Syncope

SYNCOPE

Chairperson : Prof. Dr. Ajoy KrishnamurthyPresenter: Dr. M. Ramesh Babu

Out Line

• Definition• Mechanism • Classification • Clinical features • Diagnosis • Treatment

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.

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.

• 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 periodBrignole M, Alboni P, Benditt DG, et al. Eur Heart J, 2001; 22: 1256-1306.

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.

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%

Sync

ope M

ortal

ity

Overall Due to Cardiac Causes

Impact of Syncope

1Linzer, J Clin Epidemiol, 1991.2Linzer, J Gen Int Med, 1994.

0%

20%

40%

60%

80%

100%

Anxiety/Depression

Alter DailyActivities

RestrictedDriving

ChangeEmployment

73% 171% 2

60% 2

37% 2

Prop

ortio

n of

Pati

ents

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.

Maintenance of Postural Normaltension

Neurovascular Compensation

• High pressure mechanoreceptors

• Low pressure mechanoreceptors

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.

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.

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.

Syncope: Etiology

Orthostatic CardiacArrhythmia

StructuralCardio-

Pulmonary

*

1• Vasovagal• Carotid Sinus•SituationalCoughPost-

micturition

2• Drug Induced• ANS

FailurePrimarySecondary

3• Brady Sick sinus AV block•TachyVTSVT• Long QT

Syndrome

4 • Aortic Stenosis• HOCM• PulmonaryHypertension

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

Syncope Mimics• Disorders without impairment of consciousness

Falls Drop attacksCataplexyPsychogenic pseudo-syncopeTransient ischemic attacks

• Disorders with loss of consciousnessMetabolic disordersEpilepsyIntoxicationsVertebrobasilar transient ischemic attacks

Causes of Syncope

Framingham Cohort1 (N=727) Composite Data (Linzer2) (N=1,002)

Cause Prevalence Mean % Cause  Prevalence

Mean %Vasovagal 21 Vasovagal 18Orthostatic 9.3 Orthostatic 8Cardiac 10 Cardiac 18Seizure 5.2 Neurologic 10Medication 6.8 Medication 3Stroke/TIA 4.2 Situational 5Other 7.8 Carotid Sinus 1Unknown 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.

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

.

Differential Diagnosis of Syncope: Seizures vs syncope

Observation Seizure syncope

Onset Sudden More gradualDuration Minutes SecondsJerks Frequent RareHeadache Frequent (after) Occasional (before)Confusion after Frequent RareIncontinence Frequent RareEye deviation Horizontal Vertical (or none)Tongue biting Frequent RareProdrome Aura DizzinessEEG Often abnormal Usually normal

Classification of Syncope

Etiologically classified into :• I .cardiac • II. Noncardiac• III. Undetermined

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

Non cardiac syncope

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

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

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

Cont..

b) Orthostatic syncope: 4-12% . Venous pooling or volume depletion . Drug indueced . Nuerogenic c) Anatomical: subclavean steal syndrome2) 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.

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.

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.

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.

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.

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.

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.

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.

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.

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.

Cont..

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

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.

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.

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.

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.

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.

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.

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.

• Pic vasovagal syncope

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.

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.

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.

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.

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.

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.

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.

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.

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.

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.

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.

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.

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.

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.

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.

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.

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.

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.

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.

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.

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.

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.

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.

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.

• 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.

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.

• 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).

• 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.

• 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.

• 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.

• 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.

• Family history: • Family history of epilepsy may be presnt in

seizures.• Positive family history in HOCM, long QT

syndrome.

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.

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

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

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.

• 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.

• 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.

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.

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.

- 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).

• 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.

• 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%.

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.

Method CommentsHolter (24-48 hours) Useful for infrequent events

Event Recorder Useful for infrequent eventsLimited value in sudden LOC

Loop Recorder Useful for infrequent eventsImplantable type more convenient (ILR)

Wireless (internet) Event Monitoring

In development

Ambulatory ECG

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

Patient Activator Reveal® Plus ILR 9790 Programmer

Reveal® Plus Insertable Loop Recorder

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.

Electroencephalogram

• Not a first line of testing• Syncope from Seizures• Abnormal in the interval between

two attacks – Epilepsy• Normal – Syncope

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.

• 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.

• 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.

Classification of Task Force Recommendations

Levels of Evidence

Treatment of Syncope

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

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

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.

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

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.

Cont.Cause Treatment

Drug induced autonomic failure

Eliminate the offending agent

Primary & secondary autonomic failure

Modify physical factors that influence systemic blood pressure

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.

Treatment of Cardiac Arrhythmias as primary cause

• Treatment goals: • -prevention of symptom recurrence • -improvement of quality of work• -reduction of mortality risk

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.

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.

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).

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.

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.)

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).

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.

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).

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.

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.

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.

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%.

• 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.

• 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%.

• 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.

• 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.

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 .

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