the most frecuently sustained arrhythmia managed in emergency

departments, and accounts for a high and increasing prevalence in Spain. Atrial
fibrillation is increases mortality, is associated with substantial complications and,
therefore, has a relevant impact inrunning of the health care system. Management
requires consideration of diverse clinical variables and a large number of possible
therapeutic approaches, justifying action plans that coordinate the work of medical staff
in the interest of providing appropriate care and optimizing resources. These evidencebased guidelines contain recommendations for managing atrial fibrillation in the special
circumstances of hospital emergency departments. Stroke prohylaxis, rate control,
rhtyhm control, and related diagnostic and logistic issues are discussed in detail.
[Emergencias 2012;24:300-324]

9-4-2012

ACCEPTED:
13-5-2012

Key words: Atrial Fibrillation. Emergency departments. Antiarrhythmic drugs.

Cardioversion. Heart rate control. Anticoagulation. Stroke prevention.

CONFLICT OF INTEREST:
None

Introduction
Atrial fibrillation (AF) has become a serious
public health problem in the XXI century because
of its increasing prevalence1-8, impact on survival
and quality of life9-13, and the high costs of healthcare involved11,14,15. Thus the importance of appropriate, effective and efficient strategies to manage
this arrhythmia in all types of care settings9,11,16,17.
As discussed below, this applies particularly to
hospital emergency departments (EDs), where patients with AF are usually first attended or referred
for chronic or acute disease exacerbation, especially those with symptoms suggestive of cardiovascular disease or advanced age since AF is highly prevalent in both these population groups16,18-21.
However, despite these considerations, there is
variability in the management of AF in our set-

ting, in treatment and prophylaxis of complications, including logistics (transfer and destination
of these patients) and in ED coordination with
other levels of care16-19,22-24. This is probably a consequence of the large number of clinical considerations involved, as well as the diversity of possible
treatment options, which sometimes means that
ED management of AF does not meet defined
standards18,19,22-24. All this justifies the establishment
of coordinated action and treatment strategies for
the various professionals involved, to improve and
optimize human and material resources.
Some years ago, these considerations led the
Spanish Society of Accident and Emergency Medicine (SEMES) and the Spanish Society of Cardiology (SEC), through their scientific sections specialized in cardiac arrhythmias, to define criteria for
the management of AF in the ED and publish

*Consensus document produced by the Cardiac Arrhythmia Group of the Spanish Society of Emergency Medicine (SEMES) and the
Electrophysiology and Arrhythmias section of the Spanish Society of Cardiology (SEC).

300

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ATRIAL FIBRILLATION MANAGEMENT IN THE HOSPITAL EMERGENCY DEPARTMENT: 2012 UPDATE

them as a consensus document in 200316. Since

then, abundant scientific literature has appeared,
requiring major changes, which, together with
the emergence of new drugs, have necessitated
an update on the recommendations of this consensus document. To this end, the available scientific evidence has been reviewed in depth, together with current clinical practice guidelines and
recommendations (in particular the recently published European Society of Cardiology-ESC- guidelines)9. This paper attempts to adapt the general
recommendations of international clinical practice
guidelines to the specific characteristics of Spanish
EDs. It proposes general guidelines for the management of arrhythmia, based on scientific evidence and applicable to most EDs regardless of
the level of complexity of the hospital where they
are located, and hopefully will help ensure proper
care to patients and better use of available resources. Obviously, the present guidelines are not
the only alternatives for the management of AF;
other options, based on scientific evidence, and
the recommendations of other guidelines, may be
equally valid.

Atrial fibrillation in hospital emergency

departments
Prevalence and clinical relevance
AF is an extremely serious condition; it is an independent predictor of mortality2-4,7,8,12,25 and doubles the risk of early death. It significantly affects
patient quality of life, being associated with various phenomena8-11,26-28 including hemodynamic deterioration, disturbing symptoms (palpitations,
weakness, reduced effort ability)26, increased number of hospitalizations9,10,25, increased risk of heart
failure29-34 and the development of arterial thromboembolism, primarily in the form of stroke35,36. AF
increases the risk of stroke to 5 times that of the
general population, and these embolic phenomena double the risk of early mortality, involving
more residual disability and prolonged hospital
stay in survivors, and relapse occurs more frequently than with ischemic accidents of other etiologies37-40.
ED visit rate is very high in our country (almost
24 million visits in 2009)41. Professional working
conditions and the profile of patients differ radically from those of controlled clinical trials, and
the ED is a faithful exponent of daily practice regarding the acute phase of AF 19,22. As in other
neighboring countries, the ED constitutes a gateEmergencias 2012; 24: 300-324

way to the health system, widely used by the

general population (71% of hospitalized medical
patients are admitted via an ED)20, and especially
by patients with a history of cardiovascular disease and those of advanced age, where the
prevalence of AF is high21,42,43. Thus, AF is the most
prevalent sustained cardiac arrhythmia seen in
daily ED practice, responsible for 3.6% of all general emergencies in our country19, 10% of admissions to medical departments2 and with increasing
incidence and prevalence for a multitude of reasons. Among them, an aging population (incidence and prevalence of AF increase with age)42,
improvement in survival rates after myocardial infarction44, increased number of cardiac and thoracic surgical interventions (associated with a high
rate of postoperative AF)45, correct early diagnosis
of arrhythmia7 and increased prevalence of various
risk factors related to arrhythmia (arterial hypertension, obstructive apnea, etc.)46.
At the same time, the earlier therapeutic action
is taken the greater the probability of successfully
treating such arrhythmia and recovering sinus
rhythm47,48, and the earlier thromboprophylaxis is
initiated the better, to avoid serious consequences
of arterial embolism9,36.
As mentioned, AF is a serious disease of increasing prevalence in the ED, and this explains
the extraordinary relevance of strategies for effective management in this health care setting, since
this is where patients are first attended when
symptoms begin or arrhythmia is first detected18,22, and where the greatest possibilities exist to
prevent complications and recover sinus
rhythm16,18.

Patient characteristics
The first step before planning any therapeutic
action is to determine the profile of patients treated and, based on the clinical profile, establish the
most appropriate management strategies to optimize resources. According to the GEFAUR-1 19,22
survey data, AF in Spanish EDs mainly affects the
elderly (mean age 75 years, with 57% of patients
being older) and the main factors associated with
AF are hypertension (58%), the existence of structural heart disease in 47% of patients (37% ischemic, 30%, valvular, 25% hypertensive and 8%
dilated), diabetes mellitus in 22% and hyperthyroidism in 1.5% of patients. The great majority
(89%) of ED patients present risk factors for the
development of thromboembolism which means
they are high risk subjects and, therefore, candidates for indefinite oral anticoagulation9.
301

A. Martn Martnez et al.

Of particular importance is the duration of

the AF episode: the shorter the duration, the
greater the chances of success in arrhythmia
control49,50, and in episodes lasting less than 48
hours, cardioversion is safe without previous
thromboprophylaxis51. Thus, 25-30% of episodes
last less than 48 hours, in 20% the duration is
unknown and the remainder involve longer duration. Finally, in terms of clinical presentation,
70% of patients present with acute symptoms
related to arrhythmia or complications or treatment (for the latter, the figure reaches 93% for
episodes of recent onset)18,19. These data are of
great clinical importance since the existence of
acute symptoms suggests an active management approach in the ED with prompt relief of
symptoms. Thus, AF in the ED mainly affects
elderly patients with structural heart disease,
high risk of thromboembolism, high co-morbidity, and consulting for acute symptoms related
with arrhythmia, all crucial data for the treatment plan9.

Current status of the management of atrial

fibrillation in the ED
As in other areas of care, it is important to
know the patterns of clinical management used
in daily practice, in order to translate the evidence from randomized clinical trials and the
recommendations of clinical practice guidelines
for greater effectiveness in clinical practice52.
Data from the GEFAUR-1 and 2 studies show
that most patients (89%) present a high risk of
embolism. However, prescription of anticoagulation is insufficient (39%) and does not match
the recommendations of clinical practice guidelines19,24 (in the most recent study, RHYTHM-AF,
anticoagulation was prescribed for 53% of patients at high risk)18. Regarding heart rate control, this was performed in 67% of eligible patients, but the excessive use of digoxin meant
the treatment was only effective in 43% (in the
RHYTHM-AF study, beta-blocker use reached
63%) 22. Finally, the RHYTHM-AF study showed
that restoration of sinus rhythm was attempted
in 80% of recent onset episodes, but the high
use of amiodarone reduced the effectiveness of
the strategy (72% of cases)19. It is therefore necessary to implement strategies that increase anticoagulant prescription in high risk patients, increase the effectiveness of heart rate control
using beta blockers and generalize heart rhythm
control to all eligible patients using more effective methods such as electrical cardioversion.
302

Treatment Goals
Medical action in all patients with AF must systematically consider the following objectives:
1) relieve the symptoms for which the patient
consulted the ED by controlling heart rate and/or
restoring sinus rhythm, 2) avoid complications
arising from hemodynamic deterioration caused
by the arrhythmia itself and maintain high heart
rate; and 3) prevent thromboembolic phenomena.
To achieve these general objectives, three specific management strategies are available9,16:
1) control of ventricular response (heart rate
control), which allows achieving and maintaining
heart rate that relieves symptoms associated with
the arrhythmia, allowing proper exercise tolerance
and avoiding the appearance of long-term complications such as tachycardia; 2) Heart rate control, i.e. sinus rhythm restoration and maintenance in those patients in which it is safe to
attempt cardioversion and likely to maintain sinus
rhythm in the long term, and 3) prophylaxis
against arterial thromboembolism; this should be
administered whenever there are risk factors for
this complication, whether or not the patient consulted for symptoms associated with the arrhythmia.
According to the current state of knowledge,
thromboprophylaxis and heart rate control are always therapeutic targets in the ED. Heart rate
control should be achieved with an elective strategy tailored to each patient according to the clinical profile and available treatment options9,16.

General management of atrial fibrillation

in the ED
Before reviewing management strategies, it is
necessary to deal with a set of general concepts,
such as hemodynamic instability, structural heart
disease and the electrical cardioversion procedure,
which are described in detail in the previous version of this document and remain in force16.
Initial evaluation of the patient should focus on
establishing whether the patient is stable from a
clinical and hemodynamic point of view. If the patient presents hemodynamic instability (hypotension associated with immediate life-threatening
organ dysfunction) where AF may be playing a
role, synchronized electricalal cardioversion is recommended9. Importantly, if AF recurs early or if
recovery of stable sinus rhythm appears to be
highly unlikely, then it is acceptable to try to foEmergencias 2012; 24: 300-324

ATRIAL FIBRILLATION MANAGEMENT IN THE HOSPITAL EMERGENCY DEPARTMENT: 2012 UPDATE

cus on control of heart rate only22. In stable patients, consider whether triggers exist (the most
common in the ED is febrile syndrome, especially
in the elderly) and treat them first. Finally, one
should remember that there is usually no need for
hospitalization to apply management strategies
for arrhythmia or tests. In general, hospitalization
is required for AF patients with complications
(angina, stroke, heart failure), uncontrollable heart
rate (if it causes severe symptoms), early treatment with risk of pro-arrhythmia or hemodynamic
instability16.

Prophylaxis of arterial thromboembolism

in the ED
AF favors the formation of intra-atrial thrombi,
which can break off and cause stroke, the most
serious and frequent being cerebral. AF increases
the risk of stroke five-fold with respect to the general population. Furthermore, AF-associated stroke
is more severe than stroke of other etiologies, and
largely responsible for the morbidity associated
with AF24,53-54.
The risk of stroke in AF is much higher when
associated with mitral valve disease 54,55 and increases particularly after cardioversion, whether
spontaneous, pharmacological or electricalal 9,55,
especially when AF is prolonged before cardioversion. The risk of embolism is similar in all chronic
forms of AF: paroxysmal, persistent and permanent9,56,57. Prophylactic antithrombotic agents substantially decrease the risk of stroke in AF36,37,58,59.
However, this treatment is not without complications, some severe and disabling them, such as intracranial hemorrhage. It is therefore necessary to
identify patients with increased risk-benefit profile
for each treatment, and those in which prophylaxis may not be required because of low thromboembolic risk. Regarding individual recommendations for antithrombotic prophylaxis, there are
three different clinical situations: 1) non-valvular
AF, 2) AF associated with a prosthetic valve or mitral valve disease, and 3) cardioversion of AF.

of stroke, transient ischemic accidents (TIA), or

systemic embolism, advanced age, hypertension,
diabetes, coronary heart disease, heart failure and
female gender. The importance of each of these
factors varies in published studies37,60,61. Also, some
echocardiographic factors have been described,
including left ventricular dysfunction (ejection
fraction < 40%) and, to a lesser extent, ventricular
hypertrophy60. Of these risk factors, the most important is a history of stroke, TIA or systemic arterial embolism, with a relative risk of 2.5 to 2.9
and an annual incidence of stroke of 12%60,61. Advanced age is second in importance60,61. It is estimated that as from the age of 65 years, the relative risk of developing thromboembolic events
increases each decade from 1.4 to 1.8. Importantly, although most studies and guidelines have established a minimum from which age may be
considered a risk factor, it is a constant factor, i.e.
not a qualitative factor, but the older the patient,
the higher the risk.
Thromboembolic risk in the AF patient is not
static but can change throughout life. Not only
does age change, but new risk factors often appear. Furthermore, the risk of bleeding complications may also be modified with time. Even
the expected benefit of anticoagulant therapy
may change, since the main purpose of this
treatment is maintenance of neurological functions, and in some patients these may already
be diminished or abolished by previous stroke
or other causes. From the identification of the
above risk factors, we have established multiple
risk stratification scales. The best known and
most practical is the CHADS2 scale38,62, which includes heart failure, hypertension, advanced age
( 75 years), diabetes, and prior stroke, TIA or
systemic embolism (Table 1). The higher the
score, the greater the risk of thromboembolic
events and therefore the higher the recommendation for anticoagulant treatment. Thus, for a
score of 2 or higher, anticoagulation is recommended. In younger patients (< 65 years) without risk factors, anticoagulation is not recommended.
However, a large group of patients present a

1. Prophylaxis in non-valvular AF
The incidence of stroke in non-valvular AF is 45% globally per year, but varies greatly with the
thromboembolic risk factors involved.

1.1. Risk Stratification

Many clinical factors are associated with increased risk of stroke. The main ones are a history
Emergencias 2012; 24: 300-324

Table 1. CHADS2 embolic risk stratification scheme

Risk factor
C: cardiac failure
H: hypertension
A: age 75 years
D: diabetes mellitus
S: stroke or TIA
TIA: transient ischemic attack.

Score
1
1
1
1
2

303

A. Martn Martnez et al.

Table 2. CHA2DS2-VASc embolic risk stratification scheme

CHA2DS2
Risk factor
C: cardiac failure, left ventricular dysfunction
H: hypertension
A: age 75 years
D: diabetes mellitus
S: stroke or TIA
V: vascular artery disease: myocardial infarction,
peripheral arterial disease or complicated aortic plaque
A (age): age 65 years
Sc (sex category): female
TIA: transient ischemic attack.

Score
0-1

1
1
2
1
2
1
1
1

CHADS2 score of 1, or 0-1 together with one of

the above risk factors not included in the CHADS2
scale. In this group, representing approximately
one third of patients with AF, the recommendation based on the CHADS 2 scale is ambiguous,
and one should then apply the CHADS2-VASc risk
scale (Table 2) recently agreed on by the ESC9,63.
This scale includes the same same factors as the
CHADS2 scale but attributes greater weight to advanced age, and includes other risk factors: age
between 65 and 74 years, female gender and arterial disease (myocardial infarction and/or complicated aortic plaque and/or peripheral arterial
disease). According to this scale, AF patients with
a score greater than one point should be anticoagulated, while in patients with a score of 0 it is
recommended not to administer antithrombotic
treatment or, optionally, anti-aggregation. For patients with a score of 1, oral anticoagulation is
recommended; in some cases (therapeutic compliance difficulty, patient choice) antiaggregation
can be chosen. Figure 1 summarizes the indications and modalities of thromboprophylaxis in
non-valvular AF. Risk of embolism has also been
demonstrated in patients with atrial flutter, and
the same recommendations apply9,64.

1.2. Risk of bleeding

In addition to assessing the risk of thromboembolic events, it is also important to assess
the risk of bleeding before deciding on the most
appropriate therapeutic approach. In general,
there are very few absolute contraindications for
anticoagulation. The risk of bleeding has decreased in recent years, mainly due to better control of anticoagulation and blood pressure. Furthermore, it should never be forgotten that the
consequences of not anticoagulating a patient
with AF can be devastating.
The main hemorrhagic risk factor is poor control of anticoagulant therapy; strict control may
save a lot of undesirable effects. Another risk fac304

CHADS2

2
OAC

CHA2DS2-VASc

Nothing (ASA)

OAC (ASA)

OAC

Figure 1. Recommendations for thromboprophylaxis in nonvalvular atrial fibrillation. OAC: oral anticoagulation; ASA:
acetylsalicylic acid (second choice).

tor for bleeding is advanced age: the older, the

higher the risk of bleeding, especially in those
aged 85 years or more. However, elderly patients
are also those with increased risk of ischemic
events, so in these patients anticoagulant therapy
is recommended together with strict control65. Although falls are more common in this group, the
risk of bleeding from falls does not justify withholding anticoagulation if indicated66,67.
The ESC has also defined a risk scale for
bleeding-the HAS-BLED scale, 9 which in addition
to poor control of anticoagulation (labile INR)
and advanced age, includes prior stroke, hypertension, history of bleeding, renal and/or liver
failure, and the consumption of drugs and/or alcohol (Table 3). The higher the score, the greater
the risk of bleeding, and a score 3 is considered high.
It should be noted that many hemorrhagic
risk factors are also ischemic risk factors, so it is
common for patients with a high ischemic risk
score to also score high on the HAS-BLED scale.
Therefore, a high score on this scale does not
contraindicate anticoagulant therapy, but indicates the need for tighter control of anticoagula-

Table 3. HAS-BLED hemorrhagic risk stratification

Risk factor

Score

H: hypertension
1
A: abnormal liver and/or renal function
(one point each)
1o2
S: stroke or TIA
1
B: history of bleeding
1
L: labile INR
1
E: elderly (> 65 years)
1
D: drugs or alcohol (1 point each)
1o2
TIA: transient ischemic attack. INR: international normalized ratio.
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ATRIAL FIBRILLATION MANAGEMENT IN THE HOSPITAL EMERGENCY DEPARTMENT: 2012 UPDATE

tion. And a high score on the scale should only

influence the therapeutic decision when the indication for anticoagulation is less evident
(CHADS2-VASc = 1).
In ischemic patients with high risk and a history of intracranial hemorrhage, the decision on
anticoagulation is complex and must be made
individually after consensus between specialists.
In general, the decision will be not to anticoagulate the patient, especially if prior bleeding was
lobar.

1.3. Treatment Options

As mentioned, chronic anticoagulant therapy
substantially reduces the risk of thromboembolism. The reduction of relative risk compared
to placebo is 64%, with a reduction in absolute
annual risk of stroke of 2.7%38. There are various
treatment options for chronic treatment with oral
anticoagulants in AF patients. K antagonists (VKA)
have traditionally been used, the only therapeutic
option for the past 60 years, with demonstrated
utility in stroke prevention in patients with AF.
The main vitamin K antagonists (VKA) drugs are
acenocoumarol and warfarin. Although most
studies in Spain have been performed using warfarin, acenocoumarol is the most commonly used
VKA (Sintrom). Despite its proven efficacy in the
prevention of ischemic events 37,38,58,59, there are
some major problems. On one hand, the therapeutic range is very narrow. The intensity of anticoagulation with VKA is expressed as INR (international normalized ratio), which is calculated
from the ratio between actual prothrombin time
obtained and that of standardized control serum.
For anticoagulation to be effective and at the
same time minimize the risk of bleeding, an INR
between 2 and 3 is recommended. With a lower
INR it is not recommended, even in very elderly
patients, and a higher INR is associated with increased bleeding complications. Furthermore,
VKA drugs are metabolized by cytochrome P-450,
so it interacts with many drugs and foods and
this can alter the level of anticoagulation. This
implies the need for periodic monitoring of the
INR, making anticoagulant treatment an additional burden for patients.
Recently, new evidence has appeared regarding other oral anticoagulants for the prevention
of ischemic events in AF, with dabigatran being
the first to be approved in Spain. This is a direct
inhibitor of thrombin and interferes little with
drugs or food and may be administered in a
fixed dose with no need for monitoring. The RELY study showed that dabigatran at a dose of
Emergencias 2012; 24: 300-324

150 mg/12 h was more effective than warfarin in

preventing ischemic events without increasing
the risk of bleeding69. At a dose of 110 mg/12 h,
dabigatran was as effective as warfarin with a
lower risk of bleeding. Thus, the recommended
dose for the prevention of ischemic events in FA
is 150 mg/12 h. The lower dose of 110 mg/12 h
should be reserved for patients who are elderly (>
80 years) or at high risk of bleeding, including
those with peptic disease (due to their increased
risk of digestive tract bleeding), and patients with
low body weight. Its profile of greater effectiveness (at 150 mg/12 h) and enhanced safety (at
110 mg/12 h) is the recommended treatment
option for most patients69. Dabigatran is also recommended in patients with recurrent thromboembolism despite correct use of VKA anticoagulation drugs. An alternative is to increase the
range of INR, but this entails higher risk of bleeding.
Dabigatran is eliminated via the kidneys, so in
patients with severely impaired renal function
(creatinine clearance < 30 ml/min), its use is contraindicated. Although it can be assumed that the
level of anticoagulation is correct in patients with
preserved renal function and adequate compliance, in selected cases requiring monitoring, a diluted thrombin test (Hemoclot) can be used, as
well as in cases of overdose (intentional or accidental) or hemorrhage.
There is no specific antidote for dabigatran,
but a specific monoclonal antibody that completely reverses its anticoagulant effect is being
developed. Given its short elimination half-life
and safety, cases of bleeding can generally be resolved with appropriate supportive treatment and
temporary or permanent withdrawal of the drug
(suspension of one or two doses may be sufficient to restore adequate coagulation) in cases of
serious bleeding, in addition to activated carbon,
hemodynamic supportive measures and local hemostasis (compression, endoscopy, surgical ligation). A pro-coagulant factor may be necessary to
reverse the effect, such as prothrombin complex
or activated recombinant factor VII, although
clinical experience concerning the effectiveness of
these agents is limited. In addition, in these cases
it should be remembered that dabigatran is dialyzable.
Another therapeutic alternative in oral anticoagulation is to use direct inhibitors of factor Xa,
namely rivaroxaban and apixaban. As with dabigatran, they are administered at fixed doses without monitoring. Rivaroxaban, recently approved
in Spain as prophylaxis for arterial thromboem305

A. Martn Martnez et al.

bolism in FA, a dose of 20 mg once daily (or 15

mg/day if renal clearance of creatinine is between
15-30 ml/min), has similar efficacy to VKA for the
prevention of ischemic events with a comparable
incidence of major bleeding (but with a drastic
reduction in the rate of intracranial hemorrhage
and fatal bleeding), according to the ROCKET-AF
study 70 . Apixaban, not yet approved by drug
agencies, was found to be superior to aspirin in
the AVERROES study in patients not recommended for VKA treatment, without increased risk of
bleeding 71, and superior to warfarin with fewer
hemorrhages (and a reduction in overall mortality) in the ARISTOTLE study72. Thus the new anticoagulants, for best balance between effectiveness and adverse effects, and more favorable
control profile, are currently the preferred alternative to VKA in most patients.
A meta-analysis has shown that aspirin partially reduces the risk of ischemic events in AF
(19%), a much smaller proportion than anticoagulant therapy (reduction of relative risk with
VKA versus aspirin: 39%)73. However, this treatment is not without its complications, especially
in the elderly. This group of patients, at the
greatest risk of bleeding with oral anticoagulant
therapy, also present more bleeding complications with antiplatelet therapy, and this treatment is less effective73,74. In cases where oral anticoagulation cannot be administered or the
indication is weak (CHA2DS2-VASc = 1), one can
opt for antiplatelet therapy despite it being
much less effective. The recommended dose of
aspirin is 75 to 100 mg/day. In cases of intolerance or allergy to aspirin, clopidogrel 75 mg/day
may be given.
Dual antiaggregation therapy with aspirin and
clopidogrel is generally not recommended as it
involves a small reduction of embolic risk at the
expense of an increased risk of bleeding 75. The
combination of anticoagulation and antiaggregation therapy should be reserved for patients with
acute coronary syndrome or stent carriers.
In patients without prosthetic valves scheduled for procedures involving risk of bleeding,
such as surgery or endoscopy with biopsy, one
must discontinue oral anticoagulation; other therapy is not necessary if downtime is less than one
week. In patients with very high embolic risk or
cases in which the suspension of oral anticoagulation is likely to continue for more than 1 week,
we recommend treatment with low molecular
weight fractionated heparin9.
Table 4 summarizes the recommendations for
thromboembolism prophylaxis in non-valvular AF.
306

Table 4. Summary of recommendations for thromboembolism

prophylaxis in non-valvular atrial fibrillation
1. We recommend preventive treatment with VKA or dabigatran for all
patients with AF, except those with very low embolic risk (males
with isolated AF and age under 65 years).
2. In patients with a CHA2DS2-VASc score of 1 or 0, consider aspirin at
doses of 75-100 mg / day, as an alternative to anticoagulants.
3. VKA anticoagulation should be maintained with a target INR of 2.5
(2.0-3.0).
4. The recommended dose of dabigatran is 150 mg/12 h except
where age exceeds 80 years or where the risk bleeding is very high,
in which cases a dose of 110 mg/12 h is recommended.
5. Rivaroxaban at a dose 20 mg / day has been recently approved,
except in cases of moderate or severe renal insufficiency, for whom
the dose is 15 mg / day.
6. These recommendations apply regardless of the type of AF, and they
also apply to atrial flutter.
7. The combination of anti-aggregant and anticoagulant is only
indicated in AF patients presenting acute coronary syndrome or
stent carriers.
VKA: vitamin K antagonists, AF: atrial fibrillation.

2. Prophylaxis in atrial fibrillation associated

with a prosthetic valve or mitral valve
The incidence of stroke in patients with AF
and mechanical prosthetic valves or mitral valve
heart disease (stenosis or rheumatic mitral insufficiency, degenerative mitral regurgitation, mitral valve prolapse and mitral annulus calcification) is 17%. This high risk justifies
anticoagulation in all cases9. The only drugs currently accepted for thromboprophylaxis in these
situations are VKA drugs, used to maintain a level of anticoagulation with an INR of 2 to 3, except in cases of prosthetic mitral valve, when
INR must be greater than 2.5 (2.5-3.5). Dabigatran is still not approved for thromboprophylaxis
in these clinical circumstances.

3. Prophylaxis in sinus rhythm restoration

The pro-embolic tendency increases markedly
after cardioversion, be it spontaneous, pharmacological or electricalal, especially when the period of AF before cardioversion is prolonged76,77.
This tendency constitutes the main difficulty in
the medical decision on whether to prescribe
cardioversion or not, and on when to perform
it, so it is important to ensure appropriate
thromboprophylaxis beforehand.
Embolic phenomena may occur during cardioversion, but more commonly they appear
hours or days later. This delay is explained, first,
by the fact that mechanical atrial contraction
does not normalize immediately after cardioversion, but takes some time, depending on the
degree of atrial dilatation and the duration of
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ATRIAL FIBRILLATION MANAGEMENT IN THE HOSPITAL EMERGENCY DEPARTMENT: 2012 UPDATE

prior arrhythmia, which can last up to four

weeks 78. Second, this same delay in normalization of atrial contraction (called postcardioversion atrial stunning) together with endothelial
and plasma changes induced by the cardioversion79-82, favors the emergence of atrial thrombi
after, and possibly as a result of, cardioversion.
In the case of a short episode, thromboprophylaxis is not needed for cardioversion since
the probability of atrial thrombus formation (before or after cardioversion) is low. From previous
observations, a limit of 48 hour limit has been
established to distinguish a short episode from
other more prolonged episodes 83. However, AF
evolution time is not a categorical variable but
rather a continuous variable, ie. the lower the
evolution time, the lower the possibility of postcardioversion embolism. Therefore, cardioversion should be initiated as soon as possible, bef o r e t h e 4 8 - h o u r w i n d o w, i n p a t i e n t s n o t
previously anticoagulated. In all cases of short
duration AF, we recommend a previous dose of
heparin, preferably low molecular weight heparin for its ease of administration and equivalent efficacy83-85.
If there are no risk factors for thromboembolism, it is not necessary to continue anticoagulation after cardioversion. In cases where the
duration of the episode exceeds 48 hours or is
unknown, or when there is mitral valve disease
or a history of arterial embolism, one cannot
proceed to cardioversion directly because of the
high probability of intra-atrial thrombus. In
these cases, anticoagulation during at least
three weeks before cardioversion is required,
with continued anticoagulation for at least 4
weeks thereafter9,51. It is very important to know
the duration of AF in the ED because incorrect
data can have catastrophic consequences. In
case of doubt as to the duration of AF, we must
act as if it were more than 48 hours. In these
cases, an alternative to prior anticoagulation is
to rule out atrial thrombi by means of transesophageal echocardiography 86-88. This strategy
is cost-effective, avoids delayed cardioversion
(which increases its effectiveness) and increases
the number of patients eligible for rhythm control. If we exclude the presence of thrombus in
the left atrium and the appendage, one can
proceed after heparin administration before cardioversion. Similarly, anticoagulation should be
continued for at least 4 weeks after cardioversion, since thrombus formation during this period cannot be ruled out. If thrombi are found by
transesophageal echocardiogram, one should
Emergencias 2012; 24: 300-324

prescribe oral anticoagulation for at least 3

weeks and repeat the test to confirm their disappearance before cardioversion. If the episode
of AF does not exceed 48 hours or is unknown
and the patient spontaneously reverts to sinus
rhythm, anticoagulation for 4 weeks is necessary
after cardioversion. In cases of urgent cardioversion, a dose of heparin should be administered
beforehand and oral anticoagulation should be
continued during at least 4 weeks. Recommendations on thromboprophylaxis of AF also apply
to atrial flutter9,51.
Many patients undergoing cardioversion
present one or more risk factors that make indefinite anticoagulation advisable, so long term
thromboembolic risk must be assessed in all cases.

3.1. Drugs
Anticoagulation before and after cardioversion can be achieved with heparin, VKA or dabigatran. In fact, recent guidelines of the American College of Chest Physicians 2012
recommend the use of dabigatran as first choice
for prophylaxis of arterial thromboembolism in
elective cardioversion episodes of AF lasting
more than 48 hours. This option may be very
attractive for use in the ED, since it allows
scheduling cardioversion for a fixed date (3
weeks after initiation of dabigatran), assuming
adequate compliance. This facilitates the logistics and avoids delays in attempting rhythm
control, which may help increase the number of
patients susceptible to restoration of sinus
rhythm and improve the effectiveness of this
strategy, because the earlier the attempt at cardioversion, the better the results69.
In previously anticoagulated patients, cardioversion can be performed in both those receiving VKA and dabigatran. In the first case,
one must ensure correct anticoagulation by analyzing the INR value before cardioversion, which
should be between 2 and 3. In the case of dabigatran, since its anticoagulant effect is fixed and
predictable, monitoring is not required before
cardioversion, as long as renal function is preserved and compliance is adequate.
After emergency cardioversion or cardioversion in patients with AF episodes lasting less
than 48 hours but requiring indefinite anticoagulation, if the anticoagulant is VKA drugs then
one should continue with heparin until the INR
is between 2 and 3.
Table 5 summarizes the recommendations for
anticoagulation in cases requiring cardioversion.
307

A. Martn Martnez et al.

Table 5. Summary of recommendations for anticoagulation in

cardioversion
1. In urgent cardioversion we recommend a dose of heparin
beforehand and continued oral anticoagulation (OAC) during at
least 4 weeks thereafter. If VKA drugs are used as the OAC, continue
with heparin until the INR is between 2 and 3.
2. If cardioversion is performed in AF of less than 48 hours duration
and the AF is non-valvular in a patient with no history of stroke,
heparin is recommended before cardioversion, but anticoagulation
is not necessary afterwards.
3. If cardioversion is performed in prolonged AF (> 48 h),
anticoagulation is recommended for at least 3 weeks before
cardioversion and 4 weeks thereafter.
4. In the above circumstances, anticoagulation before cardioversion
may be omitted if transesophageal echocardiogram rules out the
presence of atrial thrombi. In these cases, heparin should be
administered before cardioversion.
5. Peri-cardioversion anticoagulation can be performed with heparin,
VKA drugs or dabigatran.
6. If VKA drugs are used as the OAC, ensure that the INR is between 2
and 3 before cardioversion.
7. These recommendations are valid regardless of the type of
cardioversion (spontaneous, pharmacological or electrical).
8. These recommendations are also valid for atrial flutter.
AF: atrial fibrillation; VKA: vitamin K antagonists, INR: international
normalized ratio.

Heart Rate (HR) Control

HR control is always a therapeutic goal in AF
to alleviate symptoms, prevent hemodynamic deterioration and prevent the emergence of tachycardiomyopathy and heart failure1,4,89,90. During the
last decade, a number of studies have compared
the benefits of this strategy against the exclusive
control of rhythm91-95. Globally, they found no differences regarding long-term mortality, quality of
life or effects on remodeling, controlling different
structural substrates (heart failure, hypertension)
or cost effectiveness 96. These results validate HR
control, which has become the strategy of choice,
especially in elderly patients with high comorbidity and low probability of maintaining long-term
sinus rhythm, and who tolerate HR control well,
or in those at risk of developing serious adverse
pro-arrhythmia with antiarrhythmic drugs
(AAD)9,96. However, HR control should not be considered as an alternative to exclusive control of
the rhythm; both are compatible and should be
performed together in the ED, as recommended
by the clinical practice guidelines9,16.

Objective heart rate

With HR control we seek to maintain a heart
rate that protects the patient from the consequences of tachycardia, such as the appearance of
symptoms or the deterioration of left ventricular
function, allow adequate stress tolerance (and
therefore an active life) and preserve the quality
308

Figure 2. Objective of heart rate (HR) control in atrial fibrillation.

of life without compromising cardiac output and

avoid the appearance of adverse effects (such as
bradycardia, syncope or even the need for a pacemaker)97. Classically, objective heart rate (60-80
bpm at rest and 90-115 bpm during moderate
physical activity) is defined on an empirical basis,
not evidence-based. Recently it has been demonstrated (and thus included in clinical practice
guidelines) that less strict initial control (< 110
bpm at rest) is just as beneficial to the patient in
terms of survival and quality of life, and easier to
achieve98. In cases where symptoms persist, then
we should seek tight control of HR (< 80 bpm at
rest and < 110 bpm after moderate exercise) and,
depending on the patient profile, we should consider how to ensure safe and effective implementation of the strategy with Holter-ECG monitoring
and/or exercise test (Figure 2)9.

Heart rate control guidelines

Ventricular rate control in the absence of ventricular pre-excitation syndrome can be achieved
with four drug groups that slow nodal conduction: digitalis, beta-blockers, non-dihydropyridine
calcium
antagonists
and
amiodarone.
Dronedarone, despite its HR reducing effect99, is
contraindicated for this purpose given the results
of the PALLAS study 100. Agents with rapid and
transient effect, such as ATP and adenosine, have
no therapeutic utility in AF 101. Propafenone also
slows AV conduction, but is not indicated for this
purpose.
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ATRIAL FIBRILLATION MANAGEMENT IN THE HOSPITAL EMERGENCY DEPARTMENT: 2012 UPDATE

Figure 3. Heart rate control in atrial fibrillation. HF: heart failure, iv: intravenous. * Digoxin ( diltiazem) in patients with
very restricted physical activity. Amiodarone iv ** in critically
ill patients after failure of previous steps.

At the same time, as a general recommendation, control of ventricular rate during AF is performed intravenously although the alternative oral
route can be useful but remembering that the onset of drug action is delayed.
For HR control in AF (Figure 3), one must first
determine whether the patient presents HF at that
time, since this limits the use of drugs with negative inotropic effect. In this group of patients the
HF should be treated first. It should not be forgotten that a high HR can often be a adaptive response in this clinical setting and requires no
more than HF treatment. If, despite this, it is considered necessary to reduce the ventricular response in this situation, intravenous digoxin
should be administered together with the remaining treatment for HF 102,103. If, in spite of these
measures, HR control is not adequate, intravenous
diltiazem or verapamil may be added for acute
control104, or amiodarone as a last resort, due to
the risk of conversion to sinus rhythm if the patient is not adequately anticoagulated.
Patients who are not in HF present few restrictions on pharmacological treatment, so that one
can choose between more effective or faster acting agents, such as beta-blockers and the nondihydropyridine calcium antagonists: diltiazem and
verapamil. These drugs have proven efficacy in
controlling the ventricular response, both at rest
and during exercise, and any of them can be the
first choice105,106.
The choice of drug is made fundamentally on
the basis of its possible side effects, considering
Emergencias 2012; 24: 300-324

the patients clinical profile and concomitant diseases101,107. Thus, in the ED, calcium channel blockers are preferred for diabetic patients with
bronchial hyper-reactivity or symptomatic peripheral vasculopathy, and beta-blockers in patients
with structural coronary disease (especially ischemic). Diltiazem offers advantages for intravenous administration, to adjust the dose for continuous infusion within a wide margin, and
besides it does not elevate plasma levels of digoxin and has less negative inotropic effect108, so it is
recommended as a first choice109. In cases where
monotherapy using any of these agents is insufficient for HR control, digoxin can be added.
Digoxin has a slow onset of action and limited efficacy, especially in the presence of adrenergic
stimuli given its predominantly vagotonic action102. Thus, its use as monotherapy for chronic
control of HR is only possible in certain patients
with very limited physical activity.
When considering any combination of drugs
to control the ventricular response, one should
consider the following points:
The addition of digoxin may require lowering its dose, especially in the elderly. In this case,
increasing the interval between doses beyond 24
hours is not acceptable; rather, one should reduce
the total daily dose of digoxin.
Diltiazem and beta-blockers do not significantly increase plasma levels of digoxin, which
can occur with verapamil.
The combination of digoxin and beta blockers usually has more bradycardic effect than the
combination of digoxin and diltiazem.
Calcium channel blockers should not be used
together with beta blockers.
The usual dose of drugs used to control the
ventricular response and major adverse effects are
shown in Tables 6 and 7.

Rhythm control in the acute phase (I):

restoration of sinus rhythm
Sinus rhythm restoration and maintenance is
an option for selected patients. First, HR control
and embolic prophylaxis should be given to all
patients, then rhythm control should be tackled
on the basis of 3-level decision making (Figure 4):

1. Safety of the attempt

This refers to the risk of post-cardioversion embolism. As a general rule, and in the absence a
universal, safe and effective treatment for AF, the
309

A. Martn Martnez et al.

Table 6. Dosage of the drugs most commonly used to control ventricular response
Drug

Loading dose

Diltiazem
Verapamil
Esmolol
Metoprolol
Propranolol
Amiodarone
Digoxin

0.25 mg/kg in 2 min

0.75-0.15 mg/kg in 2 min
0.5 mg/kg in 1 min
2.5-5 mg/kg in 2 min to a maximum of 3 doses
0.15 mg/kg
5-7 mg/kg en 30 min. Then, 1,200 mg/day (continuous infusion) or 400 mg/8 h (oral)
0.50 mg initially, then 0.25/6 h to maximum 1.5 mg

Table 7. Most important adverse effects of the drugs

recommended for control of ventricular response
Drug

Adverse effects

Digoxin

AV block, bradycardia, digitalis intoxication

(gastrointestinal, ocular, neurological, proarrhythmia).
Beta blockers
Hypotension, bronchospasm, bradycardia,
AV block, heart failure.
Calcium antagonists Hypotension, AV block, heart failure,
(diltiazem and
interaction with digoxin
verapamil)
(verapamil).
Amiodarone
Pulmonary toxicity, hepatotoxicity,
photosensitivity, corneal deposits, skin
discoloration, hypo/hyperthyroidism,
polyneuropathy, optic neuropathy, interaction
with acenocoumarol, bradycardia, torsades de
pointes (rare).

safety of any strategy must always prevail over effectiveness. Therefore, the first consideration is to
ensure that AF duration is less than 48 hours, and
that the patient has been properly anticoagulated
during 3 weeks before or has undergone transesophageal echocardiography to rule out the
presence of thrombi in the left atrium9,51.
If not, safety first is the rule and the ED physician must refer the patient to the cardiology unit
for evaluation of scheduled elective cardioversion
3 weeks after anticoagulation9.

2. Does sinus rhythm persist in the ED?

If the attempt is considered safe, the following
level of decision-making is based on the question
Does sinus rhythm persist in the ED?. It is well
known that AF tends to self-perpetuate through
rapidly occurring electricalal and anatomical remodeling after the onset of the arrhythmia 29-32,
which explains why cardioversion (both pharmacological and electricalal) obtains better results
the sooner it is performed48-50. In addition, rapid
cardioversion offers clinical benefits such as earlier
relief from symptoms and earlier discharge, highly
relevant in acute clinical scenarios 110. Moreover,
newly diagnosed AF has a less benign prognosis
than is normally considered since it is associated
with a higher mortality than paroxysmal or per310

Onset of effect

Maintenance dose

2-7 mins
3-5 mins
5 mins
5 mins
5 mins

5-15 mg/h

0,05-0,2 mg/kg/min

200 mg/day
0,125-0,25 mg/day

2 hrs

manent AF90, and patients with AF of less than 48

hours duration consult the ED for acute symptoms
in 96% of cases18,22, which favors a proactive attitude to treatment in this area. Therefore, the
restoration of sinus rhythm seems reasonable in
new-onset AF, and is especially important in the
ED, as this is where such patients are first attended at the onset of symptoms16,22.
As mentioned, the major studies comparing
long-term results between heart rate control versus rhythm control strategies found no significant
differences, especially in populations of elderly patients and patients with serious structural heart
disease91-96. However, persistent AF is clearly not
beneficial at all: indeed, the most powerful predictors of increased survival in the large studies cited
are the existence of sinus rhythm and anticoagulant treatment111,112. These studies show that maintaining sinus rhythm positively influences prognosis, but the drugs available at that time were less
effective and had many adverse effects. These
facts explain the apparent non-advantages of the
rhythm control strategy111. Thus the principle of
safety prevailing over effectiveness in handling AF
seems justified. Currently there is new information
on the safety and efficacy of AAD, and also on
catheter ablation techniques that have fewer adverse effects than AAD113-115.
The classical recommendations on antiarrhythmic therapy in AF have been described as lax by
some authors, since they are applied when evolution time is prolonged (and therefore atrial remodeling also) and the existence of this atrial remodeling contributes to explain the poor results
obtained with long-term rhythm rate control116.
These authors recommend aggressive early treatment (in the first or early episodes detected), not
only with AAD but also treatment of factors that
determine the arrhythmia (very prevalent in the
population attending the ED, such as hypertension, structural heart disease, obstructive apnea,
etc.), to try to prevent the progression of atrial remodeling (and the transformation to permanent
AF) and improve treatment outcomes to maintain
long-term sinus rhythm116,117.
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ATRIAL FIBRILLATION MANAGEMENT IN THE HOSPITAL EMERGENCY DEPARTMENT: 2012 UPDATE

Hemodynamic stability

Yes
No
HF control and thromboembolism prophylaxis
Synchronized electrical cardioversion
Low molecular weight heparin
AF duration < 48 hrs, or
anticoagulation > 3 weeks, or TE-ECO ()
Admission
Yes

No

Objective sinus rhythm?

Yes

No rhythm control
No

SIGNIFICANT HEART
DISEASE?
No
Class IC drugs
(Flecainide/propaferona) iv
vernakalant iv or electrical CV

Reversion to sinus rhythm?

Yes

Discharge

*Correct control (HR, symptoms) discharge. Consider

programmed electrical CV. Outpatient control.
*Poor control or persistent symptoms - Admission

Yes

No

CHF III-V?
No

Yes

Vernakalant/
electrical CV
(*)

Electrical CV within 48h of episode onset

Figure 4. Decision factors for the restoration of sinus rhythm. HR: heart rate, TE-ECO: Transesophageal echocardiography; CV: cardioversion; CHF: congestive heart failure. *Amiodarone iv may be an alternative in cases of electrical CV rejection or contraindication
for vernakalant.

Therefore, taking into account the benefits of

rapid clinical cardioversion (and greater chance of
success), the positive influence of not losing sinus
rhythm for prognosis, the improved profile of
AADs and the ablation techniques currently available, it is considered that rhythm rate control
plays an important role in the management of AF
for a growing number of patients, especially those
with episodes of recent onset, such as those that
typically visit the ED16,19,22. The decision to control
rhythm rate should be taken per individual, based
on the possibilities of obtaining and especially
maintaining long-term sinus rhythm in each patient (Table 8)16,116-122. It is important to remember
that in episodes of paroxysmal AF with a self-limiting tendency, the purpose of rhythm control is to
shorten the duration of the crisis, promote symptom control and achieve earlier ED discharge.
Emergencias 2012; 24: 300-324

3. Structural heart disease

This is the ultimate deciding factor when
restoring sinus rhythm in the ED, since it influences the likelihood of sinus rhythm maintenance
and constitutes a limiting factor for the use of
AAD 16,118,121,122. In the absence of an echocardiogram, which is common in the ED, it can be
safely estimated that there is no significant heart
disease for use of AAD if all the following parameters are normal: anamnesis, physical examination, ECG (other than evidence of AF) and chest
x-ray123.
In the absence of significant heart disease, one
can use more potent and effective class I-C drugs
for acute cardioversion, preferably administered
intravenously (acting in 30-90 minutes)16,124, since
they are highly effective (88-90%) and well toler311

A. Martn Martnez et al.

Table 8. Factors to consider before deciding to attempt

restoration of sinus rhythm in patients with atrial fibrillation
1. Conditioning factors in favor of attempting sinus rhythm
restoration.
First episode of atrial fibrillation.
History of paroxysmal atrial fibrillation.
Atrial fibrillation secondary to a transitory or treatable disease
(hyperthyroidism, post-surgery, drugs, substance abuse, fever,
etc.).
Atrial fibrillation producing severe/limiting symptoms (angina,
heart failure, syncope, poor subjective tolerance).
Selection of the patient.
2. Factors against attempting sinus rhythm restoration.
High likelihood of early or late recurrence:
Duration of arrhythmia >2 years.
History of multiple electrical cardioversions or failure of
antiarrhythmic drugs available for maintaining sinus rhythm
(in patients ineligible for catheter ablation).
Early relapse of arrhythmia (< 1 month) after cardioversion.
Mitral valve disease.
Severely dilated left atrium (> 55 mm).
Poor tolerance or high risk of pro-arrythmia with available drugs
for maintaining sinus rhythm.
Rejection by the patient.

ated (with persistent AF, electrical cardioversion is

recommended before 48 hours) 16,22,118,119,124-126. In
cardiac patients (especially those with ischemic
heart disease or heart failure), the use of these
class I-C AAD is not safe due to their depressive
effect on contractility and increased risk of pro-arrhythmia, and are therefore not recommended9,119,119,122,124. On the other hand, amiodarone is
considered safe for patients with structural heart
disease9,16,127,128 but is less effective at restoring sinus rhythm in AF, and has certain long-term adverse effects130-133. The recent appearance of vernakalant, with greater efficacy than amiodarone,
fast onset of action (median conversion time at
10-12 minutes) and safe for use in patients with
structural heart disease (except aortic stenosis or
NYHA grade III-IV heart failure), is an alternative in
most patients with recent-onset AF, especially
those with heart disese134. Amiodarone can therefore be used in patients with structural heart disease where vernakalant is contraindicated and/or
electrical cardioversion is rejected; it is important

to remember that intravenous administration requires accurate ECG monitoring, as applies to all
AAD. We would also emphasize that if an AAD
fails to restore sinus rhythm, as a general rule another AAD should not be administered since it
greatly increases the risk of adverse effects, especially pro-arrhythmic effects9,16,135. Table 9 outlines
the dosage and adverse effects of AAD used to restore sinus rhythm.
So, if an AAD fails or is not indicated, synchronized electrical cardioversion is recommended
(biphasic with maximum power), which also constitutes an excellent first alternative for rhythm
control in the ED, especially if there is structural
heart disease or WolffParkinsonWhite syndrome,
since the technique is effective and safe for sinus
rhythm restoration16,22,136-138.
Finally, it is important to remember that arrhythmia management strategies should be integrated, and not exclusive: administer thromboprophylaxis if there are risk factors, HR control if
there is ventricular response, rhythm control if the
patient meets the criteria, and aggressive treatment of factors associated with the development
of arrhythmia (structural heart disease, hypertension, etc.).

Rhythm Control (II): Maintenance of sinus

rhythm
General considerations
Approximately 50% of patients in whom AF reverts to sinus rhythm during the first year of pharmacological treatment show AF recurrence, usually during the first month139. This figure may be as
high as 80% in patients not receiving an AAD.
This means that the treatment of AF aimed at
maintaining sinus rhythm is often unsatisfactory,
with repercussions for the quality of life10,116.
We now know that antiarrhythmic treatment
aimed at maintaining sinus rhythm has a limited
impact on prognosis96. Therefore, the main reason

Table 9. Recommended dosage and adverse effects of the drugs most commonly used for the restoration of sinus rhythm
Drug

Initial dose

Maintenance dose

Flecainide

200-300 mg (oral)
1,5-3 mg/kg iv in 20 min
450-600 mg (oral)
1,5-2 mg/kg iv in 20 min
5-7 mg/kg iv in 30 min
Then, 1200 mg/day (continuous infusion) or 400 mg/8 h (oral)
3 mg/kg iv in 10 min

100-150 mg/12 h

Propafenone
Amiodarone

150-300 mg/8 h
200 mg/day

Adverse effects

Decreased BP, 1:1 flutter

Decreased BP, 1:1 flutter

Decreased BP, Elevated QT,

Tdp, Hypotension, GI,
Sneezing, dysgeusia, paraesthesia,
Decreased BP (in CHF-III-IV)

2nd dosis: 2 mg/kg iv

in 10 min (15 min
after 1st dosis)
Min: minutes. BP: blood pressure. TdP: torsade de pointes. GI: gastrointestinal. CHF: congestive heart failure. iv: intravenous.
Vernakalant

312

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ATRIAL FIBRILLATION MANAGEMENT IN THE HOSPITAL EMERGENCY DEPARTMENT: 2012 UPDATE

Table 10. Potential causes of atrial fibrillation

Heart
Hypertension.
Heart failure.
Ischemic heart disease with prior myocardial infarction.
Ventricular systolic or diastolic dysfunction.
Cardiomyopathy.
Valvulopathy.
Congenital heart disease.
Pericardium disease of the.
Post-surgery (major) especially cardiac surgery.
Breast disease.
Ventricular stimulation.
Supraventricular tachycardia (Wolff-Parkinson-White syndrome, atrial
flutter, atrial or intranodal tachycardia).
Genetic and/or family disorders.
Non-cardiac causes
Obesity.
Obstructive sleep apnea syndrome.
Pulmonary disease, embolism, pneumonia, COPD, pulmonary
hypertension.
Excessive alcohol intake, acute or chronic.
Hyperthyroidism.
Aerobic exercise of medium-high intensity.
COPD: chronic obstructive pulmonary disease.

for establishing antiarrhythmic treatment is to

control the symptoms associated with AF. Therefore, in general, antiarrhythmics in asymptomatic
patients or those with only slight symptoms do
not appear to be justified, nor in patients that become asymptomatic after adequate control of HR.
The ideal candidate for antiarrhythmic treatment is one with overt symptoms in frequent
episodes of AF. The initial strategy (to control HR
and rhythm) after an episode of AF treated in the
ED diverges from the ultimate goal. For example,
in a particular case the initial objective may be HR
control but persistence of symptoms may mean a
subsequent decision to aim at rhythm control using antiarrhythmics. If these measures fail, one
must then decide between returning to HR control or rhythm control using catheter ablation.
In any strategy to restore or maintain sinus
rhythm, the first step should be optimal treatment
of all the precipitating or predisposing factors of
AF (Table 10). Whenever the appearance of AF
concurs with a transient or reversible factor, for
example surgery or pericarditis, our priority
should be rhythm control, including at least one
attempt at cardioversion in cases of persistent AF,
even if the patient has few symptoms, because
once the precipitating factors have been dealt
with, the probability of maintaining rhythm without using AAD is high.

1. Guiding principles for antiarrhythmic

treatment
The main purpose of antiarrhythmic treatEmergencias 2012; 24: 300-324

ment is symptom control and improved quality of

life. This does not necessarily imply the elimination of all AF episodes.
The ideal goal of completely eliminating AF
is not always achieved and therefore recurrence
should not be considered as failure provided the
antiarrhythmics result in episodes that are less frequent and/or better tolerated than before.
The efficacy of antiarrhythmic drugs at maintaining sinus rhythm is modest141.
Drug induced pro-arrhythmia and/or extracardiac adverse effects are frequent events142.
Safety must take precedence over efficacy in
guiding the choice of AAD.
The use of an antiarrhythmic should be considered before electrical cardioversion in patients
with post-cardioversion recurrence in the absence
of antiarrhythmic drugs.
The following AAD (Figure 5) are recommended for AF rhythm control after cardioversion,
and the choice of one or the other depends on
the presence and type of underlying heart disease: amiodarone, dronedarone, flecainide,
propafenone, sotalol9.
In patients without significant structural
heart disease, initial antiarrhythmic treatment
should be one of the following drugs:
dronedarone, flecainide, propafenone or sotalol.
When an antiarrhythmic is not effective at reducing AF recurrence to a clinically acceptable
level, consider using another antiarrhythmic but
always based on the avoidance of associations.
The new antiarrhythmic drug for sinus
rhythm maintenance incorporated in these guidelines is dronedarone, already marketed in Spain,
which has been developed to avoid the adverse
effects of amiodarone. Although tolerance is better because of the absence of iodinated compounds and dronedarone has a positive impact on
patient survival, it is less effective than amiodarone in the prevention of relapse and is more
costly.

2. Strategies to minimize adverse effects

a) pill in the pocket. When symptomatic
crises of paroxysmal AF occur only sporadically,
the risk of taking an AAD every day cannot be
justified. In these cases it may be recommended
that the patient take a single loading dose of flecainide propafenone only when they experience
a crisis of palpitations with the idea of shortening their duration. This strategy is safe provided
tolerance has first been checked in the ED, to
rule out adverse effects including IC-induced
313

A. Martn Martnez et al.

TREATMENT OF ASSOCIATED CONDITIONS

Evaluate beta-blocker treatment and prevention of remodeling
THROMBOPROPHYLAXIS

SIGNIFICANT HEART DISEASE?

NO
(Or hypertension with mild-moderate LVH)

YES
1st: Cardiopathy treatment

HT
(LVH > 1.4 mm)
Flecainide
Propafenone
Dronedarone
Sotalol

Dronedarone

Ischemic
cardiopathy

Heart failure
Systolic dysfunction VI

Dronedarone
Sotalol

Consider amiodarone
Non-pharmacologic therapy (RF ablation)
Figura 5. Rhythm control in atrial fibrillation (II): Post-cardioversion maintenance of sinus rhythm. HT:
hypertension. LVH, left ventricular hypertrophy. LV, left ventricle. RF: radio frequency.

flutter143.
b) Low-dose amiodarone. Due to its prolonged
half life, it is possible in some cases to achieve adequate rhythm control using less than 1g weekly
oral amiodarone. This minimizes the risk of systemic adverse effects144.

3. Choice of drug
All AADs can become pro-arrhythmogenic, especially when certain factors concur (Table 11)135.
This, together with the above, means that drug
safety should be the fundamental characteristic
for deciding on what drug to use, with effectiveness being a secondary consideration.

3.1. Concept of pro-arrhythmia

The concept of pro-arrhythmia refers to the
appearance or aggravation of preexisting arrhythmia as a result of treatment with a drug at doses
or plasma concentrations that are non-toxic135. It
includes sustained ventricular arrhythmia, conversion of a non-sustained to sustained arrhythmia,
acceleration of tachycardia to bradycardia or a
conduction disturbance, such as sinus node dysfunction, atrioventricular block or significant QRS
314

widening. The clinical impact of these new arrhythmias is variable and ranges from absence of
symptoms to heart arrest, and occasionally the
new arrhythmia may be more serious than that
we are attempting to suppress144.
All drugs that act on cardiac ion channels can
induce pro-arrhythmia, although its intended use
is different. Among AADs, the safest in this regard
is amiodarone, although not without its risks145.
To prevent pro-arrhythmia, the choice of drug
is crucial, taking into consideration general and
Table 11. Risk factors for the development of pro-arrhythmia
during pharmacological treatment of atrial fibrillation
Electrolyte disturbances: hypokalemia and hypomagnesemia.
Renal failure.
Presence of structural heart disease: ischemic heart disease, heart
failure or hypertension with moderate-severe ventricular
hypertrophy (> 1.4 mm).
Presence of bundle branch block.
A history of ventricular tachycardia or fibrillation.
Presence of long QT before or after treatment.
Bradycardia or tachycardia.
Short PR as an expression of accelerated nodal conduction.
Drug Interactions: macrolides, antihistamines or other antiarrhythmics.
Treatment with diuretics.
Prior pro-arrhythmia.
Female sex (QT physiologically longer).

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ATRIAL FIBRILLATION MANAGEMENT IN THE HOSPITAL EMERGENCY DEPARTMENT: 2012 UPDATE

Table 12. Specific contraindications for anti-arrhythmics*

Clinical situation

Contraindicated drugs

Branch block or wide

QRS complex
Propafenone, flecainide
Postinfarction scar
Propafenone, flecainide
Prolonged QT interval
Sotalol
Heart failure
Propafenone, flecainide, dronedarone
Symptomatic bradycardia
All
Hypo or hyperthyroidism
Amiodarone
Renal failure
Sotalol
*Identifies drugs with worse safety profile in this context, without
implying that the alternatives are risk-free.

specific pro-arrhythmia risk factors and avoiding

antiarrhythmic poly-therapy and combinations
with non-antiarrhythmic drugs which act on ion
channels (Table 12). An exception to this recommendation is adding beta-blockers or calcium antagonists for HR control, since they do not potentiate proarrhythmic effects, although they may
contribute to the development of bradycardia and
conduction blocks. Periodic ECG should be performed and one should suspend the drug or reduce the dose in cases of QRS prolongation
> 25% (flecainide, propafenone) or when the QT
interval reaches 500 ms (sotalol, amiodarone and
dronedarone)146,147.

4. Treatment Modalities
There are several treatment modalities for postcardioversion maintenance of sinus rhythm: nonpharmacological therapy (catheter ablation), the
use of antiarrhythmic drugs and finally treatment
to prevent remodeling (upstream therapy). Again,
as always in the management of AF, none should
be regarded as exclusive, since they can be used
at the same time in a patient or during disease
evolution. Finally, it is absolutely essential to consider long-term prophylaxis against arterial thromboembolism in all these patients, regardless of
what decision is made on sinus rhythm maintenance. The following section analyzes each of the
treatment modalities available for the maintenance of sinus rhythm.

4.1. Catheter ablation treatment

4.1.1. Ablation of the atrioventricular node.
This is a very effective method to control the ventricular frequency and symptoms with neutral effect on mortality148. It is an irreversible palliative
intervention, requiring pacemaker implantation. It
may be considered when drugs fail or are not indicated and severe symptoms persist.
The type of pacemaker implanted (mono, bi or
Emergencias 2012; 24: 300-324

Table 13. Indications for catheter ablation of the arrhythmic

substrate
Paroxysmal atrial fibrillation with symptoms uncontrolled by antiarrhythmic drugs.
Persistent atrial fibrillation with no significant symptoms and
controlled with anti-arrhythmic drugs in the absence of significant
comorbidities, advanced age or severe heart disease.
Ablation of cavo-tricuspid isthmus in cases of common atrial flutter
(1C) in relation to the use of antiarrhythmic drugs used to treat atrial
fibrillation.
Ablation of the accessory pathway in patients with pre-excited atrial
fibrillation.

tri-chamber) is chosen according to patient characteristics, type of AF, underlying heart disease,
ventricular function and presence or absence of
heart failure149. The indications for this procedure
are 9 : a) symptomatic patient with persistent
AF/permanent uncontrolled ventricular response
despite maximum tolerated drug doses, and b)
non-response to cardiac resynchronization therapy
with poorly controlled ventricular response despite optimal pharmacological treatment, which
prevents adequate ventricular pacing.
4.1.2. Ablation of arrhythmic substrate. In recent years different ablation techniques have been
developed with the aim of "curing" AF. All involve
electrical isolation of the pulmonary vein combined or not with other lesions at other atrial locations, using radio frequency energy and/or
cryoablation. Several randomized trials in selected
populations have shown that ablation is more effective than AAD at maintaining sinus rhythm in
the medium term, but 12-25% of patients require
a second operation and recurrence affects more
than 30% of patients after the first year150,151. Most
studies involve patients with frequent symptomatic episodes of paroxysmal AF in the absence
or with only minimal heart disease, without excessive left atrial dilation and in whom one or several
antiarrhythmics have failed.
Regarding indications for this procedure:
(Table 13) curative ablation should only be considered in patients who remain symptomatic despite optimal medical treatment including drugs
for HR and rhythm control9. Since it is an interventional technique, not without its complications
and very dependent on center experience, it can
only be considered as an alternative to antiarrhythmics in exceptional highly selected cases:
young patients with paroxysmal AF and without
heart disease. Curative ablation is indicated for
paroxysmal AF when the alternative is chronic use
of amiodarone with increased risk of long term
adverse effects. Ablation is not regarded as an alternative to anticoagulant treatment in patients
315

A. Martn Martnez et al.

Table 14. Dosage and adverse effects of antiarrhythmic drugs most commonly used for the maintenance of sinus rhythm
Drug

Dosage

Flecainide

100-200 mg/12 h oral

300 mg single oral dose, (pill in the pocket)
Propafenone 150-300 mg/8 h oral
600 mg single oral dose, (pill in the pocket)
Sotalol
80-160 mg/12 h oral

Adverse effects
VT (QRS increase >25% from baseline), HF, conversion to1:1 atrial flutter.
VT (QRS increase> 25% from baseline), HF, conversion to atrial flutter 1:1 GI toxicity.
HF, Tdp (QT interval > 500 ms), bradycardia, atrioventricular block,
bronchospasm (bronchial hyper-reactivity due to beta-blocker action).
Pulmonary, hepatic and GI toxicity, photosensitivity, corneal deposits,
blue-grey skin color, hypo/hyperthyroidism, polyneuropathy, optic neuropathy,
interaction with acenocoumarol, bradycardia, torsades de pointes (rare).
Interaction with digoxin and OAC (reduce dose).

Amiodarone 200 mg/24 h oral

(loading dose 600 mg/24 h during
4 weeks, 400 mg/24 h during 4 weeks
and 200 mg/24 h maintenance)
Consider reduced doses ( 5 pills/week)
to minimize adverse effects
Dronedarone 400 mg/12 h oral
Hepatotoxicity (monitor liver enzymes), HF, interaction with digoxin (reduce dose).
VT: ventricular tachycardia; Tdp: polymorphic ventricular tachycardia in torsion points (torsade de pointes), HF: heart failure; GI: gastrointestinal; OAC:
oral anticoagulation.

with moderate to high risk of embolism. When AF

is persistent, and especially if long-term or associated with heart disease, catheter ablation is less
effective and frequently requires several procedures152. In this context it should only be considered when severe symptoms persist and medication has failed.
Contraindications of catheter ablation are: a)
formal contraindication in the presence of left atrial thrombus, b) when the probability of success is
very low due to the presence of comorbidities
(chronic obstructive pulmonary disease-COPD-,
morbid obesity, uncontrolled hyperthyroidism),
severe or advanced heart disease (valvular, cardiomyopathy post-infarction ventricular dysfunction, etc..) or left atrial dilatation.

4.2. Antiarrhythmic drugs (Table 14)

4.2.1. Beta blockers. Most patients with a first
episode of AF are given beta blockers initially to
control HR and rhythm. In patients without significant heart disease, beta blockers are the first option to prevent recurrence of AF when the arrhythmia is clearly related to physical or
psychological stress (adrenergic AF)9. Beta-blockers
are only moderately effective at preventing the recurrence of AF, but they are a reasonable option,
isolated or combined with other antiarrhythmics,
with their high safety profile and positive effect
on morbidity and mortality in patients with heart
disease. Their effectiveness is greater in AF secondary to thyrotoxicosis and triggered by exercise. They are usually associated with other antiarrhythmics, except sotalol, which is also a beta,
not so much to enhance rhythm control as to reduce the ventricular frequency in case of recurrence or onset of atrial flutter.
4.2.2. Class IC drugs (flecainide and
316

propafenone). Due to their safety profile, these

are considered the drugs of choice, along with
dronedarone and sotalol, in patients without
structural heart disease, although they are less effective than amiodarone 124,125. They should be
avoided whenever there is significant structural
heart disease because of their contractility depressant effect and ventricular pro-arrhythmic effect in
this clinical context. Furthermore, these drugs can
transform AF episodes into episodes of atrial flutter, known as type IC, but also found as a result
of class IA and III drugs. The pharmacological effect of conduction velocity depression means, furthermore, that this flutter is slower than common
type atrial flutter, presenting HR around 200 bpm.
Often, particularly if nodal conduction has accelerated intrinsically or because of concomitant
treatment with sympathomimetics, the specific AV
conduction system can conduct 1:1 at these frequencies, thus paradoxically causing an increase
in heart rate involving poor hemodynamic tolerance. At the same time, elevated HR and His-Pukinje system sensitivity to these drugs frequently
lead to bundle branch block that mimicks ventricular tachycardia. Currently, to prevent 1:1 conduction, these drugs are associated with beta
blockers or calcium antagonists with AV node action. Likewise, the treatment of choice for IC flutter is catheter ablation, allowing continued use of
the same AAD after ablation. Type IC drugs have
a high safety profile in patients without structural
heart disease, are acceptably tolerated124 and can
be used outside the hospital as "pill in the pocket"
treatment. ECG monitoring is recommended at
initiation of treatment with flecainide or
propafenone. The effects of both drugs are similar; although propafenone is perhaps somewhat
less effective and less well tolerated126, it better
controls ventricular response due to its slight
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ATRIAL FIBRILLATION MANAGEMENT IN THE HOSPITAL EMERGENCY DEPARTMENT: 2012 UPDATE

betablocker effect. Both agents may be used as

pill-in-the-pocket treatment. Any increase in
length of the QRS complex greater than 25%
compared to baseline is a sign of potential risk of
pro-arrhythmia and obliges dose reduction or
withdrawal.
4.2.3. Sotalol. This is a beta-blocker with
potassium channel blocker effect. Like all the others, it is less effective than amiodarone, except in
patients with ischemic heart disease; the Sotalol
Amiodarone Atrial Fibrillation Efficacy Trail (SAFET) showed similar efficacy153. Its main drawback is
its possible pro-arrhythmic effect with occurrence
of torsade de pointes due to QT interval prolongation154. To prevent this, careful monitoring with
serial ECGs is required. Suspend treatment or reduce the dose if QT interval exceeds 500 ms155.
Also, avoid the use of other drugs that may prolong the QT interval. Except in the presence of
risk factors for pro-arrhythmia (Table 14), it is safe
to start treatment on an outpatient basis. In any
case, sotalol is contraindicated when severity or
association of risk factors makes for a high probability of pro-arrhythmia.
4.2.4. Amiodarone. Although this the most effective antiarrhythmic, it also has the highest organic toxicity, so (in the absence of significant
heart disease) it is reserved for patients with frequent, symptomatic recurrence of AF when other
treatment options (sotalol, propafenone, flecainide or dronedarone) have been ineffective or
not well tolerated141. In patients without heart disease and resistant to other antiarrhythmics, in anticipation of long years of chronic treatment with
amiodarone, one should consider the alternative:
non-pharmacologic treatment with catheter ablation.
Due to its toxicity profile, it is generally used
when other drugs have failed or are contraindicated 139. It can be administered safely in patients
with structural heart disease, including heart failure156, and is the drug of choice in patients with
ventricular dysfunction or severe NYHA functional
class III or IV heart failure or NYHA functional class
II with decompensation in the previous month157.
Pro-arrhythmic phenomena with amiodarone are
rare, so they can be initiated on an outpatient basis, but close monitoring is recommended during
loading dose, especially in patients with severe
heart disease155.
4.2.5. Dronedarone. This is a multichannel
sodium, potassium and calcium blocker with noncompetitive antiadrenergic activity. Unlike amiodarone, it has no iodine radicals, which gives it a
less toxic profile. Efficacy in maintaining sinus
Emergencias 2012; 24: 300-324

rhythm is less than that of amiodarone according

to the DIONYSOS study results (evaluation of effectiveness and safety of dronedarone versus
amiodarone) 159,160 . The safety profile of
dronedarone is advantageous in patients without
structural heart disease and in patients with stable
heart disease, and has shown little potential for
pro-arrhythmia in clinical trials.
Dronedarone was not initially indicated for the
treatment of AF in patients with severe functional
class NYHA III or IV heart failure or recently unstable NYHA functional class II (decompensation during the previous month), according to the results
of the ANDROMEDA study (Dronedarone assessment in patients with symptomatic NYHA functional class II-IV heart failure)161,162. After the PALLAS study results, dronedarone became
contraindicated in patients with any kind of heart
failure and permanent AF 99,100. In the ATHENA
study (evaluating dronedarone versus placebo in
patients with non-permanent AF and cardiovascular risk factors), a significant reduction was observed in the target primary combined events of
cardiovascular-induced hospitalization and overall
mortality, which had never been previously
demonstrated for any drug in this category.
Therefore, in patients with non-permanent AF and
cardiovascular risk factors, dronedarone should be
considered in order to reduce mortality and hospitalization for cardiovascular reasons113,162. It can
be safely used in patients with ischemic heart disease and hypertension, and in patients without
heart disease when other AADs fail. Finally,
dronedarone has not been compared with other
AADs, apart from amiodarone, nor with HR control strategy in asymptomatic patients. Therefore,
there is insufficient evidence to recommend its
use in these cases. It Is safe to start with outpatient treatment. It reduces HR and AV conduction
in cases of AF, so doses of beta-blockers or calcium blockers must be adjusted when associated
with them163.

4.3. Control of factors that condition AF

(upstream therapy)
Treatment of the causal disease may prevent or
delay myocardial remodeling associated to hypertension, heart failure or inflammation (eg. after
cardiac surgery) and prevent the development of
a new episode of AF ("primary prevention") or,
once established, reduce the rate of recurrence or
progression to permanent AF ("secondary prevention")164. Treatment with angiotensin converting
enzyme (ACE) inhibitors, angiotensin receptor II
antagonists (ARBs) and statins for the prevention
317

A. Martn Martnez et al.

of primary AF in patients without cardiovascular

disease or risk factors is not recommended. In
contrast, it is advisable to control all contributing
or precipitating risk factors (hypertension, diabetes, obstructive sleep apnea syndrome or OSAS,
hyperthyroidism, etc.) before any attempt is made
to restore or maintain sinus rhythm.
4.3.1. ACE inhibitors and ARBs. These agents
should be considered for primary prevention of
new-onset AF in patients with heart failure and reduced ejection fraction, and in patients with hypertension, and especially those with left ventricular hypertrophy165-171. Although their usefulness is
debatable for the prevention of paroxysmal AF, recurrences or persistent AF after cardioversion in
the absence of significant structural heart disease,
they may be used alone or associated with antiarrhythmics provided they are indicated for other
reasons (hypertension)172-174.
4.3.2. Aldosterone antagonists (spironolactone
and eplerenone). Their role has not been studied
specifically in humans, so we will have to wait
and see whether preliminary results of several ongoing studies are confirmed: they suggest a decrease in the incidence of recurrent AF after electrical cardioversion in patients with hypertension
and mild left ventricular dysfunction.
4.3.3. Statins. The preventive effect of statins
on AF is mediated by improvement in lipid metabolism and prevention of atherosclerosis, and of
anti-inflammatory and antioxidant actions 175,176.
Statins may be moderately effective in the prevention of recent AF onset in patients with underlying
heart disease, especially cardiac insufficiency, and
also after isolated coronary bypass surgery or
combined with valve surgery, so they should be
considered especially when there is an indication
for their use177-180. Clinical studies and randomized
controlled trials have not shown the benefit of
statin therapy after cardioversion181. In summary,
there is insufficient evidence to strongly recommend the use of statins for primary and secondary prevention of AF, except in the case of postoperative AF. Nor is there consensus on the
intensity and duration of treatment and the type
of statin182-185.
4.3.4. Polyunsaturated fatty acids (PUFA).
Omega-3 or n-3 PUFA are universal constituents
of biological membranes, where they exert a stabilizing effect. In experimental studies they have
been shown to reduce electrical atrial remodeling
and attenuate structural changes of the atria. Currently there is no firm evidence to be able to
make any recommendation for their use in the
primary or secondary prevention of AF, although
318

favorable results have been reported in sinus

rhythm maintenance after direct cardioversion
and in the prevention of recurrence of AF in patients treated with amiodarone and ACEI associated with omega-3 or n-3 PUFA. However, larger
scale and longer term studies are needed to confirm these findings. Neither the dose nor the duration of treatment for this antiarrhythmic effect
have been established186,187.
4.3.5. Corticosteroids. Evidence for their use in
the secondary prevention of AF is also extremely
low. Only two studies have provided data showing a reduction in recurrent AF in the group receiving corticosteroid therapy and antiarrhythmics
after catheter ablation 188,189. Thus, well-designed
prospective studies are necessary, with specific
doses and treatment duration times, in order to
establish the usefulness of steroids as adjuvant
therapy for the secondary prevention of AF190.

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Emergencias 2012; 24: 300-324

ATRIAL FIBRILLATION MANAGEMENT IN THE HOSPITAL EMERGENCY DEPARTMENT: 2012 UPDATE

Manejo de los pacientes con fibrilacin auricular en los servicios de urgencias hospitalarios
(actualizacin 2012)
Martn Martnez A, Fernndez Lozano I, Coll-Vinent Puig B, Tercedor Snchez L, Del Arco Galn C,
Arribas Ynsaurriaga F, Suero Mndez C, Mont Girbau L
La fibrilacin auricular (FA) es la arritmia sostenida de mayor prevalencia en los servicios de urgencias (SHU), que presentan una frecuentacin elevada y creciente en Espaa. La FA es una enfermedad grave, que incrementa la mortalidad y asocia una relevante morbilidad e impacto en la calidad de vida de los pacientes y en el funcionamiento de los
servicios sanitarios. La diversidad de aspectos clnicos a considerar y el elevado nmero de opciones teraputicas posibles justifican la implementacin de estrategias de actuacin coordinadas entre los diversos profesionales implicados,
con el fin de incrementar la adecuacin del tratamiento y optimizar el uso de recursos. Este documento recoge las recomendaciones para el manejo de la FA, basadas en la evidencia disponible, y adaptadas a las especiales circunstancias
de los SUH. En l se analizan con detalle las estrategias de tromboprofilaxis, control de frecuencia y control del ritmo,
y los aspectos logsticos y diagnsticos relacionados. [Emergencias 2012;24:300-324]
Palabras clave: Fibrilacin auricular. Servicio de urgencias. Frmacos antiarritmias. Cardioversin. Control cardiaco.
Anticoagulacin. Tromboprofilaxis.

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