American Journal of Emergency Medicine (2009) 27, 901.e1–901.
e2
Case Report
Adenosine-induced cardiopulmonary arrest in a patient
with paroxysmal supraventricular tachycardia
Abstract
Adenosine is commonly used for the chemical termina-
tion of supraventricular tachycardia. In addition, even when
it is ineffective as an agent of chemical cardioversion, it may
slow the cardiac rate to allow an analysis of the underlying
rhythm. Common adverse effects include facial flushing,
shortness of breath, and chest pain. Major contraindications
include heart blocks and known adenosine hypersensitivity.
This case report illustrates an episode of cardiopulmonary
arrest after adenosine administration and, to the authors'
knowledge, is the first occurrence reported in the literature.
Adenosine is an endogenous purine nucleoside indicated
for the treatment of paroxysmal supraventricular tachycardia
(PSVT). Adenosine receptor stimulation slows cardiac
automaticity through the sinoatrial node and causes atrio-
ventricular nodal blockade to terminate PSVT. Although
adenosine is effective for the conversion of PSVT to normal
sinus rhythm, its use is not without risk. Adenosine is
contraindicated in patients with known hypersensitivity to
the medication, patients with high-degree AV block without
a functioning pacemaker, and patients with sinus node
disease. Potential adverse effects include lightheadedness,
chest pain, and hypotension. Dyspnea has been reported in
up to 12% of patients. Bronchospasm has also been reported,
although the incidence is unknown [1]. Generally, adverse
effects associated with adenosine are self-limited because of
the rapid elimination and short half-life of the drug.
A 61-year-old man with a history of asthma, diabetes, and
hypertension presented to our emergency department (ED)
complaining of palpitations and dyspnea. These symptoms
differed from his usual asthma exacerbations. Initial vital
signs included a heart rate of 154 beats per minute (bpm),
blood pressure of 89/68 mm Hg, respiratory rate of 40 breaths
per minute, and O2 saturation of 97% on room air. The patient
was alert and conversant, and physical examination revealed
a regular tachycardia and bilateral coarse wheezes. The initial
electrocardiogram revealed a narrow-complex tachycardia at
180 bpm, which was interpreted as PSVT. Adenosine 6 mg
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was administered via intravenous push without effect.
Adenosine 12 mg was subsequently administered with
conversion to sinus tachycardia at 130 bpm and otherwise
stable vital signs. Almost immediately thereafter, the patient
complained of worsening dyspnea, and cardiopulmonary
arrest ensued. Pulseless electrical activity was noted, and
resuscitation as per advance cardiac life support guidelines
was initiated, including orotracheal intubation. The patient
developed a wide complex tachycardia, received direct
current cardioversion at 200 J, and converted back to
supraventricular tachycardia with a blood pressure of 158/
108 mm Hg. Diltiazem was administered with conversion to
sinus tachycardia. The patient was admitted to the intensive
care unit. Several days later, he was still dependent on full
mechanical ventilation and showing few signs of meaningful
neurologic recovery. He received a tracheostomy and
gastrostomy tube, and was ultimately transferred to a long-
term care facility.
The adverse pulmonary effects of adenosine remain
unclear. It is believed that adenosine may work through
indirect inflammatory mediators by activation of the
purinoreceptors, causing bronchospasm [2]. Adenosine's
effects on the pulmonary system are supported by therapeutic
use of its inhibitors. Various therapeutic agents used in the
treatment of asthma, including theophylline, function by
blocking cyclic adenosine monophosphate to prevent
bronchospasm. Thus, it is plausible that adenosine agonists
may cause bronchospasm.
One case of adenosine-induced respiratory failure has been
reported in the literature [3]. A patient with a history of chronic
obstructive pulmonary disease on a treatment regimen that
included theophylline was referred to the ED for evaluation of
PSVT. After receiving adenosine, the patient's rhythm
converted to sinus tachycardia. Shortly thereafter, the patient
became cyanotic and hypoxic, and PSVT recurred. The patient
was ultimately intubated and treated with intravenous
verapamil. Two months after hospitalization, the patient had
fully recovered. This case was interesting given the con-
comitant use of a known adenosine antagonist, theophylline.
In another study, an analysis of 100 patients who received
adenosine was performed [4]. Two major adverse events,
asystole and ventricular fibrillation, were reported after
adenosine use. These 2 cases identify the potential for serious
901.e2 Case Report

cardiac adverse events after adenosine use. However, neither Timothy J. Meehan MD
case involved treatment of PSVT, and no adverse pulmonary Toxikon Medical Toxicology Fellowship Program
effects were identified. Department of Emergency Medicine
Determining whether true bronchospasm occurs after University of Illinois at Chicago
adenosine administration has proven difficult [2]. Dyspnea is Chicago, IL 60612, USA
commonly reported after adenosine use, and studies have
attempted to differentiate dyspnea from bronchospasm. Burki Benjamin W. Stull MD
et al [5] found that although adenosine administration caused Department of Emergency Medicine
dyspnea in some patients, there were no significant changes University of Illinois at Chicago
seen in measured airway resistance. A similar study involving Chicago, IL 60612, USA
patients receiving adenosine during myocardial perfusion E-mail address: bstull1@uic.edu
imaging found that there were no significant differences in
spirometric parameters of dyspneic patients compared with Heather M. Schumann PharmD
controls [6]. These studies demonstrate that, although Department of Pharmacy Practice
dyspnea is reported by a significant number of patients University of Illinois at Chicago
receiving adenosine, bronchospasm may not be the cause. Chicago, IL 60612, USA
Adenosine treatment of PSVT has previously been
described in a case that resulted in respiratory failure with John L. Zautcke MD
full recovery. The case we report describes cardiopulmonary Department of Emergency Medicine
arrest shortly after adenosine administration for treatment of University of Illinois at Chicago
PSVT, and it is the only adverse event of its kind described in Chicago, IL 60612, USA
the literature. Adenosine has been frequently implicated in
reports of dyspnea. However, studies using airway resistance
and spirometric analysis have demonstrated that this dyspnea
may not reflect true bronchospasm. The exact mechanism by doi:10.1016/j.ajem.2008.11.008
which adenosine may contribute to the development of
respiratory compromise is still ambiguous. Whether the References
developments of the current case were incidental findings
temporally associated with the administration of adenosine [1] Adenocard package insert. Deerfield, IL: Astellas Pharma US Inc.;
or a very rare complication remains to be defined. 2005.
[2] Polosa R, Rorke S, Holgate ST. Evolving concepts on the value of
adenosine hyperresponsiveness in asthma and chronic obstructive
R. Carlin Walsh PharmD
pulmonary disease. Thorax 2002;57:649-54.
Department of Surgery [3] Burkhart KK. Respiratory failure following adenosine administration.
University of Cincinnati Medical Center Am J Emerg Med 1993;11:249-50.
Cincinnati, OH 45267, USA [4] Knight BP, Zivin A, Souza J, et al. Use of adenosine in patients
hospitalized in a university medical center. Am J Med 1998;105:
Kristen L. Felice PharmD 275-80.
[5] Burki NK, Dale WJ, Lee L. Intravenous adenosine and dyspnea in
Department of Pharmacy humans. J Appl Physiol 2005;98:180-5.
Advocate Lutheran General Hospital [6] Balan KK, Critchley M. Is the dyspnea during adenosine cardiac stress
Park Ridge, IL 60068, USA test caused by bronchospasm. Am Heart J 2001;142:142-5.