CLINICAL MEDICINE JIACM 2003; 4(24): 286-91
Pushpa Yadav*, Arvind Sethi**, AK Agarwal***, Arun Jain*
Syncope is a term applicable to sudden and transient loss vasovagal, situational (e.g., in response to micturition,
of consciousness alongwith postural tone with rapid cough, or defecation), and carotid sinus syncope. Syncope
spontaneous recovery. It is due to transient but sudden associated with pain, neuralgia, or panic and episodes
decrease or brief cessation of cerebral blood flow. Brain is associated with exercise in athletes without heart disease
an organ which cannot tolerate even a brief deprivation are also included in this category. The compensatory
of oxygen and blood derived nutrients. Syncope is a response to the patient’s assuming an upright posture is
common problem and produces tremendous anxiety interrupted and replaced by a paradoxical withdrawal of
among patients and their families. Evaluation of syncope sympathetic activity and an increase in parasympathetic
is particularly a challenging task because its causes are (vagal) activity. Characteristically, there is severe reduction
multiple and often difficult to diagnose. A lot of money in blood pressure and decrease in heart rate. The
could be spent while evaluating the cause of syncope, with mechanism of neurally mediated syncope is poorly
no positive test results. The aim of this article is to help understood. In some cases fainting may be triggered in
clinicians maximise the diagnostic yield in the work-up of central nervous system (emotional upsets). Activation of
syncope, help to assess risks which suggest a guideline to receptors in the ventricular wall or in other organs
hospitalise those patients of syncope who are at high risk (bladder, oesophagus, respiratory tract) may cause
for an adverse outcome and require invasive testing. increase in vagal efferent activity and sympathetic
withdrawal. The role of neurohormonal agents such as
It is important first to distinguish syncope from many other
epinephrine, serotonin, and endorphins is being
symptoms. Dizziness, vertigo, and pre-syncope do not
investigated. Endogenous nitric oxide is also an inhibitor
result in loss of consciousness. It may at times be difficult
of sympathetic activity and considered to be mediator of
to distinguish syncope from seizures. Aura, disorientation
central inhibitory influence.
after the event, slowness in returning to consciousness,
and unconsciousness lasting more than five minutes Table I : Causes of syncope.
suggests a seizure. A loss of consciousness that is Cause Mean prevalence
precipitated by exercise, pain, cough, micturition, (Range %)
defecation, or any stressful event is usually syncope. Some Neurally–mediated syncope
rhythmic movements or jerks though typical of seizures Vasovagal attack 18 (8-37)
can occur in syncope too. Rarely, the only way to Situational syncope 5 (1-8)
differentiate between the two is by direct observation Carotid sinus syncope 1 (0-4)
during tilt testing or by prolonged electroencephalo- Psychiatric disorders 2 (1-7)
graphy. Drop attacks cause fall without loss of Orthostatic hypotension 8 (4-10)
consciousness. Medications 3 (1-7)
Neurologic disease 10 (3-32)
Differential diagnosis Cardiac syncope
Table I summarises the causes of syncope. Neurally Organic heart disease 4 (1-8)
Arrhythmias 14 (4-38)
mediated syncope is the most common cause of syncope
and is mediated by reflex mechanisms causing changes Unknown 34 (13-41)
in vascular tone, heart rate, or both. This category includes Reproduced from Linzer et al12.
* Senior Physician, ** Senior Resident, *** Consultant,
Department of Medicine, Dr. Ram Manohar Lohia Hospital, New Delhi-110 001, India.
Psychiatric disorders such as anxiety, depression, and arrhythmias will guide further evaluation that may detect
conversion disorders is the next category. Patients with life threatening disorders.
psychiatric disorders are younger, generally do not have
underlying heart disease, and have more frequent Patients where initial assessment suggests a
Orthostatic hypotension is another common cause of Specific testing is carried out to confirm or rule out the
syncope which may result from age related physiologic diagnosis (e.g., lung scanning for pulmonary emboli,
changes, volume depletion, medications which have effect echocardiography or cardiac catheterisation for serious
on vascular tone, heart rate, and autonomic insufficiency2,3. heart disease like aortic stenosis, coronary artery disease).
Exercise related syncope always requires investigations
Neurologic disorders rarely cause syncope. Transient because it may be the only symptom that precedes a
ischaemia almost exclusively involving the vertebrobasilar sudden cardiac death 7. Syncope that occurs during
territory, migraines involving basilar artery, and certain exercise tends to be more ominous than that occurring
types of seizures, i.e., atonic seizures, temporal lobe in the post-exertional state.
epilepsy, and unwitnessed grandmal seizures4 are some
of the common conditions mimicking syncope. Patient having unexplained syncope when
Cardiac diseases manifesting as syncope include coronary initial assessment does not lead to diagnosis
artery disease, congestive heart failure, valvular heart Such patients could be broadly categorised into :
disease, or congenital heart disease. The presence of
I. Those with structural heart disease or
structural heart disease irrespective of the cause of
syncope has emerged as the most important factor for
predicting the risk of death as well as likelihood of II. Those with no heart disease and normal
arrhythmia5,6. Exertional syncope may be the outcome of electrocardiogram
fixed cardiac output that does not increase with exercise, III. Elderly individuals.
due to arrhythmia, neurocardiogenic disorders, or
anomalous coronary artery. Patients with structural heart disease or
The cause of syncope may not be determined in some
patients. Proportion of patients with unexplained syncope Structural heart disease is often suspected in patients who
is lower now because of wider use of various investigative have sudden or exertional syncope. Because structural
tools. heart disease is a strong predictor of mortality among
patients with syncope, an echocardiogram or an exercise
Approach to syncope stress test or both are required to determine the
Figure 1 highlights the work-up of a case of syncope. As underlying heart disease and to quantify it. If the results
there is no diagnostic gold standard, history, physical of these tests are negative, no further testing may be
examination, and electrocardiography (ECG) are the core required. Echocardiography reveals unsuspected findings
of the syncope work-up and combined diagnostic yield is in only 5-10% of patients8.
80%. Electrocardiography should be done in almost all
Exercise testing : is indicated for evaluation of ischaemia
patients – although it may be positive only in a minority
or exercise induced tachyarrhythmia. In patients with
of patients – because the test is inexpensive and risk free.
exertional syncope, echocardiography should be done
The findings in the electrocardiogram can lead to
first to exclude hypertrophic cardiomyopathy.
decisions about immediate management of underlying
disease (e.g., pacemaker for complete heart block) or 24-hour Holter monitoring : is indicated when
further tests may be planned (e.g., for bundle branch symptoms suggest arrhythmic syncope (palpitations with
block). Evidence of previous myocardial infarction or syncope, episodic unconsciousness with no prodrome),
Journal, Indian Academy of Clinical Medicine Vol. 4, No. 4 October-December 2003 287
Fig. 1 : Syncope work-up.
or those with abnormal ECG, heart disease, or unexplained 4% of patients had symptoms in conjunction with
syncope because of the episodic nature of arrhythmias. arrhythmias and in about 15% of patients symptoms were
One may not be able to exclude arrhythmic syncope, if no not associated with arrhythmia (thereby ruling out
arrhythmias are found and no symptoms occur during 24 syncope due to arrhythmia)9. Extending monitoring to as
hours Holter monitoring. In studies of Holter monitoring, long as 72 hours did not increase the yield for arrhythmias
288 Journal, Indian Academy of Clinical Medicine Vol. 4, No. 4 October-December 2003
associated with symptoms10. patients with unexplained recurrent syncope in whom
cardiac cause of syncope, including arrhythmias, has been
Continuous loop – event monitoring : is recommended
excluded. It generally involves the use of provocative
in patients with recurrent syncope and a normal heart,
agents such as isoproterenol or nitroglycerine in patients
syncope of unexplained cause, heart disease and
with negative result on a passive tilt-table test and who
abnormal ECG. These recorders are used for monitoring
have a high pretest probability of neurally mediated
lasting weeks or months. The monitor can be activated
syncope. Positive responses using either agent are
by the patient or observer after symptoms occur, thereby
reported in approximately 66% with specificity
freezing its memory for previous 2-5 minutes and
approaching 90%15. Women of child bearing age should
subsequent 60 seconds. There is need of compliance on
have a pregnancy test and men older than 45 yeas of age
the part of the patient for this test. An implantable
and women older than 55 years of age have stress testing
continuous–loop recorder, which is inserted
before tilt-table testing.
subcutaneously, and cardiac monitoring can be done upto
18 months, has been used in patients with recurrent Carotid sinus syncope, a neurally mediated syncope,
syncope of unexplained cause 11. Further studies are should be considered in patients with spontaneous
needed to define its exact role. suggestive symptoms, e.g., syncope while shaving or while
turning the head, and in elderly patients with recurrent
Electrophysiologic studies : Patients with normal heart
syncope and a negative diagnostic work-up.
and normal electrocardiograms do not require
electrophysiological studies. Patients who have syncope
and serious organic heart disease and those whose hearts
are normal but electrocardiograms show conduction It is not routinely required in diagnostic evaluation of
disturbances, i.e., first degree heart block, bundle branch syncope. An electroencephalogram (EEG) aids in
block, etc., should undergo electrophysiological studies. diagnosing less than 2% of cases of syncope16, almost all
Yield of this test in patients with organic heart disease of whom have symptoms suggestive of seizure. CT scan
shows that 21% have inducible ventricular tachycardia of the head helps in another 2% of cases17.
and 34% have bradycardia12, 3% patients have inducible
ventricular tachycardia, and 19% have bradycardia Psychiatric evaluation
(patients with electrocardiograms revealing conduction Syncope due to psychiatric disorders is usually
disturbances)12. In patients with normal heart and normal recurrent in younger patients with no heart disease. It
electrocardiogram, yield is very low. For bradyarrhythmias, is a known presentation of somatisation disorder and
electrophysiological studies have low specificity and may be precipitated by anxiety, panic, or major
sensitivity13. depression as a neurally mediated response18. Alcohol
and drug dependence and abuse may also lead to
Signal–averaged electrocardiography syncope.
The role of signal–averaged electrocardiography in
unselected patients of syncope is yet not known. It is Exercise–related syncope in young athletes
useful in selecting patients for electrophysiological Exercise related syncope, while generally a benign
studies in presence of ischaemic heart disease when event, can signal sudden death in young adults. It
ventricular tachycardia is suspected. occurs either during or immediately after a period of
exercise. Most authors conclude that young and
Evaluation for neurally mediated syncope otherwise healthy adults who present with exertional
Head up tilt–table testing : is a widely used method to syncope, have a greater probability of organic
determine a patient’s predisposition to autonomically pathology and require a thorough investigation for a
mediated hypotensive syncope14. It is recommended in pathologic aetiology19. In one study, it was concluded
Journal, Indian Academy of Clinical Medicine Vol. 4, No. 4 October-December 2003 289
that collapse occurring before the finish line is a much Treatment
more ominous event than that occurring after the
Not all patients with syncope require hospital admission.
Disorders with potential for adverse outcomes, should be
The various causes of exercise related syncope are evaluated earliest with hospitalisation, e.g., aortic stenosis
depicted in Figure 2. The most common cause of exercise and hypertrophic cardiomyopathy, severe orthostasis, or
related syncope is neurocardiogenic syncope. For adverse drug reactions. Neurally mediated syncope and
evaluation, after electrocardiography and a thorough patients with neither heart disease nor an abnormal ECG
history and physical examination, laboratory tests should may be evaluated as out-patients.
be ordered as clinically indicated (serum Na+ levels for
Treatment depends on identifying the mechanisms and
suspected exertional hyponatraemia, glucose levels in
factors that contribute to syncope. Orthostatic syncope
suspected cases of hypoglycaemia). Potentially life
being the commonest form, measures to minimise the
threatening abnormalities include arrhythmogenic right
effects of gravity are usually recommended. Sitting or lying
ventricular dysplasia, hypertrophic cardiomyopathy,
down at the onset of an episode may prevent it and if
prolonged QT syndrome, and heat stroke. These patients
one must keep standing, then avoiding a still posture may
should be restricted from strenuous exercise pending
help. Standing and straining must not be done at the same
completion of evaluation for syncope. Non-life-
time especially by the persons prone to ‘micturition
threatening abnormalities include hypoglycaemia, mild
syncope’. Such patients should sit to urinate. Treatment of
hyponatraemia, neurocardiogenic syncope, and mild heat
the primary problem, i.e, prostate surgery, or treating
exhaustion. In all cases of unexplained exertional and pre-
bronchitis, eliminates the trigger in such patients.
exertional syncope, an echocardiogram followed by stress
Maintenance of adequate hydration is also important in
test should be done. In such individuals temporary
preventing orthostatic hypotension. Diuretics may, hence,
restriction from vigorous activity should be considered.
precipitate such an episode and thus may be used with
Diagnostic evaluation should be ordered as indicated
caution. In cases of autonomic failure, increasing the intake
according to the possible diagnosis, possibly in
of salt and fluid and using waist high support stockings
consultation with a cardiologist, neurologist, and
and abdominal binders may be beneficial. Fludrocortisone
psychiatrist, if required. Reassuring clinical features are
may also be used in such cases.
syncope occurring after exercise, it being non-recurrent,
there being no family history and a normal cardiac Very few trials of treatment for neurally mediated syncope
examination with ECG, echo, and stress test being normal. have been reported using atenolol19, paroxetine20, and
Such athletes may return to vigorous activity with an etilefrine 21, an alpha-adrenergic agonist, with varied
appropriate follow-up plan. responses. Case series have also tried salt plus
Fig. 2 : Exercise – related syncope.
290 Journal, Indian Academy of Clinical Medicine Vol. 4, No. 4 October-December 2003
fludrocortisone, metoprolol, midodrine, disopyramide, electrocardiographic (Holter) monitoring. Ann Intern Med
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Syncope related to arrhythmias requires specific therapy. monitoring in patients with syncope : is 24 hours enough ?
Arch Intern Med 1990; 150: 1073-8.
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