This document provides an outline on syncope (transient loss of consciousness). It defines syncope, describes the mechanisms, classifications, clinical features, diagnosis and treatment. Key points include: - Syncope is caused by transient global hypoperfusion of the brain due to low cardiac output or systemic vascular resistance. - Causes are classified as cardiac (e.g. arrhythmias, structural issues), non-cardiac (e.g. neurological, metabolic), or unknown. - Common causes include vasovagal, orthostatic hypotension, arrhythmias, and carotid sinus hypersensitivity. - Evaluation involves history, physical exam, ECG and sometimes tilt table testing or cardiac

1. SYNCOPE
Chairperson : Prof. Dr. Ajoy Krishnamurthy
Presenter: Dr. M. Ramesh Babu

2. Out Line
• Definition
• Mechanism
• Classification
• Clinical features
• Diagnosis
• Treatment

3. Syncope (Greek – to interrupt)
• Syncope is the sudden
transient loss of
consciousness and postural
tone with spontaneous
recovery.
• Loss of consciousness
occurs within 10 seconds of
hypoperfusion of the
reticular activating system in
the mid brain.

4. Cont.
• A syncopal prodrome (presyncope) is
common, although loss of consciousness may
occur without any warning symptoms.
• Typical presyncopal symptoms include
dizziness, lightheadedness or faintness,
weakness, fatigue, and visual and auditory
disturbances.

5. • Individuals <18 yrs
• Military Population 17- 46 yrs
• Individuals 40-59 yrs*
• Individuals >70 yrs*
15%
20-25%
16-19%
23%
Syncope
Reported Frequency
*during a 10-year period
Brignole M, Alboni P, Benditt DG, et al. Eur Heart J, 2001; 22: 1256-1306.

6. The Significance of Syncope
• 500,000 new syncope patients each year 5
• 170,000 have recurrent syncope 6
• 70,000 have recurrent, infrequent, unexplained syncope 1-4
explained:
53% to 62%
infrequent, unexplained:
38% to 47% 1-4
1 Kapoor W, Med. 1990;69:160-175.
2 Silverstein M, et al. JAMA. 1982;248:1185-1189.
3 Martin G, et al. Ann Emerg. Med. 1984;12:499-504.
4 Kapoor W, et al. N Eng J Med. 1983;309:197-204.
5 National Disease and Therapeutic Index, IMS America, Syncope and Collapse #780.2; Jan 1997-Dec 1997.
6 Kapoor W, et al. Am J Med. 1987;83:700-708.

7. 1 Day SC, et al. Am J of Med 1982;73:15-23.
2 Kapoor W. Medicine 1990;69:160-175.
3 Silverstein M, Sager D, Mulley A. JAMA. 1982;248:1185-1189.
4 Martin G, Adams S, Martin H. Ann Emerg Med. 1984;13:499-504.
• Some causes of syncope are potentially fatal
• Cardiac causes of syncope have the highest mortality rates
The Significance of Syncope
0%
5%
10%
15%
20%
25%
SyncopeMortality
Overall Due to Cardiac Causes

8. Impact of Syncope
1Linzer, J Clin Epidemiol, 1991.
2Linzer, J Gen Int Med, 1994.
0%
20%
40%
60%
80%
100%
Anxiety/
Depression
Alter Daily
Activities
Restricted
Driving
Change
Employment
73% 1
71% 2
60% 2
37% 2

9. Maintenance of Postural Normal tension
• Standing  pooling of 500–1000 mL of blood
in the lower extremities and splanchnic
circulation.
• There is a decrease in venous return to the
heart and reduced ventricular filling that result
in diminished cardiac output and blood
pressure.
• These hemodynamic changes provoke a
compensatory reflex response, initiated by the
baroreceptors in the carotid sinus and aortic
arch, resulting in increased sympathetic
outflow and decreased vagal nerve activity .
• The reflex increases peripheral resistance,
venous return to the heart, and cardiac output
and thus limits the fall in blood pressure.

10. Maintenance of Postural Normaltension
Neurovascular
Compensation
• High pressure
mechanoreceptors
• Low pressure
mechanoreceptors

11. Cont.
• Typically cerebral blood flow ranges from 50 to 60
mL/min per 100 g brain tissue and remains relatively
constant over perfusion pressures ranging from 50 to
150 mmHg.
• Cessation of blood flow for 6–8 seconds will result in
loss of consciousness, while impairment of
consciousness ensues when blood flow decreases to 25
mL/min per 100 g brain tissue.
• From the clinical standpoint, a fall in systemic systolic
blood pressure to ~ 50 mmHg or lower will result in
syncope.
• A decrease in cardiac output and/or systemic vascular
resistance—the determinants of blood pressure—thus
underlies the pathophysiology of syncope.

12. Cerebral perfusion and autoregulation
• The cranial cavity normally contains a brain weighing
approximately 1400 g, 75 mL of blood, and 75 mL of
spinal fluid.
• Because brain tissue and spinal fluid are essentially
incompressible, the volume of blood, spinal fluid, and
brain in the cranium at any time must be relatively
constant (Monro–Kellie doctrine).
• More importantly, the cerebral vessels are compressed
whenever the intracranial pressure rises. Any change in
venous pressure promptly causes a similar change in
intracranial pressure.
• Thus, a rise in venous pressure decreases cerebral
blood flow both by decreasing the effective perfusion
pressure and by compressing the cerebral vessels.

13. Autoregulation
• This process, by which the flow to many tissues is maintained
at relatively constant levels despite variations in perfusion
pressure. In the brain, autoregulation maintains a normal
cerebral blood flow at arterial pressures of 65 to 140 mm Hg.

14. Syncope: Etiology
Orthostatic
Cardiac
Arrhythmia
Structural
Cardio-
Pulmonary
*
1
•Vasovagal
•Carotid Sinus
•Situational
Cough
Post-
micturition
2
•Drug
Induced
• ANS
Failure
Primary
Secondary
3
•Brady
Sick sinus
AV block
•Tachy
VT
SVT
•Long QT
Syndrome
4
•Aortic Stenosis
•HOCM
• Pulmonary
Hypertension
5
•Psychogenic
•Metabolic
e.g. hyper-
ventilation
•Neurological
Non-
Cardio-
vascular
Neurally-
Mediated
Unknown Cause = 34%
24% 11% 14% 4% 12%
DG Benditt, UM Cardiac Arrhythmia Center

15. Syncope Mimics
• Disorders without impairment of consciousness
Falls
Drop attacks
Cataplexy
Psychogenic pseudo-syncope
Transient ischemic attacks
• Disorders with loss of consciousness
Metabolic disorders
Epilepsy
Intoxications
Vertebrobasilar transient ischemic attacks

16. Causes of Syncope
Framingham Cohort1 (N=727)
Composite Data (Linzer2)
(N=1,002)
Cause
Prevalence
Mean %
Cause
Prevalence
Mean %
Vasovagal 21 Vasovagal 18
Orthostatic 9.3 Orthostatic 8
Cardiac 10 Cardiac 18
Seizure 5.2 Neurologic 10
Medication 6.8 Medication 3
Stroke/TIA 4.2 Situational 5
Other 7.8 Carotid Sinus 1
Unknown 35.9 Unknown 34
1Soteriades ES, et al. NEJM. 2002;347:878-885.
2 Linzer M, et al. Ann Intern Med. 1997;126:989-996.

17. Causes of Syncope by Age
Younger Patient
• Vasovagal
• Situational
• Psychiatric
• Long QT*
• Brugada syndrome*
• WPW syndrome*
• RV dysplasia*
• Hypertrophic cardiomyopathy*
• Catecholaminergic VT
• Other genetic syndromes
Older Patient
• Cardiac**
– Mechanical
– Arrhythmic
• Orthostatic hypotension
• Drug-induced
• Neurally mediated
• Multifactorial
.

18. Differential Diagnosis of Syncope: Seizures vs syncope
Observation Seizure syncope
Onset Sudden More gradual
Duration Minutes Seconds
Jerks Frequent Rare
Headache Frequent (after) Occasional (before)
Confusion after Frequent Rare
Incontinence Frequent Rare
Eye deviation Horizontal Vertical (or none)
Tongue biting Frequent Rare
Prodrome Aura Dizziness
EEG Often abnormal Usually normal

19. Classification of Syncope
Etiologically classified into :
• I .cardiac
• II. Noncardiac
• III. Undetermined

20. Cardiac syncope
1. cardiac syncope (10-20%)
i. Due to stuctural abnormalities (3-11%) leading to decrease cardiac out
put:
- left ventricular outflow obstuction(LVOTO)
- right ventricular outflow obstruction(RVOTO)
- coronary artery disease (CAD)
- cardiac tamponade
- aortic dissection.
ii. Due to arrythmias (5-30%)
-tacharrthmias
-bradyarrthmias
-pacemaker related.
iii. Neurally mediated syncope
-during and fallowing catherization
- nitrate syncope

21. Non cardiac syncope
• 40-50% of all causes of syncope
• Divided into 4 groups
1. vascular
2.nuerological
3.metabolic
4. psycogenic

22. Cont.
1. Vascular causes : most common causes of
syncope and consitute 1/3rd of all syncopes.
divide into 3 groups:
a)reflex mediated
b)orthostatic
c)anatomical

23. Cont.
a)Reflex mediated syncope:
i) Neurally mediated : nuerocardiogenic/vaso vagal syncope (the commonest
cause)
ii)Neurally indueced:
a)carotid sinus syncope/carotid sinus hypersensitivity:
.cardioinhibitory
.vasodepressor
. Mixed
b)situational syncope(1-8%):
. Micturation syncope
. Defecation syncope
. Cough syncope
. Swallowing syncope
. Divers
. Postprandial syncope
. Valsalva syncope
iii) Neuralgias:
. Glossopharyngeal
. Trigeminal

24. Cont..
b) Orthostatic syncope: 4-12%
. Venous pooling or volume depletion
. Drug indueced
. Nuerogenic
c) Anatomical: subclavean steal syndrome
2) Nuerologic syncope:( <10%)
i) cerebrovascular syncope
ii) seizure disorders
iii) migraine (12-13%)
3) Metabolic syncope: (<5%)
4) Psychogenic syncope
(3) Undertermined (syncope of unknown origin) 13-41% of all
syncopes.

25. 1. Cardiac syncope
• Severe obstuction to cardiac output or rhythm
disturbace can lead to syncope.
• a) Due to structural abnoramalites leading to
flow: exertional syncope is a common
manifestation of all types of heart diseases in
which cardiac output is fixed and does not rise
or may fall with exercise.
• i) LVOTO : common conditions AS, HCM.

26. AS
• Aortic stenosis: syncope occurs in <42% with
severe AS , ususally with exertion.
• Mechanism of syncope:
• Due to fixed CO, CO decreases on exertion due
to reflex fall in peripheral vascular resistance.

27. Hypertrophic cardiomyopathy
In 30 %
• Mechanism: Dynamic LVOTO is worsened by an
increase in LV contractility (stimulating the LV
mechanoreceptors),decrease in chamber size, or
decrease in after-load. (Hence , a Valsalva
maneuver, severe cough or drugs precipitates
hypotension and syncope.)
• VT reported in 25% of adults pts.
• Predictors of syncope : include age < 30 yrs . LVED
volume index <60 ml/m2 and unsustained VT.

28. LV inflow obstruction
• LV infow obstuction can also cause syncope.
• MS it rarely leads to syncope and it could be due to :
• Decreased LV filling which in turn may lead to
decreased CO and syncope.
• AF with rapid ventricular rate.
• PH
• Pulmonary embolism
• Cerebral embolic event
• Ball valve thrombus
• Associated AS or CAD.
• Atrial myxomas: it result in obstuction of MV or TV and
may obstuctive ventricular filling leading to decrease
CO and syncope especially with change in position.

29. RVOTO
• Causes: Pulm.HTN secondary to CHD (TOF and
eisenmenger complex ), Pulm.Stenosis ,
Pulm.embolism.
• Mechanism :inability to increase CO in
association with a reflex fall of peripheral
resistance results in hypotension and syncope.
• In CHD right to left shunt as in TOF results in
marked arterial hypoxia which may precipitate
syncope.

30. CAD
• Syncope can occur in 5-12% in AMI especially in elderly
pts. , while syncope in unstable angina and coronary
spasm is rare.
• Mechanism: sudden pump failure producing
hypotension and decreased perfusion of the brain.
• Others: acute mechanical complications – MR,VSD,
ventricular wall rupture.
• Cardiac tamponade.
• Drug induced: vasodilators (nitrates,CCBs, morphine);
volume depletion due to diuretics.

31. Syncope due to arrhythmias
• Tachyarrhythmias : VT, SVT, AF and AV nodal
reentrant tachycardia are common causes of
syncope.
• Ventricular tachycardia: is commonest arrythmia
(39%) of cardiac syncopes.
• VT generally occurs in known organic heart
disease and long QT syndrome which could be
congenital or acquired.
• Commonly associated ventricular arrythmia is
Torsade De Pointes, sometimes polymorphic VT.

32. Cont.
• SVT: 8% of cardiac syncopes.
• SVT occurs mostly in known organic heart
diseases like AS, HCM, restrictive CM,PS and LV
dysfunction.
• Syncope in WPW syndrome is related to rapid
rate of reciprocating SVT or rapid ventricular over
the accessory pathway during AF and also in
vasomotor factors.

33. Bradyarrythmias and Adv. AV block
• Accounts for 31% of cardiac syncopes.
• Profound sinus bradycardia ,SA exit block ,high
AV block and sick sinus syndrome (SSS) are
common causes.
• Sinus bradycardia: It may be due excessive
vagal tone , decreased sympathetic tone or
sinus node disease itself.

34. Cont..
• Sick sinus syndrome(SSS): 25-70% of SSS
pateints which is charecterized by
disturbances of SA impulse formation or
conduction.

35. Cont.
• Complete heart block: syncope is common in
Stokes – Adams syndrome.
• Progression to high grade AV block or CHB in pts.
with conduction defects: RBBB+LAH,RBBB+1ST AV
block , LBBB+1ST AV block, fascicular blocks with
Mobitz type II AV block or with prolonged PR
interval can occur.
• iii) Pacemaker related:syncope in pts. With
pacemaker implantation is due to pacemaker
malfunctioning or pacemaker syndrome.

36. Cont..
• Mechanism of syndrome in arrhythmias:
• In Tacharrhythmias: mild-moderate
tachycardias increase CO, where as marked
tachycardia (>140/min) leads to decrease in
diastolic filling and CO (Raul’s effect) resulting
in hypotension and syncope.
• In Bradyarrythmias :Usually, bradycardia leads
to prolonged ventricular filling resulting in
increased stroke volume to maintain CO.

37. Neurally mediated syncope
• Following cardiac catheterisation:
• Pain associated with femoral puncture and groin
compression after sheath removal may produce
vasovagal episode and result in syncope.
• Prophylactic measures to prevent vasovagal episode:
• Adequate explanation of the procedure to the patient.
• IV atropine in anxoius bradycardia pts. Prior to removal
of the sheath.
• Patient should monitored for rhythm and BP during the
sheath removal and immediately afterwards.

38. Cont.
• Nitrate syncope: nitrates causes marked
venodilatation, decrased CO results in
tachycardia and increased cardiac inotropic
state.
• However, in susceptible individuals and
presence of predisposing factors leads to
stimulation of cardiac mechanoreceptors and
syncope.

39. Non cardiac syncope
• Non cardiac syncope include vascular, metabolic and
psychogenic.
• a) vascular syncope : include reflex mediated and
othostatic.
• 1) reflex mediated:
• i)Nuerocardiogenic syncope (vasovagal /vasodepressor
syncope/common faint):
• Most common causes of syncope .
• It is characterized by a sudden fall of BP with or without
bradycardia, often preceded by a constellation of prodromal
symptoms such asnausea, headache, sweatings,
hyperventilation, parasthetia chest pain and palpitation.
• These symptoms may persist minutes or hours after the
syncope.
• Often occurs in youngers and resolves spontaneously once
the pt. assumes supine position.

40. Vasovagal syncope
• Phases:
• 1st phase: BP and heart rate increases largely
due to baroreceptor mediated rise in
sympathetic tone.
• 2nd phase: abrupt fall in the BP and heart rate
with prodromal symptoms culminating in
syncope.
• 3rd phase: rapid recovery on assuming supine
position.

41. Pathophysiology of vasovagal syncope
• Normal response to upright position (standing):
• The decrease in venous return, stroke volume
and arterial pressure lead to increase
sympathetic and decrease parasympathetic
acitivity, thereby maintaining BP and heart rate.
• In vasovagal syncope: facilitating factors trigger
baroreceptors and medullary centers through
afferent fibres, activating the parasymapthetic
tone but inhibiting the sympathetic tone through
vagal efferent fibres resulting in hypotension and
bradycardia and there by syncopy.

42. • Pic vasovagal syncope

43. Situational syncope
• 1-8% includes : micturition, defecation, swallowing,
coughing, valsava manuever.
• Micturational syncope: often seen in younger men
after rising from the bed in early morning and men
who with sudden LOC during or immediately following
voiding.
• Mechanism: similar to vasovagal. The
mechanoreceptors in bladder are triggered in the
presence of predisposing factors, causing syncope.
• Predisposing factors: fatigue, decreased food intake,
alcohol ingestion, recent UTI, bladder pathology.
• Falicitating factors: changes during micturition i.e.
sudden decompression of bladder, and possible
valsalva maneuver, orthostatic hypotension in elderly,
physiological changes during sleep.

44. Defecation syncope
• Occurs mostly in elders, usually arising from the
bed at night or during manual disimpaction of the
rectum.
• Mechanism: triggering of mechanoreceptors in
the gut wall in the presence of predisposing and
facilitating factors.
• Predisposing factors: fatigue, decreased food
intake, alcohol consumption, GIT pathology.
• Facilitating factors: change in the sleep, valsalva
manuever during defecation, orthostatic
hypotension.

45. Swallowing or deglutition syncope
• Mechanism: occurs in pts. associated with
structural abnormalities of esophagus or heart
due to triggering of mechanoreceptors in
upper GIT, especially esophagus.
• Predisposing factors: esophagus abnormalities
(diverticula, achalasia, stricture,tumor etc.)
• Cardiac causes like AMI, acute rhuematic
carditis, sinus arrest or high degree AV blocks.

46. Cough syncope
• Tussive / post tussive / laryngeal vertigo
• Syncope following a paroxysm of severe cough usually
occurs in the middle aged men who drink alcohol, smoke
and have a chronic lung disease.
• Mechanism: reflex triggering of pulmonary
mechanoreceptors.
• Severe coughing increases intrathoracic pressure which
decreases venous return and in turn CO.
• Transmission of high intrathoracic pressure to the
subarachnoid space during coughing may increase the
cerebrovascular resistance and reduce the cerebral blood
flow.
• Rarely associated with Mobitz II or complte heart block,
obstuctive cardiomyopathy and severe cerebrovascular
disease.
• Similar mechanism during endotrachial intubation or
bronchoscopy and sneeze syncope associated with Arnold-
Chari malformations.

47. Cont..
• V) Valsalva syncope: usually in the presence of
predisposing factors (such as cerbrovascular
disease or sick sinus syndrome) causes syncope
due to progressive fall in venous return , arterial
pressure and CO as a result of prolonged increase
in the intrathoracic pressure.
• VI) Divers syncope: underwater diving leads to
sudden death. It could be a form of
nuerocardiogenic syncope and hypoxia and
bradycardia of diving reflex may contribute.

48. Cont.
• Postprandial syncope: postprandial
hypotension (usually 45-60 min after meals)
due to splanchanic blood pooling and
peripheral vasodilatation may lead to syncope
especially in the elderly pts.
• Impaired baroreflex function and thereby
inadequate sympathetic acitivity and release
of gastrointestinal peptides could be the
contributing factors.

49. Carotid sinus hypersensitivity / carotid
sinus syncope
• Profound bradycardia and / or hypotension with
compression of carotid sinus suspceptible individuals.
• Asymptomatic elder males ; spontaneous fainting,
occurs in 5-20% of the individuals with abnormal
carotid sensitivity.
• Mechanism: triggering of carotid sinus (located in the
ICA just above the bifurcation of CCA) and medullary
centers via afferent fibres (glossopharyngeal and vagus
nerves) activates parasympathetic and inhibits
sympathetic tone via vagal and sympathetic efferent
fibers results in profund bradycardia and hypotension.

50. Types of carotid sinus hypersensitivity
• Cardioinhibitory type: defined as cardiac
asystole of >3 sec. Most common type;
• secondary to marked sinus bradycardia, SA block,
and high degree AV bloCK.
• Vasodepressor type: defined as a SBP decline of
> 50mmhg, in the absence of significant
bradycardia. Presyncopal symptoms/signs not
usually observed.
• Mixed type: combination of cardioinhibitory and
vasodepressor response, with bradycardia and
hypotension.

51. Cont..
• Predisposing factors:
• For carotid syncope: CAD and hypertension in majority,
neck pathology (enlarged neck L/N,carotid boby
tumors, parotid tumors, thyroid tumors, head and neck
tumors).
- posssible association with digitalis, alpha-methydopa
and propranolol intake have been reported.
For carotid sinus hypersensitivity: sinus node dysfunction
and AV node conduction abnormalities are often
noted in the pts.
Precipitating factors: factors which exert pressure on the
carotid sinus may precipitate syncope,e.g. tight collar,
shaving, sudden turning of the head.

52. Orthostatic syncope
• A decline of >20mmhg in systolic or >10mmhg
in diastolic BP upon assuming upright posture
is often defined as orthostatic hypotension.
• It is a disorder in which assumption of upright
posture results hypotension associated with
light-headness, blurring of vision and sense of
profound weakness.
• These symptoms are often worst on arising in
the morning or after meals or exercise.

53. cont..
• Mechanism: normally, upright posture results in
pooling of 500-700ml of blood in lower limbs and
splanchnic circulation leads to decrease venous
return and CO, and triggering of aortic, carotid
and cardiopulmanory baroreceptors.
• This reflexly increases sympathetic outflow and
inhibit parasympathetic acitivity, resulting in
increase in heart rate and vascular resistance to
maintain systemic BP on standing upright.
• Hence, orthostatic hypotension occurs when a
defect exist in the regulation of systemic BP in
any element of this system.

54. Cont..
• Etiology and classification: divided into 3 groups:
• A)Due to venous pooling and/ or blood volume
depletion:
• Prolonged bed rest, prolonged standing, pregnancy,
venous varicosities, blood loss, dehydration.
• B)Neurogenic causes:
• General medical causes: DM , renal failure,
amyloidosis, and alcoholic nueropathy.
• Autoimmune diseases: mixed connective tissue
diseases, SLE, rheumatoid arhtritis, GB Syndrome,
Eaton-Lambert syndrome.

55. Cont.
• Central brain lesion: multiple cerebral infarcts,
multiple sclerosis, craniopharyngioma.
• Autonomic failure: Shy-Drager syndrome(
multiple system atrophy), Parkinson’s disease.
• Tabes dorsalis, syringomyelia.
• Circulating endogenous vasodilatators:
hyperbradykinism, carcinoid syndrome,
mastocytosis.
• Idiopathic orthostatic hypotension.

56. Cont.
• C)Drug induced: it accounts for 2-9%.
• Vasodilators: Ca channel blockers, nitrates,
hydralazine, ACE inhibitors, and prazosin.
• Other antihypertensives: methyldopa, clonidine,
labetelol, and diuretics.
• Antidepressants: mono amino oxidase (MAO)
inhibitors, and antidepressants.
• Tranquilizers: phenothiazines and barbiturates.
• Antiparkinsonian drugs.

57. Idiopathic orthostatic hypotension
• Is a rare disorder, common in males.
• Often associated with other autonomic
disturbances such as impotence, impaired
erection and ejaculation, impaired sweating
and sphincter malfunction.

58. Neurological syncope
• Infrequent causes of syncope (<10%)
• i) cerebrovascular syncope: 6% of CVA and TIA
• Vertebrobasilar system: in almost all the pts.
atherosclerotic occlusive disease of vertebrobasilar
system is involved in this type of syncope, with
compromised perfusion to the medullary centers,
which is usually preceded by symptoms of vertigo,
diplopia, dysarthria and ataxia.
• Subclavian atrery: subclavian steal syndrome due to
occlusive disease of the subclavian artery to the origin
of the vertebral artery may give rise to syncope.

59. Cont.
• Brachiocephalic artery : in the occlusive disease
of the origins of the brachiocephalic vessels e.g.
aortic arch syndrome, Takayasu’s arteritis,
syncope is not uncommon.
• Syncope is a rare manifestation: of SLE, gaint cell
arteritis, sickle cell disease, embolic
complications of rheumatic heart disease and
myxoma, dissection of extracranial arterics.
• Syncope may occur in the anomalies of cervical
spine or cervical spondylosis.

60. Reflex mediated syncope
• It includes neuralgias:
• Glossopharyngeal neuralgia: severe unilateral
paroxysmal pain in oropharynx, tonsillary fossa, base of
the tongue, or ear precipitated by swallowing,
chewing, or coughing, occasionally results in syncope
and seizure during the attack.
• Syncope is mostly caused by asystole or bradycardia
and rarely due to vasodepressor response.
• It is associated with neoplasms of neck or lymphomas
with meningeal involvement in 1/6 th of the pts. with
syncope.
• Trigeminal neuralgia: it may also be associated with
syncope due to bradycardia asystole or vasodepressor
response.

61. Seizure diorders
• <2% of seizure pts. have syncope.
• Temporal lobe syncope: temporal lobe epilepsy is
rarely associated with bradyarrthmias and is the
most likely form of epilepsy to masquerade as
syncope.
• Hence, the term temporal lobe syncope is used
for partial complex seizures when pts. Have drop
attacks resembling syncope.
• Non convulsive seizures i.e. atonic seizures or
epileptic drop attacks which are common with
secondary generalized seizures or partial epilesy
affecting mesial frontal or central cortical regions
may masquerade as syncope.

62. Migraine related syncope
• 12-18% of pts. With migraine may have syncope
and orthostatic hypotension due to
hyperresponsiveness of dopamine receptors with
the inhibition of vasomotor center and vasovagal
reaction secondary to pain.
• Syncope usually occurs in less form of migraine
due to basilar arterial system involvement.
• This type of migraine usually afflicts young
women and has a strong menstrual association.

63. Metabolic syncope
• Hypoglycemia related syncope: is associated
with weakness, sweating , sensation of hunger,
confusion and altered consiousness, which are
not related to posture and usually promptly
respond to food ingestion or IV glucose
administration.
• Most common causes: due to insulin or OHA’s,
alcohol, prolonged fasting and rarely,
insulinomas.
• It is gradual in onset and is associated with sinus
tachycardia and rarely, hypotension.
• However, hypoglycemia may trigger
neurocardiogenic syncope.

64. Cont..
• Hypoxia related syncope: may occur in young healthy
adults exposed to moderate to very high altitudes due
to:
- Reflex bradycardia, hyperventilation, and subsequent
hypocapnia, resulting a reflex cerebral vasoconstriction
which decreases cerebral oxygen delivery.
- mild volume depletion due to diuresis at high altitudes
or due to physical activity may lead to vasovagal
syncope.
• In presence of cardiovascular disease, pulmonary
insufficiency and anemia; syncope may occur at lesser
levels of 02 deprivation.
• It is associated with sinus tachycardia while BP is
usually normal.

65. Psychogenic syncope
• Syncope may be manifestation of generalized
anxiety disorder, major depression or panic
disorder, especially in young females by
precipitating vasovagal reactions.
• During hyperventilation seen in psychiatric
pts., there is tachycardia and slight
hypotension but no fall of BP.
• Complete loss of consciousness rarely occurs.

66. Exercise induced syncope
• Syncope may occur during or immediately after
exercise. The most common causes are:
• 1) underlying cardiac diseases: most common are:
• Structural abnormalities:
- LVOTO: AS, HCM.
- RVOTO: PH
- Cardiomyopathy: DCM, HCM, RV dysplasia
- CAD: atherosclerotic, anamolous origin of coronary
arteries(in young).
• Arrthmogenic: VT, SVT, accessory pathways, long QT
syndrome.
• Underlying cardiac diseases have a potential for
sudden cardiac death.

67. • 2) Underlying neurological causes subclavian
steal syndrome.
• 3) Neurocardiogenic: exercise syncope without
structural heart disease is due to the increase
in catecholamines and force of ventricular
contraction results in triggering of cardiac
mechanoreceptors in the setting of mild
volume depletion and shifts of blood flow to
dissipate heat.

68. Evaluation of syncope
• 1)Clinical history:
• Mode of onset
• Duration of episode
• Precipitating factors (triggers)
• How was consciousness regained?
• Associated factors- before (prodromes, aura),
during , and after (postictal)
• Predisposing factors
• Family history.

69. • Mode of onset:
• Rapid sudden onset in cardiac and vasovagal syncope
and seizure disorder.
• Gradual onset in hypoglycemia, during related syncope
and hyperventilation.
• Unrelated posture: arrythmogenic and seizure disorder.
- prolong standing facilitates vasovagal syncope.
- after arising: in orthostatic hypotension.
- syncope on changing position ( from sitting to lying,
bending, turning over in bed).

70. • Duration of episode: in syncope, duration of
the event is usually ≤1 min and duration of
episode usually lasts ≤ 5 min; while seizure,
the duration of unconsciousness is usually ≥ 5
min.
• Restoration factors: regained consciousness
promptly in syncope ( of cardiac origin); while
in seizure disorder, it occurs slowly.

71. • Trigerring factros:
• i)On exertion: cardiac syncope occurs due to LVOTO
(AS,HCOM),RVOTO(PH,PE), CAD and sometimes due to
arrythmias.
• With arm exercise: subclavian steal syndrome.
• After exercise in well trained athletes: exercise induced
syncope.
• ii) with head rotation /pressure on carotid sinus:
carotid sinus syncope / hypersensitivity.
• iii) pain, grief, emotional stress, unpleasant sight,
sound or smell: vasovagal syncope.
• iv) during or immediately after micturition , defecation,
swallowing, coughing: situational syncope.

72. • V) Associations:
• a) association with aura: in seizure disorders.
• b) prodromes of warmth, nausea, sweating, light
headiness: they occur in vasovagal syncope.
• Sweating or nausea before the event sometimes in cardiac
syncope.
• Preceded by vertebrobasilar symptomssuch as vertigo,
diplopia, dysarthria, ataxia: CVA in vertebrobasilar system.
• c) episode associated with blue face, frothing at the mouth,
toungue biting, urinary incontinence, convulsive
movements in seizure disorders.
• d) postictal confusion state, sleepiness, aching muscles in
seizure disorders.

73. • Vi) predisposing factors:
• a) fatigue, surgery(eye, dental), exposure to heat: vasovagal
syncope.
• b) in situational syncope:
- fatigue, alcohol ingestion, UTI,bladder pathology (
micturition syncope)
- fatigue, alcoholintake, GIT pathology( defecation syncope).
- esophgeal pathology (swallowing syncope)
- smoking, chronic lung dieseases, alcohol intake (cough
syncope).
• c) neck pathology, CAD, hypertension: carotid sinus syncope
• d) concomitant use of drugs: postural hypotension, nitrate
syncope( diuretics, vasodilators, betablockers).
• e) head inhury: seizure disorders.

74. • Family history:
• Family history of epilepsy may be presnt in
seizures.
• Positive family history in HOCM, long QT
syndrome.

75. Blood pressure measurement
• 2) BP measurement for detection of
orthostatic hypotension: supine BP and heart
rate are measured after the pt. has been lying
down for at least for 5 min.
• Standing measurements should be obtained
immediately and for at least for 2 min., and
should be continued for 10 min when there is
a high suspicion of orthostatic hypotension.

76. 3)Carotid Sinus Massage (CSM)
• Method
– Massage, 5-10 seconds
– Don’t occlude
– Supine and upright
posture
(on tilt table)
• Outcome
– 3 second asystole
and/or 50 mmHg fall in
systolic BP with
reproduction of
symptoms = Carotid
Sinus Syndrome
• Absolute
contraindications
– Carotid bruit, known
significant carotid
arterial disease,
previous CVA, MI last 3
months
• Complications
– Primarily neurological
– Less than 0.2%
– Usually transient

77. 4)Head-up Tilt Test (HUTT)
• Unmasks VVS
susceptibility
• Reproduces symptoms
• Patient learns VVS
warning symptoms
• Physician is better able to
give prognostic /
treatment advice

78. Head up tilt test (HUTT)
• Standard diagnostic test for evaluating pts.
• i) indications:
• Recurrent syncope or a single syncopal episode in a
high risk pt. who either has no evidence of structural
heart disease or in whom other causes of syncope have
been excluded.
• Evaluation of pts. In whom an apparent cause of
syncope has been established ( e.g. asysole, AV block)
but in whom the presence of neurally mediated
syncope would influence the treatment.
• As a part of the evaluation of pts. With exercise –
related syncope.

79. • ii) potential emerging indications:
• Recurrent idiopathic vertigo in whom neurally
mediated bradycardia and hypotension may be
the cause.
• Recurrent TIAs especially if Doppler, U/S, carotid
angiography and TEE have failed to disclose an
etiology for the symptoms.
• Chronic fatigue syndrome: in some, neurally
mediated bradycardia and hypotension may
contribute to the symptom complex.

80. • iii) relative contraindications:
• Syncope with clinically severe LVOTO.
• Syncope in presence of critical MS.
• Syncope in setting of known critical proximal coronary
artery stenosis.
• Syncope in conjunction with known critical
cerebrovascular stenosis.
• iv) not warrented:
• Single syncopal episode which is highly typical of
neurally mediated syncope without an injury and also
not in a high risk setting.
• Syncope in which an alternative specific cause has
been established.

81. Technique
• Preparation:
• The test is performed in a quiet room, minimizing
the surrounding noise which ample lighting and
comfortable temperature in a fasting state ( 75ml
of NS for each hour of fasting may be infused to
decrease the possibility of false positive result).
• All non essential and vasoactive drugs should be
withheld for about 5 half-lives.
• Tilt table with foot board support is used.
• Simultaneously and continues monitoring of
minimum 3 ECG leads and BP is done.

82. Procedure
• 20-45 min supine equilibrium period before
start the test. HUTT has 2 protocols.
- passive tilt testing: table is tilted to an angle
of 60◦-80◦ (usually 70◦ )for 30-45 min. if there
is no positive response i.e. syncope or
presyncope in association with hypotension
and / or bradycardia, proceed with
pharmacological provocation.

83. - provocative tilt testing: usually isoproternol,
nitroglycerine or edrophonium are used.
• 1 µg/min of isoproternol infusion is started while the
pt. is in supine position and then pt. is tilted for 10-15
min and watched for any positive response.
• If there is no response, the pt. is again brought to
supine position and the procedureis continued with
increasing dosage and pt. is tilted for similar duration
till the positive response ( max. dosage 3-5µg/min or
adverse effects or severe tachycardia ) is reached.
• Altenatively, increasing bolus dosages may be given
instead of continuous infusion. (each increament 1-
2µg).

84. • Positive response: 3 types
• Type 1 : mixed response
• Heart rate initialy raises and then falls, but the
ventricular rate does not fall to <40/min or fall to
40/min for <10sec or asystole for <3sec.
• BP raises initially and then falls before heart rate falls.
• Type2 : cardioinhibitory response – heart rate rises
initially and then falls to a ventricular rate <40/min for
>10sec or asystole occurs for <3sec.
• Type2A: BP rises initially and then falls before heart
rate falls.
• Type2B: BP rises initially and falls to <80mmhg systolic
at or after the onset of rapid and severe fall in heart
rate.

86. • Type 3 : pure vasodepressor response:
• Heart rate rises progressively and does not fall
>10% from peak at the time of syncope.
• BP falls to cause syncope.
• The estimated sensitivity and specificity for
passive tilt test is 65% and 90% respectively while
with pharmacalogic provacation, sensitivity is
75% and specificity 80% with overall
reproducibility of 67-85%.

87. 5)ECG
• i) standard ECG: for diagnosis of syncope due
to arrythmias.
• ii) signal averaged ECG: for the detection of
late potentials for prediction of inducible
ventricular tachycardia in pts. with syncope.
• iii) Holter monitoring: it determines the
presence or absence of arrythmias in pts. Who
develop symptoms during ambulatory
monitoring.

88. Method Comments
Holter (24-48 hours) Useful for infrequent events
Event Recorder Useful for infrequent events
Limited value in sudden LOC
Loop Recorder Useful for infrequent events
Implantable type more
convenient (ILR)
Wireless (internet)
Event Monitoring
In development
Ambulatory ECG

89. Heart Monitoring Options
ILR
Event Recorders
(non-lead and loop)
Holter Monitor
12-Lead
2 Days
7-30 Days
Up to 14
Months
10 Seconds
OPTION
TIME (Months)
0 1 2 3 4 5 6 7 8 9 10 11 12 13 14

90. Patient Activator Reveal®
Plus ILR 9790 Programmer
Reveal®
Plus
Insertable Loop Recorder

91. 6)Electrophysiological (EP) Studies
• It is indicated in pts. with suspected structural
heart disease and unexplained syncope and it
should not be performed in pts. with known
cause of syncope for whom treatment will not
be influenced by the finding of the test.
• EP studies are helpful in establishing the
diagnosis of sick sinus syndrome, heart block,
SVT or VT in pts. with syncope.

92. Electroencephalogram
• Not a first line of testing
• Syncope from Seizures
• Abnormal in the interval between
two attacks – Epilepsy
• Normal – Syncope

93. 7)CT scan , Carotid duplex scan
• These are helpful in establishing neurological
causes of syncope and seizure disorders with
careful history and neurological examination.
• 8)Echocardiography : for detection of occult
cardiac disease and impaired ventricular
function to suggest a cardiac cause of
syncope.

94. • 9)Stress testing: it is reserved for pts. In whom
syncope or pre-syncope occurred during or
immediately after exertion or in association with
chest pain.
• It is indicated in young individuals with recurrent
syncope during exertion when other causes of
syncope have been excluded and rule out
anomalous coronary arteries.
• It is contraindicated in pts. Suspected of having
severe AS or HOCM.

95. • 10)Cardiac catheterization : for establishing
the diagnosis of structural heart diseases and
anomalous coronary arteries with syncope.
• 11)Routine blood tests: such as serum
electrolytes, glucose and heamatocrit levels
may be heplful, but have a low diagnostic
value in evaluation.

98. Classification of Task Force
Recommendations

99. Levels of Evidence

100. Treatment of Syncope
• Principal goals of treatment:
- prevent recurrences.
- reduce risk of mortality
• Adiitonal goals:
- prevent injuries assoicated with recurrences
- improve quality of life.

101. Neurally mediated syndromes: therapy
Recommendations
Initial treatment:
Education and reassurance
Sufficient for most
No treatment Single syncope and no high
risk settings
Additional treatment High risk or high frequency
settings

102. Neurally mediated syndromes :
therapy
Additional treatment( high risk or high frequency):
• Syncope is very frequent, e.g. alters the quality of
life.
• Syncope is recurrent and unpredictable ( absence
of premonitory symptoms) and exposes patients
to “ high risk” of trauma.
• Syncope occurs during the prosecution of a “ high
risk” activity (e.g. driving, machine operation,
flying, competitive athletics, etc.

103. Neurally mediated syndromes :
therapy
• Class I:
• Explanation and reassurance.
• Avoidance of trigger events
• Modification or discontinuation of hypotensive drug treatment.
• Cardiac pacing in CI or M carotid sinus syndrome.
Class II:
• Volume expansion by salt supplements, an exercise program
• or head-up tilt sleeping (>10) in posture-related
• syncope
• Tilt training in patients with vasovagal syncope
• Isometric leg and arm counter-pressure manoeuvres in
• patients with vasovagal syncope
• Cardiac pacing in patients with cardioinhibitory vasovagal
• syncope with a frequency >5 attacks per year or
• severe physical injury or accident and age >40

104. Treatment of orthostatic hypotension
• Treatment goals:
- prevention of symptom recurrence and
associated injuries.
- improvement of quality of life
- establishment of quality of the underlying
diagnosis.

105. Cont.
Cause Treatment
Drug induced autonomic
failure
Eliminate the offending
agent
Primary & secondary
autonomic failure
Modify physical factors
that influence systemic
blood pressure

106. Treatment of Orthostatic Hypotension
class I recommendations:
• Syncope due to orthostatic hypotension
should be treated in ALL pts. . In many
instances, treatment entails only modification
of drug treatment for concomitant conditions.

107. Treatment of Cardiac Arrhythmias as
primary cause
• Treatment goals:
• -prevention of symptom recurrence
• -improvement of quality of work
• -reduction of mortality risk

108. Cont.
• Class I recommendations:
• Syncope due to cardiac arrhythmias must
receive appropriate to the cause in all pts. In
whom it is life- threatening and when there is
a high risk of injury.

109. Cont.
• Class II Recommendations:
• Treatment may be employed when culprit
arrhythmia has not been demonstrated and a
diagnosis of life threatening arrhythmia is
presumed from surrogate data.
• Treatment may be employed when a culprit
arrhythmia has been identified but is not life-
threatening or presenting a high risk of injury.

110. Cont..
Sinus node dysfunction
(including brady & tachycardia syndrome)
• Cardiac pacemaker therapy is indicated and is proven
highly effective when bradyarrhythmias is documented
as the cause of the syncope.( class I, level B).
• Physiological pacing ( atrial or dual-chamber) is
superior to VVI pacing.(class I, level A).
• Elimination of drugs that may increase susceptibility to
bradycardia should be considered (level C).
• Catheter ablation for control of atrial arrhythmias may
have role in selected pts. With brady-tachy syndrome(
level C).

111. Cont.
AV conduction system disease
• Cardiac pacing is first-line therapy for treatment
of syncope AV block(class I,level B).
• Pacing improves survival and prevents syncopal
recurrence in pts. With heart block (level B).
• Pacing may be life saving in pts. with BBB and
syncope in these pts.(If suspected mechanism is
intermittent AV block)(level C).
• Consider VT or VF as a possible cause of syncope
in these pts. If they also have LV dysfunction.

112. Cont.
paroxysmal SVT and VT
• SVT s are uncommon as a cause of syncope.
• Syncope due to acquired Torsades de Pointes as a
result of drugs is not uncommon. The causal drug
should be eliminated immediately.
• In syncope due to VT, amiodarone may provide
benefit in the absence of heart disease. If LV
function is depressed , as ICD is warranted.
• The RV outflow tract and bundle-branch reentry
forms of VT may be amenable to catheter
ablation. ( an ICD is also indicated with LV
dysfunction.)

113. Indications for ICD therapy
• Class I Recommendations:
• Documented syncopal VT or VF (level A)
• Undocumented syncope, previous MI and
inducible SMVT (level B)
• Established long QT syndrome, Brugada
syndrome, ARVD or HOCM with a family
history of sudden death ( level C).
• Brugada syndrome or ARVD and inducible
VT/VF.(Level C).

114. Implanted device (pacemaker, ICD)
malfunction
• Implanted pacing systems are rarely the cause of
syncope or near-syncope.
• If syncope is attributed to the implanted device:
-evidence of battery depletion/failure, or lead
failure device or lead replacement is indicated.
- evidence of pacemaker syndrome , device
reprogramming or replacement is indicated.
- in the event an ICD fails to detect and / or treat
an arrhythmia, reprogramming generally resolve
the problem.

115. Treatment of Steal Syndromes
• Syncope associated with upper extremity
exercise in the setting of subclavian steal
syndrome may warrant surgery or angioplasty.
• Direct corrective angioplasty or surgery Is
usually feasible and effective( class I,level C).

116. Metabolic Disturbances:
Hyperventilation
• Hyperventilation resulting in hypocapnia and
transient alkalosis may be responsible for
confusional states or behavioral disturbances.
• Clearcut distinction between such symptoms and
syncope may be difficult.
• Frequently associated with anxiety episodes
and/or ‘panic’ attacks.
• Recurrent faints associated with hyperventilation
should justify a psychiatric consultation.

117. When to Hospitalise a pateint with
Syncope (for Diagnosis)
• Suspected or known significant heart disease
• ECG abnormalities suggesting an arrhythmia
• Syncope during exercise
• Syncope occuring in supine position
• Syncope causing severe injury
• Family history of sudden death
• Sudden onset of palpitations in the absence of
heart disease
• Frequent recurrent episodes.

118. When to Hospitalise a pateint with
Syncope (For Treatment)
• Cardiac arrhythmias as cause of syncope
• Syncope due to cardiac ischeamia
• Syncope secondary to structural cardiac or
cardiopulmonary diseases
• Stroke or focal neurologic disorders
• Cardioinhibitory neurally-mediated syncope
when a pacemaker implant is planned.

119. Pharmacological Therapy
• Many pharmacalogical agents have been used
in the treatment of neurocardiogenic syncope.
• Studies are limited by 2 factors:
• 1) problems with reproducability of tilt-table
testing.
• 2)the relatively favorable natural history of
neurocardiogenic syncope, with spontaneous
remission rate of 91%.

120. • Only 4 pharmacalogical agents have been showed to
be effective in randomized clinical trails: atenolol,
paroxetine, midodrine, and enalapril.
• Mahanonda et al, randomized trail on 42 pts. With
syncope or presyncope and positive tilt-table testing to
atenolol or placebo.
• At follow-up tilt testing after 1 month, response rate
were 62% and 5% in atenolol and placebo groups
respectively.
• Many nonrandomized trails shown the ability of β-
blockers to reduce the response to tilt-table tests or
reduce symptom recurrence during follow-up.

121. • Ward et al, randomized 16 pts. With frequent
syncope (>2 syncopal episodes per month,
reproducibility +ve tilt test) to midodrine, an α-
agonist, and placebo in a cross trail.
• Response rates to repeat tilt test were 63% with
midodrine and 13% with placebo.
• Di Girolamo et al randomized trail 68 pts. With
refractory vasovagal syncope and a +ve tilt-table
test to paroxetine or placebo.
• After 1 month repeat testing, response rates
were 62% and 38%.

122. • Another study randomized 30 pts. With consistently
+ve tilt-table test to receive enalapril or placebo.
• Repeat tilt testing 1 week later showed a 100%
response to enalapril in the 14 pts. and 20% to placebo
group.
• During 13 month follow up, none of the pts. On
enalapril had a recurrence of syncope or presyncope;
recurrence rate of placebo not reported.
• Larger studies and more clinical experience with ACE-
inhibitors are necessary before they can be considered
first-line agents for pts. With neurocardiogenic
syncope. The mechanism of action is unknown.

123. • Other agents:
• Used in in the treatment of vasovagal syncope include:
• Disopyramide
• Scopolamine, anticholenergic agent
• Theophylline
• Clonidine
• Fludrocortisone has not been tested in randomized
trails but has been used extensively because of its
emperical benefits and lack of toxicity.

125. References
• 1. Guidelines on Management (Diagnosis and
Treatment) of Syncope – Update 2004,Executive
Summary, The Task Force on Syncope, European
Society of Cardiology.
• 2)Adam’s and Victor’s text book of Nuerology,
• 3)Clinical examination of Cardiology – B.N.Raghava rao,
• 4)Cardiac Arrhythmias- R.K.Thakur.
• 5)Harrison’s principles of internal medicine,
• 6)Oxford Text Book of Medicine.
• 7) Ganong's Review of Medical Physiology .

126. THANK YOU