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SELECTED PAPER – ATRIAL FIBRILLATION
Cardioversion in atrial fibrillation. Focus on recent-onset atrialfibrillation
Andrea Tampieri • Anna Maria Rusconi •
Tiziano Lenzi
� SIMI 2012
Abstract Atrial fibrillation is the most common sustained
arrhythmia encountered in clinical practice. Its prevalence
is rising due to an increasing elderly population and the
improvement in management of life-threatening diseases
such as myocardial infarction and heart failure. Over the
past few years effective non-pharmacological treatments,
new antiarrhythmics drugs, and anticoagulants have been
introduced. Regardless of rate-control or rhythm control
strategy, adequate stroke prevention still remains a cor-
nerstone in the treatment of this arrhythmia. This review
aims to illustrate the main practical issues in the manage-
ment of atrial fibrillation, focusing on patients with recent-
onset and hemodynamically stable atrial fibrillation.
Keywords Atrial fibrillation � Recent-onset �Cardioversion
Epidemiology
Atrial fibrillation (AF) is the most common arrhythmia in
clinical practice, accounting for one-third of hospitaliza-
tions for cardiac arrhythmia, and being responsible for
3–6 % of all medical causes of admission in the Emer-
gency Department (ED) [1, 2]. The estimated prevalence of
AF in the general population was found to be approxi-
mately 1 % and ranges from 0.1 % in individuals under
55 years, increasing with age up to 9 % in the ultra-octo-
genarians [1]. Data appearing in recent publications seem
to confirm predictions of a gradual increase in the number
of patients with AF, reporting a prevalence in the general
population of the United States (US) of up to 2.5 % [3, 4].
The overall prevalence has been reported from European
studies to be about 6 % and increases with age rising from
1 % in people aged 55–59 years to 18 % in the elderly over
85 years [5, 6].
The incidence rate of AF was found to be about 10/1000
person/year in the Rotterdam study and ranges from 1/1000
person/year in the age group 55–59 years to 21/1000 per-
son/year in those aged 80–84 years. Both prevalence and
incidence were higher in men than in women. The life-time
risk of developing AF at the age 55 was approximately
23 %, similar to the epidemiological estimate in North
America [7]. With regard to mortality and morbidity, AF is
recognized as an independent risk factor for death, with a
relative risk of 1.5 for men and 1.9 for women [8]. In the
AFFIRM study the 5-year mortality of patients older than
65 years with AF reaches values of about 4.5 % per year.
The mortality rate is obviously higher in patients with
heart failure and is related to the underlying heart disease.
Although the presence of AF in subjects without significant
disease appears to result, in itself, in an increased risk of
death stroke is still the major determinant of mortality: in
more than 50 % of cases the cause of death in fibrillating
patients was ischemic stroke [9].
AF has gained importance as a social and financial burden
on public health in recent years. Community surveys have
documented that during the past 20 years the incidence of AF
has increased by 13 % and have projected that people suf-
fering from this arrhythmia in the US will reach 16 million in
2050 [4]. Consistently ED visit rates increased by 88 %,
while the rate of in-hospital admissions remained stable at
approximately 64 %, resulting in a subsequent increase in
hospitalization of 60 % [10, 11]. This development poses a
significant challenge to health systems in the coming decades
A. Tampieri (&) � A. M. Rusconi � T. Lenzi
Emergency Department, Ospedale Civile Santa Maria della
Scaletta, via Montericco 4, 40026 Imola (Bo), Italy
e-mail: [email protected]
123
Intern Emerg Med (2012) 7 (Suppl 3):S241–S250
DOI 10.1007/s11739-012-0863-0
in relation to the high baseline annual costs per patient and
average costs of hospitalization [12].
Electrophysiology and hemodynamic effects
Atrial fibrillation is a cardiac arrhythmia characterized
by chaotic electrical activity in the atria, causing a loss of
atrial mechanical contraction and an irregular ventricular
response. Among the theories proposed to explain the elec-
trogenesis of AF, two are the most reliable: in the ‘‘multiple
wavelet hypothesis’’ small and contemporary reentrant cir-
cuits give rise to many depolarization wavefronts that per-
petuate the arrhythmia [13]. The second theory assumes the
existence of atrial foci with increased automaticity which
may trigger AF after a brief burst of ectopic activity. They are
usually located near the pulmonary veins, and transcatheter
ablation of these foci may terminate the arrhythmia [14].
However, these theories are not mutually exclusive.
Atrial fibrosis is the most evident histopathological
change in AF. It replaces the conduction tissue, causing the
substrate to fragmentary and irregular activation of the atria
from multiple foci of reentry. AF itself results in structural
and functional changes in the atrium, leading to atrial
remodeling of both anatomical, electrical and mechanical
aspects that maintain the arrhythmia [15]. The electrophys-
iological effects of these changes induce the development of
sustained AF and reduce the likelihood of conversion to sinus
rhythm, whereby it is assumed that ‘‘AF begets AF’’.
The adverse hemodynamic consequences determined by
the FA are represented by a loss of synchronized atrial
contraction, irregular ventricular response, elevated heart
rate, and impairment of coronary flow. The loss of atrial
contribution to ventricular filling may result in a significant
reduction in cardiac output, especially when hampered by
the presence of mitral stenosis, hypertension, hypertrophic,
or restrictive cardiomyopathy. The irregularity of the ven-
tricular rate may also contribute to hemodynamic impair-
ment. Furthermore, a persistently elevated heart rate during
AF may produce a tachycardia-mediated cardiomyopathy,
increasing both atrial and ventricular size [16]. Myocardial
ischemia may be induced by higher oxygen requirements and
by reduction of coronary blood flow caused by tachycardia.
The absence of a mechanical contraction causes blood stasis
and promotes the formation of thrombi in the left atrium,
which represents the most frequent source of cardio-embolic
ischemic stroke in patients with AF [17].
Diagnostic criteria and classification
Diagnosis of AF requires an electrocardiographic (ECG)
finding of the arrhythmia. Therefore, in patients with
symptoms suggestive of AF but in sinus rhythm (SR) at the
time of consultation, 24-h ECG Holter monitoring may be
necessary to confirm the diagnosis. Electrocardiographic
diagnostic criteria of AF are summarized in Table 1.
Usually, AF presents itself with the appearance of nar-
row QRS complex arrhythmia and thus can be confused
with supra-ventricular tachycardia. The main differential
diagnoses are atrial flutter and atrial tachycardia. Espe-
cially if the ventricular rate is high, it may not be easy to
distinguish these arrhythmia, but usually atrial tachycardia
and atrial flutter have a frequency of\300 bpm, and vagal
maneuvers may help to bring out any atrial activity.
Sometimes AF may present itself with broad QRS com-
plexes in the case of frequency-dependent or pre-existing
bundle branch block, as well as in the appearance of links
and the Ashman’s phenomenon. A wide complex tachy-
arrhythmia also occurs when atrial impulses are conducted
through an accessory pathway (Wolf–Parkinson–White
syndrome): the ventricular rate can be very high (over
300 bpm) and the risk of degenerating into ventricular
fibrillation is consistent (Fig. 1). Rarely, AF can be asso-
ciated with atrio-ventricular-block presenting a low ven-
tricular rate, so it may be difficult to identify the
irregularity of RR intervals and differentiate it from a
junctional escape rhythm or idioventricular rhythm.
The classification of atrial fibrillation is normally made
according to the onset and duration of the arrhythmia,
because these factors have several important effects on
subsequent management. Different temporal patterns of AF
[18] are described in Table 1.
Table 1 Diagnostic criteria and classification
Electrocardiographic diagnostic criteria
Absolutely irregular RR interval
Chaotic atrial activity with the absence of distinct P waves
If atrial electrical activity is visible in some ECG leads (usually
V1), the duration of the atrial cycle is irregular and\200 ms (the
frequency of atrial activity is [300 beats per min)
Classification
New onset or first diagnosed: the first episode diagnosed
regardless of the duration of onset
Paroxysmal: an episode that spontaneously regresses within
7 days of onset (usually within 48 h)
Persistent: an episode that lasts more than 7 days or requires
pharmacologic or electrical cardioversion
Long-standing persistent: cardioversion was ineffective and the
arrhythmia has lasted for over a year
Permanent: the presence of AF is accepted by the patient and
physician, the therapeutic strategy adopted is no longer rhythm
control, but, if necessary, rate control
Recent-onset: usually refers to the onset and duration of
symptomatic AF of \48 h, irrespective of whether it is newly
detected, recurrent paroxysmal or persistent episodes
S242 Intern Emerg Med (2012) 7 (Suppl 3):S241–S250
123
Regarding the prevalence of different types of AF, it
was found to be paroxysmal in 36 % of patients, persistent
in 28 %, and permanent in the remaining 36 % of cases. It
has also been documented that new-onset AF occurs in
18 % of patients and 15 % of subjects with paroxysmal AF
develop a persistent (46 % of cases) or permanent form
(54 %) within 1 year [19, 20]. However, the recurrence of
AF episodes is frequent over the years.
Clinical manifestation and symptoms
Atrial fibrillation may occur with different clinical mani-
festations, appearing asymptomatic, presenting with simple
palpitations, or as a real medical emergency. About 70 % of
patients report symptoms; the most commonly reported are
palpitations (54 %), dyspnea (44 %), asthenia and fatigue
(14 %), chest pain (10 %), dizziness, and syncope (10 %).
The intensity of the presenting symptoms is generally
related to the degree of associated tachycardia.
The European Heart Rhythm Association (EHRA) has
recently proposed a classification of disability and
impairment of daily activities caused by AF, distinguishing
four classes of disabilities related to the strength of
symptoms [21].
The hemodynamic instability is the most important
element to recognize in a first assessment, as it is a
potential life-threatening condition. The main signs and
symptoms of hemodynamic instability are the following:
• Low cardiac output with systolic blood pressure
\90 mmHg.
• Pulmonary edema.
• Angina with or without ischemic ECG findings.
• Ventricular rate [150 bpm or \40 bpm.
When AF is asymptomatic and was discovered acci-
dentally in a routine ECG or because of related compli-
cations (ischemic stroke or other thromboembolic event), it
is defined ‘‘silent’’ AF. The rate of diagnosis of silent AF
varies depending on the method of recording ECG used
and ranges from 15 % if it has been found by ECG stan-
dard to over 50 % when detected by Holter ECG or
through a monitoring device [22].
Asymptomatic AF in addition to being a common con-
dition, though unrecognized, is frequently associated with
cardio-embolic events. The Canadian Registry of Atrial
Fibrillation and different studies [23] have reported that
‘‘silent’’ AF amounts to about 21 % of first diagnoses of
AF. Moreover, even among patients with note symptomatic
paroxysmal AF, asymptomatic recurrences are more fre-
quent than those with symptoms. The first manifestation of
a ‘‘silent’’ AF is often devastating: in the Framingham
Study among patients with AF associated stroke, the
arrhythmia was a ‘‘new diagnosis’’ in 24 % of cases.
Fig. 1 AF in patient with pre-excitation syndrome (Wolf–Parkin-
son–White). Irregular wide complex tachycardia with left bundle
branch block aspect is recorded during conduction through the
accessory pathway. Delta wave is visible in a narrow complex (blackarrow) during conduction through AV node when the heart rate slows
down
Intern Emerg Med (2012) 7 (Suppl 3):S241–S250 S243
123
Causes and associated conditions
The onset of AF may be favored by a broad spectrum of
clinical conditions, including various heart diseases, sys-
temic diseases, and individual factors. Among cardiovas-
cular risk factors related to arrhythmia, the most involved
are hypertension, which is associated with the FA in
50–65 % of cases, diabetes (present in about 20 % of
cases), obesity, and smoking. The age is an independent risk
factor, even in the absence of underlying heart disease
[1, 4]. The most common cardiac causes of AF are repre-
sented by hypertensive cardiomyopathy (involved in
approximately 60 % of cases of AF) and valvular disease.
In particular, AF occurs in 50 % of patients with mitral
valve disease. In these cases it is currently defined as
‘‘valvular AF’’. In addition, heart failure and ischemic heart
disease are often responsible for the development of AF and
influence the prognosis. Sick sinus syndrome and pre-
excitation syndrome are also concerned in exacerbating AF.
In the post-operative setting AF is frequent especially after
cardiothoracic surgery, affecting about 27 % of patients and
leading to an increased risk of complications and prolonged
hospital stay [24]. Among the underlying non-cardiac cau-
ses of AF, the most commonly encountered are pneumonia,
acute infections, electrolyte depletion, pulmonary embo-
lism, lung cancer, pleural effusion, COPD exacerbations,
anemia, and thyrotoxicosis. These co-existing medical
conditions are usually reversible and should be recognized
since treatment of the trigger often resolves the arrhythmia,
while a ‘‘purely’’ antiarrhythmic treatment might be scar-
cely effective, as well as potentially damaging (i.e., in the
course of hypokalemia). The intake of drugs, dietary and
lifestyle factors (i.e., alcohol, caffeine, cocaine, ampheta-
mines, beta-stimulants) may trigger AF usually temporarily
and reversibly. Alterations of autonomic tone may also
contribute to the onset of arrhythmia [25]. The term ‘‘lone
AF’’ refers to AF in patients younger than 60 years without
underlying heart disease or comorbidities. It is defined by a
normal clinical history and examination, normal ECG, chest
X-rays, laboratory tests, and echo cardiogram. It is therefore
a diagnosis of exclusion in the absence of notes or other
identifiable causes of AF. Lone AF accounts for between 5
and 10 % of all forms of AF and mostly affects young male
subjects [26]. Although the prognosis appears to be more
favorable in terms of lower incidence of stroke, heart fail-
ure, and mortality, some studies have questioned the benign
features of lone AF.
Initial assessment and investigations
Clinical assessment of patients with AF requires a careful
history and physical examination focused on determining
the need for appropriate timing and method of restoring
sinus rhythm, rather than rate control, as well as to ensure
adequate prophylaxis of cardio embolic stroke. In partic-
ular, the physician should recognize the hemodynamic
impact of arrhythmia, the date of onset and duration, any
potentially reversible causes, cardioembolic risk stratifica-
tion, and underlying heart diseases. Indeed, these are the
main issues that influence the treatment strategy of AF, as
shown in Fig. 2. Determining the time of onset of an AF
episode is essential to decide an attempt to restore normal
sinus rhythm or rate control. Patients with AF \48 h
duration may be cardioverted on low-molecular-weight
heparin (LMWH) without risk of stroke, whereas a duration
[48 h contraindicates an immediate cardioversion.
Hemodynamicallystable condition
andabsence of WPW Sdr.
Absence of underlying reversibile causes
AF onset < 48 hrs
If AF is still persisting after 6-12 hrs consider enhanced-DCC
UnderlyingHeart disease
Lone AF oronly Hypertension
Patient characteristics:- low risk of recurrence
- without previous stroke- not tolerated syptoms
Immediate DCC
Treat reversibile cause
Rate-controlor
elective-DCC
Rate-control
Consider PCV
amiodaronei.v
propafenoneor flecainide
i.v
yes
no
yes
yes
yes
no
no
no
Fig. 2 Proposed approach to the management of patients with
recent-onset AF. Stratify thromboembolic risk and initiate appropriate
prophylaxis in all patients. When elective DCC is considered in
patients with AF [48 h or after a failed attempt at cardioversion,
OAC treatment is required for at least 3 weeks before and 4 weeks
after cardioversion
S244 Intern Emerg Med (2012) 7 (Suppl 3):S241–S250
123
In this case because the high risk of thromboembolism,
the patient should start anticoagulation with warfarin, and,
if necessary, a therapy for rate control. After 3 weeks of
proper anticoagulation (INR persistently between 2 and 3)
the patient may undergoes elective cardioversion, contin-
uing to take the anticoagulant for another 4 weeks.
Previous episodes, cardiac and noncardiac diseases,
cardiovascular risk factors, and a history of taking drugs or
alcohol should be investigated to identify possible precip-
itating factors and associated conditions. It is important to
note antiarrhythmic drug intake, which is relevant to avoid
proarrhythmic effects in case of attempted pharmacological
cardioversion.
Vital signs, blood pressure, heart rate, oxygen saturation,
heart murmurs, and lung sounds should be evaluated to
determine the hemodynamic impact. Symptoms such as
chest pain and syncope should be carefully considered
because they may be related to myocardial ischemia,
pulmonary embolism, and pre-excitation syndrome. An
ECG baseline is necessary for diagnosis. Laboratory mea-
surements of electrolytes, blood count, liver and kidney
function, blood glucose levels, and thyroid function are
recommended to identify possible treatable causes. A trans-
thoracic echocardiogram is also recommended for detecting
valvular disease, atrial and ventricular size, hypertrophy,
EF, and other underlying heart disease. Chest radiography is
justified if suggested by clinical findings.
Specialist referral may be required for additional tests, as
in the case of a trans-esophageal echocardiogram to exclude
intra-cardiac thrombus in selected patients in whom
cardioversion of AF [48 h with previous abbreviated
anticoagulation is considered (TEE-guided approach). An
exercise test and/or coronary angiography is indicated to
evaluate myocardial ischemia when suspected. Holter-ECG
or loop-recorder could be considered to define the type and
temporal pattern of arrhythmic events if unknown [18].
Prevention of thromboembolism
Anti-thrombotic therapy for prevention of stroke is a cor-
nerstone in the management of AF, independent of other
adopted strategies, AF being responsible for 15–18 % of all
cases of stroke and associated with a worse prognosis [27,
28]. The annual rate of ischemic stroke in patients with
non-valvular AF increases from 5 to 7 % compared with
the population without AF. It also increases with ageing up
to 23 % in patients over 80 years. Furthermore, the inci-
dence of systemic embolism consistently increases in cases
of AF associated with rheumatic heart disease, valvular
disease, and mitral stenosis. The risk of stroke varies sig-
nificantly among different classes of patients with AF.
Prevention of thromboembolism is the primary goal in the
management of patients with AF, irrespective of clinical
presentation and the strategy adopted. The current guide-
lines recommend different regimes of thromboembolic
prophylaxis in relation to the individual base-line stroke
risk [18, 29, 30].
Rhythm control and rate control strategies
The goal of rhythm control is to restore and maintain sinus
rhythm using pharmacological or electrical cardioversion,
whereas the purpose of rate control strategy is to slow the
heart rate and prevent embolism. In early 2000, a heated
debate about the best management strategy for AF devel-
oped [31]. Several randomized studies have compared
rhythm and rate control, but no significant difference was
found between the two strategies in terms of mortality,
major cardiovascular events, or stroke [32], even in
patients with associated congestive heart failure [33].
Thromboembolic events occurred most frequently among
patients managed with rhythm control who discontinued
oral anticoagulant, probably due to asymptomatic recur-
rences of AF despite antiarrhythmic drugs assumption [34].
Currently, the debate seems to be outdated consistently
with the strong recommendation of long-term antithrom-
botic prophylaxis, irrespective of strategy considered.
Moreover, AFFIRM and AF-CHF trials have compared the
two strategies in poorly symptomatic patients with persis-
tent or permanent AF, and do not define the optimal
management of symptomatic patients with recent-onset AF
presenting to the ED. Definitely an individualized approach
should be regarded in the selection of rhythm or rate
control strategy, taking into account the conditions asso-
ciated with a high likelihood of relapse.
Rate control strategy is generally recommended in the
following conditions:
• Persistent AF of long duration.
• Elderly, well-tolerated symptoms or silent AF.
• High rate of recurrence and refractory to antiarrhythmic
treatment.
• Left atrium size C5.5 cm.
• Concomitant underlying heart disease, congestive heart
failure.
• Mitral stenosis or severe valvular heart disease.
However, the rhythm-control strategy is recommended
in the first episode of AF, in young patients, in cases of
symptomatic episodes of recurrent AF lasting \48 h, or
when AF causes hemodynamic deterioration. In addition,
the patient’s wishes should be considered in the choice of
treatment strategy. After successful cardioversion, long-
term treatment with oral anti-arrhythmic agents for pro-
phylaxis of AF relapses should be required.
Intern Emerg Med (2012) 7 (Suppl 3):S241–S250 S245
123
Pharmacological cardioversion
Pharmacological cardioversion (PCV) is generally rec-
ommended as first-line treatment in patients with AF of
recent onset (\48 h), hemodynamically stable and poorly
tolerated symptoms. Several antiarrhythmic drugs have
demonstrated proven efficacy in converting AF to SR and
have been proposed with different classes of recommen-
dations in the guidelines. They are usually administered
intravenously for more rapid action than oral administra-
tion. Among these flecainide, propafenone, and ibutilide
have proven to be more effective than amiodarone and
procainamide [35, 36]. Physicians should be aware of
possible pro-arrhythmic effects of these drugs in patients
with underlying heart disease. In the absence of under-
lying heart disease, class IC antiarrhythmic agents (pro-
pafenone or flecainide) should be the drug of choice,
while amiodarone (class III agent) should be the drug of
choice in the presence of coronary artery disease or left
ventricular dysfunction. The characteristics of antiar-
rhythmic agents are summarized in Table 2. When
administered in patients with recent-onset AF, propafen-
one and flecainide were proved to be the most effective
drugs in restoring the SR, reaching conversion rates up to
88 and 91 %, respectively, during the first 8 h. Amioda-
rone is not superior to placebo after a single loading dose
administration and in the first 6 h; however, after con-
tinuous infusion during an interval of 24 h a conversion
rate of up to 95 % has been documented, indicating a
slow onset of action. Ibutilide, a class III antiarrhythmic
agent, has been effective in converting each recent onset
and long-standing permanent AF and flutter. It can be
used in the treatment of AF recurrence during Ic antiar-
rhythmic drug assumption. Conversion rate is up to
75–80 % in recent onset arrhythmias, and it is higher for
atrial flutter than for AF. However, administration of i-
butilide is associated with a 4–5 % risk of torsades de
pointes occurring most frequently in the first 6 h. Its use is
contraindicated in patients with long QT interval and in
patients with structural heart disease. Pre-treatment with
intravenous magnesium reduces the risk of ventricular
arrhythmias. Compared with flecainide for immediate
(within 90 min) cardioversion of recent onset AF showed
the same safety and efficacy [22, 37, 38]. Procainamide is
less effective than other antiarrhythmic agents and its use
is regarded with a level IIb of recommendation in con-
verting AF. However, a recent study reported an efficacy
of 60 % and an excellent safety profile in patients taking
other antiarrhythmic drugs [39]. Vernakalant is a new
atrial-selective drug, which blocks multiple sodium and
potassium channels regulating the atrial depolarization
and conduction. It has recently been approved in Europe
for investigational use only, while in the US it is not yet
available and is under consideration for approval by the
FDA. In the AVRO trial, a multicenter randomized blin-
ded phase III clinical study, vernakalant was compared to
amiodarone for conversion of new-onset AF. Structural
heart disease was an exclusion criterion in this study.
Vernakalant was more effective than amiodarone in
restoring SR within 90 min (conversion rate 52 vs. 5 %),
confirming its safety and efficacy observed in previous
trials and nothing more, because amiodarone is not
superior to the placebo in this span of time [40]. A ‘‘pill-
in-the pocket’’ approach may be considered in selected
patients without structural heart disease and previously
treated in hospital settings with no evidence of side
effects. It consists in taking an oral loading dose of class
IC drugs (flecainide or propafenone) as outpatients,
resulting in a marked reduction in emergency room visits
and hospital admission [41].
Table 2 Antiarrhythmic drugs with proven efficacy for pharmacological cardioversion
Drug Class i.v-dose Oral-dose First-line choice Warnings/caution
Procainamide IA 15–17 mg/kg over 60 min Absence of structural heart
disease
Hypotension; torsades de pointes; suspend
if prolonged QT/QRS
Propafenone IC 2 mg/kg over 10–20 min 450–600 mg Lone AF, absence of
structural heart disease
Suspend if QRS widens [25 %; risk of
flutter 1:1; hypotension; proarrhythmic
on diseased heart
Flecainide IC 2 mg/kg over 10–20 min 300–400 mg As above As above
Amiodarone III 5–7 mg/kg over 30 min
followed by 15 mg/kg
infusion in 24 h
Structural heart disease Suspend with QT lengthening; torsades de
pointes; hypotension; avoid in
hyperthyroidism.
Ibutilide III 0.01 mg/kg over 10 min
(max 1 mg)
Second-line PCV attempt;
no structural hearth
disease; atrial flutter
Torsades de pointes; prolonged QT; avoid
in LV disfunction, hypokalemia–
hypomagnesemia
Vernakalant III 3 mg/kg over 10 min
followed by 2 mg/kg over
10 min after 15 min rest
Approved only for
investigational use
Structural heart disease; prolonged QT;
hypotension; Torsades de pointes;
requires adequate hydration
S246 Intern Emerg Med (2012) 7 (Suppl 3):S241–S250
123
Synchronized electrical cardioversion
Synchronized direct-current cardioversion (DCC) is
highly effective in terminating AF, whereas adverse
events related to an adequate procedure are uncommon.
DCC is contraindicated in cases of digitalis toxicity,
atrioventricular block, or severe electrolyte abnormalities
by the risk of inducing ventricular arrhythmias or asystole
[42, 43].
Shock is painful and therefore conscious patients require
a sedation, usually using propofol 1 mg/kg boluses until
they are unresponsive or midazolam 0.1 mg/kg. The elec-
tric current must be delivered in synchronization with the R
wave through properly placed pads. The recommended
starting dose of energy delivered with a biphasic wave-
forms device is 120–200 J to be increased if the initial
shock fails [43]. Nevertheless, the delivery of higher
biphasic energy at the first shock as well as a front-rear pad
placement has shown to increase the likelihood of initial
success and limit the cumulative dose of energy delivered
with multiple attempts [44].
Hemodynamically unstable patients with potentially
life-threatening conditions should undergo immediate
DCC. In delayed cardioversion, patients can undergo
elective DCC either after adequate anticoagulation or TEE-
guided approach. In this condition DCC has a well-recog-
nized superiority over PCV since antiarrhythmic drugs lose
efficacy when AF lasts more than 48 h.
DCC has recently been compared with PCV in symp-
tomatic and hemodynamically stable patients with recent-
onset AF, both in an ED and short observation unit settings.
DCC with or without pharmacological pre-treatment has
proved safe, more effective than PCV (conversion rates up
to over 90 %), and associated with shorter length of stay in
ED, and lower rates of hospitalization [45–53]. Moreover,
pre-treatment with antiarrhythmic agents has demonstrated
a role in facilitating DCC and in promoting the mainte-
nance of SR [54]. Both class IC and class III drugs as well
procainamide have documented a DCC-enhancing property
resulting in a higher conversion rate and a reduction of
energy delivered. Therefore, in patients with stable recent-
onset AF, physicians have the option of proceeding directly
to DCC or starting a PCV and then executing an enhanced
DCC if AF persists.
Preservation of sinus rhythm after cardioversion
PCV and ECV are usually effective to restore sinus rhythm.
However, the recurrence of AF is frequent: if untreated,
only 20–30 % of patients will remain in sinus rhythm
1 year after cardioversion [55, 56]. The risk of recurrence
is dependent on age, duration of atrial fibrillation, exis-
tence, and severity of structural damage to the heart [57,
58]. Amiodarone seems to be the most effective antiar-
rhythmic drug in preventing recurrences of atrial fibrilla-
tion if compared with class I and other class III drugs,
produces no significant proarrhythmia, and causes no
increase in all-cause mortality [59, 60]. The most suitable
antiarrhythmic drug for the prophylaxis of AF recurrences
(amiodarone vs. class IC) will be chosen according to
patient characteristics (structural heart disease versus
healthy heart) and according to individual tolerability, and
side effects. Class IA and sotalol should be used most
carefully because a trend to increased mortality exists [59].
Dronedarone is a new antiarrhythmic drug similar to ami-
odarone recently studied in patients with AF. It seems to
reduce recurrence of AF [61–63], but is less effective than
amiodarone, with respect to which it showed only a modest
reduction in side effects [64]. Also two recent studies of
patients at high cardiovascular risk or with heart failure
were stopped early because of increased adverse events
bringing out serious doubts about its safety [65–67].
Rate control
A sustained and uncontrolled tachycardia may lead over
time to a hemodynamic deterioration due to left ventricular
dysfunction. Achieving an adequate rate control is essential
in patients with AF; however, the parameters to define an
optimal heart rate remain controversial. Recent updates of
AF guidelines highlighted that in relation to mortality,
hospitalization, symptoms, and major complications, a strict
rate control (resting heart rate \80 bpm, and \110 bpm
during moderate exercise) is not beneficial compared with a
lenient rate control (resting heart rate\110 bpm) in patients
with persistent/permanent AF with stable ventricular func-
tion [68]. The drugs most commonly used to reduce the
heart rate are beta-blockers, calcium channel blockers, and
digoxin. The characteristics of drugs for heart rate control
are summarized in Table 3. These drugs slow atrioventric-
ular conduction, so are contraindicated in WPW syndrome
because they do not slow conduction through the accessory
pathway and thus may precipitate life-threatening ventric-
ular tachycardias. Beta-blocker agents are the first drugs of
choice in patients with concomitant coronary artery disease,
whereas calcium channel blockers are especially useful in
patients with COPD or asthma. Both should not be used in
patients with heart failure. Digoxin has a slower onset
of action, but it may be useful in patients with left ventric-
ular dysfunction, or as an additional agent to beta blockers
or calcium channel blockers to achieve a targeted
rate\110 bpm.
Intern Emerg Med (2012) 7 (Suppl 3):S241–S250 S247
123
Recent updates
Catheter ablation has proven to be useful and effective in
maintaining SR in selected patients with symptomatic par-
oxysmal AF without significant underlying heart disease and
who have failed prophylactic treatment with antiarrhythmic
agents. Currently it is recommended with a class IA level of
evidence [68], and long-term antithrombotic therapy is rec-
ommended according to base-line risk of patient, regardless
of apparent persistence of normal SR [30].
Proposed approach to management
Clearly hemodynamically unstable patients and those with
pre-excitation syndrome (WPW) at high risk of developing
ventricular arrhythmias should be treated urgently with
synchronized DCC, and heparin administration should not
delay time to shock (Fig. 2). Conversely, in patients with
symptomatic bradycardia due to AF with AV block,
administration of atropine and transcutaneous pacing
should be considered [43]. On the other hand, the latest
guidelines agreed in recommending a strategy of rate
control for patients with AF onset of more than 48 h or
unknown duration and those with a high likelihood of
relapse [18, 29]. Recognition and treatment of potentially
reversible conditions such as infections, anemia, impaired
electrolyte balance especially hypokalemia, pulmonary
embolism, or coronary artery disease may promote the
resolution of AF.
In hemodynamically stable patients with symptomatic
recent onset AF the physician has several treatment
options, from the ‘‘wait and see’’ approach to directly
executing DCC. We suggest an attempt to PCV to alleviate
symptoms and restore SR. If the pharmacological attempt
fails, enhanced-DCC can be performed as a second-line
treatment. A time of 6–12 h before executing DCC can be
considered reasonable for the onset of action of IC anti-
arrhythmic agents and the spontaneous resolution of
paroxysmal AF, without causing ED overcrowding. After
successful cardioversion patients should take OAC for the
first 4 weeks and then a long-term antithrombotic therapy
according to their base-line risk [30]. If the DCC attempt
also fails, the patient could be discharged home, and rate
control strategy, delayed DCC or catheter ablation may be
considered.
Conclusion
Stable recent onset AF, both first detected or recurrent
episodes, is one of the most commonly encountered
arrhythmia in the ED. Current guidelines do not clearly
define a univocal approach for the management in this
subgroup of patients. This leads to wide disparities in the
management of recent-onset AF in various ED. The het-
erogeneity of treatment provided depends mainly on the
resources available, hospital policies and protocols, and the
standard of training of emergency physicians [69]. Con-
siderable controversy arises from the opposition of con-
servative strategies such as rate control, a ‘‘wait and see’’
approach or even the direct admission to hospital, to
aggressive strategies which aim to cardiovert the eligible
patients to SR, either electrically and/or pharmacologically.
Conservative strategies as well as routine hospital care
generally result in a prolonged length of stay in the ED or
in a loss of available hospital beds, and certainly affect
overcrowding [70]. A routine DCC protocol-based
approach in the ED setting or outpatient management as the
‘‘pill in the pocket’’ approach has proven to be safe for
patients and effective in increasing the rate of discharge
and shortening the length of stay in ED, as well as in
reducing the number of ED visits. Considering the trend of
increasing hospital visits for AF, the implementation of
shared protocols including DCC in the ED for management
of selected patients with recent-onset AF should be pro-
moted in coming years to reduce hospitalization rates and
costs related to this arrhythmia.
Table 3 Drugs slowing AV node conduction recommended for rate-control
Drug Class i.v dose Oral dose First-line choice Warning/caution
Metoprolol Beta-blocker 2.5–5 mg up to 3 doses 25–100 mg twice
daily
CAD and
hyperthyroidism
Asthma and COPD
Diltiazem Calcium-channel
blocker
0.25 mg/kg 120–360 mg Asthma, COPD Hypotension; bradycardia
Verapamil As-above 0.075–0.15 mg/kg 120–360 mg As-above As-above
Digoxin 0.25 mg each 2 h up a total
dose 1.5 mg
Digoxinemia
based
Heart failure Ischemic heart disease; toxicity;
avoid DCC
Caution: All these drugs are contraindicated in cases of pre-excitation syndrome because they may trigger ventricular arrhythmias, promoting
conduction through accessory pathway
S248 Intern Emerg Med (2012) 7 (Suppl 3):S241–S250
123
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