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(Acta Anaesth. Belg., 2014, 65, 1-8)
Junctional Ectopic Tachycardia after Congenital Heart Surgery
E. Cools and C. Missant
Abstract : Purpose : In this literature review, we try
to give anesthesiologists a better understanding about
Junctional Ectopic Tachycardia (JET), a narrow complex
tachycardia that frequently occurs during and after surgery for congenital heart disease.
Source : Information was found in the databases of
Pubmed, Science Direct, Medline and the Cochrane
Library, by using the mesh terms “Tachycardia, Ectopic
Junctional”, combined with “Diagnosis”, “Etiology”,
“Physiopathology”, “Complications” and “Therapy”.
The publication date of the articles ranged from 1990
to 2012.
Principal Findings : Risk factors for the development
JET are surgery near the AV node, a duration of cardiopulmonary bypass longer than 90 minutes, young age,
the use of inotropic drugs and hypomagnesaemia.
The diagnosis of Junctional Ectopic Tachycardia can
be made on a 12-lead ECG, demonstrating a narrowcomplex tachycardia with inverted P-waves and VA
dissociation. Adenosine administration and an atrial
electrocardiogram can help to confirm the diagnosis.
If JET has a minimal impact on the hemodynamic status of the patient, risk factors should be avoided and
the adrenergic tonus should be reduced. Hemodynamic
unstable JET can be treated by amiodarone, hypothermia and pacing. Extracorporeal membrane oxygenation
(ECMO) and radiofrequency or cryoablation are treatment options for life-threatening and resistant JET.
Conclusion : JET is the most frequent arrhythmia during
and after congenital cardiac surgery. The ECG is the
only available method to diagnose JET, demonstrating
inverted P-waves and VA-dissociation. Amiodarone
seems to be the most effective treatment option, because
it can restore sinus rhythm and reduces the JET rate.
Keys words : Junctional Ectopic Tachycardia ; Con­
genital Cardiac Surgery ; Tachycardia.
important cause of morbidity and mortality related
to congenital heart surgery. The tachycardia and
the loss of atrial-ventricular synchrony can lead to
severe hemodynamic instability (2).
JET arises near the AV node (junctional), where
an ectopic focus starts to fire automatically with a
frequency of 170 to 260 beats per minute (tachycardia). The impulses can be conducted to the atria
and ventricle at the same time (ventriculo-atrial
association­) or more impulses can be conducted to
the ventricle than to the atria (ventriculo-atrial dissociation) (3). Frequently, another supraventricular
tachyarrhythmia precedes JET. With an incidence
reported ranging from 2 to 11.2%, JET is the most
frequent arrhythmia after congenital cardiac surgery (4) and mortality rates have been reported
to vary from 3 to 13.5% (5, 6). In the majority of
cases, JET occurred immediately after surgery or
during the first post- operative day (5). In very rare
occasions, JET can occur as late as 50 days after
surgery (7).
The diagnosis of JET can be difficult. Some
medications which are used to treat tachyarrhythmia
that have a strong resemblance with JET, can cause
an aggravation of the arrhythmia and should be
avoided (8). The exact cause of JET is not known,
but several associations and predictors of JET
have been studied and identified. Early attention to
these factors makes it possible to avoid them when
possible and to create preventive strategies. While
there are many ways to successfully treat JET, there
is no consensus about the best treatment options.
Many anti- arrhythmic drugs have been used, but
some of them have important side- ffects and should
be avoided. JET is a self- imiting arrhythmia. In
Introduction
Junctional Ectopic Tachycardia (JET) or Hisbundle tachycardia is a narrow complex tachycardia
that can present as a primary idiopathic arrhythmia
during infancy (so called congenital JET), but
most often occurs in the postoperative period
after congenital cardiac surgery (1). JET is an
Evelien Cools, MD ; Carlo Missant,MD, PhD.
Department of Anesthesiology, University Hospitals Leuven
and the Department of Cardiovascular Sciences, KU
Leuven, Belgium
Correspondence address : Prof Dr Carlo Missant, Department
of Anesthesiology, University Hospitals Leuven, Herestraat
49, 3000 Leuven, Belgium. Tel : +32 16 34 42 70. Fax :
+32 16 34 42 45. E-mail : [email protected]
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e. cools and c. missant
most instances it will resolve spontaneously, within
2 or 3 days (9). It is, however, difficult to predict
when the resolution of the arrhythmia will occur.
Pathophysiology
The exact cause of JET is still not completely
understood. Surgery near the AV node or the
proximal conduction system (such as VSD closure
or RV outflow tract repairs) seems to be an important
factor in the pathogenesis and increases the risk of
JET (8). During surgery, direct manipulation of the
heart can result in myocardial injury and increase
the electrical excitability (10). Indeed, autopsy
reports have mentioned hemorrhagic tracts that
invaded the tissue near the AV node (11). The
surgeon can reduce the incidence of JET by trying
to minimise the traction and manipulation of the
heart (8). However, this can be difficult to achieve
and furthermore, JET has also been reported in
operations which don’t take place in the area of the
AV node (7).
Risk factors
One can distinguish pre-, per- and postoperative
risk factors for the development of JET.
The age of the patient and surgery near the
AV-node, are preoperative risk factors. The younger
the patient (or the lower the weight of the patient),
the greater the risk of developing JET with associated hemodynamic compromise. Manipulation and
trac­tion during surgery are relatively greater in a
small heart (8, 12). Moreover, the myocardium of
the young child has an increased non-contractile
tissue mass (13) and a sarcoplasmatic reticulum
with a reduced storage capacity for calcium (14).
In addition, the first hours after surgery, systolic
and diastolic function of the heart is impaired due
to postoperative myocardial oedema. Hence, the
cardiac output (which is determined by heart rate
and stroke volume) is more dependent on the heart
rate in these circumstances. During tachycardia, the
ventricle has not enough time to fill in, which will
have a negative impact on the cardiac output. There
is some evidence that JET is more frequently observed in children who have experienced an episode
of heart failure before the actual surgery (5).
Cardio- pulmonary bypass (CPB) and aortic
cross clamping, commonly used during congenital
heart surgery, result in decreased myocardial
perfusion, which possibly can cause myocardial
damage although cardioprotective strategies are
being applied in clinical practice. Per-operatively,
the aortic cross clamp time is the best predictor of
JET (4, 5). It has been reported that a total duration
of CPB longer than 90 minutes, is associated with
an elevated risk to the development of JET and
other heart rhythm disorders (3, 8). Surgeries with
a higher grade of complexity, e.g. redo surgery,
need more manipulation of the heart, have a longer
CPB-time and therefore lead to a higher incidence
of JET (3, 15). To have an idea about the extent
of myocardial injury due to trauma and ischemia,
creatinine kinase (CK-MB), troponin-I and -T can
be measured after CPB. Elevated levels of these
markers have been reported to be associated with an
increased risk of JET (6, 16).
Positive inotropic drugs, hyperthermia, anae­
mia and electrolyte imbalances are all associated
with JET in the per- and postoperative setting.
During weaning from, and sometimes after,
CPB, inotropes such as dobutamine and epinephrine
can be necessary to increase the contractility
of the heart. An important side-effect of these
medications however is their positive chronotropic
and arrhythmogenic effect. This effect is even
more pronounced in the immature myocardium of
the young child and during heart failure, thereby
diminishing the cardiac output and increasing
myocardial oxygen consumption (5).
In addition to positive inotropic drugs, hyper­
thermia and anaemia can also increase the heart
rate and have been shown to be associated with an
increased incidence of JET (1, 7).
While acute electrolyte imbalances definitely increase the incidence of arrhythmias, hypo­
magnesaemia seems to be the most essential in
the pathogenesis of JET (15). Hypomagnesaemia
causes an intracellular potassium deficiency and
an augmented intracellular calcium concentration, leading to an increase in myocardial excitability (17). In addition­, magnesium attenuates the
degree of myocardial necrosis and plays a cardioprotective role in ischemia-reperfusion injury by
decreasing the catecholamine release from the adrenal medulla and adrenergic nerve endings (14).
Many factors can cause hypomagnesaemia during
surgery, e.g. hemodilution, blood loss and transfusions, large amounts of intravenous fluids, increased
urinary loss, catecholamine-induced lipolysis and
ischemia (14, 17). Consequently, magnesium and
the other electrolytes should be measured and corrected repetitively during surgery.
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junctional ectopic tachycardia3
Fig. 1. — Diagnosis of Junctional Ectopic Tachycardia based
on the electrocardiogram. Since JET arises near the AV-node,
it’s a small-complex tachycardia with a ventricular rate ranging
from 170 to 260 bpm. Because of the retrograde activation of
the atrium, the P-wave is negative (18).
Reproduced with permission from RnCeus.com
Fig. 2. — The difficult differential diagnosis with other supraventricular tachycardia. On this ECG, you can see a smallcomplex tachycardia with a heart rate of 260 beats per minute.
P-waves aren’t visible. This narrow-complex tachycardia can
be Junctional Ectopic Tachycardia or another supraventricular
tachycardia. Afterwards, it proved to be Junctional Ectopic
Tachycardia. If the focus of the junctional rhythm lies low
nodal or in the proximal His bundle, the P-wave will coincide
with the T-wave on the ECG (19).
Reproduced with permission from Bash S., M.D.
Diagnosis
The 12-lead electrocardiogram (ECG) is the
only and therefore most important tool to diagnose
JET. Since JET arises near the AV node, it is a
small-complex tachycardia (Fig. 1) (18). Because
of the retrograde atrial activation, the P-wave will
typically be inverted. The timing of the P-wave
depends on the specific location of the ectopic focus.
If the ectopic focus arises at the top of the AV-node,
the P-wave takes place prior to the QRS-complex.
In case of an ectopic focus that lies in the centre
of the AV node, the P-wave will disappear into the
QRS-complex. If the focus lies low nodal or in the
proximal His-bundle, the P-wave will coincide
with the ST-segment or the T-wave (Fig. 2) (3, 19).
Depending on the electrical conduction pattern,
2 types of JET occur in clinical practice. There can
be ventricular-atrial association (VA-association),
where every ectopic beat will be conducted to the
ventricle and atrium : ventricular and atrial rate
are thus equal (1:1). This is more frequently seen
in the younger patients. Most of the time, however,
VA-dissociation occurs and more impulses will be
conducted to the ventricle than the atria and the
atrial frequency will therefore be lower than that of
the ventricle (Fig. 3) (1, 10).
Frequently, other supraventricular tachycardias
or a transient AV block precede JET. In contrast to
other supraventricular tachycardias where the heart
rate suddenly increases (e.g. from 120 to 200 beats
per minute), the heart rate gradually increases over
time in JET. For this reason, JET is said to have a
“warm-up pattern” (1). Hence, the ECG-pattern in
JET isn’t uniform at all. Moreover, a bundle branch
block can also coincide with JET, leading to a broadcomplex tachycardia (Fig. 4A) (1, 20). Therefore,
the differential diagnosis with other arrhythmias
can be difficult.
Fig. 3. — The effect of adenosine on Junctional Ectopic
Tachycardia. During the first 4 ventricular complexes, there
is VA-association : every QRS-complex is followed by an
inverted P-wave. After the 4th and 5th ventricular complex, the
P-wave disappears. This can be normal in Junctional Ectopic
Tachycardia, or can be caused by adenosine. VA-association
occurs more frequently in younger patients (1, 10).
A strategy that is frequently used to
discriminate JET from other forms of tachycardia
is the use of adenosine. Adenosine blocks the
conduction through the AV node and suppresses the
automaticity of the atrial and Purkinje tissue (21).
By blocking the AV node, an atrial tachycardia can
be unmasked and a paroxysmal supraventricular
tachycardia, in which the AV node is a component
of the re-entry circuit, can be terminated. Adenosine
can suppress JET for a very short time, but does
not terminate it (22). In JET with VA-association,
adenosine blocks retrograde atrial conduction and
VA-dissociation appears (Fig. 3) (1, 10, 20). The
recommended dose of adenosine in the diagnosis of
JET is 0.1-0.4 mg/kg intravenously, with a maximum
dose of 6 mg. Because of the short half-life of 20
seconds, adenosine will be preferably administered
via a central venous catheter (21). Side effects of
adenosine are sinus bradycardia, flushing, dyspnea
and nausea. Adenosine should be used with caution
in patients with asthma, sinus node dysfunction and
orthotopic cardiac transplantation (23).
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An important difference between JET and
paroxysmal supraventricular tachycardia is the
response to electrical cardio-version. While PSVT is
sensitive to cardio-version, JET doesn’t react (22).
When the diagnosis of JET remains unclear,
the temporary epicardial pacing wires, which are
placed during surgery, can be used to create an atrial
electrocardiogram (ACG). An ACG can unmask
the P-waves that disappear in the QRS-complex or
T-wave (Fig. 4) (1, 20) and, in addition, demonstrate
VA-dissociation (24). An atrial ECG can be taken
by placing one atrial pacing wire underneath the gel
pad of a precordial chest lead, such as precordial
lead V1. In this way, the ACG and ECG can be
recorded simultaneously and the P-waves will be
augmented on the ECG (20, 25).
Treatment
JET is a self-limiting arrhythmia. However,
no one can predict when exactly the arrhythmia
will resolve. Hence, the loss of VA-synchrony
and tachycardia can cause a severe hemodynamic
instability needing urgent medical treatment.
The pivotal step in the management of JET
consists of correction and avoidance of all possible
risk factors associated with JET and which are
mentioned above.
First, increased adrenergic tone should be
avoided whenever possible as it will accelerate the
JET rate. Therefore, routine critical care (anxiolysis
and continued postoperative sedation) is the
cornerstone measure in the prevention of JET (1).
Similarly, positive inotropic drugs can have
arrhythmic side effects. Although it can be difficult
to avoid these drugs during surgery for congenital
heart disease, they should be used at a dosage as
low as possible. Milrinone, a positive inotropic
drug with phosphodiesterase inhibitor activity can
also be arrhythmogenic, but has the advantage
to have relatively less effect on the heart rate in
comparison to dobutamine and epinephrine because
it acts independently of the β-adrenergic receptor.
Therefore, milrinone should be the positive
inotropic drug of choice, despite the side effect of
severe hypotension (7, 26). Vagolytic drugs, e.g.
pancuronium, mepiridine and barbiturates, should
also be used with caution, as they can increase
the JET rate. Other causes of tachycardia, e.g.
hypovolemia, fever and anaemia, should be avoided
or immediately corrected (26).
During every congenital cardiac surgery,
the haemodynamic status of the patient should be
adequately monitored using invasive arterial blood
pressure, assessment of serum lactate levels, urine
output and (whenever possible) transoesophageal
echocardiography and mixed venous oxygen
(24). While only hypomagnesaemia
saturation proved to be a risk factor of JET, all acute
electrolyte and pH disturbances should immediately
be treated, because they can lead to other forms of
arrhythmias (4).
Amiodarone, a type III anti-arrhythmic
agent with both alpha- and beta receptor blocking
properties, prolongs the action potential and refrac­
tory period of every ventricular contrac­tion (24).
It has the highest efficacy rate for the treatment
of JET and is therefore the first-line treatment
option to restore sinus rhythm and slow the heart
rate (1, 8, 27). Amiodarone should be administered
whenever JET leads to hemodynamic instability.
Possible dosing regimens include the intravenous
administration of one or two loading boluses of
5 mg/kg with a maximum bolus dose of 15 mg/
kg/day. If necessary, these loading boluses can be
followed by a continuous infusion of 10-20 µg/
kg/min, diluted in dextrose 5% (1, 28, 29). The
use of amiodarone in hemodynamic stable JET is
controversial, due to the associated side effects such
as hypotension, bradycardia, AV block and torsade
de pointes (Table 1) (1, 27, 30). The hypotension
can be treated by volume boluses (1) or calcium
gluconate 10% (24). Amiodarone seems to be
effective in the treatment of JET in 80-90% of the
cases (24, 29, 31). A lower body temperature and
a large difference between the arterial and venous
oxygen saturation, which is related to a low cardiac
output, are predictors of failure of amiodarone
therapy. In these particular patients, amiodarone
could be combined with hypothermia to have a
more adequate first line approach (see below) (8).
Once the sinus rhythm has been restored, the
amiodarone infusion can then gradually be weaned.
Because of the prolonged half-life of amiodarone
after prolonged infusion or during hemodynamic
instability, one should monitor for late sinus
bradycardia (24).
Other anti-arrhythmic drugs have only been
tested in small series. The beta-blockers esmolol
and sotalol have both successfully been used in
the treatment of JET, mainly by reducing the JET
rate (1, 5, 24), but have the disadvantage to have a
negative inotropic effect (1). Propanolol only has a
minimal effect when administered during an episode
of JET, but it has been reported that the preoperative
use of propanolol seems to reduce the incidence
of JET (1, 28). Recently, the alpha-2 adrenergic
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junctional ectopic tachycardia5
Table 1
Treatment options for Junctional Ectopic Tachycardia. The most relevant side- effects are mentioned. JET :
Junctional Ectopic Tachycardia, SR : Sinus Rhythm, TdP : Torsade de Pointes, IV : intravenous, ECMO :
extracorporeal membrane oxygenation (1, 8, 19, 22, 24, 27, 32)
Treatment
Effect
Side- effects
Amiodarone
Restoration of SR, reduces JET- rate
Hypotension, bradycardia, AV block, TdP
Beta- blockers
Reduces JET- rate
Negative inotrope
Dexmedetomidine
Restoration of SR, reduces JET- rate
Hypotension, bradycardia, nausea, dry mouth
Hypothermia
Decreases automaticity of ectopic focus,
reduces JET rate and metabolic oxygen
requirements
Metabolic acidosis, peripheral vasoconstriction,
cardiac arrhythmias, coagulation abnormalities
and impaired immunity
Pacing
Establish AV synchrony
ECMO
Extracorporeal heart support
Thrombosis, bleeding, infections and exposure to
additional blood products
Ablation
Destroys the ectopic focus
Complete AV block
agonist dexmedetomidine has drawn quite some
attention. Dexmedetomidine seems to be effective
to restore sinus rhythm during JET by its depressive
effect on the AV node. Advantages compared
with amiodarone are that dexmedetomidine’s side
effects are less pronounced. Dexmedetomidine has
a faster onset of action, prevents shivering during
hypothermia and has sedative, analgesic and anxio­
lytic properties (33). In a very recent paper, Le
Riger and co-workers have successfully used dex­
medetomidine to control JET in an infant after
tetralogy of Fallot repair (32). Unfortunately, the
number of studies about the use of dexmedetomidine
in JET are limited, but its promising effects clearly
makes it an interesting drug for the treatment of JET
in the future (33).
Importantly, certain drugs that are used in
the treatment of supraventricular tachycardia,
can aggravate JET. Supraventricular tachycardia
can be treated with vagal manoeuvers, adenosine,
beta-blockers, amiodarone and calcium channel
blockers. In JET, calcium channel blockers should
be avoided because of the negative inotropic effect
that can induce atrial fibrillation (1, 17, 34). While
digoxine was used years ago to treat JET, it has no
place anymore in the treatment of JET, because of
the increase in JET rate and the myocardial cell
excitability (6, 24). Another difference between
JET and PSVT is the response to electrical cardioversion. While PSVT can be converted to normal
sinus rhythm by electrical cardioversion, JET is
resistant (22).
If amiodarone therapy fails, another treatment
option might be the induction of hypothermia to
32-34°C as it will decrease the automaticity of
ectopic pacemaker cells (1, 6, 22). A decreased
core temperature cannot restore sinus rhythm, but
it can significantly slow the ventricular rate, thereby
ameliorating diastolic filling and hemodynamic
stability. In addition, hypothermia reduces the
metabolic oxygen requirements and the myocardial
work (24). Hypothermia can be induced by cooling
blankets, ice packs or by the administration of
cooled infusion solutions (19). Only a few studies
examined the best way of cooling during JET but it
has been reported that cooling with intravenous cold
saline has the advantage to have less side-effects, to
generate a more homogenous cooling and to have a
better temperature control (35). It is important that,
during hypothermia, the patient must be sedated,
paralyzed and mechanically ventilated to prevent
shivering (1, 8). Hypothermia has a range of sideeffects such as metabolic acidosis, peripheral
vasoconstriction, cardiac arrhythmias and impaired
(19, 24). Therefore,
coagulation and immunity antibiotic prophylaxis should be administered (1).
The duration of cooling varies among the studies :
most of the time, cooling during 1-3 days resolves
JET, but there are case reports where cooling was
necessary for one week (1).
Procainamide, a type I anti- arrhythmic, has
a higher efficiency in the treatment of JET when
combined with hypothermia (28). A bolus of 515 mg/kg, if necessary followed by a continuous
infusion of 20-120 µg/kg/min seems to be effective
in controlling JET. Adverse effects of procainamide
are bradycardia, hypotension and proarrhythmic
effects (24). Procainamide combined with hypo­
thermia could resolve JET in 50-80% of the
cases (31, 35).
If the haemodynamics do not improve after
amiodarone-therapy or hypothermia, cardiac pacing
should be initiated in an effort to establish atrioventricular synchrony (24). Some authors start pacing
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Fig. 5 — Flowchart of the management of JET. JET : Junctional Ectopic Tachycardia, CPB : Cardiopulmonary Bypass, CK- MB :
Creatinine- Kinase, Bpm : beats per minute, VA : Ventriculo- Atrial, ACG : Atrial electrocardiogram, ECMO : Extracorporeal
Membrane Oxygenation.
before inducing hypothermia (1). The pacing rate
should be 5 to 10 beats per minute higher than the
actual JET rate. Pacing can be performed by using
the temporary pacing wires placed during surgery,
by external pads or by trans-oesophageal pacing.
Atrial (AAI), synchronous (DDI) and paired ventricular pacing (in which two stimuli are delivered
to the ventricle in close succession to slow the heart
rate (36) can all be tried to achieve atrio­ventricularsynchrony (1, 24). Pacing should however be
stopped frequently to evaluate the under­lying heart
rate, cardiac output and rhythm. Flecainide, a type
Ic anti-arrhythmic drug, decreases the automaticity
of the ectopic focus and improves the outcome of
JET when combined with atrial pacing. The used
dose of flecainide in JET is a bolus of 2 mg/kg followed by a continuous infusion of 0.40 mg/kg per
hour. Flecainide has a fast onset of action, but it’s
myocardial depressive effect should be closely
monitored (1, 28, 31).
If the JET remains resistant to all of the above
mentioned treatment options or the haemodynamic
imbalance creates a serious life-threatening situa­
tion, the circulation of the child can be supported
by extracorporeal membrane oxygenation (ECMO).
The deleterious side-effects of ECMO should be
outweighed by the life-saving nature of this treatment
strategy (30). Besides ECMO, radiofrequency or
cryoablation might be the ultimate treatment for
JET (24). An important complication of ablation is
the creation of a complete AV block, which needs
pacemaker implantation. Complete AV block has
less frequently been reported after radiofrequency
ablation. ECMO is a more attractive technique
for the treatment of severe hemodynamic unstable
JET (30).
An overview of all possible treatment options
for JET with the associated side effects is given
in Table 1. Figure 5 provides a flowchart of the
management of JET in the perioperative phase.
Conclusion
JET is the most frequent arrhythmia during
and after congenital cardiac surgery. Therefore,
it is important for everybody involved in the
operative care of congenital heart surgery
peri­
patients to recognise and treat JET early. The
ECG is the only available method to diagnose
JET. Adenosine and an atrial electrocardiogram
can help to confirm the diagnosis. Risk factors
are surgery near the AV node, duration of CPB
longer than 90 minutes, a young age, heart failure
before surgery, electrolyte disturbances (especially
hypomagnesaemia), hyperthermia and anaemia. If
JET occurs, the hemodynamic impact should be
examined thoroughly. Many treatment options have
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junctional ectopic tachycardia7
been studied. Of these, amiodarone seems to be the
most effective because it can restore sinus rhythm
and reduces the JET rate. Hypothermia and pacing
are second-line treatment options. Extracorporeal
membrane oxygenation or ablation are necessary
if the hemodynamic status of the patient is really
compromised.
Acknowledgements
This review was funded with instutional grants
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