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The Management of Atrial Fibrillation in the ICU
Paul E. Marik, MD, FCCM,
and Gary P. Zaloga, MD, FCCM
Marik PE, Zaloga GP. The management of atrial fibrillation in
the ICU. J Intensive Care Med 2000;15:181–190.
Atrial tachyarrhythmias are the most frequent arrhythmias
occurring in ICU patients, being particularly common in
patients with cardiovascular and respiratory failure. Unlike
ambulatory patients in whom atrial fibrillation/flutter (AF)
is likely to be short lived, in the critically ill these arrhythmias
are unlikely to resolve until the underlying disease process
has improved. Urgent cardioversion is indicated for hemodynamic instability. Treatment in hemodynamically stable patients includes correction of treatable precipitating factors,
control of the ventricular response rate, conversion to sinus
rhythm, and prophylaxis against thromboembolic events in
those patients who remain in AF. Diltiazem is the preferred
agent for rate control, while procainamide and amiodarone
are generally considered to be the antiarrhythmic agents of
choice.
From the Department of Internal Medicine, Washington Hospital
Center, Washington, DC.
Received Nov 29, 1999, and in revised form Jan 31, 2000. Accepted for publication Feb 4, 2000.
Address correspondence to Dr Marik, Department of Internal
Medicine, RM-2A-68, Washington Hospital Center, 110 Irving St.
NW, Washington, DC 20010–2975, or e-mail: [email protected].
Atrial tachyarrhythmias are the most common arrhythmias occurring in ICU patients, with a reported
prevalence of 28% [1]. Atrial fibrillation is the most
common atrial arrhythmia, followed by atrial flutter
and multifocal atrial tachycardia (MAT). Since the
etiology and management strategies of atrial fibrillation and atrial flutter overlap, for the purposes of
this discussion they will be considered as one entity
(AF). Patients who develop AF in the ICU have a
worse prognosis than those who remain in sinus
rhythm (SR); however, the attributable mortality of
AF is unclear [1].
Pathophysiology
Atrial fibrillation is a rhythm in which atrial activation is disorganized and the atria do not contract
effectively. It is probably caused by a variant of
reentry in which one or more activation wavefronts
travel in endlessly varying paths, giving rise to subsidiary wavelets [2–4]. Atrial enlargement helps sustain AF by accommodating more wavelets [5].
AF is particularly common in ICU patients with
cardiovascular disorders, respiratory failure, and
sepsis [1,6]. The etiology is largely multifactorial,
with hypoxia, electrolyte disturbances (hypokalemia, hypomagnesemia), myocardial ischemia,
anemia, increased sympathetic tone, ‘‘cardiotonic
drugs,’’ and atrial distention being implicated [1].
Pulmonary hypertension with right atrial distention
may be an important precipitant in patients with
respiratory failure and sepsis [6]. Underlying cardiovascular disease, diabetes, and advanced age increase the risk of developing atrial arrhythmias [1].
Drugs such as catecholamines and theophylline increase the risk of developing atrial tachyarrhythmias and increase the ventricular response, making
rate control more difficult [7–10]. Patients with sudden onset of AF and no obvious underlying cause
should be investigated for the possibility of pulmonary embolism. The natural history of untreated
AF in critically ill patients has not been studied.
However, it is unlikely that spontaneous conversion
will occur until the underlying disease process has
improved or resolved [6]. This contrasts with noncritically ill patients admitted with recent onset AF,
Copyright q 2000 Blackwell Science, Inc.
181
182 Journal of Intensive Care Medicine Vol 15 No 4 July/August 2000
in whom spontaneous conversion will occur in up
to 67% of patients [11]. The development of AF in
critically ill patients is frequently associated with
increased pulmonary capillary wedge pressure, decreased cardiac output, pulmonary hypertension,
and worsening respiratory failure. In addition, AF
increases morbidity and mortality in critically ill patients as a result of systemic emboli.
In critically ill patients, the development of AF
is often associated with significant hemodynamic
compromise [6]. The decrease in cardiac output that
accompanies AF may cause or exacerbate tissue
hypoxia. AF results in a decrease in cardiac output
as a consequence of reduced diastolic filling time
and loss of atrioventricular synchrony [12]. Loss of
atrioventricular synchrony compromises stroke volume and cardiac output to a variable degree depending upon ventricular compliance, venous
filling pressure, ventricular rate, and other hemodynamic factors. The importance of atrioventricular
synchrony is illustrated in the study of Donovan et
al. [13], who demonstrated an increase in the mean
cardiac output from 4.5 to 5.3 L/min when critically
ill patients were switched from ventricular demand
pacing to atrioventricular pacing.
studies of the treatment of AF in ICU patients. The
treatment algorithm outlined in this article is based
on the synthesis of data from the above cited studies
[12,14–16], as well as those randomized controlled
studies that have enrolled patients presenting to the
hospital with new onset AF [17–27]. AF is a common
complication in postoperative coronary artery bypass patients; this is a distinct clinical problem
which will not be reviewed in this article.
The components of the acute management of AF
include assessment of the need for urgent cardioversion, correction of treatable precipitating factors,
control of the ventricular response rate, conversion
to sinus rhythm, and prophylaxis against thromboembolic events in those patients who remain in AF.
Rate control and correction of treatable precipitating factors is essential in all patients. Conversion
to sinus rhythm may be important in patients who
remain in AF, as AF is usually associated with a
significant decrease in cardiac output which may
be poorly tolerated in critically ill patients. Furthermore, prompt termination of AF may obviate the
need for anticoagulation. In addition, prolonged
AF causes electrophysiologic alterations in cardiac
tissue that can perpetuate the arrhythmia, a process
known as electrophysiologic remodeling [28].
Management of AF
Urgent Cardioversion. Electrical cardioversion is
a time-honored, highly effective method for converting AF to sinus rhythm. It is probably underutilized in ICU patients. Urgent cardioversion is
indicated when the ventricular response is greater
than 130 beats/min in association with angina,
acute cardiac failure, hypotension [mean atrial pressure (MAP) < 70 mmHg or decrease in MAP > 15
mmHg], or indices of inadequate tissue perfusion
[28–30].
Patients should be well sedated and given an
analgesic prior to cardioversion. The combination
of midazolam (2–10 mg) and fentanyl (50–150 mg)
may be used in nonintubated patients. Ketamine (a
neuroleptic anesthetic agent with potent analgesic
properties) is an alternative in patients in whom
respiratory depression [e.g., chronic obstructive
pulmonary disease (COPD)] needs to be avoided.
It should be emphasized that in ICU patients AF is
a multiple disease process whose management may
differ depending on the underlying etiology (i.e.,
sepsis, pericarditis, acute myocardial infarction,
acute respiratory failure, pulmonary embolism,
etc.). However, on the basis that most episodes of
AF in critically ill patients are associated with some
degree of hemodynamic compromise, we believe
that all patients with this arrhythmia should be
treated.
Despite the high prevalence of AF in ICU patients, only two prospective studies [14,15], and two
retrospective studies [12,16] (a total of 91 patients)
have reported on the management of AF in critically
ill ICU patients (Table 1). Of note, there have been
no placebo-controlled, prospective randomized
Table 1. Trials of Acute AF in ICU Patients
Reference
Year
Number
of Patients
P/R*
14
15
16
12
1993
1995
1998
1996
24
21
38
8
P
P
R
R
*P 4 prospective; R 4 retrospective.
Drugs Studied
Procainamide versus amiodarone
Magnesium versus amiodarone
Amiodarone
Amiodarone
Conversion
Success Rate (%)
71 versus 70
78 versus 50
48
87
Marik and Zaloga: Atrial Fibrillation in the ICU
The combination of propofol and fentanyl is useful
for short-duration hypnosis and analgesia for cardioversion in intubated patients.
The aim of electrical therapy is to provide a current through the myocardium to change enough
myocardial cells to the same electrical state for a
sufficient time to break the reentrant circuits or
produce electrical homogeneity. This allows a stable rhythm to be reestablished from the sinus node.
Animal experiments have shown that the period of
homogeneity needs to be 4–12 msec. More organized arrhythmias such as AF require less energy to
break the circuit (5–10 J internal, 20–100 J external)
compared to disorganized rhythms (e.g., ventricular
fibrillation, 10–13 J internal, 200–300 J external).
The current delivered to the heart is determined by
both the energy chosen (J) and the transthoracic
impedance [31,32]. The use of bare paddles without
a couplant (gel/cream) results in very high transthoracic impedance [31,32]. Impedance may be
reduced by strong pressure on the paddles, anteroposterior positioning of the paddles, repetitive
shocks, and delivery of the shock during expiration
[31,32]. Various types of electrodes may be used for
cardioversion, including the traditional handheld
electrode paddles and self-adhesive monitor-defibrillator pads. The paddles/pads should be placed
in a position that will maximize current flow
through the myocardium. The most commonly employed placement is apex–anterior. The anterior
electrode should be placed on the right of the upper
sternum below the clavicle; the apex electrode
should be placed to the left of the nipple, with the
center of the electrode in the midaxillary line [33].
In women, placement of paddles on the breast
should be avoided, since in this position transthoracic impedance is high. Placement of the apex
electrode adjacent to or under the breast is preferable [31].
Synchronization of shocks is extremely important. Properly synchronized shocks rarely, if
ever, induce ventricular fibrillation; failure to synchronize shocks on the R wave may lead to inadvertent delivery of a shock in the vulnerable period
and is likely to produce ventricular fibrillation [33].
Because some defibrillators default to an unsynchronized mode after each shock, the operator
must remember to reenable the synchronizer before
each subsequent shock. Shocks to convert atrial
fibrillation should begin at energy levels of 100 J,
with the energy for subsequent shocks increased
in increments of 50–100 J. Atrial flutter is an easier
rhythm to convert and shocks should begin at 50
J [33].
For those patients who fail cardioversion, pace
termination of AF may be effective. Recently Oral
183
et al. [34] have demonstrated that pretreatment of
patients with ibutilide increased the efficacy and
decreased the mean energy required for successful
transthoracic cardioversion. The role of this approach in ICU patients remains to be determined.
In the ICU setting it is highly likely that AF will
recur soon after successful cardioversion, as the
precipitating conditions still exist. Consequently
antiarrhythmic drugs, such as procainamide or amiodarone, administered before or soon after the
cardioversion may be useful for prevention of recurrence. Due to the risk of torsades de pointe, all
antiarrhythmics should be avoided for at least 4–6
hours in patients who have received ibutilide.
Rate Control. Rate control can improve hemodynamics even if the patient remains in AF. Digoxin
is commonly used in the treatment of AF in ICU
patients. Yet in the critically ill ICU patient, digoxin
is probably the most ineffective drug in controlling
the ventricular response in AF. Digoxin decreases
ventricular response in AF by vagotonic mechanisms [35,36]. In critically ill patients, AF occurs in
the setting of high sympathetic tone and frequently
with the use of vasopressors and inotropic agents, a
situation in which digoxin is likely to be ineffective.
Digoxin has been demonstrated to have limited
value in the management of patients presenting to
hospital with acute AF and in AF after coronary
artery bypass graft surgery. Schreck et al. [37] compared the effects of intravenous diltiazem with digoxin for ventricular rate control in the emergent
treatment of acute atrial fibrillation and flutter. By
60 minutes, the mean ventricular response had decreased from 150 to 99 beats/min in the diltiazem
group and 144–129 beats/min in the digoxin group
(p 4 0.01, for differences between groups). Tisdale
et al. [38] demonstrated that ventricular rate control
occurs more rapidly with intravenous diltiazem
than digoxin in AF after coronary artery bypass graft
surgery. Other studies have similarly demonstrated
poor rate control in patients treated with digoxin
[27,39,40]. Furthermore, it is important to emphasize that digoxin does not increase the rate of conversion to sinus rhythm. The Digitalis in Acute Atrial
Fibrillation (DAAF) Trial Group randomized 239
patients (non-ICU) with new onset atrial fibrillation
to receive digoxin or placebo [27]. At 16 hours, 46%
of the placebo group and 51% of the digoxin group
had converted to sinus rhythm (not significant). As
digoxin provides poor rate control and has a very
narrow therapeutic index, we believe that this drug
should be avoided except in ICU patients with poor
left ventricular function [40].
Diltiazem appears to be an effective alternative
to digoxin for rate control. Ellenbogen et al. [41]
184 Journal of Intensive Care Medicine Vol 15 No 4 July/August 2000
reported that 79 of 84 patients (94%) with acute AF
responded to a bolus dose of 20 or 25 mg diltiazem
with a greater than 20% reduction in heart rate from
baseline, conversion to sinus rhythm, or a heart rate
less than 100 beats/min. Hypotension was the most
common side effect, occurring in 13% of patients.
In an additional report, these authors demonstrated
that a 10 to 15 mg/hr continuous infusion of intravenous diltiazem was effective in maintaining rate
control [42]. Additional studies have demonstrated
a response rate of 93 and 97% [43–45]. Coadministration of calcium is effective in limiting hypotension in diltiazem-treated patients.
Esmolol, an ultrashort-acting, nonselective bblocker has also been demonstrated to be effective
in controlling the ventricular response in AF [46–48].
Metoprolol (intravenously or orally) is an alternative agent. b-blockers are particularly effective in
patients with increased sympathetic tone. These
agents may cause hypotension, particularly in unstable ICU patients. Magnesium has been shown to
reduce the ventricular response in AF, with a greater
effect when combined with digoxin [49,50]. Magnesium may act by increasing the atrio-His interval
and atrioventricular nodal refractoriness [51,52].
Adenosine has virtually no role in the acute treatment of AF, given its very short half-life [33]. The
agents used for rate control are listed in Table 2.
Pharmacologic Cardioversion. A number of antiarrhythmic drugs including procainamide, amiodarone, flecainide, propafenone, sotalol, and
ibutilide have been studied in patients with acute
atrial fibrillation in a non-ICU setting [17–27]. These
trials are listed in Table 3 (inadequately powered,
uncontrolled studies after cardiac surgery were excluded from this analysis). The length of observation in many of these studies was short (i.e., 2.5
hours). Only two studies have prospectively investigated the management of AF in ICU patients (Table
1). Procainamide and amiodarone are generally
considered to be the antiarrhythmic agents of
choice in acutely ill ICU patients [12,14,16]. However, the efficacy of these agents in critically ill ICU
patients has never been tested in a randomized
controlled study. These agents might best be used
in patients with persistent atrial fibrillation in preparation for direct-current cardioversion. The choice
between amiodarone and procainamide is determined largely by the drugs side-effect profile and
cost, with amiodarone being recommended in patients with severe left ventricular dysfunction.
Clemo et al. [16] described 38 critically ill patients
with AF who were resistant to conventional heart
rate control measures and who were treated with
amiodarone. An infusion of amiodarone (over 1
hour) was associated with a significant decrease in
heart rate of 37 5 8 beats/min and a significant
increase in systolic blood pressure of 24 5 6
mmHg. In the 22 patients with indwelling pulmonary artery catheters, the cardiac index increased
over the first 2 hours from 2.4 5 0.3 L/min/m2 to
2.8 5 0.3 L/min/m2 (p < 0.05). In the first 24 hours
of the infusion 18 patients (48%) converted to sinus
rhythm. Kumar [12] studied the efficacy of intravenous amiodarone in eight patients with severely
compromised left ventricular function who developed AF in the ICU. Intravenous amiodarone was
effective in seven of the eight patients. Six of the
seven patients reverted to sinus rhythm within 30
minutes, with the cardiac index, pulmonary capillary wedge pressure and mean arterial pressure remaining stable during the infusion.
Oral and intravenous amiodarone increase atrioventricular nodal refractoriness and intranodal conduction [53–55]. These changes are thought to be
mediated by the drug’s calcium channel blocking
action and its noncompetitive antiadrenergic effect.
Intravenous amiodarone has a minimal effect on
the effective refractory periods of atrial, ventricular,
and His-Purkinje tissues, and it does not prolong
the H-V interval, the QRS interval, or the QTc duration. One hypothesis for this difference is that many
of amiodarone’s electrophysiologic effects require
long-term administration, which allows greater
penetration of the drug and its active metabolite
into these tissues [56]. The typical adverse effects
seen with chronic use of oral amiodarone (dermato-
Table 2. Parenteral Agents Used for Rate Control in AF
Agent
Loading Dose
Maintenance Dose
Digoxin
10–15 mg/kg LBW
(8–10 mg/kg)*
0.5 mg/kg over 1 minutes
5 mg over 2–4 minutes
May repeat every 5 minutes to 15 mg
0.25–0.35 mg/kg over 2 minutes
0.125–0.25 mg/day
Esmolol
Metoprolol
Diltiazem
*Patients over 70 years of age and with renal failure.
0.05–0.2 mg/kg/min
5–10 mg every 6 hours
5–15mg/hr
Marik and Zaloga: Atrial Fibrillation in the ICU
185
Table 3. Trials of Patients with Recent Onset AF that Developed Outside the ICU
Reference
Year
Number
of
Patients
17
18
19
20
21
22
23
24
25
26
27
1991
1993
1996
1998
1998
1997
1998
1998
1998
1996
1997
102
80
266
262
127
240
117
156
123
100
239
Drugs Studied
Flecainide versus placebo
Flecainide versus procainamide
Ibutilide versus placebo
Ibutilide versus placebo
Ibutilide versus procainamide
Propafenone versus placebo
Propafenone versus procainamide
Propafenone versus placebo
Propafenone versus digoxin versus placebo
Amiodarone versus placebo
Digoxin versus placebo
logic, ophthalmologic, central nervous system,
thyroid) are not observed with intravenous amiodarone [57,58]. Hypotension and bradycardia, the
most common adverse events reported with intravenous amiodarone, usually occur during the loading infusion [57]. However, acute hepatotoxicity
with liver function test abnormalities has been reported in 9–17% of patients [57,59]. Hepatic dysfunction appears to be short lived and reversible.
The early acute hepatitis reported with parenteral
amiodarone may be a toxic effect of the carrier
vehicle polysorbate 80 [60,61]. Amiodarone has
been associated with acute pulmonary toxicity presenting as acute respiratory distress syndrome
(ARDS). This syndrome has been reported after thoracic surgery and in infants [62–65]. Donaldson et
al. [66] described three patients with ARDS who
were treated with amiodarone and had histologic
changes of widespread lipoid pneumonia at autopsy. These authors suggest that high oxygen concentrations may be a risk factor for acute
amiodarone pulmonary toxicity, while preexisting
pathology such as ARDS may mask its development. Amiodarone should therefore be used with
caution in this group of patients. It is important to
note that amiodarone has been shown to significantly increase plasma concentrations of digoxin by
60–70% within 24 hours of coadministration [67,68].
This interaction is clinically significant and result in
signs and symptoms of digitalis toxicity.
Procainamide is one of the oldest antiarrhythmic
drugs, having been used in 1936 (where it was
applied topically to the heart during surgery) [69].
Procainamide is a class IA antiarrhythmic drug with
wide antiarrhythmic indications. Intravenously the
drug has negative inotropic and hypotensive effects
[70]. Nearly half of the administered dose is eliminated unchanged in the urine, with 10–23% of the
drug being acetylated to produce N-acetylprocaineamide (NAPA). The elimination of the drug is pro-
Length of
Observation
(Hours)
Conversion
Success Rate
(%)
6
2.5
1.5
1.5
1.5
8
48
2
1
24
16
67 versus 35
92 versus 65
47 versus 2
35 versus 0
58 versus 18
76 versus 37
49 versus 70
70 versus 17
49 versus 32 versus 14
68 versus 60
51 versus 46
longed by both renal and hepatic disease. A close
relationship has been found between the plasma
concentration and the therapeutic effects of procainamide, with a suggested therapeutic range varying
from 4 to 8 mg/ml [69]. QT prolongation and polymorphic ventricular tachycardias (torsades de
pointes) may occur with this drug, necessitating
close monitoring of both drug levels and the QTc
interval on a 12-lead electrocardiogram.
Ibutilide fumarate is a new class III intravenous
antiarrhythmic agent indicated for the acute termination of atrial fibrillation and flutter [71,72]. It has
a short half-life due to extensive tissue distribution
and is available only for administration as an intravenous bolus (1 mg dose) [73]. The drug has minimal hemodynamic effects, even in patients with
depressed ventricular function [74]. Ibutilide prolongs repolarization in the atria and ventricle by
enhancing the inward depolarizing, slow sodium
current and by blocking Ikr [71–73]. Ibutilide causes
a dose-dependent prolongation of the QT interval,
which is maximal at the end of the infusion and
returns to baseline within 2–4 hours following infusion [71–73]. Torsade de pointes is the most clinically important adverse effect, being reported in
4.3% of patients [75]. The role of ibutilide in critically
ill patients remains to be determined. This drug
may have a role in enhancing termination of AF
in patients undergoing electrical cardioversion or
atrial overdrive pacing [34,76].
Based on the above information we suggest the
following approach to the critically ill patient with
AF. Hemodynamically unstable patients should be
electrically cardioverted followed by an infusion of
procainamide or amiodarone (as outlined above).
A loading dose of procainamide, amiodarone, or
ibutilide followed by repeated attempts at directcurrent cardioversion should be considered after
three failed attempts at cardioversion. In ‘‘hemodynamically stable’’ patients with AF, all correctable
186 Journal of Intensive Care Medicine Vol 15 No 4 July/August 2000
factors such as hypokalemia (K < 4 mmol/L), anemia, and hypoxemia should be corrected. Magnesium supplementation (2 g magnesium sulfate in
10 ml dextrose in water over 5 minutes) should
be considered except in hypermagnesemic patients
(serum magnesium > 2.5 mg/dl). Drugs such as
aminophylline and dopamine should be stopped.
Pain and anxiety, which increases sympathetic activity, should be treated. We then suggest rate control with diltiazem (5 mg boluses every 5 minutes
until rate control is achieved or a maximal dose of
Fig 1. Atrial fibrillation/flutter treatment algorithm.
15 mg is administered, followed by an infusion
of up to 15 mg/hr). Procainamide or amiodarone
should be considered in patients who remain in
AF. Amiodarone should be avoided in patients receiving high inspired oxygen concentrations. In patients who remain in AF after 12–24 hours we
suggest direct-current electrical cardioversion. This
algorithm is outlined in Figure 1. The dosages of
the agents used for cardioversion of AF are listed
in Table 4. There are no data on the optimal duration of antiarrhythmic therapy. However, as AF is
Marik and Zaloga: Atrial Fibrillation in the ICU
187
Table 4. Agents Used for Cardioversion in AF
Agent
Loading Dose
Maintenance Dose
Procainamide
5–15mg/kg over 15 minutes
(max. 1000 mg)
2–4 mg/min
Amiodarone
150 mg over 20–30 minutes
Ibutilide
1 mg over 10 minutes
(may be repeated in 10 minutes
if necessary)
50–150 mg every 8 hours orally
130–300 mg every 8 hours orally
1 mg/min for 6 hours
then 0.5 mg/min
None
Flecainide
Propafenone
50–100 mg every 12 hours orally
130–300 mg every 8 hours orally
likely to recur if the drug is terminated prematurely,
we suggest continuation of the drug (intravenously
or orally) until the precipitating factors have either
improved or resolved.
Atrial Fibrillation and Acute Myocardial
Infarction
Atrial fibrillation associated with acute myocardial
infarction (AMI) most often occurs within the first
24 hours and is usually transient but may recur. The
incidence of AF in AMI ranges from 9 to 16% [77–81].
Its etiology includes left ventricular dysfunction,
pericarditis, metabolic abnormalities, excess catecholamine release or iatrogenic factors (e.g., use of
sympathomimetic drugs) [77,80–82]. The appearance of atrial fibrillation, however, is often a manifestation of extensive left ventricular systolic
dysfunction [77,78,82]. Data from the GUSTO-1
study suggest that patients who develop AF frequently have extensive coronary artery disease with
poor reperfusion of the infarct-related artery [77].
Patients who develop AF in the setting of AMI are at
an increased risk of ischemic strokes [77,78]. Atrial
fibrillation in the setting of AMI independently predicts 30-day and 1-year mortality rates [77,78].
If AF causes hemodynamic compromise or ongoing ischemia, direct-current cardioversion should
be performed. In the absence of congestive heart
failure, bronchospastic disease, or atrioventricular
block the most effective means of slowing the ventricular rate in AF is the use of intravenous b-adrenoceptor blocking agents such as atenolol, esmolol,
or metoprolol. Rapid digitalization will control the
ventricular rate and improve left ventricular function. This method provides a slower response than
intravenous b-adrenoceptor blocking agents. Acute
digitalization, however, may cause coronary and
splanchnic vasoconstriction. Rate slowing may also
be achieved with intravenous diltiazem. However,
Half-Life
(Hours)
3–4
SS
(Hours)
12
3–21
(acute)
NA
6
NA
16–20
2–10
48–72
24–36
because of their negative inotropic effect and concerns regarding the use of calcium channel blockers
in acute AMI, these agents are not recommended
as first-line agents. The roles of class I and class III
antiarrhythmic agents and electric shock for converting persistent AF are unclear as is the role of
antiarrhythmic agents for the prevention of further
episodes of AF in patients who convert to sinus
rhythm. Anticoagulation with heparin is indicated
in patients who remain in AF for more than 24
hours or have recurrent episodes of AF.
Anticoagulation
According to the most recent guidelines on antithrombotic therapy from the American College of
Chest Physicians, anticoagulation is not required
for AF of less than 48 hours [83]. This recommendation is supported by the study of Weigner et al. [11]
who demonstrated 3 thromboembolic events in 357
patients (1%) with new onset AF (<48 hours) who
converted to sinus rhythm. On the other hand, full
anticoagulation is required in patients in whom AF
has been present for more than 48 hours or its
duration is uncertain. In patients planned for pharmacologic cardioversion in whom AF has been
present for more than 48 hours and who have not
been on chronic anticoagulation, transesophageal
echocardiography should be performed to exclude
the presence of an atrial thrombus [84].
Conclusion
Atrial fibrillation is a common and clinically important arrhythmia in critically ill patients. As this
arrhythmia is likely to persist until the underlying
medical disorder has resolved, medical management is almost always required. The management
of AF includes correction of correctable factors such
188 Journal of Intensive Care Medicine Vol 15 No 4 July/August 2000
as electrolyte abnormalities, elimination of sympathomimetic drugs, rate control, and either pharmacologic or electrical cardioversion.
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