Introduction
Transient loss of consciousness is a dramatic symptom due to many causes. Syncope is a symptom defined as, transient loss of consciousness resulting from global hypoperfusion and associated with generalized loss of postural tone with subsequent recovery which is prompt, spontaneous, and complete. Syncope accounts for 5% of hospital visits and 1 to 3% of all hospital admissions in United States.1 It must be distinguished from other causes of loss of consciousness, particularly seizures which is manifestation of paroxysmal excessive discharge of cortical neurons. It has also to be differentiated from Drop attacks which lead to fall without loss of consciousness.

Involuntary movements, often refer to as myoclonic jerks, may accompany syncope due to cardiovascular causes (convulsive syncope) can create diagnostic problem. Some anti-epileptic drugs started with a wrong diagnosis of seizure in a patient with bradycardia induced syncope can potentiate bradycardia and lead to syncope. Thus it is important to distinguish syncope from seizure. Features that help to distinguish the two are the precipitants of the episode, the premonitory or the prodormal symptoms, the symptoms that accompany the episode, and the event that follow it. A loss of consciousness that is precipitated by pain, exercise, micturition, defaecation, or stressful event is usually syncope rather than seizure. Symptoms of nausea, sweating that occur before or during the episode is usually syncope, whereas aura is typically seen in seizure. Disorientation after the event, slowness in returning to consciousness, and unconsciousness lasting for more than five minutes is suggestive of seizure. Rhythmic movement in form of tonic-clonic type is commonly associated with seizures.

The causes of syncope can be broadly divided into:-

1. Cardiac Causes : -
   a) Rhythm abnormality (Brady-arrhythmias, Tachyarrhythmias)
   b) Structural heart disease (Aortic stenosis, mitral stenosis, HOCM, Pulmonary hypertension, etc.)
2. Non-cardiac Causes: -
   a) Vasovagal (Vsodepressor/Neurally mediated syncope)
   b) Orthostatic hypotension.
   c) Carotid sinus hypersensitivity.
   d) Neurogenic causes: - T.I.A, vertebro-basilar insufficiency.
   e) Situational syncope: - micturition, defaecation, coughing.
   f) Conditions simulating syncope:- metabolic (hypoglycaemia), drugs (alcohol) etc.

Non-cardiac Causes

1. Neurocardiogenic syncope : (Vasovagal/Vasodepressor Syncope)This disorder results from reflex mediated change in vascular tone or heart rate.Vasovagal syncope is associated with sympathetic withdrawal (Vasodilatation) and increase in parasympathetic activity (Bradycardia).6,7 Neurally mediated syncope comprises largest group of disorders causing syncope.6-8 It often occurs when upright, some times while sitting; it will never occur in lying down position. Attacks are more likely to occur in certain situations like large meal in warm restaurant, hot and crowded environment, alcohol, after prolonged standing. If syncope ensues, the individual usually lies still while unconscious, though occasionally may convulse briefly. On recovery of consciousness which is prompt and complete the person may complain of nausea, clumsiness, light headedness, headache. Interestingly co-existing heart disease is rare. In some cases of emotional upset, fainting may be triggered in CNS while in others by receptors in the bladder, respiratory centres, may lead to reflex increase in vagal activity and sympathetic withdrawal (situational syncope).7,8
2. Postural/Orthostatic hypotension : This occurs in patients with defect in vasomotor reflexes.9 Systemic blood pressure falls on assumption of upright posture due to loss of vasoconstrictor reflexes in resistance and capacitance vessels of lower limbs. It accounts for 8% of patients (range 4-12%).2 Most common causes of orthostatic hypotension include chronic diseases of peripheral nerves such as diabetes mellitus, nutritional,amyloid polyneuropathy9 which causes secondary autonomic dysfunction.19
3. Carotid sinus hypersensitivity : Carotid sinus syndrome is rare under 50years of age. Syncope is precipitated by pressure on carotid sinus baroreceptors. Syncope can be precipitated by manoeuvre which can cause mechanical stimulation of the carotid sinus such as turning the head, shaving, looking up, and wearing tight collars.
   
   Cardiac Causes
   Cardiovascular causes of syncope : Cardiac arrhythmias like various tachy-arrhythmias, bradyarrhythmias can precipitate syncope. With bradyarrhythmias stroke volume can no longer increase to compensate adequately for decreased heart rate. With tachyarrhythmia ventricular filling time is inadequate to maintain adequate stroke volume.
   
   Bradyarrhythmia such as sick-sinus syndrome (sinus pause > 3 sec.), Stokes-Adams syndrome (high degree Av block), Tachycardia-Bradycardia syndrome can be associated with syncopal episode. Syncope due to tachyarrhythmia is usually preceded by palpitations, lightheadedness, but may occur without warning symptoms. Syncope can be due to supraventricular tachyarrhythmias like atrial flutter, atrial fibrillation, and W.P.W syndrome with rapid ventricular rate.
   
   Patients with structural heart diseases like Aortic stenosis, Hypertrophic obstructive cardiomyopathy, Pulmonary stenosis, Mitral stenosis, Pulmonary hypertension can precipitate syncope.
   
   
4. Cerebrovascular diseases : They are rare causes of syncope, usually due to Vertebro-basilar territory insufficiency.
   
   Approach to patient with Syncope : The key initial step is to classify syncope as cardiac or non-cardiac. Patients with a structural heart disease or an abnormal E.C.G have an increase likelihood of arrhythmia and increased risk of death.20

History taking
History taking is of paramount importance, despite its low specificity the history taking can provide a general direction to the evaluation and may yield a diagnosis. Specific attention should be directed towards prodromal symptoms, duration, situation, and circumstances and associated symptoms of syncope, which often give vital clues to diagnosis to syncope.

Physical Examination
Physical examination should be done to disclose the cause of syncope.

Laboratory and diagnostic testing
E.C.G is recommended in all patients; despite its low yield because it can lead to decisions about immediate management of underlying disease (Pacemaker implantation for CHB). Routine lab tests are not indicated and are done only if specifically indicated by history or clinical examination. If the patient has evidence of cardiac disease then following investigations are recommended,

Echocardiography : If E. C. G or clinical examination is suggestive of structural heart disease then echocardiography is indicated in patients with suspected structural heart diseases which cannot be diagnosed clinically.

Electrophysiologic studies: Electro-physiologic studies are used to diagnose structural heart disease and arrhythmias. Approximately 21% have inducible ventricular tachycardia and 34% have bradycardia.3 In patients with abnormal electrocardiogram 3% have inducible ventricular tachycardia and 19% have bradycardia.3 In patients with normal heart and normal electrocardiogram 1% have inducible ventricular tachycardia and 10% have bradycardia.3 Electrophysiologic tests have a poor sensitivity and specificity for bradyarrhythmias.

Holter/Ambulatory monitoring : It involves continuous E.C.G monitoring to establish cause of syncope. Symptoms are found to occur in conjugation with arrhythmia in 4% of patients, leading to diagnosis of arrhythmic syncope, and symptoms occur without arrhythmia in 17%, potentially ruling out arrhythmic syncope.13 In 79% of patient’s brief arrhythmia or no arrhythmia are found.13

External loop monitor : (Continuous loop event monitor)It is used for long term monitoring in which the patient or the observer can activate the monitor after the symptoms appear, freezing in its memory the recording from the previous 2 to 5 minutes and subsequent 60 seconds. In patients with frequent syncope arrhythmia are found in 8 to 20% and normal rhythm in 12 to 27% of patients.14,15 Limitations include compliance of the patient and problems in using the device. An implantable continuous loop recorder that can be inserted sub-cutaneously can monitor up to 18 months.

Tilt-table testing : Patients who appear to have no cardiac disease but no clue to aetiology to syncope is found then HUT is most rewarding. It involves motorized table capable of tilting patient between 60 and 80 degree, with continuous E.C.G and blood pressure monitoring. In susceptible patients tilt at an angle between 60 and 80 degree for 30 to 60 minutes induces a vasovagal syncope.Tilt-table generally involves provocative agents like Isoproterenol or Nitroglycerine.11,12 Among patients with unexplained syncope positive responses with isoproterenol are reported in approximately 66%.10,12 To date tilt-table is the only diagnostic tool accurate for providing direct diagnostic evidence indicating susceptibility to vasovagal syncope.

C.T/M.R.I imaging /E.E.G : should be avoided unless physical or historical features of central nervous system focality are present. An electroencephalogram provides diagnostic information in less than 2% of cases of syncope.16

Treatment
Treatment depends on cause of syncope. Patients with vasovagal syncope are instructed to avoid situations and stimuli, which can precipitate syncope and are advised to assume recumbent position. Drug therapy is advised in patient’s resistant to above line of therapy. Atenolol has showed to reduce symptoms after 1 month.17 Atenolol attenuates discharge frequency of mechanoreceptors because of its negative inotropic effect. Serotonin reuptake inhibitor such as Paroxitine 20 to 40 mg/day reduces rate of recurrence after 2 yrs. of therapy.18 Case series have used salt plus fludrocortisone or have used metoprolol, midodrine, disopyramide, theophylline but the effectiveness of these medications cannot be determined because of lack of controls. Currently there is interest in investigation of neurohumoral agents like serotonin, endorphins, epinephrine in neurocardiogenic syncope.

Permanent pacemakers which provide pacing at a high rate if a predetermined drop in heart rate occurred in patients with severe symptoms and bradycardia on a tilt-table testing, has an 85% of reduction in relative risk of recurrent syncope.19

Treatment of orthostatic hypotension includes volume replacement in patients with hypovolaemia and avoidance of drugs responsible for orthosis.

Carry home message
Syncope is a common clinical symptom and manifestation of many disease processes due to cerebral hypoperfusion more commonly due to vasovagal, postural, carotid sinus hypersensitivity and less often due to more serious causes such as cardiac arrhythmias, organic heart diseases, which can be diagnosed and treated in systemic clinical and investigational approach. However it is utmost important to identify patients with cardiac causes of syncope as they are associated with high risk of death.

References

1. George M. Tadros, Jess W. Oren, John M Costella. Syncope in young patients:-An approach to a patient with Syncope: Hospital Physician 2002.
2. Linzer M, Young EH, Estes NA III, Wang P, Vorperian VR. Diagnosing Syncope I: - Clinical efficacy assessment project of American college of Physicians. AnnIntern Med 1997; 126 : 989-96.
3. Linzer M, Young EH, Estes NA III, Wang P, Vorperian VR. Diagnosing Syncope II :- Clinical efficacy assessment project of American college of Physicians. Ann Intern Med 1997; 127 : 76-86.
4. Silverstein MD, Singer DE, Mulley AG, Thibaulty GE, Barnett GO. Patient with syncope admitted to medical intensive care unit. JAMA 1982; 248 ; 1185-9.
5. Kapoor WN, Hansa BH, Schulberg HC. Psychiatric illness in patients with syncope. Am J Med 1995; 19 : 505-12.
6. Benidtt DG, Remde S, Bailins S, Dunnigan A, Asso A, Milstein S. Tilt-table test for evaluation of neurally mediated syncope; rationale and proposed protocols. Pacing Clin Electrophysiol 1991; 14 : 1528-37.
7. Abbound FM. Neurocardiogenic syncope. NEJM 1993; 328 : 1117-20.
8. Kapoor WN, Smith MA, Mille NL. Upright tilt testing in evaluation of syncope. Comprehensive literature review. Am J Med 1994; 97 : 78-88.
9. Bannister R. Autonomic failure a textbook of clinical disorders of Autonomic nervous system. 2nd ed Oxford England: Oxford university press 1988: 1-20.
10. Fujimara O, Yee R, Klein GJ, Sharma AD, Boahene KA. The diagnostic sensitivity of electrophysiologic testing in patients with syncope caused by transient Bradycardia. N Engl J Med 1989; 321 : 1703-07.
11. Kapoor WN, Smith MA, Miller Nl. Upright tilt-table testing in evaluating Syncope:A comprehensive literature review. Am J Med 1994; 97 : 78-88.
12. Beneditt DG, Fergmann DW, Grubb BP. Tilt-table testing for assessing syncope. J Am Coll Cardiol 1996; 28 : 263-75.
13. Diamarco JP, Philbrick JT. Use of ambulatory E.C.G monitoring. Ann Intern Med 1990; 113 : 53-68.
14. Linzer M, Pritchett EL, P Antinem M, Mc carthy E. Incremental Diagnostic yield of a loop electrocardiographic recorders in unexplained syncope. Am J Cardiole 1990; 66 : 214-9.
15. Brown AP, Dawkins KD, Davis JK. Detection of arrhythmia, Use of patient activated ambulatory E.C.G device with a solid state memory loop. Br Heart J 1987; 58 : 251-3.
16. Kapor. Evaluation and outcome of patients with syncope. Medicine (Baltimore) 1990; 69 : 160-75.
17. Mahananda N, Bhuripanya K, Kangkayate C. Randomised double blind placebo controlled trial of oral atenolol in patients with unexplained syncope and positive upright tilt-table result. Am Heart J 1995; 130 : 1250-3.
18. Di Girolamo E, Di Iorioc. Effect if Paroxitine hydrochloride a selective reuptake inhibitor, on refractory vasovagal syncope, placebo-controlled study. J Am Cardiol 1999; 33 : 1227-31.
19. Connolly SJ, Sheldon R, Roberts RS, Gent M. The north American Vasovagal pacemaker Study (VPS): A randomized trial of permanent cardiac pacing for prevention of the vasovagal syncope. J Am Cardiol 1999; 33 : 16-20.
20. Martin TP, Hanusa BH, Kapoor WN. Risk stratification of patient with syncope. Ann Emerg Med 1997; 29 : 459-66.