ILLUSTRATIVE CASE
Supraventricular Tachycardia Associated With Severe Anemia
Daniel J. Corwin, MD* and Richard J. Scarfone, MD*†
Abstract: We present the unusual case of a 7-year-old girl with severe
iron-deficiency anemia who concurrently was determined to be in a supra-
ventricular tachycardia (SVT) rhythm. To our knowledge, the association
of anemia with SVT has not been reported previously. We review the
presentation of SVT, management strategies for treating both severe
anemia and SVT, risks and benefits of using the classic treatments for
SVT in a severely anemic patient and discuss iron-deficiency anemia–related
cardiac disease.
Key Words: anemia, supraventricular tachycardia, iron-deficiency
(Pediatr Emer Care 2017;00: 00–00)
CASE
A 7-year-old African American girl with no chronic medical
conditions presented to our emergency department with a com-
plaint of “heart racing.” She noted that for the past 3 to 5 days,
she was experiencing shortness of breath and a sensation that
her heart was “beating fast.” She also reported 2 days of feeling
more tired than normal. She had never experienced this sensation
before. She denied any fever or decreased oral intake. She denied
vomiting or diarrhea. Her past medical history was notable for a
small bowel obstruction that was repaired with jejunal resection
and jejunoplasty with primary anastomosis on her first day of
life. She had no known sequelae after this surgery. Her mother
reported a well-balanced diet without excessive milk intake.
She had no family history of any hemoglobinopathies or
cardiac arrhythmias.
Her initial physical examination was notable for an extremely
pale child who was awake, alert, and talkative. Her vital signs were
notable for a temperature of 36.5°C, a heart rate of 206 beats
per minute, a respiratory rate of 24 breaths per minute, a blood
pressure of 111/55 mm Hg, and an oxygen saturation of 100%
on room air. Her initial cardiac examination was notable for
tachycardia without murmurs or gallops. Her lungs were clear
without crackles. She had no hepatosplenomegaly or lymphade-
nopathy. Her skin examination was notable for extreme pallor.
She was placed on a cardiac monitor and an electrocardio-
gram (EKG) was obtained (Fig. 1), notable for narrow-complex
tachycardia without clear p-waves; therefore, supraventricular
tachycardia (SVT) was the initial clinical impression. Vagal ma-
neuvers were attempted without a change in the patient's heart
rate. Point-of-care laboratory testing revealed a hemoglobin (Hg)
of 3.7 g/dL and a hematocrit (HCT) of 11% (Table 1). Having
confirmed the clinical impression of severe anemia and not
being aware of any association between anemia and SVT, it was
decided to administer a 10-mL/kg normal saline fluid bolus and
judge her clinical response. Shortly after receiving the fluid
From the *Division of Emergency Medicine, The Children's Hospital of
Philadelphia; and †Perelman School of Medicine, University of Pennsylvania,
Philadelphia, PA.
Disclosure: The authors declare no conflict of interest.
Reprints: Daniel Corwin, MD, Division of Emergency Medicine, The
Children's Hospital of Philadelphia, Colket Translational Research Bldg,
3501 Civic Center Blvd, 9th Floor/CTRB 9013B, Philadelphia, PA 19104
(e‐mail: corwind@email.chop.edu).
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ISSN: 0749-5161
Pediatric Emergency Care • Volume 00, Number 00, Month 2017
Copyright © 2017 Wolters Kluwer Health, Inc. Unauthorized reproduction of this article is prohibited.
bolus, her heart rate decreased to the 180s, seeming to make
SVT less likely and pointing to anemia with compensatory sinus
tachycardia as a possible alternative explanation for her clinical
picture. At this point, her complete blood count results returned
and were notable for an Hg of 2.3 g/dL, HCT of 9.6%, mean
corpuscular volume of 59.3 fL, reticulocyte count of 0.2%, and
a red blood cell distribution width coefficient of variation of
33.3% (Table 1). Other cell lines were normal, and the peripheral
smear revealed 3+ anisocytosis, 3+ poikilocytosis, 3+ hypochromia,
and 3+ microcytosis.
Shortly after the laboratory values resulted, the patient's
blood pressure began slowly decreasing, eventually reaching sys-
tolic pressures of 72 to 78 mm Hg. She maintained normal mental
status and peripheral perfusion. A type and screen result was
pending, thus she was transfused with O negative blood at a rate
of 2.5 mL/kg per hour. Her heart rate was stable in the 180s and
her blood pressure improved to 80s/50s. She was transferred to
the pediatric intensive care unit with a heart rate in the 180s with
a stable blood pressure.
Approximately 6 hours after emergency department arrival,
while in the intensive care unit, the patient coughed, and her heart
rate abruptly dropped to 84 beats per minute. A second EKG was
obtained, which showed a sinus rhythm without evidence of
preexcitation (Fig. 2). Her heart rate remained between 80 and
120 beats per minute during the remainder of the hospital stay.
Based on this abrupt resolution of tachycardia, coupled with
the inability to discern p-waves and the regularity of the rhythm on
the initial EKG, a reciprocating tachycardia (either atroventricular
reentry tachycardia [AVRT] or atrioventricular nodal reentry
tachycardia [AVNRT]) was thought to be the etiology of her
clinical presentation. An echocardiogram showed mildly dimin-
ished left ventricular systolic shortening, mild dilation of the left
ventricle, mild dilation of the right ventricle, mild right ventric-
ular hypertrophy, and pulmonary artery pattern suggestive of
elevated pulmonary artery pressure.
During the hospitalization, she was transfused with a total of
20 mL/kg of packed red blood cells over 48 hours, and her Hg
was 9.0 g/dL before discharge. Iron studies had confirmed the
diagnosis of iron-deficiency anemia with a transferrin satura-
tion of 3% and a ferritin of 1.7 ng/mL. She was noted to have
a negative hemoccult testing of her stool and no signs of bleeding
on rectal examination. The result of screening for celiac disease
was negative. She was discharged home to continue iron supple-
mentation in addition to atenolol for her newly recognized SVT.
She has followed up with gastroenterology service, and it
was presumed that either small bacterial overgrowth or primary
jejunal malabsorption secondary to her previous surgery was
the etiology of her severe iron deficiency. However, given that
iron is predominantly absorbed in the proximal duodenum and
that the patient was not previously anemic, this explanation
seems less likely. On follow-up with the cardiology service
2 months after her initial visit, she had remained well, and her
atenolol was discontinued.
DISCUSSION
This was an unusual case of a child who presented with ex-
treme pallor and tachycardia who was subsequently diagnosed
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Corwin and Scarfone Pediatric Emergency Care • Volume 00, Number 00, Month 2017

FIGURE 1. Initial EKG.

with both iron-deficiency anemia and SVT. To our knowledge, Most of the cases of SVT in pediatrics (>90%) are due to either
there have not been previous reports of these 2 conditions existing an extranodal accessory pathway (atrioventricular reentrant
concurrently in the same patient. tachycardia, which includes Wolff-Parkinson-White syndrome)
Supraventricular tachycardia, an abnormally fast rhythm or a reentry circuit using the atrioventricular node (atrioventricu-
originating above the ventricles, is the most common dysrhythmia lar nodal reentrant tachycardia).2 In AVRT, the accessory path-
seen in pediatrics.1 The incidence is estimated to be between 1 in way may either conduct antegrade (defined as preexcitation, as
250 and 1 in 1000 children.2 The peak age ranges at initial diag- in Wolff-Parkinson-White syndrome) or retrograde (in which
nosis are infancy, early childhood (6–9 years), and adolescence. case the pathway is “concealed,” because the EKG in sinus
rhythm appears normal) but uses the atrioventricular (AV) node
as 1 arm of the conduction pathway. In AVNRT (more likely to
TABLE 1. Laboratory Values occur in older children and adolescents), 2 conducting pathways,
a “fast” and a “slow” pathway, create a reentrant loop within the
Normal Range AV node.
Test Value and Units Treatment of SVT is focused on interrupting the reentrant cir-
White blood cell count 8.8 4.27–11.40 thou/uL cuit that passes through the AV node and is based on the physio-
Hg 2.3 11.5–15.5 g/dL
logical stability of the patient.3,4 Stable patients can be converted
to sinus rhythm using vagal maneuvers (ie, Valsalva maneuver,
HCT 9.6 35.0%–45.0%
ice to the face to induce the diving reflex) or pharmacologically
Platelets 718 150–400 thou/uL with adenosine. Unstable patients with poor perfusion, congestive
Mean corpuscular volume 59.3 77.0–95.0 fL heart failure, or altered mental status should be treated emergently
Red blood cell distribution width 33.3 12.2%–14.4% with synchronized cardioversion.
coefficient of variation This case presented several diagnostic and management
Reticulocyte count 0.2 0.98%–1.94% challenges including distinguishing sinus tachycardia from SVT
Lactic dehydrogenase 720 420–750 U/L in a patient with obvious and extreme pallor. Generally, heart rates
Uric acid 2.4 2.0–5.0 mg/dL above 220 beats per minute in children younger than 1 year and
Iron 11 25–140 mcg/dL above 180 in children older than 1 year are consistent with
Transferrin 278 180–370 mg/dL SVT.1,3 With SVT, p-waves are not visible, as opposed to sinus
TFN Saturation 3 6%–40% tachycardia where they theoretically should be observed. How-
Calculated TIBC 389 250–520 mcg/dL
ever, with a very rapid sinus rhythm, it can be difficult to distin-
guish p-waves on a cardiac monitor or EKG. Typically, both rate
Ferritin 1.7 10–70 ng/mL
and beat-to-beat intervals are fixed in SVT, as opposed to varying
HgA 98.3 96.4%–98.2% in sinus tachycardia.3 Thus, the fact that this patient's heart rate did
HgA2 1.7 1.8%–3.6% decrease substantially upon receiving intravenous fluid seemed to
Parvovirus B19 PCR Negative be more consistent with the response expected with sinus tachy-
Hg indicates hemoglobin; HCT, hematocrit; TFN, transferrin; TIBC, total
cardia and not typically seen with SVT. In addition, postulating
iron binding capacity; PCR, polymerase chain reaction. that she had both extreme anemia and SVT would mean that she
had 2 seemingly unrelated conditions presenting concurrently.

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Pediatric Emergency Care • Volume 00, Number 00, Month 2017
FIGURE 2. Second EKG.
On the other hand, the initial heart rate above 200 was more con-
sistent with SVT, and had this patient's relative hypotension been
purely due to acute blood loss and hypovolemic shock, one would
have expected a more rapid and pronounced decrease in her
degree of tachycardia in response to fluids.
One management consideration is the safety and efficacy of
trialing adenosine as both a diagnostic and therapeutic measure in
this setting. In a multicenter review on the use of adenosine, only
minor adverse events were observed in 98 cases of use (including
nausea, flushing, and dyspnea) without any hemodynamically sig-
nificant arrhythmias or bronchospasm.5 Patients with congenital
heart disease were included in this sample. However, it should
be noted that all patients in this study presented with SVT. In this
particular patient, concern was raised that the transient asystole
resulting from adenosine use might adversely affect a child with
severe anemia who was relying on tachycardia to adequately
perfuse her end organs.
Another management consideration for this case was the
transfusion rate of packed red blood cells in a severely anemic
patient. Transfusion-associated circulatory overload, which can
lead to heart failure and pulmonary edema, can occur in children,
although it is more common in adults.6 Severely tachycardic pa-
tients have brief diastolic filling times, and the rapid administra-
tion of crystalloid or colloid may precipitate congestive heart
failure. For these reasons, by convention, it is common practice
to slowly transfuse packed red blood cells to prevent volume
overload. We elected to transfuse slowly in this situation, because
even in the setting of relative hypotension, our patient was other-
wise stable with a normal mental status. In addition, the cause of
her anemia and the rate at which it evolved were unclear at the
time of transfusion.
This is the first reported case describing a child with se-
vere iron-deficiency anemia presenting with AVRT or AVNRT.
Schinasi et al7 reported a child with transient erythroblastopenia
of childhood presenting with ectopic atrial tachycardia. Ectopic
atrial tachycardia, as opposed to AVRT or AVNRT, is the result
of rapid, automatic discharge from a focus distinct from the
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Supraventricular Tachycardia
sinoatrial node. The proposed mechanism in that case was re-
duced tissue oxygenation leading to a neurohormonal response
and elevated catecholamines, triggering latent atrial ectopic foci.
In addition, there are cases in the adult literature of iron-
deficiency anemia associated with cardiomyopathy and left ven-
tricular dysfunction, thought to be secondary to either elevated
sympathetic tone due to high-output heart failure or primary
myocyte dysfunction.8 For those cases, iron replacement was
found to reverse cardiomyopathy.9 Our patient did have evi-
dence of left ventricular dysfunction on initial echocardiogram;
second echocardiogram on iron therapy has not been obtained. Ar-
rhythmias as a result of iron-deficiency anemia seem to be less
common, and when occurring, tend to present in elderly patients
and as ventricular premature contractions.10 It is unclear if the
SVT in our patient was secondary to iron-deficiency anemia it-
self or was a preexisting condition unrelated to her
severe anemia.
CONCLUSIONS
The etiology of extreme tachycardia in this patient with
severe iron-deficiency anemia was supraventricular, rather
than sinus, tachycardia. Her tachycardia resolved without pharma-
cologic intervention or signs of end-organ damage. This case
illustrates that these 2 conditions may coexist and highlights
the importance of maintaining a broad differential diagnosis
of the etiology of tachycardia even in the presence of severe anemia.
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