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					                                         CLINICAL MEDICINE                                        JIACM 2003; 4(24): 286-91



                                                        Syncope
                            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
syncope.                                                           diagnosis
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
                                                                         electrocardiographic abnormalities.
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
                                                                   electrocardiographic abnormalities
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
                                                                  Neurologic testing
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.
finish line20.
                                                                        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
                                                                           1990; 113: 53-68.
theophylline, and other drugs.
                                                                       10. Base EB, Curtiss EI, Arena VC et al. The duration of Holter
Syncope related to arrhythmias requires specific therapy.                  monitoring in patients with syncope : is 24 hours enough ?
                                                                           Arch Intern Med 1990; 150: 1073-8.
Electrophysiological studies often provide important clues
                                                                       11. Krahn AD, Klein GJ, Yee R et al . Use of an extended
and thus guide therapeutic intervention. Supraventricular                  monitoring strategy in patients with problematic syncope.
tachycardia may respond to drugs or radiofrequency                         Circulation 1999; 99: 406-10.
ablation. Bradyarrhythmias require pacing. Implantable                 12. Linzer M, Yang EH, Estes NA III et al. Diagnosing syncope 2.
defibrillators are helpful in treatment of both ventricular                Unexplained syncope : Clinical Efficacy Assessment Project
                                                                           of the American College of Physicians. Ann Intern Med 1997;
tachy- and brady-arrhythmias. However, their role in the                   127: 76-86.
therapy of vasovagal syncope is unclear.                               13. Fujimura O, Yee R, Klein GJ et al. The diagnostic sensitivity
                                                                           of electrophysiological testing in patients with syncope
The treatment of patients with structural heart disease                    caused by transient bradycardia. NEJM 1989; 321: 1703-7.
requires specific corrective surgeries.                                14. Benditt DG, Ferguson DW, Grubb BP et al. Tilt table testing
                                                                           for assessing syncope. J Am Coll Cardiol 1996; 28 (1): 263-75.
Syncope may result from diseases involving many
                                                                       15. Grubb BP, Kosinuski D. Current trends in aetiology, diagnosis
specialities. It is important for the primary care physician               and management of neurocardiogenic syncope. Curr Opin
to act in conjunction with relevant specialists to formulate               Cardiol 1996; 11: 32-41.
a strategy for directed testing and diagnosis in the                   16. Davis TL, Freemon FR. Electroencephalography should not
                                                                           be routine in the evaluation of syncope in adults. Arch Intern
evaluation of syncope as also the subsequent
                                                                           Med 1990; 150: 2027-9.
management of the individual.
                                                                       17. Kapoor WN. Evaluation and outcome of patients with
                                                                           syncope. Medicine (Baltimore) 1990; 69: 160-75.
References                                                             18. Kapoor WN, Fortunato M, Hanusa BH, Schulberg HC.
1.   Kapoor WN, Fortunato M, Hanusa BH, Schulberg HC.                      Psychiatric illness in patients with syncope. Am J Med 1995;
     Psychiatric illnesses in patients with syncope. Am J Med              99: 505-12.
     1995; 99: 506-12.                                                 19. When does fainting represent a deadly condition ?
2.   Lipsitz LA. Orthostatic hypotension in the elderly. NEJM              Exertional syncope : benign hypotension or life threatening
     1989; 321: 952-7.                                                     abnormality ? Part I. Sports Med Diag 1997; 19: 118-20.
3.   Bannister SR ed. Autonomic failure A Textbook of Clinical         20. Holzhausen LM, Noakes TD, Kroning B et al. Clinical and
     Disorders of the Autonomic Nervous System 2nd ed. New                 biochemical characteristics of collapsed ultra-marathon
     York: Oxford Univ Pr. 1988; 1-20.                                     runners. Med Sci Sports Exerc 1994; 26: 1095-1101.
4.   Davidson E, Rotenbeg Z, Fuchs J et al. Transient ischaemic        21. Mahanonder N, Bhuripanyo K, Kankagate C et al .
     attack – related syncope. Clin Cardiol 1991; 14: 141-4.               Randomised double blind, placebo controlled trial of oral
                                                                           atenolol in patients with unexplained syncope and positive
5.   Martin TP, Hanusa BH, Kapoor WN. Risk stratification of
                                                                           upright tilt test results. Am Heart J 1995; 130: 1250-3.
     patients with syncope. Ann Emerg Med 1997; 29: 459-66.
                                                                       22. DiGierolamo E, Di Iorio C, Sabatini P et al . Effects of
6.   Kapoor WN, Hanusa B. Is syncope a risk factor for poor
                                                                           paroxetine hydrochloride, a selective serotonine reuptake
     outcomes ? Comparison of patients with and without
                                                                           inhibitor, on refractory vasovagal syncope : a randomised,
     syncope. Am J Med 1996; 100: 646-55.
                                                                           double blind, placebo-controlled study. J Am Coll Cardiol
7.   Maron BJ, Shirani J, Poliac LC et al. Sudden death in young           1999; 33: 1227-30.
     competitive athletes. Clinical, demographic, and
                                                                       23. Raviele A, Briguole M, Sutton R et al. Effect of etilefrine in
     pathological profiles JAMA 1996; 276: 199-204.
                                                                           preventing syncopal recurrence in patients with vasovagal
8.   Recchia D, Barzilai B. Echocardiography in the evaluation of          syncope : a double-blind, randomised, placebo-controlled
     patients with syncope. J Gen Intern Med 1995; 10: 649-55.             trial : the vasovagal syncope intervention study. Circulation
9.   DiMarco     JP, Philbrick    JT. Use     of   ambulatory              1999; 99: 1452-7.




 Journal, Indian Academy of Clinical Medicine              Vol. 4, No. 4   October-December 2003                                   291

				
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