Download Arrhythmias in the intensive care patient

Arrhythmias in the intensive care patient
Hans-Joachim Trappe, Bodo Brandts and Peter Weismueller
Purpose of review
Atrial fibrillation, atrial flutter, AV–nodal reentry tachycardia
with rapid ventricular response, atrial ectopic tachycardia, and
preexcitation syndromes combined with atrial fibrillation or
ventricular tachyarrhythmias are typical arrhythmias in intensive
care patients. Most frequently, the diagnosis of the underlying
arrhythmia is possible from the physical examination, the
response to maneuvers or drugs, and the 12-lead surface
electrocardiogram. In all patients with unstable hemodynamics,
immediate DC-cardioversion is indicated. Conversion of atrial
fibrillation to sinus rhythm is possible using antiarrhythmic
drugs. Amiodarone has a conversion rate in atrial fibrillation of
up to 80%. However, caution in the use of short-term
administration of intravenous amiodarone in critically ill patients
with recent-onset atrial fibrillation is absolutely necessary, and
the duration of therapy should not exceed 24 to 48 hours.
Ibutilide represents a relatively new class III antiarrhythmic
agent that has been reported to have conversion rates of 50%
to 70%; it seems that ibutilide is even successful when
intravenous amiodarone failed to convert atrial fibrillation.
Recent findings
Newer studies compared the outcome of patients with atrial
fibrillation and rhythm- or rate-control. Data from these studies
(AFFIRM, RACE) clearly showed that rhythm control is not
superior to rate control for the prevention of death and
morbidity from cardiovascular causes. Therefore, rate-control
may be an appropriate therapy in patients with recurrent atrial
fibrillation after DC-cardioversion. Acute therapy of atrial flutter
in intensive care patients depends on the clinical presentation.
Atrial flutter can most often be successfully cardioverted to
sinus rhythm with energies less than 50 joules. Ibutilide trials
showed efficacy rates of 38–76% for conversion of atrial
flutter to sinus rhythm compared with conversion rates of
5–13% when intravenous flecainide, propafenone, or
verapamil was administered. In addition, a high dose (2 mg) of
ibutilide was more effective than sotalol (1.5 mg/kg) in
conversion of atrial flutter to sinus rhythm (70% versus 19%).
Summary
There is general agreement that bystander first aid,
defibrillation, and advanced life support is essential for
neurologic outcome in patients after cardiac arrest due to
ventricular tachyarrhythmias. The best survival rate from
cardiac arrest can be achieved only when (1) recognition of
early warning signs, (2) activation of the emergency medical
services system, (3) basic cardiopulmonary resuscitation,
(4) defibrillation, (5) management of the airway and ventilation,
and (6) intravenous administration of medications occurs as
rapidly as possible. Public access defibrillation, which places
automatic external defibrillators in the hands of trained
laypersons, seems to be an ideal approach in the treatment of
ventricular fibrillation. The use of automatic external
defibrillators by basic life support ambulance providers or first
responder in early defibrillation programs has been associated
with a significant increase in survival rates. Drugs such as
lidocaine, procainamide, sotalol, amiodarone, or magnesium
were recommended for treatment of ventricular
tachyarrhythmias in intensive care patients. Amiodarone is a
highly efficacious antiarrhythmic agent for many cardiac
arrhythmias, ranging from atrial fibrillation to malignant
ventricular tachyarrhythmias, and seems to be superior to other
antiarrhythmic agents.
Keywords
atrial fibrillation, arrhythmias, amiodarone, ibutilide, automatic
external defibrillators
Curr Opin Crit Care 9:345–355. © 2003 Lippincott Williams & Wilkins.
Department of Cardiology and Angiology, Ruhr-University Bochum, Germany
Correspondence to Hans-Joachim Trappe, MD, Department of Cardiology and
Angiology, Ruhr-University Bochum Hoelkeskampring 40, 44625 Herne, Germany
E-mail: [email protected]
Current Opinion in Critical Care 2003, 9:345–355
© 2003 Lippincott Williams & Wilkins
1070-5295
Introduction
Emergency medicine and critical care are fields that
often require rapid diagnosis and intervention for specific situations [1]. These critical interventions can be
life-saving or severely debilitating, depending on their
appropriateness and timeliness. In cardiac emergencies,
accurate differentiation of ventricular and supraventricular tachyarrhythmias is essential for appropriate management [2]. Most frequently, the diagnosis of the underlying arrhythmia is readily apparent, but occasionally it is
necessary to use clues from the physical examination,
the response to maneuvers or drugs, in addition to the
12-lead surface electrocardiogram [3,4]. Treatment of
cardiac arrhythmias in intensive care and emergency
medicine is sometimes difficult. Correct therapy based
on an understanding of the mechanism that caused the
arrhythmia may not only be lifesaving in the immediate
situation, but may also improve the quality of life. The
purpose of the present chapter is to summarize new
strategies for patients with supraventricular or ventricular tachyarrhythmias in intensive care or cardiac emergencies.
345
346 Cardiovascular system
Types of tachyarrhythmias
Supraventricular tachyarrhythmias include atrial fibrillation, atrial flutter, AV-nodal reentrant tachycardia with
rapid ventricular response, atrial ectopic tachycardia, and
preexcitation syndromes combined with atrial fibrillation. Ventricular tachyarrhythmias still remain the main
cause of death; these arrhythmias include monomorphic
and polymorphic ventricular tachycardia, torsade de pointes
tachycardia, ventricular flutter, and ventricular fibrillation. In the assessment of patients with life-threatening
supraventricular or ventricular arrhythmias, attention
should be given to identify whether the tachycardia is
associated with worsening angina or low cardiac output.
There is general agreement that many cardiac or extracardiac causes can lead to supraventricular or ventricular
tachyarrhythmias and to cardiac arrest; left ventricular
function (or dysfunction) plays an important role in prognosis and outcome (Fig. 1).
Incidence and type of cardiac arrhythmias
in critically ill or elderly patients
It has been well known for many years that cardiac arrhythmias can occur in healthy people or in patients with
cardiac or extracardiac diseases. Arrhythmias are well defined in patients after myocardial infarction, in patients
with underlying cardiac or pulmonary disease, and in
patients after cardiac surgery or heart transplantation [5].
However, only few data are available regarding incidence
and type of arrhythmias in critically ill patients. Reinel et
al. studied all consecutive arrhythmia episodes in critically ill patients in a medical–cardiologic intensive care
unit between 1996 and 1999 [5]. All episodes of patients
with new-onset, sustained arrhythmias (duration ⱖ30
seconds) were included that were either self-terminated or that required intervention. A total of 310 ar-
rhythmia episodes were assessed during the study period
in 133 patients, with a mean of 2.91 episodes per patient
(range 1–14). Admission diagnoses were cardiac (n = 48),
cardiac surgery (n = 45), resuscitation (n = 12), pulmonary
(n = 15), sepsis (n = 5), neurologic (n = 2), and others
(n = 6). Among the 310 arrhythmia episodes, there were
278 tachycardia (179 episodes regular, 97 episodes irregular) and 32 bradycardia events (heart rate <40 beats/min).
There were 108 narrow-QRS complex tachycardia and
168 wide-QRS complex tachycardia with two episodes of
primary ventricular fibrillation. Among the 278 tachycardias, 135 episodes (48.6%) were ventricular, 13 episodes
(4.7%) were torsade de pointes tachycardia, and 83 episodes (29.8%) were atrial fibrillation, 10 episodes were
atrial flutter (3.6%), 21 were supraventricular tachycardia
(7.6%), and 2 were ectopic atrial tachycardia (0.7%). It
seems that in critically ill patients, two types of arrhythmias are dominantly visible: sustained ventricular tachycardia and atrial fibrillation. Lampert and Ezekowitz reported recently that the aging heart is susceptible to
diverse cardiac arrhythmias, and in many of these arrhythmias intensive care medicine is mandatory [6].
Baine et al. studied the incidence of arrhythmia types,
hospital and intensive care stay in 144,512 elderly patients (age 65 years or older) with cardiac arrhythmias
(time interval 1991–1998) [7]. In 1998, atrial fibrillation
was the most frequent arrhythmia and accounted for
44.8% of the relevant discharges. Atrial flutter was observed in 5.2%, sinoatrial node dysfunction in 13.2%, and
complete AV block in 5.8%. Supraventricular tachycardia
was observed in only 3.8%. Cardiac arrest was present in
1.3%, ventricular tachycardia in 6.9%, and ventricular fibrillation in 1.3%. It is interesting to note that lengths of
stay in hospital and intensive care are determined by the
underlying arrhythmia: mean hospital stay was 7.8 days
Figure 1. Diagnostic methods in intensive care patients after cardiac arrest caused by ventricular fibrillation
Mechanisms and diagnostic methods in intensive care
patients after cardiac arrest caused by ventricular
fibrillation. Angio, angiography; BRS, baroreflex sensitivity;
ECG, electrocardiogram; EPS, programed electrical
stimulation; HRV, heart rate variability; LVEF, left
ventricular ejection fraction.
Arrhythmias in intensive care patient Trappe et al. 347
in ventricular fibrillation, 7.0 days in ventricular tachycardia in contrast to 4.7 days in atrial fibrillation, 4.5 days
in atrial flutter, or 5.6 days in complete AV block. Mean
intensive care stay was 2.7 days in ventricular fibrillation,
1.7 days in ventricular tachycardia, 0.9 days in atrial fibrillation, 1.0 days in atrial flutter, or 1.5 days in complete AV block. In addition to the study by Reinelt et al.,
management of atrial fibrillation is also a major problem
in elderly patients.
Atrial fibrillation
Since the time of Hippocrates, there has been interest
in how the heartbeat is initiated. It was concluded that
the nervous system initiates the heartbeat. In 1907,
Keith and Flack described the sinus node and suggested
it as the site of initiation within the atrium. It became
clear that electrical disturbances in the atrium (disruptions in the normal spread of activation) will lead to atrial
arrhythmias. Clinical, there is an increased interest in
atrial arrhythmias, particularly atrial fibrillation, because
the incidence of this arrhythmia is high and the associated morbidity and mortality higher than previously
recognized.
Acute management
Atrial fibrillation or flutter is the most frequent arrhythmia in emergency rooms and intensive care units, both in
surgical and cardiologic intensive care units [8]. Knotzer
et al. found that 14.8% of surgically ill patients developed
atrial tachyarrhythmias compared with 47.4% of patients
treated in a cardiologic intensive care unit [5,9]. The goal
of acute treatment of atrial fibrillation with rapid ventricular response is to restore sinus rhythm or to control
the ventricular rate (Fig. 2). If cardioversion to sinus
rhythm is not possible, the secondary goal is to slow the
ventricular response, usually to a rate of less than 100 beats
per minute. Patients who are hemodynamically unstable
(significant hypotension, severe angina, pulmonary
edema) should be promptly cardioverted after administration of an anesthetic agent. Cardioversion should always be performed in a synchronized mode.
Hemodynamically stable situation: restoration of
sinus rhythm
In patients in whom atrial fibrillation is of known acute
onset (present for less than 48 hours) DC-cardioversion
should be considered early. Pharmacologic conversion to
sinus rhythm with antiarrhythmic drugs is a widely used
Figure 2. Stored electrocardiogram in a patient with an implanted automatic cardioverter defibrillator
Patient was admitted to an intensive care unit because of frequent episodes of implanted automatic cardioverter defibrillator (ICD) discharges. The electrocardiogram
clearly shows atrial fibrillation with rapid ventricular response (heart rate 175 beats per minute) without successful ICD therapy. Postshock persistence of atrial
fibrillation with a heart rate of 187 beats per minute.
348 Cardiovascular system
therapeutic alternative with different efficacy rates [10].
Amiodarone has a conversion rate in atrial fibrillation of
up to 80% [11]. However, only a single retrospective
study has been published that includes intensive care
unit patients with left ventricular dysfunction, although
this is frequent in critically ill or even in elderly patients
with recent onset of atrial fibrillation [12]. In critically ill
patients, amiodarone is indicated for a wide range of
arrhythmias including recent-onset atrial fibrillation. Despite many published reports on safety and efficacy of
intravenous amiodarone in the treatment of patients with
recent-onset atrial fibrillation, there are an increasing
number of reports in critically ill patients highlighting
occasional serious acute pulmonary toxicity [13]. Therefore, caution in the use of short-term administration of
intravenous amiodarone in the critically ill patient with
recent-onset atrial fibrillation is absolutely necessary,
and the duration of therapy should not exceed 24 to
48 hours, except when absolutely necessary. In contrast
to amiodarone, ibutilide represents a relatively new class
III antiarrhythmic agent that has been reported to have
high conversion rates [14]. Proarrhythmic effects occur in
5 to 8% of patients, and careful monitoring is required.
The conversion rates of recent-onset atrial fibrillation to
sinus rhythm with ibutilide range from 50 to 70%, and it
seems that ibutilide is even successful when intravenous
amiodarone failed to convert atrial fibrillation [15]. Hennersdorf et al. studied 26 patients in whom atrial fibrillation or flutter persisted for a maximum of 6 hours. All
patients initially received amiodarone (150 mg IV) and
after 2 hours of persistent arrhythmia ibutilide (1 mg IV;
in the case of persisting arrhythmia and body weight
> 70 kg, a second infusion of 1 mg ibutilide was administered after 30 minutes). Before the administration of
ibutilide, magnesium (1 g) was administered, and high
normal levels of potassium serum levels were achieved
(4.5 to 5.0 mmol/L). After amiodarone administration,
atrial flutter persisted in 73% and atrial fibrillation in
27% of patients. After administration of ibutilide, conversion to sinus rhythm was achieved in 82% patients
after a median time of 7 minutes (range 3 to 12 minutes).
The rate of cardioversion with ibutilide was higher
in atrial flutter (84% patients) than in atrial fibrillation
(71% patients). Therefore, in implanted automatic cardioverter defibrillator patients with atrial fibrillation or
flutter, ibutilide is an effective drug even when amiodarone failed. Ibutilide seems to be well suited for cardioversion of recent-onset atrial fibrillation or flutter [15].
Hemodynamically stable situation: rate control or
rhythm control?
In every intensive care unit, there are many patients with
recent-onset atrial fibrillation. Within the last few years,
cardioversion to sinus rhythm was the goal to treat these
patients. However, there are new important studies reporting the role of rate control in these patients: the
AFFIRM and the RACE studies [16•,17•]. Although
these studies are not performed in critically ill patients,
they have many implications for the management of patients with atrial fibrillation, arriving in an intensive care
unit. A total of 4060 patients (mean age 69.7 ± 9.0 years)
with atrial fibrillation and a higher risk of stroke or death
were enrolled in the AFFIRM study [16•]. Patients were
assigned to rhythm-control (2033 patients) or to ratecontrol therapy (2027 patients). The primary endpoint of
this study was overall mortality. In the rhythm-control
group, more than two thirds of patients started therapy
with amiodarone or sotalol. By the end of the study almost two thirds of the patients in this group had undergone at least one trial of amiodarone. In the rate-control
group, beta-blocking agents were used initially in nearly
one half of the patients, and of the calcium-channel
blockers, diltiazem was used more frequently than verapamil. In this study, there were 356 deaths among
the patients assigned to rhythm-control therapy and
310 deaths among patients assigned to rate-control
therapy (P = 0.08). The prevalence of sinus rhythm in
the rhythm-control group at follow-up was 82.4%, 73.3%,
and 62.6% at 1, 3, and 5 years, respectively. In the ratecontrol group, at 5 years, 34.6% of the patients were in
sinus rhythm, and over 80% of those in the atrial fibrillation group had adequate heart rate control. More patients in the rhythm-control group than in the rate-control
group were hospitalized, and there were more adverse
drug effects in the rhythm-control group as well. In both
groups, most strokes occurred after warfarin had been
stopped or when the international normalized ratio was
subtherapeutic. From this study it seems clear that management of atrial fibrillation with the rhythm-control
strategy offers no survival advantage over the rate-control
regimen. In the RACE study, 522 patients with persistent
atrial fibrillation after a previous electrical cardioversion
were randomized to a rhythm-control (266 patients) or a
rate-control group (256 patients) [17••]. The endpoint
was a composite of death from cardiovascular causes,
heart failure, thromboembolic complications, bleeding,
implantation of a pacemaker, and severe adverse effects
of drugs. Patients in the rhythm-control group were
treated with sotalol (160 to 320 mg daily), flecainide (200
to 300 mg daily), or propafenone (450 to 900 mg daily). If
there was a recurrence within 6 months after start of the
drug treatment, a loading dose of amiodarone was given
(600 mg daily for 4 weeks) and thereafter continued with
200 mg daily. Rate control was achieved with the administration of digitalis, calcium channel blockers, and betablocking agents, alone or in combination. After a mean of
2.3 ± 0.6 years, 39% of patients in the rhythm-control
group had sinus rhythm, as compared with 10% of patients in the rate-control group. The primary endpoint
occurred in 22.6% of patients in the rhythm-control
group and in 17.2% of patients in the rate-control group.
The distribution of the various components of the primary endpoint was similar between both groups. Data
from this study clearly showed that rhythm control is not
Arrhythmias in intensive care patient Trappe et al. 349
superior to rate control for the prevention of death and
morbidity from cardiovascular causes. Therefore, rate
control may be an appropriate therapy in patients with a
recurrence of atrial fibrillation after electrical cardioversion.
Alternatives for rate control in atrial fibrillation with
rapid ventricular response
Both a loss of atrial synchrony and the rapid ventricular
response may be poorly tolerated in hemodynamically
compromised patients [3]. Attempts to restore sinus
rhythm are frequently unsuccessful or (after AFFIRM
and RACE) even debatable [16•,17••]. Heart rate control becomes the main therapeutic goal in this situation.
The optimal regimen for pharmacologic rate control during atrial fibrillation in critically ill patients is unclear. It
has been well known for many years that treatment with
intravenous digoxin, verapamil, beta-blocking agents, or
diltiazem is effective in patients with atrial fibrillation
and rapid ventricular response [1]. Digoxin may be helpful for rate control, with an initial dose of 0.5 mg. After
30 minutes, 0.25 mg digoxin should be administered
again. In intensive care and emergency medicine, other
therapeutic strategies are verapamil (5 to 10 mg IV), diltiazem (20 mg IV), or beta-blocking agents as such as propranolol (1 to 5 mg IV, additional infusion of 10 to 120 mg
per day) and esmolol (500 µg/kg over 1 minute, followed
by a 4-minute maintenance infusion of 50 µg/kg/min
with further dose adjustment as necessary) [11]. However, beta-blocking agents or calcium channel blockers
may cause additional hypotension. Just recently, Delle
Karth et al. compared another pharmacologic approach
for rate control in critically ill patients: these authors
studied the role of amiodarone or diltiazem in a prospective, randomized trial [18]. Sixty patients with atrial tachyarrhythmias (atrial fibrillation 57 patients, atrial flutter 2
patients, atrial tachycardia 1 patient) were randomized to
diltiazem (25 mg bolus followed by a continuous infusion
of 20 mg/h for 24 hours) (group I), amiodarone (300 mg
bolus) (group II) or amiodarone (300 mg bolus followed
by 45 mg/h for 24 hours) (group III). The primary endpoint was a >30% heart rate reduction within 4 hours.
The secondary endpoint was a heart rate <120 beats/min.
Tachyarrhythmias were considered uncontrolled if the
heart rate was >120 beats/min four hours after study drug
administration. The primary endpoint was achieved in
70% of group I patients, 55% of patients in group II, and
in 75% of patients in group III (P = 0.38). In patients
achieving heart rate control, diltiazem showed a significantly better rate reduction when compared with group
II and III (P < 0.01). However, premature drug discontinuation due to hypotension was required significantly
more often in group I (30%) than in group II (0%) or
group III (5%) (P < 0.01). Uncontrolled tachyarrhythmias
were observed more frequently in group II (45%) than in
group I (0%) or group III (5%). This study shows that
sufficient rate control can be achieved in critically ill
patients with atrial tachyarrhythmias using either diltia-
zem or amiodarone. Although diltiazem allowed significantly better 24-hour heart rate control, this effect was
offset by a significantly higherincidence of hypotension
requiring discontinuation of the drug. It seems clear that
amiodarone may be an alternative in patients with severe
hemodynamic compromise.
Atrial flutter
Acute therapy for patients with atrial flutter in intensive
care depends on the clinical presentation. If the patient
presents with acute hemodynamic collapse or congestive
heart failure, emergent direct-current synchronized
shock is indicated. Atrial flutter can most often be successfully cardioverted to sinus rhythm with energies less
than 50 joules. A number of drugs have been shown to be
effective in conversion of atrial flutter to sinus rhythm.
Placebo-controlled intravenous ibutilide trials showed
efficacy rates of 38 to 76% for conversion of atrial flutter
to sinus rhythm [19,20]. For those who responded to
ibutilide, the mean time interval to conversion was
30 minutes. In the largest available study, the efficacy of
intravenous ibutilide (76%) was significantly higher than
that of intravenous procainamide (14%) [21]. Several
single-blinded, randomized control trials comparing intravenous flecainide with either intravenous propafenone or intravenous verapamil have shown relatively
poor efficacy for acute conversion (5 to 13%); in addition,
the conversion rate of intravenous sotalol varied from 20
to 40%, depending on the sotalol dose, but was not different from placebo. High dose (2 mg) of ibutilide was
more effective than sotalol (1.5 mg/kg) in conversion of
patients with atrial flutter to sinus rhythm (70% versus
19%) [22].
Narrow-QRS complex tachycardia
Narrow QRS tachycardia is a cardiac rhythm with a rate
faster than 100 beats per minute and a QRS duration
of less than 0.12 seconds. The patient with narrow
QRS tachycardia usually seeks medical attention because of palpitations, light-headedness, shortness of
breath, or anxiety. In many patients with narrow-QRS
complex tachycardia, the tachycardia rate is very high
(180-240 beats per minute) and therefore, after onset of
the tachycardia the patient will arrive very soon in an
intensive care unit for diagnosis and treatment. In intensive care and emergency medicine, narrow QRS complex
tachycardia is a common problem [1].
Acute management
The definitive diagnosis can be made in most of the
patients based on 12-lead electrocardiogram and clinical
criteria. Acute (and chronic) treatment should be initiated based on the underlying mechanism. In regular narrow QRS complex tachycardia, vagal maneuvers should
be initiated to terminate the arrhythmia or to modify
AV conduction. If this fails, intravenous antiarrhythmic
drugs should be administered for arrhythmia termination
350 Cardiovascular system
in hemodynamically stable patients. Adenosine, calcium
channel blockers, or beta-blocking agents are the drugs
of first choice. The advantage of adenosine relative to
intravenous calcium antagonists or beta-blockers relates
to its rapidity of onset and short half-life [3,4]. Longer
acting agents (intravenous calcium channel blockers or
beta-blocking agents) are of value, particularly for patients with recurrences of narrow QRS tachycardia. It is
clearly necessary to avoid concomitant use of intravenous
calcium channel blockers and beta-blocking agents because of possible increase of hypotensive and/or bradycardiac effects [23].
The “pill-in-the-pocket” concept
In patients who arrive in an intensive care unit or even in
critically ill patients who develop narrow QRS complex
tachycardia, the “pill-in-the-pocket” concept may be of
interest. This concept means single-dose administration
of the drug only during an episode of tachycardia for the
purpose of termination of the arrhythmia when vagal
maneuvers alone are not effective. This approach may
be considered for patients with infrequent episodes of
AV nodal reentrant tachycardia that are prolonged but
yet well tolerated, and obviates exposure of patients to
chronic and unnecessary therapy between their rare arrhythmic events [24]. However, patients should be free
of significant left ventricular dysfunction, sinus bradycardia, or preexcitation. It has been reported by Musto et al.
[23] and Alboni et al. [24] that a single dose of flecainide
(3 mg/kg) terminated acute episodes of AV nodal reentrant tachycardia. Single-dose therapy with diltiazem
(120 mg) combined with propranolol (80 mg) was superior to both placebo and flecainide [20]. In addition, longterm follow-up of single-dose therapy with diltiazem
plus propranolol was associated with a significant reduction in emergency room visits.
Ventricular tachyarrhythmias
One of the most important problems in intensive care,
emergency medicine, and cardiac rhythmology is to manage patients with recurrent ventricular tachycardia, ventricular flutter, or ventricular fibrillation [25]. Management of cardiac arrest due to life-threatening ventricular
tachyarrhythmias is one of the most important goals in
these patients to avoid serious problems and to avoid
sudden cardiac death [26]. However, treatment of the
underlying arrhythmia requires correct diagnosis; in most
patients this is possible using the 12-lead surface electrocardiogram [27]. Nevertheless, it is necessary to understand in every patient why the arrhythmia was initiated and what the trigger of initiation was in any patient
(Fig. 3).
Cardiac arrest
Patients who are successfully resuscitated from out-ofhospital cardiac arrest have a high rate of mortality after
hospital discharge. Unfortunately, we are not able to rec-
ognize high-risk patients with subsequent cardiac arrest.
Therefore, it is necessary to treat cardiac arrest patients
in the emergency situation as well as possible and to
develop algorithms for long-term therapy.
General considerations
Approximately 1000 people in the United States experience cardiac arrest each day, most often as a complication
of acute myocardial infarction with accompanying ventricular fibrillation or unstable ventricular tachycardia
(Fig. 4). In the year 2000, the American Heart Association reported again the chain-of-survival concept, with
four links—early access, cardiopulmonary resuscitation,
defibrillation, and advanced care—as the way to approach cardiac arrest [28,29]. This publication presents
the conclusions of the International Guidelines 2000
Conference on Cardiopulmonary Resuscitation and
Emergency Cardiovascular Care. It has been pointed out
that the highest potential survival rate from cardiac arrest
can be achieved only when the following sequence of
events occurs as rapidly as possible: (1) recognition of
early warning signs, (2) activation of the emergency
medical services system, (3) basic cardiopulmonary resuscitation, (4) defibrillation, (5) management of the airway and ventilation, and (6) intravenous administration
of medications. It is impossible to review all guideline
changes related to basic life support; this has been described in detail elsewhere [29]. However, it seems important to stress some important issues: change ventilation volumes and inspiratory times for mouth-to-mask or
bag mask ventilation without oxygen ventilation should
have a tidal volume of approximately 10 mL/kg (700 to
1000 mL) over 2 seconds; oxygen supplementation of a
smaller tidal volume of 6 to 7 mL/kg (approximately 400
to 600 mL) may be delivered over 1 to 2 seconds. The
compression rate for adult cardiopulmonary resuscitation
should be approximately 100 per minute and the compression–ventilation ratio for one and two rescuers
should be 15 compressions to 2 ventilations when the
victim’s airway is unprotected (not intubated).
Neurologic outcome
There is general agreement that bystander first aid, defibrillation, and advanced life support are essential for
neurologic outcome in patients after cardiac arrest. Bur
et al. evaluated the effects of basic life support, time to
first defibrillation, and emergency medical service arrival
on neurologic outcome in 276 patients after cardiac arrest
[30]. In contrast to intubation (odds ratio 1.08; 95% CI,
0.51–2.31; P = 0.84), basic life support (odds ratio 0.44;
95% CI 0.24–0.77; P = 0.004) and time to first defibrillation (odds ratio 1.08; 95% CI 1.03–1.13; P = 0.001) were
significantly correlated with good neurologic outcome. In
addition to the better neurologic outcome, among the
patients who did not receive basic life support, the av-
Arrhythmias in intensive care patient Trappe et al. 351
Figure 3. Holter recording in a 64-year-old patient who developed torsade de pointes tachycardia while in
intensive care
At 11.44 hours, sinus rhythm with deep ST-segment
depression is visible combined with some premature
ventricular beats. At 11.53 hours, a torsade de pointes
tachycardia occurs degenerating into ventricular
fibrillation.
erage cost per patient with good neurologic outcome significantly increased with the delay of the first defibrillation (P < 0.001) [30]. The importance of cerebral
perfusion and pressure and cerebral tissue oxygen tension during cardiopulmonary resuscitation has been described recently [31].
Early defibrillation
Public access defibrillation, which places automatic
external defibrillators (AED) in the hands of trained
laypersons, has the potential to be the single greatest
advance in the treatment of ventricular fibrillation since
the development of cardiopulmonary resuscitation.
Time to defibrillation is the most important determinant
of survival from cardiac arrest [32]. The earlier the defibrillation is performed the better the success rates for
resuscitation, irrespective of who is doing the first defibrillation [33]. In the last few years, there has been a
significant increase in the use of AEDs in early defibrillation programs in a variety of settings, including hospitals, emergency medical service, police departments, casinos, airport terminals, and commercial aircraft, among
others. In most of these settings, use of AEDs by basic
life support ambulance providers or first responder in
early defibrillation programs has been associated with a
significant increase in survival rates [34–36•].
352 Cardiovascular system
Figure 4. Holter recording in a patient who had cardiac arrest while in the intensive care unit
Fast monomorphic ventricular tachycardia degenerates into ventricular flutter and ventricular fibrillation. Termination was possible by DC countershock.
World-wide experience
Automatic external defibrillators were used in 105 patients with ventricular fibrillation occurring in casinos
[34]. Fifty-six of the patients (53%) survived to discharge
from the hospital. Among the 90 patients whose collapse
was witnessed (86%), the clinically relevant time intervals were a mean of 3.5 ± 2.9 minutes from collapse to
the delivery of the first defibrillation shock, and 9.8 ± 4.3
minutes from collapse to the arrival of the paramedics.
The survival rate was 74% for those who received their
first defibrillation no later than 3 minutes after a witnessed collapse and 49% for those who received their
first defibrillation after more than 3 minutes. AEDs were
used in a US airline study in 200 patients, including 99
patients with documented loss of consciousness. The administration of shock was advised in all 14 patients with
documented ventricular fibrillation, and no shock was
advised in the remaining patients. The first shock successfully defibrillated the heart in 13 patients, and defibrillation was withheld in one patient at the family’s
request [35]. Recently, Caffrey et al. reported the public
use of AEDs in three Chicago airports [36•]. During a
2-year period, 21 persons had nontraumatic cardiac arrest, and 18 of them had ventricular fibrillation. In the
case of four patients with ventricular fibrillation, defibrillators were neither nearby nor used within 5 minutes,
and none of these patients survived. Three others remained in ventricular fibrillation and eventually died
later, despite the rapid use of a defibrillator within 5
minutes. Eleven patients with ventricular fibrillation
were successfully resuscitated, including eight who regained consciousness before hospital admission. No
shock was delivered in four cases of suspected cardiac
arrest, and the device correctly indicated that the problem was not due to ventricular fibrillation.
Defibrillation in hospitals and intensive care units
Hospitals need to pay attention to the timeliness of defibrillation including monitored and unmonitored ward
settings, intensive care units, and ambulatory care facilities. There is a prevalent misconception that hospitals
inherently provide rapid defibrillation followed by
prompt advanced life support. In addition, many hospitals both in the United States and in Europe have been
Arrhythmias in intensive care patient Trappe et al. 353
slow to accept and implement the readily available technology that allows defibrillation to be performed before
arrival of a physician. Until recently, hospitals and intensive care units have been staunchly reluctant to evaluate
critically their process for providing early defibrillation
[37]. It is well known from previous studies that delays of
5 to 10 minutes can be expected before the conventional
in-hospital code teams deliver the first shock to patients
with ventricular fibrillation. It has been shown that
nurses in the hospital setting can be easily trained to use
an AED and to safely and effectively operate the device.
Role of antiarrhythmic drugs in intensive
care and emergencies
Prompt cardiopulmonary resuscitation and early defibrillation either by DC-countershock or an AED significantly improve the likelihood of successful resuscitation
from ventricular fibrillation [38]. Despite these circumstances, there is still a place for antiarrhythmic drugs to
treat patients with life-threatening ventricular tachyarrhythmias such as monomorphic or polymorphic ventricular tachycardia in intensive care or emergencies [4•].
The American Heart Association has clearly defined
when and how to use these agents [29]. Drugs such as
lidocaine, procainamide, sotalol, amiodarone, or magnesium were recommended for treatment of ventricular
tachyarrhythmias in intensive care or emergencies.
Class I drugs
In summary, there is still a place for lidocaine in the
treatment algorithm for stable, monomorphic, or polymorphic ventricular tachycardia, and lidocaine is acceptable for these arrhythmias with normal or impaired cardiac
function. In contrast, there is little evidence supporting a
benefit from treatment with lidocaine for cardiac arrest.
Lidocaine seems to be more effective during acute myocardial infarction. However, the US guidelines postulated that lidocaine is a second-tier choice and other
drugs are preferred over lidocaine in each ventricular
tachycardia scenario. In addition, the prophylactic use of
lidocaine is not recommended. Use of procainamide is
indicated in patients with ventricular tachycardia and is
an alternative in pulseless ventricular tachycardia/ventricular fibrillation. Its utility in pulseless cardiac arrest is
less well studied and limited by the need for a relatively
slow infusion (maximum rate 50 mg/min) and the achievement of potentially toxic concentrations if administered
more rapidly. Procainamide should be avoided in patients with preexisting QT prolongation and torsade de
pointes tachycardia. The electrocardiogram and blood
pressure must be monitored continuously during procainamide administration. Precipitous hypotension may
occur if the drug is injected too rapidly [29]. Propafenone
and flecainide are class I antiarrhythmic drugs with significant conduction-slowing and negative inotropic effects. In addition, propafenone has nonselective betablocking properties. Intravenous propafenone is used for
the same indication as flecainide and is acceptable for
treatment of both supraventricular and ventricular tachycardia. Because of significant negative inotropic effects,
propafenone and flecainide should be not given to patients with impaired left ventricular function. In addition, both propafenone and flecainide should be avoided
when coronary artery disease is suspected.
Class III drugs
Sotalol prolongs action potential duration and increases
cardiac tissue refractoriness. In addition, it has nonselective beta-blocking properties. Sotalol is effective in both
supraventricular and ventricular tachycardia. Side effects
include bradycardia, hypotension, and torsade de pointes
tachycardia. Intravenous sotalol in intensive care medicine is limited by its need to be infused relatively slowly.
This may be impractical and has uncertain efficacy in
emergent circumstances, particularly under compromised circulatory conditions [29]. Amiodarone is a complex
drug with effects on sodium, potassium, and calcium
channels as well as alpha- and beta-adrenergic-blocking
properties. Amiodarone is a highly efficacious antiarrhythmic agent for many cardiac arrhythmias, ranging
from atrial fibrillation to malignant ventricular tachyarrhythmias [39]. In most published studies, intravenous
amiodarone has been administered in patients with ventricular tachyarrhythmias only after failure of other antiarrhythmic drugs. In 1999, Kudenchuk described in 504
randomized patients with out-of-hospital cardiac arrest
due to refractory ventricular arrhythmias (ARREST
study) that treatment with amiodarone (single 300-mg
dose of intravenous amiodarone) resulted in a higher rate
of survival to hospital admission (44%) compared with
placebo (34%) (P = 0.03) [40]. The role of amiodarone
as an emergency drug has been reported recently by
Taylor [39].
Magnesium
Severe magnesium deficiency is associated with cardiac
arrhythmias, symptoms of heart failure, and sudden cardiac death. Hypomagnesemia can precipitate refractory
ventricular fibrillation and can hinder the replenishment
of intracellular potassium. Magnesium deficiency should
be corrected in intensive care and emergencies if present. Magnesium is not usually categorized as an antiarrhythmic agent. However, it has been known for a long
time that in emergent circumstances, magnesium sulfate
1 to 2 g is helpful to suppress life-threatening ventricular
tachyarrhythmias and should be administered over 1 to
2 minutes [4•]. The role of magnesium in intensive care
and emergency medicine was described by Kaye and
O’Sullivan in 2002 [41]. These authors concluded that
magnesium should be the first-line therapy in eclampsia
and torsade de pointes tachycardia. Data from other studies show that magnesium has a clearly defined role as a
second-line therapy in acute severe bronchial asthma
354 Cardiovascular system
References and recommended reading
[42]. Hypomagnesemia should be considered in patients
with biventricular failure presenting with malignant ventricular tachyarrhythmias. Magnesium should be considered as a temporizing measure in cases of severe digoxin
toxicity while using antibodies as the specific antidote.
They pointed out that magnesium is safe and easy to use
and should be available for immediate use in all intensive care units and emergency departments [41].
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Atrial fibrillation, ventricular tachycardia, and patients
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“classical” patients in intensive care units and emergencies. It has been shown that evaluation of history, physical examination, and the 12-lead-surface electrocardiogram are essentials for correct diagnosis and treatment.
In all patients with cardiac arrhythmias in intensive care
and emergencies who have unstable hemodynamics, external DC cardioversion is the method of choice. In patients with atrial fibrillation, there are numerous studies
that analyzed outcome and recurrences after antiarrhythmic drug treatment. However, recently published studies showed that rhythm control is not superior to rate
control and, therefore, a new strategy seems to be advisible to treat these patients. Nevertheless, there is general
agreement that rate control is necessary in patients with
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different studies are very promising.
Papers of particular interest, published within the period of review, have
been highlighted as:
•
Of special interest
••
Of outstanding interest
Conclusion
Emergency medicine and critical care are fields that often require rapid diagnosis and intervention for specific
situations. It is well known that in all patients with tachyarrhythmias, evaluation of the underlying etiology and
the degree of left ventricular function (dysfunction) is
essential. Correct treatment of arrhythmias in the intensive care patient is based on an understanding of the
mechanism that caused the situation. The therapeutic
role of antiarrhythmic drugs in the management of atrial
fibrillation or cardiac arrest is debatable. After the AFFIRM
and RACE studies, the restoration of sinus rhythm is not
the goal in any patient, and rate control is an alternative
way for these patients. The prophylactic administration
of antiarrhythmic drugs has never been studied formally
in victims of cardiac arrest. The optimal dose of antiarrhythmic drugs, whether best given before or only after
multiple defibrillation shocks have failed to restore circulation, is not yet known.
16. The Atrial Fibrillation Follow-up Investigation of Rhythm Management
(AFFIRM) Investigators: A comparison of rate control and rhythm control in
•
patients with atrial fibrillation. N Engl J Med 2002, 347:1825–1833.
This randomized, multicenter study compared two different treatment strategies in
patients with atrial fibrillation and high risk of stroke or death. The primary endpoint
was overall mortality. A total of 4060 patients were enrolled in the study and randomized to rhythm control or rate control. The study showed that rhythm-control
strategy offers no survival advantage over the rate-control strategy in patients with
atrial fibrillation.
Van Gelder IC, Hagens VE, Bosker HA, et al.: Crinhs HJGM for the Rate
Control versus Electrical Cardioversion for Persistent Atrial Fibrillation Study
Group: A comparison of rate control and rhythm control in patients with recurrent persistent atrial fibrillation. N Engl J Med 2002, 347:1834–1840.
In this randomly assigned study, 522 patients with persistent atrial fibrillation were
included after a previous electrical cardioversion. Patients were randomized to
rhythm control or rate control. The endpoint of this study was a composite death
from cardiovascular causes, heart failure, thromboembolic complications, bleeding, implantation of a pacemaker, or severe adverse effects of drugs. It was shown
that rate control was not inferior to rhythm control.
17
••
18
Delle Karth G, Geppert A, Neunteufl T, et al.: Amiodarone versus diltiazem for
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2001, 29:1149–1153.
19
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20
Ellenbogen KA, Stambler BS, Wood MA: Efficacy of intravenous ibutilide for
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21
Volgman AS, Carberry PA, Stamber BS: Conversion efficacy and safety of
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34
Valenzuela TD, Roe DJ, Nichol G, et al.: Outcomes of rapid defibrillation by
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35
Page RL, Joglar JA, Kowal RC, et al.: Use of automated external defibrillators
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26
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37
27
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41
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42
Stuehlinger HG, Thell R, Laggner AN: Magnesium in emergency medicine.
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30
31
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36 Caffrey SL, Willoughby PJ, Pepe PE, et al.: Public use of automated external
defibrillators. N Engl J Med 2002, 347:1242–1247.
•
Automatic external defibrillators save lives when they are used by designated personnel in certain public settings. This study was performed at three Chicago airports in a prospective way during a 2-year period. It was pointed out that automatic
external defibrillators deployed in readily accessible, well-marked public areas were
used effectively to assist patients with cardiac arrest. In the cases of survivors, most
of the users had no duty to act and no prior training in the use of these devices.