Vol.1, No.2, 8-10 (2013) Open Journal of Emergency Medicine
http://dx.doi.org/10.4236/ojem.2013.12003
Tako-tsubo syndrome after administration of
intravenous adrenaline during atrioventricular block
Manuel Calvo-Taracido, Manuel Almendro-Delia, Juan C. Garcia-Rubira*
Unidad de Gestion de Cardiologia, Hospital Universitario Virgen Macarena, Sevilla, Spain;
*Corresponding Author : [e-mail]
Received 20 October 2013; revised 22 November 2013; accepted 17 December 2013
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ABSTRACT
We describe the clinical case of a 70-year-old
woman with complete atrioventricular block that
after administration of intravenous adrenaline,
developed electrocardiographic changes sug-
gestive of acute coronary syndrome, together
with apical dyskinesia of the left ventricle. After
ruling out the existence of coronary lesions, and
after total recovery of the echocardiographic al-
terations in segmental contractility, she was di-
agnosed as Tako-tsubo syndrome induced by
administration of adrenaline. This is the first re-
port of this syndrome in the scenario of atrio-
ventricular block treated with adrenaline infu-
sion.
Keywords: Adrenaline; Asystole; Atrioventricular
Block; Tako-Tsubo Syndrome
1. CASE REPORT
A 70-year-old woman suffered two episodes of syn-
cope of a few seconds duration at home, with no prior
chest pain. She had a previous history of hypertension,
and no other significant pathologies. At the arrival of the
emergency team, an electrocardiogram was performed,
showing a complete atrioventricular block with episodes
of asystole (Figure 1). Two milligrams of atropine and
adrenaline infusion were administered immediately and
the patient was then carried to the ambulance. A new
electrocardiogram performed then showed intraventricu-
lar conduction disturbance and ST segment elevation in
inferior and anterolateral leads together with the atrio-
ventricular block (Figure 2). The patient suffered several
episodes of syncope in the ambulance, with hemody-
namic instability dur ing all the transport time. On arrival
at the emergency room, a temporary pacemaker was im-
planted, and the adrenaline infusion was retired. De-
creased level of consciousness was the dominant symp-
tom. Serial analysis revealed a modest rise of myocardial
injury markers: Maximum CPK 92 U/L (normal < 195),
Troponine-T 0.64 ng/ml (upper limit 0.05). Transthoracic
echocardiography showed mild concentric hypertrophy
(interventricular septum 13 mm, posterior wall 14 mm),
and dyskinesia of the apical segments. Global systolic
function was moderately depressed (left ventricular ejec-
tion fraction 0.45). Coronary angiography showed no an-
giographic lesions. On the third day she recovered sinus
rhythm at 88 beats per minute with deep T-wave inver-
sion in precordial leads (Figure 3). She underwent a
permanent DDD pacemaker implantation, and was dis-
charged fully asymptomatic. Control echocardiography 4
weeks later showed normal contractility.
2. DISCUSSION
Tako-tsubo syndrome was first described in Japan by
Sato et al. [1]. It is characterized by a transitory ven-
tricular dysfunction associated with elevation of myo-
cardial damage enzymes in small amount in the absence
of coronary lesions. Prognosis seems to be better with
thi s syn drome than with the acute coronary synd rome [ 2] .
ST-segment elevation is one of the characteristic presen-
tations of this syndrome, and frequently involves anterior
and inferior derivations [3], as it occurred in our case in
the electrocardiogram of the early hours after admission.
Other patients do not show this pattern, but only have
T-wave inversion. The T-wave inversion presentation
seems to be more frequent in Caucasian people [4].
There are several hypotheses about the pathophysiol-
ogy of this syndrome; the most accepted is the catechol-
aminergic hypothesis. According to it, high levels of ca-
thecolamines induced by stress result in myocardial

M. Calvo-Taracido et al. / Open Journal of Emergency Medicine 1 (2013) 8-10 9
Figure 1. First electrocardiogram showed complete atrioventricular block.
Figure 2. After adrenaline infusion, ST segment suggestive of myocardial infarction was observed (see leads DII, DIII and aVF).
Figure 3. After recovering atrioventricular conduction, right bundle branch block and deep negative T waves appeared.
toxicity, either by excesive stimulation of adrenorecep-
tors and by microvascular dysfunction [5]. Plasma cate-
cholamine levels have been found 3 times higher in pa-
tients with stress-related myocardial dysfunction com-
pared with those in patients with Killip class III myocar-
dial infarction [6]. Such levels overcome the physiologi-
cal activation of beta adrenergic receptors in myocytes,
and their coupling switches from Gs protein to Gi protein.
As a consequence, the contractility is reduced, and the
cell is protected from necrosis by this mechanism. The
greater beta adrenergic receptor density in apical myo-
cardium might explain the typical distribution of con-
tractility alterations in Tako-Tsubo ca rd iomyopat hy [7].
A few cases have been reported following administra-
tion of intravenous adrenaline under specific situations,
as for treating anaphylactic reaction [8], but not in the
scenario of atrioventricular block and asystole. Adrena-
line, isoprenaline, and dopamine, are the recommended
drugs in the treatment of symptomatic bradycardia not
responsive to atropine, despite the well-known potential
adverse effects, because of the need of restoring a stable
heart rhythm [9]. Our case report calls for attention about

M. Calvo-Taracido et al. / Open Journal of Emergency Medicine 1 (2013) 8-10
10
the convenience of recommending an electrocardiogram
whenever adrenaline treatment has been administered,
and perform an echocardiogram and determinations of
troponine or othe r necros is mark ers if significant ch an g es
are found on them. Although a single case report does
not have strength to generalize such a recommendation,
clinicians involved in emergency departments should be
aware of this possibility.
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