(Circulation. 2000;102:742.)
© 2000 American Heart Association, Inc.
Clinical Investigation and Reports |
Treating Electrical Storm
Sympathetic Blockade Versus Advanced Cardiac Life Support–Guided Therapy
From the Electrophysiology and Pacing Center, Division of Cardiology, School of Medicine, University of Southern California, Los Angeles.
Correspondence to Koonlawee Nademanee, MD, 1450 San Pablo St, Suite 5501, Los Angeles, CA 90033. E-mail nademane{at}hsc.usc.edu
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Abstract |
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Background—Electrical storm (ES), defined as recurrent multiple ventricular fibrillation (VF) episodes, often occurs in patients with recent myocardial infarction. Because treating ES according to the Advanced Cardiac Life Support (ACLS) guidelines yields a poor outcome, we evaluated the efficacy of sympathetic blockade in treating ES patients and compared their outcome with that of patients treated according to the ACLS guidelines.
Methods and Results—Forty-nine patients (36 men, 13 women, mean age 57±10 years) who had ES associated with a recent myocardial infarction were separated into 2 groups. Patients in group 1 (n=27) received sympathetic blockade treatment: 6 left stellate ganglionic blockade, 7 esmolol, and 14 propranolol. Patients in group 2 (n=22) received antiarrhythmic medication as recommended by the ACLS guidelines. Patient characteristics were similar in the 2 groups. The 1-week mortality rate was higher in group 2: 18 (82%) of the 22 patients died, all of refractory VF; 6 (22%) of the 27 group 1 patients died, 3 of refractory VF (P<0.0001). Patients who survived the initial ES event did well over the 1-year follow-up period: Overall survival in group 1 was 67%, compared with 5% in group 2 (P<0.0001).
Conclusions—Sympathetic blockade is superior to the antiarrhythmic therapy recommended by the ACLS guidelines in treating ES patients. Our study emphasizes the role of increased sympathetic activity in the genesis of ES. Sympathetic blockade-not class 1 antiarrhythmic drugs-should be the treatment of choice for ES.
Key Words: fibrillation • antiarrhythmia agents • myocardial infarction
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Introduction |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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Electrical storm (ES) describes the phenomenon of rapidly clustering ventricular fibrillation (VF) that necessitates multiple cardioversions (Figure 1
). The
conventional antiarrhythmic drug therapy for ES recommended by the
American Heart Association Advanced Cardiac Life Support (ACLS)
guidelines often fails to maintain sinus rhythm.1 The
unfolding scenario is swift and desperate. Patients repeatedly go into
VF, are given antiarrhythmic medication serially, and receive repeated
electrical shocks in an attempt to cardiovert the arrhythmia.
Despite these efforts, most ES patients die—many within minutes or
hours—especially if they have had a recent myocardial infarction (MI)
or ongoing myocardial ischemia.1 2
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Other phenomena probably bear on the development of ischemic VF. Increased sympathetic activity is known to contribute to it3 4 5 6 ; sympathetic blockade is known to prevent ventricular arrhythmias in the same animal model.5 6 7 8 9 These complementary observations in animals support the finding from clinical trials of post-MI patients that sympathetic blockade, either in the form of ß-blockade or left stellate ganglionic blockade (LSGB), prevents episodes of VF and sudden death.10 11 12 13 We therefore postulated that sympathetic blockade would be effective for treatment of ES in patients with a recent MI or ongoing myocardial ischemia. We prospectively evaluated the efficacy of sympathetic blockade in treating patients with ES and compared the outcome with that of patients with ES treated according to ACLS guidelines.
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Methods |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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Patients
Patients included in this study all had ES with a recent MI. ES was defined as
20 ventricular
tachycardia (VT)/VF episodes per day or 4 VT/VF episodes
per hour. Recent MI was defined as occurring within 72 hours to 3
months before the onset of ES. We excluded patients in whom the onset
of MI was <72 hours and those with acute pulmonary edema,
previous treatment with intravenous amiodarone,
acute respiratory failure, acquired or congenital long QT syndrome, or
recent coronary revascularization (<1 week
before the onset of ES).
We studied 49 patients with recent MI (36 men, 13 women; mean age
57±10 years) who had ES in the hospital. The ES occurred a mean of
11±10 days after MI (range 4 to 52; median 8 days). The location of
the MI was anterior wall in 28 patients, inferior wall in
6, non–Q-wave in 5, and inferior and anterior walls in 10.
Nineteen patients received acute thrombolytic therapy
at the onset of the MI (Table).
Left ventricular dysfunction was detected in all 49
patients either by angiography or 2D
echocardiography; mean ejection fraction was
32±8% (range 18% to 48%). Twenty-seven patients underwent
coronary artery angiography, which revealed 3-vessel disease in
14 patients, 2-vessel disease in 8, and 1-vessel disease in 5.
Thirty-two patients had evidence of mild congestive heart failure.
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Treatment Protocol
ES is, by nature, refractory to antiarrhythmic therapy; the
cardiac arrest code is always called. Thus, almost all study patients
initially received antiarrhythmic medication according to the ACLS
guidelines before the Arrhythmia Service was consulted.
Forty-one patients also received general endotracheal
anesthesia for 24 to 48 hours after the onset of ES. After
initial treatment during the code, 2 treatment approaches were used.
Patients in group 1 (n=27) received sympathetic blockade treatment
within 1 hour after all of the antiarrhythmic medications initiated
during the code were discontinued. Of these patients, 6 were treated
with LSGB, 7 with esmolol, and 14 with propranolol.
Patients in group 2 (n=22) continued to receive conventional
ACLS-guided therapy. Treatment with sympathetic blockade or ACLS-guided
therapy was determined by physician preference and predilection for the
use of either approach.
ACLS Protocol
In accordance with the ACLS guidelines,14 lidocaine
(1 mg/kg IV bolus) was the first antiarrhythmic drug given to treat VF.
This was repeated if VF continued and was followed by a continuous
infusion of lidocaine (1 to 4 mg/min). If sinus rhythm was not
restored, a 100-mg bolus dose of procainamide was given every 5
minutes up to a total dose of 500 to 1000 mg, followed by a continuous
infusion of 2 to 4 mg/min. Alternatively, an initial 5-mg/kg IV dose of
bretylium tosylate was given and repeated every 5 minutes to the
maximum of 25 mg/kg if VF episodes continued.
All 22 patients in group 2 were treated with lidocaine. Sixteen were also treated with procainamide and 18 with bretylium. Twelve patients received all 3 drugs at a given period of the treatment.
Sympathetic Blockade
The choices for sympathetic blockade therapy were LSGB or
ß-blockade. Either intravenous esmolol or
propranolol was the ß-blocking agent used.
Intravenous propranolol was given as a
0.15-mg/kg dose over a period of 10 minutes and then as a 3- to 5-mg
dose every 6 hours to maintain sinus rhythm unless the heart rate
dropped below 45 bpm. Intravenous esmolol was given as a
300- to 500-mg/kg loading dose for 1 minute followed by a
maintenance dose of 25 to 50 mg ·
kg-1 ·
min-1. The
maintenance infusion was titrated upward if necessary at 5- to
10-minute intervals until a maximum dose of 250 mg ·
kg-1 ·
min-1 was reached.
After informed consent was obtained, LSGB was performed by the anterior paratracheal approach. A 21-gauge needle was passed anteriorly between the trachea and the carotid artery to within several millimeters anterior to the lateral process of the spine. Ten to 20 mL of 1% xylocaine (without epinephrine) was injected until Horner’s syndrome or partial Horner’s syndrome developed. A repeat injection with 10 mL of 0.25% marcaine or xylocaine (without epinephrine) was given as needed.
The choice of sympathetic blockade therapy was based on the circumstances. Intravenous propranolol was used most often because of its ease of use and ready availability; LSGB required consultation with an anesthesiologist knowledgeable about the procedure, which was impractical for many of our ES patients.
Long-Term Care
After the initial acute sympathetic blockade treatment, patients
who were able to take oral drugs were also given oral
amiodarone. A 1200- to 1600-mg/d loading dose was given for 4
to 7 days. This was followed by a 600- to 800-mg/d intermediate dose
for 1 week. A 200- to 400-mg/d maintenance dose was continued
for the duration of the study. Group 1 patients who survived continued
to take oral ß-blocking agents (either 40 to 120 mg/d
propranolol or 50 to 100 mg/d atenolol). We did not perform
permanent sympathectomy in our patients. Implantation
of an internal cardioverter-defibrillator or myocardial
revascularization after ES subsided was performed
at the physician’s discretion.
Data and Statistical Analysis
Continuous variables are presented as
mean±SD. A Student’s t test and Fisher’s exact test were
performed when appropriate. The Kaplan-Meier life-table
analysis compared the cumulative survival rates of the 2
groups. The start time of the life-table analysis began at 4
hours after the initiation of the cardiac arrest code; this excluded
the possibility of treatment bias by avoiding inclusion of patients
whose arrhythmias were too severe and irrecoverable. For this
reason, 3 group 2 patients who died within that period were excluded
from the analysis. A value of P <0.05 (2-tailed)
was considered significant.
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Results |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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Group 1 (patients treated with sympathetic blockade) and group 2 (patients treated according to the ACLS guidelines) were similar with regard to clinical characteristics and the location of MI (Table
). Most of our patients were receiving calcium
antagonists (73%), but only 18% and were receiving
ß-blockers and 53% were receiving ACE inhibitors. There
were no differences in the relative risk of death among the patients
taking calcium antagonists, ß-blockers, or ACE
inhibitors compared with those who were not. The degree of
left ventricular dysfunction based on ejection fraction was
comparable between the 2 groups (Table). The
QTC interval was normal in both groups.
VF Episodes and Associated Factors
The first VF episode occurred 12±10 days after the onset of MI in
group 1 and 11±12 days after the onset of MI in group 2. All group 1
patients continued to have multiple VF episodes before sympathetic
blockade (25±12). The mean period from the onset of VF to
administration of sympathetic blockade was 20±21 hours (median 11
hours); for ß-blockade it was 17±14 hours (median 10.5 hours) and
for LSGB it was 35±32 hours (median 18 hours). After sympathetic
blockade therapy was initiated, the mean number of VF episodes was
reduced to 2.6±1.7 in group 1 (P<0.01). In contrast, 91%
of patients in group 2 continued to have VF episodes. The total VF
episodes were 28±15 for group 1 and 38±20 for group 2
(P<0.01). Both groups had sinus tachycardia;
mean baseline heart rate was 109±18 bpm in group 1 and 103±14 bpm in
group 2, suggesting the presence of increased sympathetic activity.
Atrial tachyarrhythmias occurred in 26% of group 1
patients and 45% of group 2 patients (difference not significant).
Figure 1 is an example of ES in 1 of our patients. This
patient had sinus tachycardia and runs of nonsustained
polymorphic VT, many degenerating to VF requiring multiple
cardioversions over 5 minutes. After intravenous lidocaine
and bretylium were given, multiple VF episodes continued until
intravenous propranolol abolished the VF
episodes (Figure 2).
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Figure 3 shows the effects of LSGB on a
patient who had VT/VF episodes 12 days after MI. Twenty minutes before
the first VF episode, the patient learned that a family member had
died; he became agitated and depressed and had VF shortly thereafter.
Lidocaine and procainamide increased the number of VT/VF
episodes. LSGB was performed and abolished the VT/VF. When the effects
of the LSGB dissipated, VT/VF recurred. When the stellate ganglia were
blocked, VT/VF again subsided. This patient was subsequently discharged
and remained arrhythmia-free during follow-up.
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Clinical Outcomes
First Week
Twenty-four of the 49 patients died within 1 week of the onset of
ES (Figure 4). The mortality rate within
1 week of treatment was substantially higher in group 2 than in group
1. Eighteen (82%) group 2 patients died, all of refractory VF. Only 6
(22%) group 1 patients died: 3 of refractory VF, 2 of
electromechanical dissociation, and 1 of anoxic encephalopathy and
resulting in asystole. The relative risk of dying within 1 week for the
group 2 patients was 3.68 compared with the group 1 patients (range
1.77 to 7.66; P<0.0001). Twenty of the 27 group 1 patients
and 5 of the 22 group 2 patients were also treated with oral
amiodarone after endotracheal anesthesia was
terminated. A larger proportion of group 1 patients was treated with
concomitant amiodarone because most group 2 patients died or
failed to respond to the antiarrhythmic therapy guided by ACLS,
continued to have multiple VF episodes, and continued be treated with
endotracheal anesthesia for the necessity of multiple
cardioversions, whereas group 1 patients had a drastic reduction of the
number of VF episodes and could be off the ventilators.
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Figure 5 shows the Kaplan-Meier survival
curves for the 2 groups. Group 1 patients (sympathetic blockade) had a
dramatically better outcome than group 2 patients (ACLS treatment).
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One Year
Twenty patients from group 1 survived and were discharged from the
hospital. Two group 2 patients who survived the first week had
recurrent VF and died; thus, only 2 group 2 patients survived to
discharge from the hospital. All patients were followed at the
Arrhythmia Clinic (follow-up 17±8 months; range 6 to 34
months). Nine patients underwent coronary
revascularization (6 coronary artery bypass
graft surgery and 3 angioplasty); all procedures were performed within
3 months after discharge from the hospital for documented recurrent
ischemia. One group 1 patient died of complications of
coronary artery bypass graft surgery. Four patients who
underwent the coronary artery bypass graft surgery showed
dramatic improvement, and their left ventricular function
returned to almost normal (ejection fraction increased from 29±5% to
51±4%); this suggests the possibility of "hibernating"
myocardium.15 Two patients (1 from each group)
died of congestive heart failure. There was no arrhythmic death during
the follow-up period, and the 7 patients who had received an
implantable cardioverter-defibrillator did not receive shocks from the
device. Eighteen of the 27 group 1 patients continued to fare well
during the follow-up period, compared with 1 of the 22 group 2
patients.
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Discussion |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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Patients with ES have a very high mortality rate, especially when treated according to the ACLS antiarrhythmic medication guidelines. The short-term outcome (1 week) is much better in patients treated with sympathetic blockade; the 1-week survival rate for group 1 (patients treated with sympathetic blockade) was 82%, compared with 22% for the group 2 (patients treated according to the ACLS guidelines). Patients who survived the first week after the onset of ES continued to do well during the 1-year follow-up period (Figure 4
). Therefore, the
data forcefully argue against using the ACLS guidelines to treat ES.
Sympathetic blockade (ß-blockade or LSGB), particularly when combined
with oral amiodarone, is much more effective than class I
antiarrhythmic drugs or bretylium. The finding that sympathetic
blockade dramatically improves the mortality rate fits with the
evidence that when post-MI patients are treated with
ß-blockade,11 13 they live longer and fare better.
Why does sympathetic blockade succeed when ACLS-guided
antiarrhythmic treatment fails? Abundant evidence in postinfarct animal
studies show that class 1 drugs can increase the propensity for
VF.16 17 18 Moreover, class I drugs exert negative inotropic
effects and worsen cardiac function, leading to more heart failure,
more VF episodes, and, eventually, death in patients who have left
ventricular dysfunction and mild congestive heart failure,
as did our patients.19 20 21 Conversely, sympathetic
blockade exerts beneficial effects in post-MI patients. Lombardi et
al6 demonstrated that sympathetic activity reflexively
increased during myocardial ischemia; this in turn contributed
to a decreased VF threshold during coronary artery occlusion.
Sympathetic blockade or vagal stimulation increase the VF threshold in
the same model.6 Schwartz et al10 showed that
oxprenolol (160 mg) or a surgically selective left stellate
sympathectomy prevented sudden cardiac death in
high-risk post-MI patients compared with placebo. Even though LSGB had
an 
-blocking effect in addition to ß-blocking effect, our data and
those of Schwartz et al demonstrated that LSGB and ß-blockade are
equally effective in treating post-MI life-threatening
ventricular tachyarrhythmias.
These findings indicate that post-MI patients with ES have significantly increased sympathetic activity, which plays a major role in the pathophysiology of ventricular arrhythmogenesis. Zipes4 reported that MI and myocardial ischemia affected the denervation of sympathetic-parasympathetic fibers, which enhanced sympathetic activity, thereby increasing the propensity for ventricular tachyarrhythmias. Our patients who had left ventricular dysfunction also manifested clinical signs of congestive heart failure and increased sympathetic activity. Sympathetic blockade therapy, while preventing ventricular tachyarrhythmias, did not worsen either cardiac function or heart failure. This finding confirms that of the Beta-Blocker Heart Attack trial that the more severe the left ventricular dysfunction, the more beneficial ß-blockade is.11 13 However, in 2 of our study patients who received ß-blocking agents, electromechanical dissociation developed and the patients died. Nevertheless, the data argue strongly that patients who have had a recent MI and profound left ventricular dysfunction should receive ß-blockade or sympathetic blockade immediately after the onset of VF rather than some time later.
All study patients who were able to take oral drugs were immediately started on oral amiodarone along with ß-blockade medication; amiodarone was continued during the follow-up period. All patients who survived the first week after ES did well over the long term. This observation dovetails with the finding of recent major trials on the beneficial effects of oral amiodarone in post-MI patients.22 Patients who received a combination of oral amiodarone and ß-blockade had the best outcome. There is also evidence supporting the hypothesis that intravenous amiodarone helps these patients.23 24 The data did not show, however, that intravenous amiodarone yielded a better survival rate than bretylium.24 Randomized trials comparing intravenous amiodarone and ß-blockade therapy are needed to determine whether sympathetic blockade is better than intravenous amiodarone.
Our data also confirm the findings from the studies by Lie et al25 and Braat et al26 that the presence of malignant ventricular arrhythmias during the subacute phase of MI in patients with poor ventricular function portends a grave outcome. Despite the initial fury of the VF episodes during ES, if the patient weathers the storm, most stay arrhythmia-free over the long term. It is widely known from animal experiments in the ischemic MI model that after the infarction, the myocardium heals and associated electrophysiological abnormalities develop, serving as a substrate for ventricular tachyarrhythmias.5 23 This is especially true when modulating factors (eg, increased sympathetic activity and heart failure) are present. After the myocardium is completely healed, many of these electrophysiological abnormalities disappear. This improvement, in tandem with the favorable changes in modulating factors (ie, decreased sympathetic tone or myocardial ischemic episodes), cause the life-threatening ventricular arrhythmias to disappear. One could speculate that our study patients fit this model. If these patients survive ES, the myocardium heals; when the ischemia is subsequently treated either by revascularization or medication, the arrhythmias then subside.
Study Limitations
Our study protocol was limited in that patients could not be
randomly assigned to a treatment arm because of the emergent nature of
ES. Because there are no data showing the relative efficacy of either
treatment arm, treatment selection (either sympathetic blockade or
ACLS-guided therapy) was determined by physician preference. However,
there were no differences in the clinical characteristics between the 2
groups. Also, group 1 patients continued to have multiple VF episodes
before sympathetic blockade was initiated. Thus, it is unlikely that
patients whose arrhythmias were less recalcitrant had been
selected for sympathetic blockade treatment.
Summary
Although ACLS-guided therapy is most often used to treat patients
who have ES, overwhelming data in both animal experiments and clinical
trials show that class 1 antiarrhythmic drugs are harmful rather than
helpful.21 Our study suggests an alternative course:
sympathetic blockade. Sympathetic blockade along with oral
amiodarone unequivocally improves the survival rate of these
patients. If they survive ES, these patients do well over the long
term. We propose that patients with ES, even if they have mild
congestive heart failure, left ventricular dysfunction, or
hemodynamically compromised arrhythmias, should
be given ß-blockers. Further, patients who have had an MI and left
ventricular dysfunction should receive ß-blockers whether
or not they have ventricular
arrhythmias11 13 Doing so may prevent ES
altogether. On the basis of the evidence from our study, this new
direction, although in the past the path less traveled, is the better
way to save lives.
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Acknowledgments |
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We thank Shahbudin H. Rahimtoola, MD, for his critique of the manuscript. We also thank Mary Kolb and Margaret Inman for their editorial assistance.
Received December 8, 1999; revision received March 1, 2000; accepted March 10, 2000.
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D. Bansch, F. Oyang, M. Antz, T. Arentz, R. Weber, J. E. Val-Mejias, S. Ernst, and K.-H. Kuck Successful Catheter Ablation of Electrical Storm After Myocardial Infarction Circulation, December 16, 2003; 108(24): 3011 - 3016. [Abstract] [Full Text] [PDF]
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