Initial Workup for Syncope in Children
From The Child's Doctor, Spring 2006
- Sabrina Tsao, MD
- Attending physician, Cardiology; Assistant Fellowship Director, Pediatric Cardiology, Ann & Robert H. Lurie Children's Hospital of Chicago; Assistant professor of Pediatrics, Northwestern University Feinberg School of Medicine
- Disclosure: Dr. Tsao has no industry relationship to disclose and does not refer to products that are still investigational or not labeled for the use in discussion.
Other Disclosure Information
the conclusion of this activity, participants will be able to:
- Differentiate cardiac and non-cardiac causes of syncope
- Recognize "red ﬂags" in history and history that
suggests vasodepressor syncope
- Describe the mechanism of vasodepressor syncope and oral fluid
Syncope is a relatively common, but complex presenting symptom, deﬁned as "a sudden loss of consciousness associated with the inability to maintain postural tone, followed by spontaneous recovery." The term syncope may have different meanings to different people, therefore speciﬁc questions should be asked to help differentiate cardiac causes of syncope from neuropsychogenic and metabolic conditions that can cause a similar symptom. The evaluation starts with a detailed history, physical examination and an electrocardiogram (ECG). Certain "red ﬂags" in the history deserve a more urgent referral to cardiology for additional evaluation, whereas simple vasodepressor syncope can be managed in primary care.
taking history, clarifying the following points should help pediatricians gather
important details about the context and experience of
- What does "black out" mean?
- Was the patient aware of what was going on?
- Could the patient hear people?
- What was the duration of the episode?
- Were there any witnesses?
- Did the patient sustain any injury?
- In what position was the patient when the vasodepressor syncope and oral
ﬂuid management episode occurred?
- What activity was the patient doing when it happened?
"red ﬂags" in the history that signal a need for an urgent pediatric cardiology
referral are described in Table 1.
history that suggests vasodepressor or benign syncope includes triggers such as
positional changes, prolonged standing or sitting, or obnoxious stimuli (eg,
pain, sight of blood). Patients may report seeing sparks, tunnel vision, or
nausea. Vasodepressor syncope also may be associated with a feeling of fast
heartbeat after the onset of these symptoms. Recovery of consciousness is prompt
after the patient falls or lies down.
information on the vasodepressor syncope is discussed in later sections.
Serious cardiac causes of syncope
initial evaluation of syncope, pediatricians need to carefully consider the
cardiac causes, and rule out the possible neuropsychogenic and metabolic
explanations (see Table 2).
is a brief overview of the serious cardiac conditions that may involve syncope.
Patients with syncope due to ventricular ﬁbrillation may have long QT syndrome
(Figure 1), Wolff-Parkinson-White (WPW) syndrome (Figure 2) with atrial
ﬁbrillation, or repaired congenital heart disease. The differential diagnosis
for children exhibiting ventricular tachycardia is long QT syndrome,
cardiomyopathy, or repaired congenital heart disease. Supraventricular
tachycardia may present as syncope in children with a prolonged episode or in
children with WPW who have rapid ventricular response during atrial ﬁbrillation.
FIGURE 1: Patient with long QT syndrome; note abnormal broad tall T waves
FIGURE 2: Note short PR interval and delta wave in a patient with WPW
If it develops suddenly, bradyarrhythmia can signiﬁcantly reduce cardiac output,
and may result in syncope. Heart block may be due to congenitally corrected
transposition of the great arteries (L-TGA), acute rheumatic fever, myocarditis,
or Lyme disease. Sick sinus syndrome may be found in patients with a history of
congenital heart surgeries. Sinus bradycardia or junctional bradycardia may
develop before progressing to sick sinus syndrome.
is the most common cause of sudden cardiac death in athletes.
However, there are clues that point to the diagnosis on physical examination. On
cardiac examination, the patient may have a forceful point of maximal impulse.
The classic auscultatory ﬁnding is a crescendo-decrescendo systolic murmur along
the left sternal border. The intensity of the murmur, unlike most other cardiac
murmurs, increases with Valsalva maneuvers or with rising from squatting to
standing. These maneuvers decrease preload resulting in reduced ﬁlling of the
left ventricle, which results in increased obstruction and therefore, a louder
murmur. The ECG usually shows left ventricular hypertrophy (LVH) with or without
patients may initially present with vague complaints of fever,
vomiting, and abdominal pain. On physical examination, murmur of mitral
regurgitation (holosystolic murmur at the apex radiation to the left axilla)
with a displaced maximal point of impulse may be present prior to signs of
congestive heart failure. These patients are at a risk of developing life
threatening ventricular arrhythmias (Figure 3).
FIGURE 3: Spontaneous non-sustained monomorphic ventricular tachycardia in a
patient with dilated cardiomyopathy
Severe aortic stenosis
patients will have an abnormal cardiac examination. Bicuspid
aortic valve has a systolic click, usually audible at the apex. However, with
progressive stenosis, the click may become softer or inaudible. A thrill may be
palpated in the upper
right sternal border or in the suprasternal notch and the carotids. This becomes
impalpable with increasing level of stenosis. A crescendo-decrescendo systolic
murmur is heard loudest in the aortic area with radiation to the apex and the
carotids. Depending on the degree of stenosis, the pulse pressure may be
reduced. ECG shows LVH.
Congenital heart disease
history discovered in a child presenting with syncope (Figures
4-6) requires referral to a pediatric cardiologist.
FIGURE 4: Automated external deﬁbrillator (AED) recording of a patient
with tetralogy of Fallot successfully resuscitated from VF arrest
FIGURE 5: Atrial tachycardia with rapid ventricular response in an adult
patient with D-TGA status post Mustard operation
FIGURE 6: Atrial tachycardia with variable AV conduction in an adult Fontan
patient; note the subtle small negative P waves in II, III, aVF
Abnormal coronary artery
accounts for the second most frequent cause of sudden cardiac
death in athletes. The most common abnormality is the anomalous origin of the
left main coronary artery from the right sinus of Valsalva.
Primary pulmonary hypertension
may present with exercise-induced syncope or may present
as sudden death. On physical examination, patients have a loud P2 and ECG may
show signs of right ventricular hypertrophy.
Cause of vasodepressor syncope
are many synonyms for vasodepressor syncope, including vasovagal syncope,
neurally mediated vasodepressor syncope, the simple faint, neurocardiogenic
syncope, "church" syncope, "hair-grooming" syncope or benign syncope. Its
pathophysiology is incompletely understood. The Bezold-Jarisch reﬂex with an
exaggerated negative feedback loop has been commonly attributed to causing
normal circumstances, there is gravity-driven venous pooling during standing.
This results in reduced ventricular ﬁlling pressures (preload), stroke volume
and arterial blood pressure. The compensatory mechanisms of sympathetic
stimulation and withdrawal of parasympathetic stimulation result in reﬂex
tachycardia and vasoconstriction. The underﬁlled and hypercontractile left
ventricle stimulates the mechanoreceptors, which transmit impulses via
unmyelinated C-ﬁbers from the ventricle to the central nervous system, causing
vagally mediated bradycardia and vasodilatation.
patients with vasodepressor syncope, this vagal response is thought to be
exaggerated, leading to signiﬁcant bradycardia (Figure 7), even transient
asystole, thereby causing transient decrease in cerebral perfusion and possible
loss of consciousness.
FIGURE 7: Reﬂex sinus tachycardia with abrupt drop to sinus bradycardia in a
patient during a positive tilt table test for vasodepressor syncope
Management of vasodepressor syncope
vasodepressor syncope is suspected, a full dietary and ﬂuid history should be
obtained. A 2-week ﬂuid diary may be helpful in documenting the overall ﬂuid
ﬂuid guidelines for managing vasodepressor syncope include a target daily ﬂuid
intake of 1 oz/kg. Additional ﬂuid, in the form of water or sports drinks, is
recommended with vigorous exercise. The patient should aim to drink 1⁄4 of the
total daily ﬂuid requirements with breakfast, 1⁄4 with lunch, 1⁄4 after school,
and 1⁄4 in the evening. Most of the ﬂuid intake should be during daytime when
the patient is active.
patients hydration status should be monitored by ensuring that the urine is
dilute, either by using urine dipstick to check whether speciﬁc gravity is less
than 1.010 speciﬁc-gravity unit or by observation. Dilute urine is either
colorless or very light yellow in color. The patient needs to drink enough to
abolish sensation of thirst and avoid caffeinated drinks.
ﬂuid therapy is an effective therapy in the majority of patients diagnosed with
vasodepressor syncope. If the patient feels onset of symptoms, the patient
should either put his or her head down on the lap or even lie down horizontally
in order to avoid a syncopal episode.
however, despite increasing salt and ﬂuid intake, the patient continues to have
symptoms, then it is appropriate to refer to pediatric cardiology for further
evaluation. The pediatric cardiologist may determine the need for
table testing, echocardiography, trans-telephonic monitoring, and 24-hour
ambulatory monitoring can be done more cost-effectively in conjunction with
pediatric cardiology consultation. These are not always necessary in patients
with simple vasodepressor syncope.
initial evaluation of syncope, pediatricians need to differentiate between the
serious cardiac causes of syncope and various other neuropsychogenic and
metabolic possibilities. Syncope during exercise, exertion, or accompanied by
intense emotion requires urgent referral to pediatric cardiology. Family history
that may signal cardiac conditions includes early sudden death, long QT
syndrome, cardiomyopathy, sensorineural deafness, drowning, single car accident.
Pediatricians should also refer patients with an abnormal physical examination
or ECG, and patients with vasodepressor syncope that is resistant to oral ﬂuid
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Incidence and prognosis of syncope. N Engl J Med 2002;347:878-885.
Hosey RG, Armsey TD. Sudden cardiac death. Clin Sports Med 2003 Jan;22(1):51-66.
Grimm DR. Neurally mediated syncope: A review of cardiac and arterial receptors.
J Clin Neurophysiol 1997 May;14(3):170-182.
Younoszai AK, Franklin WH, Chan DP, Cassidy SC, Allen HD. Oral ﬂuid therapy. A
promising treatment for vasodepressor syncope. Arch Pediatr Adolesc Med 1998