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Syncope

Article  in  Critical Care Medicine · November 2000

DOI: 10.1097/00003246-200010001-00002 · Source: PubMed

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Scientific Reviews

Syncope
David J. Heaven, MB, ChB, FRACP; Richard Sutton, DScMed, FRCP, FESC, FACC

Syncope is a common clinical presentation. Although most
commonly benign, it may herald a pathology with a poor prog-
nosis. The work-up of syncope includes a careful history, physical
examination, electrocardiogram, risk stratification, and appropri-
ately directed testing. The key factor in the investigation of
syncope is the presence (or absence) of structural heart disease
or an abnormal electrocardiogram. The most useful investigation
in unexplained syncope with a normal heart is the tilt table test for
evaluating predisposition to neurocardiogenic (vasovagal) syn-
cope. In the setting of structural heart disease or an abnormal
electrocardiogram, electrophysiologic studies play a more impor-
tant role. The utility of noninvasive cardiac monitoring for symp-
tom-rhythm correlation may be limited by infrequent symptoms.
The availability of external and implantable loop recorders allows
prolonged periods of monitoring to increase diagnostic yield. The
management of patients with syncope may be complex. Early
referral to a cardiac electrophysiologist is warranted in patients
who are at high risk. (Crit Care Med 2000; 28[Suppl.]:N116 –N120)
KEY WORDS: syncope; investigation; tilt table testing; carotid
sinus massage; implantable loop recorder; electrophysiology
study; arrhythmia; management

S yncope is defined as “sudden
transient loss of consciousness
with concurrent diminution in
postural tone followed by spon-
taneous recovery” (1). Syncope is a com-
mon clinical occurrence accounting for
up to 3% of emergency room visits and
6% of hospital admissions. The mortality
rate is generally low, but may be up to
33% at 1 yr in patients with a cardiac
origin (2, 3). The differential diagnosis is
broad (Table 1) (4). Diagnosis may be
made difficult by the intermittent nature
of the symptoms, the large number of
potential causes, and the lack of a crite-
rion for clinical investigation. The cost of
investigation of recurrent unexplained
syncope can be high, particularly if a be-
nign cause of syncope is overlooked in
the process of excluding life-threatening
disorders (5).
HISTORY, PHYSICAL
EXAMINATION, AND CLINICAL
INVESTIGATION
For a detailed review of the literature,
readers are directed to a report by the
From the Electrophysiology Laboratory (Dr. Heaven),
Section of Cardiology, Rush-Presbyterian-St. Luke’s
Medical Center, Chicago, IL, and the Department of
Pacing and Electrophysiology (Dr. Sutton), Royal Bromp-
ton Hospital, London, UK.
Address requests for reprints to: David J. Heaven,
MB, ChB, FRACP, Cardiology Department, Middlemore
Hospital, Private Bag 93311, Otahuha, Auckland 1006,
New Zealand.
Copyright © 2000 by Lippincott Williams & Wilkins
Clinical Assessment Project of the Amer-
ican College of Physicians (4, 6 ). The
suggested diagnostic algorithm (Fig. 1)
provides a useful framework for clinical
evaluation of syncope (4).
History and Physical Examination.
Clinical history, physical examination,
and electrocardiography form the corner-
stone of the initial evaluation of a patient
with syncope. After these are completed,
⬃45% of patients have a primary diagno-
sis made and a further 8% have a pre-
sumptive diagnosis that can be confirmed
by directed testing. “Organic” cardiac dis-
ease, where syncope is associated with
adverse outcome, is frequently suspected
on the findings of a careful history and
examination.
History taking should focus on pos-
tural symptoms, exertional symptoms,
family history (long QT syndrome, Bru-
gada syndrome, hypertrophic cardiomy-
opathy), palpitations, situational symp-
toms (Table 1), and prior organic heart
disease. Medications, such as antihyper-
tensive agents and antidepressants, may
not only cause orthostatic hypotension,
particularly in the elderly, but also favor
neurocardiogenic syncope. Antiarrhyth-
mic agents may cause proarrhythmia
with loss of consciousness or even cardiac
arrest. A variety of medications can cause
QT prolongation and torsades de pointes
(Table 2). Focal neurologic or postictal
symptoms suggest a neurologic cause.
The clinician must, however, be aware
that seizures related to cerebral hypoper-
fusion frequently accompany other
causes of syncope (7). A history obtained
from a witness may help distinguish a
seizure from cardiovascular loss of con-
sciousness. Physical examination should
concentrate on orthostatic changes and
cardiovascular and neurologic signs. Car-
diovascular examination may suggest an
“obstructive” cause, such as aortic steno-
sis, mitral stenosis, atrial myxoma or hy-
pertrophic cardiomyopathy. Signs of con-
gestive heart failure suggest significant
organic heart disease.
Electrocardiography. Electrocardiog-
raphy identifies a direct cause of syncope
in only 5% of patients. However, electro-
cardiograms (ECGs) are inexpensive and
can identify serious causes of syncope,
such as ventricular tachycardia, brady-
cardia, and (less commonly) acute myo-
cardial ischemia. Preexcitation may sug-
gest an accessory pathway with rapid
antegrade conduction. A long QT interval
or identification of the Brugada syn-
drome (partial right bundle branch block
and ST elevation in leads V1–3) may sug-
gest rare ion channel abnormalities asso-
ciated with sudden cardiac death. A QRS
duration ⬎110 msecs in leads V1–3, right
bundle branch block, precordial T wave
inversion or an epsilon wave may be
present in arrhythmogenic right ventric-
ular dysplasia. Findings of first degree
atrioventricular (A-V) block, bundle
branch block, or sinus bradycardia may
suggest bradyarrhythmic syncope,
whereas previous myocardial infarction

N116 Crit Care Med 2000 Vol. 28, No. 10 (Suppl.)

Table 1. Origin of syncope

Mean Prevalence
Origin Characteristics Severity (Range) %a

Reflex mediated Warmth, nausea Benign 18 (8–37)

Vasovagal
Situational Cough, micturition, swallow, defecation 5 (1–8)
Carotid sinus syndrome Neck pressure/head turning 1 (0–4)
Orthostatic hypotension Symptoms with standing Benign 8 (4–10)
Medications Medication use 3 (1–7)
Orthostatic Benign
Arrhythmic Torsades de pointes Severe
Psychiatric Frequent symptoms, lack of injury Benign 2 (1–7)b
Neurologic Seizure activity (atonic/temporal lobe/unwitnessed), Moderate 10 (3–32)c
Migraines (basilar) headache, neurologic symptoms or signs
Transient ischemic attacks (vertebrobasilar)
(Seizures)
Subclavian steal
Cardiopulmonary disease Chest pain, exertional syncope, dyspnea, Severe 4 (1–8)
Obstructive (aortic/mitral stenosis, myxoma, postoperative
hypertrophic cardiomyopathy)
Ischemic (MI, spasm)
Pulmonary (embolism, hypertension)
Arrhythmias Sudden syncope, injury 14 (4–38)
Bradycardia (sick sinus syndrome, heart block, drug Moderate/severe
induced, pacemaker malfunction)
Tachycardia (VT, torsades de pointes, SVT) Palpitations Severe
Unknown Negative work-up Benign to moderate 34 (13–41)d

MI, myocardial infarction; VT, ventricular tachycardia; SVT, supraventicular tachycardia.

a
Prevalence determined from pooled data from five population-based studies (n ⫽ 1002) conducted from 1984 to 1990; bpsychiatric causes occur at
higher rates in contemporary series; cTIAs and basilar migraine are a very uncommon cause of syncope (this prevalence includes seizures that by definition
are not syncope); dthere is a reduced incidence of negative work-up in current practice with increasing use of event monitoring and tilt table testing with
isoproterenol and nitrates, etc. Adapted from Linzer et al (4).

or left ventricular hypertrophy could in- Table 2. Drugs that may prolong the QT interval and potentially cause torsades de pointes
dicate ventricular tachycardia.
Inotropic agents Epinephrine
Neurologic Testing. Although electro-
Antihistamines Terfenadine
encephalography was widely used in the Astemizole
1980s, several studies have shown it is of Diphenhydramine
little use in unselected patients without Antibiotics Erythromycin
seizure activity. The yield of neurologic Trimethoprim and sulfamethoxazole
imaging studies is also very low unless Pentamidine
there is a history of seizures or focal Antiarrhythmic agents Quinidine
Procainamide
neurologic signs are demonstrated on
Disopyramide
clinical examination. Transcranial Dopp-
Sotalol
ler studies may be useful to document Amiodarone
decreased cerebral perfusion in a small Dofetilide
group of patients who have syncope dur- Other cardiac drugs Probucol
ing tilt table testing without peripheral Bepridil
hemodynamic changes (8). Gastrointestinal Cisapride
Antifungal drugs Ketoconazole
Echocardiography and Exercise
Fluconazole
Stress Testing. When there is no evidence
Itraconozole
of heart disease by history, physical ex- Psychotropic drugs Tricyclic antidepressants
amination, and electrocardiogram, the Phenothiazines
diagnostic yield of echocardiography is Haloperidol
low. Normal echocardiograms (63%) or Resperidone
studies producing no additional useful in- Diuretics Indapamide
formation (37%) were found in one large Any agent that causes hypokalemia
series (9). Echocardiography is important
where there is evidence of structural
heart disease, suspected arrhythmic syn- cardiac cause of syncope. Limiting the sidered if ischemic heart disease is sus-
cope, or an abnormal electrocardiogram. use of echocardiography to such patients pected or there is a history of exertional
It enables assessment of left ventricular can reduce the cost of investigation (10). syncope and echocardiography excludes
function and can exclude an obstructive Exercise stress testing should be con- an obstructive cardiac lesion or hypertro-

Crit Care Med 2000 Vol. 28, No. 10 (Suppl.) N117


Figure 1. Algorithm for diagnosing syncope. *Carotid sinus syndrome should be diagnosed only if the
history is suggestive and massage is diagnostically positive (asystole of ⱖ3 secs, hypotension, or both).
†
May be replaced by inpatient telemetry if there is concern about serious arrhythmia. OHD, organic
heart disease. Figure reproduced with permission from Linzer et al (4).
phic cardiomyopathy. In unselected pa-
tients, the diagnostic yield of exercise
stress testing is very low (2).
Cardiac Monitoring. Cardiac monitor-
ing is indicated when symptoms suggest
arrhythmic syncope (brief loss of con-
sciousness, palpitations with syncope, ab-
sence of prodrome, and prompt recovery
of clear mentation), in the presence of
structural heart disease or an abnormal
electrocardiogram, and in unexplained
syncope. Inpatient telemetry is required
if hospital admission is necessary (see
“Emergency Room Triage” section). Dur-
ing 24-hr ambulatory monitoring, 4% of
patients have correlation of symptoms
with arrhythmia (true positive) and 15%
have symptoms without arrhythmia (false
positive)—a diagnostic yield of 19%. An-
other 14% have asymptomatic arrhyth-
mia that can occasionally suggest the
cause (sinus pauses, Mobitz II A-V block,
nonsustained ventricular tachycardia). In
the majority of patients, symptom-
rhythm correlation is limited by sporadic
symptoms. Extended monitoring with ex-
ternal loop recorders increases the diag-
nostic yield, ⱕ47%. Diagnostic efficacy
may be limited because of patient diffi-
culties in using such a device (6). The
ability to undertake extended cardiac
monitoring has been advanced by the
availability of an implantable loop re-
corder able to provide monitoring for up
N118
to 14 months. Extended implantable loop
recorder monitoring in 85 patients with
recurrent unexplained syncope (mean
duration, 10 months) enabled symptom-
rhythm correlation in 58 patients (68%)
with an arrhythmia documented in 21
patients (25%) (11).
Tilt Table Testing and Carotid Sinus
Massage. Tilt table testing, introduced
into clinical practice in 1986 (12), has
become a widely accepted tool in the in-
vestigation of syncope, particularly where
there is no evidence of structural heart
disease (13). It is a provocative test, using
orthostatic stress to determine suscepti-
bility to neurocardiogenic syncope.
In 1996, the American College of Car-
diology published an expert consensus on
the use of tilt table testing (13). Tilt table
testing is indicated when there is recur-
rent syncope (or a single episode accom-
panied by injury, a motor vehicle acci-
dent, or syncope in a high-risk setting),
and no evidence of structural heart dis-
ease. Tilt table testing is also warranted
when an apparent syncopal cause has al-
ready been established, if demonstration
of neurally mediated syncope would alter
management. It may also be cautiously
included as part of the work-up of exer-
cise-associated syncope. Tilt table testing
is not warranted in the investigation of a
single syncopal episode with clear vaso-
vagal features. Tilt table testing may be
helpful in differentiating convulsive syn-
cope from true seizures, evaluating re-
current falls in the elderly, and investi-
gating near syncope or syncope in
patients with autonomic neuropathy.
Patients are tilted head-up on a table,
with straps and a footplate, at an angle
between 60° and 80° for 30 – 45 mins. We
prefer 45 mins, which is two standard
deviations from the mean time to syn-
cope and captures 95% of patients who
will faint (14). If the passive stage of the
test is negative, the use of provocative
agents, such as isoproterenol or nitro-
glycerin may increase the diagnostic yield
from 30% to 50% up to 40% to 80%. This
may, especially with isoproterenol, be at
the cost of reduced specificity (15).
Collapse patterns during tilt table test-
ing were defined by the Vasovagal Syn-
cope International Study investigators
(16) and have been recently updated (15).
Vasovagal responses were divided into
mixed, cardioinhibitory, and vasodepres-
sor. Two additional responses are seen:
dysautonomic response (autonomic neu-
ropathy), where the blood pressure con-
sistently falls without significant heart
rate rise; and postural orthostatic tachy-
cardia syndrome, where there is exces-
sive sinus tachycardia in response to or-
thostatic stress. Precise classification
requiring beat-to-beat blood pressure
monitoring (preferably achieved noninva-
sively with the Finapres device) may al-
low better therapeutic strategies (15).
Carotid sinus massage has its greatest
utility in elderly patients. Carotid sinus
syndrome may be underdiagnosed in this
population. Carotid sinus massage is con-
traindicated in patients with cerebrovas-
cular disease or carotid bruits. It can be
performed in the office with cardiac mon-
itoring but ideally should be undertaken
supine and during head-up tilt with non-
invasive beat-to-beat blood pressure
monitoring (4, 17).
Electrophysiology Study. Electro-
physiology studies use programmed elec-
trical stimulation and monitoring with
intracardiac (and surface ECG) electrodes
to assess cardiac impulse formation, con-
duction abnormalities, and the propen-
sity for developing tachyarrhythmias. Al-
though relatively safe, electrophysiology
studies are invasive and expensive. Elec-
trophysiology studies can be useful for
evaluating sinus node function; however,
most patients with sick sinus syndrome
and syncope have clear evidence of sinus
node dysfunction on 12-lead ECG or am-
bulatory monitoring. A-V nodal and His-
Crit Care Med 2000 Vol. 28, No. 10 (Suppl.)
Purkinje conduction may also be as-
sessed. Tachycardia may be induced by
programmed electrical stimulation (6,
18).
The diagnostic yield of electrophysiol-
ogy studies in patients with a structurally
normal heart and a normal ECG is low
(1% ventricular tachycardia, 10% brady-
cardia) whereas in patients with organic
heart disease, the yield is over 50% (21%
ventricular tachycardia, 34% bradycar-
dia). Patients with an abnormal ECG also
have a significant diagnostic yield (17%
ventricular tachycardia, 19% bradycar-
dia) (6). A negative electrophysiology
study does not necessarily exclude an ar-
rhythmic cause of syncope and has a poor
predictive value in nonischemic cardio-
myopathy, the long QT syndrome (18),
mitral valve prolapse, and the Brugada
syndrome.
EMERGENCY ROOM TRIAGE
Decisions regarding disposition of the
patient with syncope have important clin-
ical and economic implications. Because
a large number of people will experience
a syncopal event in their lifetime, empir-
ical hospitalization is not mandatory or
cost effective. Predictors of significant ar-
rhythmia or 1-yr mortality include an
abnormal ECG, history of congestive
heart failure or organic heart disease,
chest discomfort, history of arrhythmia,
and age ⬎45 yrs (19). Hospital admission
to a monitored setting is indicated where
there is a concern about patient risk. Im-
mediate investigation or therapy may be
warranted (Table 3) (20).
MANAGEMENT
A comprehensive review of the man-
agement of the many conditions that
cause syncope is beyond the scope of this
discussion. The following is a brief sum-
mary of the management of reflex syn-
cope, orthostatic hypotension, and car-
diac causes of syncope.
Reflex Syncope and Orthostatic Hypo-
tension. The majority of patients with
vasovagal syncope or orthostatic hypo-
tension are successfully managed with re-
assurance, simple measures (adequate
hydration and salt intake), and avoidance
of precipitating stimuli. Medications
causing vasodilation or volume depletion
may need to replaced with alternative
agents. Medical therapy is indicated in a
minority of patients—those at high risk
(syncope with injury) or with recurrent
Crit Care Med 2000 Vol. 28, No. 10 (Suppl.)
Table 3. Indications for hospital admission
Definite
Known cardiovascular disease (coronary
artery disease, heart failure, arrhythmia)
Chest pain with syncope
New physical examination findings of
cardiovascular or neurologic disease
Abnormal ECG (ischemic changes,
tachycardia, bradycardia, prolonged QT,
Bruguda syndrome, bundle branch block,
Wolff-Parkinson-White syndrome)
Suspected pulmonary embolism
Likely
Syncope associated with injury, tachycardia,
or exertion
Frequent events
Suspicion of coronary artery disease or
arrhythmia (medication effect causing
torsades de pointes)
Orthostatic hypotension resistant to fluid
therapy
Older patients (⬎60 yrs old)
ECG, electrocardiogram.
Adapted from Hayes (20).
or disabling symptoms. ␤ blockers may
be useful in vasovagal syncope (21), espe-
cially for patients with prominent sinus
tachycardia on the tilt table before syn-
cope (22). The serotonin reuptake inhib-
itors, paroxetine (23) and fluoxetine, have
also shown promise and may act centrally
in the reflex arc. Expansion of the intra-
vascular volume with fludrocortisone and
use of the ␣-agonist (vasoconstrictor)
midodrine can be helpful for both vaso-
vagal syncope and orthostatic hypoten-
sion (24, 25). Implantation of a dual
chamber pacemaker with a “rate drop re-
sponse” algorithm is indicated in carotid
sinus syndrome and in selected patients
with disabling symptoms from vasovagal
syncope with a bradycardic component
(26 –28).
Arrhythmia. Permanent pacing is in-
dicated for patients with syncope and
atrioventricular block or sinus node dys-
function. Patients with syncope and bifas-
cicular block who have intermittent com-
plete heart block or type II second degree
A-V block should also be referred for
pacemaker implantation. In other pa-
tients with syncope and bifascicular
block, electrophysiological study may be
useful to demonstrate a prolonged HV
interval or inducible ventricular tachy-
cardia (28).
Patients with syncope and tachycardia
should be referred for electrophysiologi-
cal evaluation. Syncope in patients with
preexcitation mandates an electrophysi-
ology study because there may be a risk of
S
yncope may her-
ald an ominous
prognosis in pa-
tients with structural heart
disease.
sudden cardiac death and the accessory
pathway may be readily eliminated by ra-
diofrequency catheter ablation. Most su-
praventricular tachycardias and idio-
pathic ventricular tachycardias can also
be cured by radiofrequency catheter ab-
lation (29). In the presence of structural
heart disease, patients with ventricular
tachycardia and syncope should be con-
sidered for an implantable cardioverter-
defibrillator (ICD) (28).
Patients with the long QT syndrome
are often treated with ␤ blockers and
pacing, but an ICD is usually recom-
mended if the presentation is aborted car-
diac arrest or there is a strong family
history of sudden cardiac death (30). ICD
implantation is the only effective way to
prevent sudden death in the Brugada syn-
drome (28).
Structural Heart Disease. When syn-
cope occurs in the setting of ischemic
cardiomyopathy or previous myocardial
infarction, inducible ventricular tachy-
cardia at electrophysiology study predicts
a high risk of sudden death. Such pa-
tients benefit from ICD therapy (31). An
electrophysiology study is less useful to
stratify sudden death risk, which may be
up to 45% at 1 yr, in nonischemic car-
diomyopathy. After ICD implantation in
patients with syncope and nonischemic
cardiomyopathy, the frequency rate of ap-
propriate device therapy is similar to pa-
tients with aborted cardiac arrest. Many
electrophysiologists recommend ICD im-
plantation in this patient group although
in the absence of controlled data, this
remains controversial (32, 33). Syncope
in hypertrophic cardiomyopathy may be
related to ventricular tachycardia, left
ventricular outflow tract obstruction, or
neurocardiogenic syncope. Such patients
should be referred for evaluation and pos-
sible treatment with amiodarone or an
ICD. Syncope in arrhythmogenic right
ventricular dysplasia suggests hemody-
namically unstable ventricular tachycar-
dia and ICD implantation should be con-
N119
sidered (28). Obstructive cardiac lesions
(aortic stenosis, mitral stenosis, atrial
myxoma) and syncope herald a poor
prognosis without surgical intervention
and these patients should be referred for
urgent evaluation.
CONCLUSIONS
Syncope is a common presentation.
The majority of these patients have a be-
nign cause. Syncope may herald an omi-
nous prognosis in patients with struc-
tural heart disease. The key to the initial
work-up is a detailed history and physical
examination followed by directed investi-
gation.
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