Approach to Syncope by Dr. Meghana

1. Syncope
– Dr. Meghana
2nd yearPG

2. Overview
I. Definition
II. Epidemiology
III. Pathophysiology
IV. Classification
V. Etiology
VI. Features
VII.Treatment
VIII.Differential Diagnosis
IX. Approach

3. I. Definition
• Transient self limited loss of
consciousness due to acute global
impairment of cerebral blood flow
• Onset – rapid
• Duration – brief
• Recovery – spontaneous and complete

4. Presyncope
• Dizziness
• Light headednessfaintness
• Weakness
• Fatigue
• Visual and auditory disturbances

5. Other causes for T-LOC
• Neurologic or cerebrovascular
• Metabolic syndromes and coma
• Psychogenic syncope
a) Epilepsy
b) Vertebrobasilar ischemia
a) Hyperventilation with hypocapnia
b) Hypoglycemia
c) Hypoxemia
d) Intoxication of drugs or alcohol
e) Coma
a) Anxiety
b) Panic disorder
c) Somatization disorder

6. II. Epidemiology
• Account for 1% of hospital admissions
and 3% of emergency visits
• Bimodal distribution by age, first episode
between 10 – 30 years peak around 15
years age, second episode peak around
≥65 years and especially ≥75 years
• MC etiology Neurally mediated syncope
• Second MC etiology cardiac syncope

7. Prognosis
• A single syncopal event for all ages –
benign
• Syncope of non cardiac and unexplained
origin in young – excellent prognosis
• Syncope due to cardiac cause – risk of
sudden cardiac death

8. III. Pathophysiology
Standing posture
↓
500 – 1000 ml pooling of blood in lower extremities and splanchnic circulation
↓
Decrease in VR to the heart
↓
Reduced Ventricular filling
↓
Decrease in cardiac output & BP
↓
Compensatory reflex by baroreceptorts
↓
Increased sympathetic & decreased vagal activity
↓
Increased peripheral resistance and increases venous return
↓
Increased CO & BP

9. Baroreceptors

10. Baroreflex

11. • Latency of autoregulatory responses → 5 – 10
sec
• Typically cerebral blood flow ranges from 50 –
60 ml/min/100g brain tissue remains relatively
constant over perfusion pressure b/n 50 – 150
mm hg
• Impairment of consciousness → when blood
flow decreases to 25ml/min/100g brain tissue
• Cessation of blood flow for 6 – 8 sec → LOC
• A fall in SBP to 50 mm Hg or lower → syncope

12. • SBP fall due to
↓cardiac output ↓Systemic vascular
resistance
Determinants of BP
• ↓ effective circulating blood
volume
• ↑ thoracic pressure
• Massive pumonary embolus
• Brady and tachy arrythmias
• Valvular heart diseases
• Myocardial dysfunction
• Central and peripheral ANS diseases
• Sympatholytic medications
• Transiently during neurally mediated
syncope

13. EEG
Two patterns
1. Slow-flat-slow pattern
2. Slow pattern
Indicates more
severe cerebral
hypoperfusion

14. EEG

15. IV. Classification
• Temporary failure of reflexes
responsible for maintaining
cardiovascular homeostasis
Neurally
mediated
syncope
• Cardiovascular homeostatic
reflexes are chronically impaired
• Autonomic failure
Orthostatic
hypotension
• Arrhythmias
• Structural cardiac diseases
Cardiac
syncope

16. Neurally mediated syncope
a) Classification and causes
b) Features
c) Treatment

17. Neurally mediated syncope
Sudden, transient change in the autonomic efferent activity
with ↑ parasympathetic and sympatho inhibition
↓
Bradycardia and vasodilatation and reduced
vasoconstrictor tone
↓
Decrease in SBP
↓
Cerebral hypoperfusion below compensatory limits of
autoregulation
• Inorder to NMS, a functioning ANS is necessary,
incontrast to syncope resulting from autonomic failure

18. a) Classification - NMS
• Based on afferent and provocative trigger
• Based on efferent pathway
i. Vasovagal syncope
ii. Situational syncope
i. Vasodepressor syncope
ii. Cardioinhibitory syncope
iii. Mixed syncope
Sympathetic
vasoconstrictor
failure
Increased vagal
outflow –
bradycardia/asystole
Both vagal and
sympathetic reflex changes

19. Vasovagal syncope
• Neuro cardiogenic syncope
• Provoked by fear, pain, anxiety, intense
emotion, sight of blood, unpleasant sights
and odours, orthostatic stress

20. Position Usually standing or sitting but may occur in supine position
(as during cardiac catheterisation)
Prodrome Few seconds to minutes
Weakness, light-headedness, sweating, nausea, yawning,
pallor or the sensation of impending doom
Urge to pass urine or motion
The event Loss of consciousness, with a fall to the ground or may just
slump to one side while sitting
Pallor, sweating, dilated pupils
Pulse is slow or of low volume
Urinary incontinence may occur
Total duration is most often less than a minute, rarely 2-5
minutes
Post event Awakens with a feeling of dizziness and nausea, sweating,
and the urge to defecate
Orients to surroundings within seconds after gaining
consciousness
Total duration of episode 5 – 10 minutes
If tries to stand up immediately, may fall again
Vasovagal syncope

21. Situational reflex syncope
• Specific localised stimuli that provoke the
reflex, vasodilatation and bradycardia
• Causes -
a. Pulmonary
b. Urogenital
c. Gastrointestinal
d. Cardiac
e. Carotid sinus
f. Ocular
• Cough syncope
• Wind instrument
player’s syncope
• Weightlifter’s syncope
• Mess trick and
fainting lark
• Sneeze syncope
• Airway
instrumentation
• Postmicturition
syncope
• Urogenital tract
instrumentation
• Prostatic
massage
• Swallow syncope
• Oesophageal
stimulation
• Glossopharyngeal
neuralgia
• GIT
instrumentation
• Rectal examination
• Defecation syncope
• Bezold-jarisch
reflex
• Cardiac outflow
obstruction
• Carotid sinus
sensitivity
• Carotid sinus
massage
• Ocular pressure
• Ocular
examination
• Ocular surgery

22. Carotid sinus sensitivity
• It results from the stimulation of the
carotid sinus baroreceptors located in the
internal carotid artery above the
bifurcation of the common carotid artery
• It is defined a sinus pause of >3 sec in
duration or a fall in SBP of 50 mm Hg or
more

23. Carotid sinus massage
• Should be performed after checking the bruits in
patients with syncope older than 40 yrs
• Done by applying gentle pressure over the carotid
pulsations for 5 – 10 sec in both supine and upright
positions
• The response – Cardioinhibitory (asystole)
Vasodepressive (fall in SBP)
Mixed
• Diagnosis of Carotid sinus hypersensitivity as
reproduction of patient symptoms during massage
• Contraditications – Prior TIA
Carotid bruit

24. b) Features - NMS
• Symptoms of Orthostatic intolerance → dizziness, light
headedness, fatigue + Autonomic activation features →
diaphoresis, pallor, palpitations, nausea,
hyperventilation & yawning
• Proximal and distal myoclonus may occur
• Eyes remain open and deviated upwards
• Pupils dilated & rowing eye movements occur
• Grunting , moaning, snorting & stertorous breathing
• Urinary incontinence
• Fecal incontinence and post ictal confusion → rare

25. c) Treatment - NMS
• Reassurance
• Avoidance of provocative stimuli
• Plasma volume expansion with fluid and salt
• Isometric counter pressure maneuvers of limbs – leg
crossing or hand grip & arm tensing (raise BP by
increasing central blood volume and cardiac output)
• Fludrocortisone, vasoconstriction agents, β blockers –
for refractory patients
• Dual chamber pacing – more than 40 years patients
syncope with asystole/severe bradycardia &
prominent cardioinhibition due to carotid sinus
syndrome

26. Orthostatic hypotension
a) Definition
b) Variants
c) Features
d) Causes
e) Treatment

27. a) Definition - OH
• Reduction in systolic blood pressure of at
least 20 mm of Hg or diastolic blood
pressure of at least 10 mm of Hg within 3
min of standing or head-up tilt on a tilt
table
• It is a manifestation of sympathetic
vasoconstrictor failure (autonomic failure)

28. • Gradual fall in BP without a compensatory heart rate
increase → characteristic

29. b) Orthostatic variants
Variant Feature Diagnosis
Classical OH ↓SBP > 20mm Hg or ↓DBP > 10
mm Hg within 3 min of
standing
Active standing or tilt table
Intial OH ↓ BP immediately on standing
of >40 mmHg with BP
spontaneously and rapidly
returning to normal
Period of symptoms < 30 sec
Active standing
Reflex or Vasovagal Syncope Intial normal adaptation reflex
followed by rapid fall in venous
return and vasovagal reaction
Tilt table
Delayed OH Slowly progressive ↓ SBP with
no bradycardiac reflex > 3 min
Tilt table
Delayed OH + Reflex syncope When vasovagal reaction
follows delayed OH
Tilt table
Postural Orthostatic
Tachycardia Syndrome (POTS)
Severe Orthostatic intolerance
(not syncope) with marked ↑ in
Heart rate > 30 beats/min and
instability of BP
Tilt table

30. c) Features - OH
Specific :
• Light headedness
• Dizziness
• Presyncope
Absent/nonspecific :
• General weakness
• Fatigue
• Cognitive slowing
• Leg bulking
• Headache
• Visual blurring → retinal or occipital ischemia
• Neck pain → Coat Hanger Headache – sub occipital, post
cervical, shoulder region
→ Due to neck muscle ischemia
• Orthostatic dyspnoea → inadequate perfusion of ventilated lung apices
• Angina → impaired myocardial perfusion with normal coronaries
Due to sudden postural
change

31. • Symptoms exacerbated by
exertion
prolonged standing
↑ ambient temp
meals
• Syncope usually preceded by warning
symptoms; but can occur suddenly →
indicates seizure/cardiac cause

32. d) Causes - OH
• Primary autonomic failure
• Secondary autonomic failure
• Postprandial hypotension
• Iatrogenic
• Volume depletion
Due to idiopathic central and
peripheral neurodegenerative
diseases - Synucleinopathies
 Lewy body diseases
Parkinson’s disease
lewy body dementia
pure autonomic failure
 Multiple system atrophy (the Shy
– Dragers syndrome)
 Diabetes
 Hereditory amyloidosis (familial
amyloid polyneuropathy)
 Primary amyloidosis (AL
amyloidosis; immunoglobulin light
chain associated)
 Hereditory sensory and autonomic
neuropathies (HSAN) (type ш –
familial dysautonomia)
 Idiopathic immune – mediated
autonomic neuropathy
 Autoimmune autonomic
ganglionopathy
 sjÖgren’s syndrome
 Paraneoplastic autonomic
neuropathy
 HIV neuropathy
Due to autonomic
peripheral neuropathies
α – adreno receptor
antagonists
Nitrates and other
vasodilators
Tricyclic agents
Phenothiazines
Iatrogenic – diureses
Medical – haemorrhage, vomting,
diarrhoea and ↓ fluid intake

33. e) Treatment - OH
• Remove reversible causes – vasoactive medications
• Non pharmacological interventions
patient education
warning about large meals
isometric counter pressure maneures
rising the head of the bed to reduce supine HTN
increased dietary salt and fluid intake
• Pharmacological interventions
Fludrocortisone acetate
vasoconstricting agents – midodrine
L-dihydroxyphenyl-serine
pseudoephedrine
• Intractable symptoms – pyridostigmine
yohimbine
desmopressin acetate
erythropoietin

34. Cardiac syncope
• Due to arrhythmias and structural heart
diseases
• These are responsible for only 13% cases
of syncope out of which 80% are due to
arrhythmias

35. Causes - arrhythmia
Bradyarrhythmias Sinus bradycardia
acute ischemic syndrome
sick sinus syndrome
hyperkalemia
acute intra cranial HTN
Complete heart block
congenital
acquired
acute ischemic syndrome
drug induced
degenerative diseases
diptheretic myocarditis
Tachyarrhythmia Supraventricular
Ventricular
Conditions predisposing to arrhythmias MI
Ventricular aneurysm
Structural defect with chamber enlargement
Mitral valve disease
ASD
Ebstein anomaly
Heart failure
Hypo and hyperkalemia
Prolonged QT syndromes
Pre excitation syndromes
Renal failure
Severe emotion
Carotid sinus hypersensitivity
Intramyocardial tumors

36. Causes – structural defects
• Severe AS
• HOCM
• Acute ischemic syndrome
• Acute pulmonary embolism
• Primary pulmonary arterial HTN
• Cardiac tamponade
• Mitral stenosis
• Severe PS
• Atrial myxoma
• Acute myocarditis
• Severe TOF
• Eisenmenger syndrome

37. Bradyarrhythmias
• Bradyarrhythmias and advanced AV blocks – 31% of CVS
causes Syncope
• Following the relief of a sudden onset palpitation, if the
patient has syncope – Sick Sinus Syndrome
• It is important to rule out SSS in all patients presenting with
SVT – verapamil given for SVT may aggrevate
bradyarrhythmia – fatal asystole
• In any SVT with HR < 200/min, recurrent syncope and
normal heart – suspect SSS
• Stoke Adams attack – syncope due to bradycardia or asystole

38. • Bradyarrhythmia due to sinus node
dysfunction associated with atrial
tachyarrhythmia → tachycardia –
bradycardia syndrome – prolonged
pause following the termination of
tachycardiac episode leads to syncope

39. Complete heart block
• Syncopal attack is rare in congenital CHB – ventricular rate
adequate
• Syncope with CHB – conduction defect
• ECG features –
• Prodromal symptoms often absent
• Unconsciousness supervenes within 5 sec in standing or
within 15 sec in recumbent position
• Bowel and bladder incontinence with fits may occur
 RBBB + Left ant. hemiblock
 Alternating BBB
 RBBB with first degree AV block
 LBBB with first degree AV block
 Fascicular block with Mobitz π AV
block

40. Tachyarrhythmias - VT
• Commonest in syncope – VT
• Syncope in VT depends on ventricular rate – rate < 200/min –
less likely to cause syncope
• Compromised hemodynamic function during VT is caused by
ineffective ventricular contraction, reduced diastolic filling due
to abbreviated filling periods, loss of AV synchrony, and
concurrent MI
• Features of VT → mostly no prodromal symptoms
a brief episode of dizziness may present
a preceding history of palpitation may occur

41. Tachyarrhythmia – SVT
• Less common than VT
• Conditions predispose to syncope in SVT
Underlying heart disease
AS
PS
HOCM
Restrictive cardiomyopathy
Rate of SVT (>200/min)
Underlying preexcitation
Advanced age
standing position at time of onset of SVT
• When rates are exceedingly high as in preexcitation, diastolic filling is
impaired, cardiac output and arterial pressure fall to below the critical
level
• Advanced age with CVA – predispose to syncope even with a slight
fall in arterial pressure

42. Inherited chanellopathies
• Mutations in ion channel sub unit genes →
cardiac electrophysiologic instability and
arrhythmogenesis
• Include
Long QT Syndrome
Brugada Syndrome
Catecholaminergic Polymorphic VT

43. Long QT Syndrome
• Genetically heterogenous disorder
• Prolonged cardiac repolarisation → VT
• Syncope and sudden death → due to unique
polymorphic VT called torsades des pointes →
degenerates into VF
• Genes involved → α and β subunits of K channels,
voltage gated Na channels scaffolding Ankyrin B
protein (ANK2)
• Idiopathic long QT syndrome → common, bizarre T
wave morphologies
• Syncope or cardiac arrest can occur under physical or
emotional stress – first episode before the age of 20 yrs
+
+

44. Acquired QT syndrome

45. Brugada syndrome
• Genetically heterogenous
• Idiopathic VF + Rt. ventricular ECG
abnormalities without structural heart
disease
• Mutations → Na channel α sub unit,
SCN5A
+

46. Brugada syndrome

47. Catecholaminergic polymorphic VT
• Genetically heterogenous disorder
• Exercise or stress induced → Syncope and
Death

48. Structural defects - AS
• Commonest cause for syncope
• Syncope indicates severe obstruction or arrhythmia
• Mechanism –
- fall in systemic vascular resistence
(vasodilatation in skeletal muscles)
- failure of forearm vasoconstriction
during leg exercise (Ventricular Bezold – jarisch
reflex)
- cardiac output fails to rise due to severe
fixed obstruction

49. Structural defects - AS
• Exercise induced syncope – occurs in 2
stages
First stage (20 – 40 sec) Second stage
Sudden fall in BP
Pallor
Light headedness
Inattention
Sinus rhythm
Reduced intensity of heart
sounds
Unconsiousness
Cyanosis
Absent pulse and heart
sounds
Apnoea
Twitching of body or
seizures
Bladder and bowel
incontinence
Abnormal ECG
Sinus tachycardia
VT, VF, AF, AV block
Asystole

50. • HOCM – due to restricted ventricular filling
or arrhythmia
• CAD – Due to arrhythmias, large area of
myocardium at risk, vasospastic angina,
postural hypotension after prolonged bed
rest, during or after coronary angiography
• Syncope with chest pain – ? H/o fall
• Nitrate syncope – a new onset of nitrate
syncope in a pt. with chronic stable angina –
progression of disease to unstable angina
evolving MI

51. • Syncope can be the presenting feature of the
Acute Pulmonary Embolism
• Syncope is rare in MS even when it is severe
• Causes of syncope in MS – Lt. atrial myxoma,
untreated critical disease, paroxysmal atrial
arrhythmias, severe pul. ar. HTN, PE, Ball
valve thrombus, with AS
• Recurrent syncope in MS – Lt. atrial myxoma
as a cause of mitral obstruction

52. TREATMENT
• Depends on the underlying disorder
• Sinus node disease and AV block - cardiac
pacing
• Atrial and ventricular tachyarrhythmias-
Ablation , antiarrythmic drugs and
cardioverter defibrillators.

53. DIFFERENTIAL DIAGNOSIS

54. HYPOGLYCEMIA
• Typically in individuals with Type I /II DM
treated with insulin
• Clinical features- tremors, palpitations,
anxiety, diaphoresis, hunger,
paresthesias.
• Repeated hypoglycemia impairs counter
regulator response which leads to a loss of
characteristic warning symptoms , that are
Hallmark of hypoglycemia.

55. CATAPLEXY
• Patients with CATAPLEXY experience
complete or partial loss of muscle tone,
which is triggered by strong emotions.
• Consciousness is maintained throughout
the episode.
• Attacks typically last between 30 sec to 2
mins.
• No premonitory symptoms.
• Seen in patients with narcolepsy

56. VIII. Approach to a patient with SYNCOPE

58. Feature Significance
Clinical significance
Diabetic patient Hypoglycemia
CAD
CVA
TIA
Postural hypotension due to autonomic neuropathy
Hypertension Postural hypotension (drugs)
Encephalopathy
Intracranial haemorrhage
TIA
CAD
Alcoholism Intoxication
Autonomic neuropathy
CAD Arrhythmias
Acute ischemic syndromes
Mechanical complication
Drugs
Postoperative or prolonged rest Pulmonary embolism
Postural hypotension
Peptic ulcer GI bleeding
Acute perforation
The deaf patient Prolonged QT syndrome
Painful/unpleasant event/sight Vasovagal
History of fall or head injury Subdural hematoma
a) Important aspects in history

59. Feature Significance
Related to physiological act
Exertional syncope Left ventricular outflow
obstruction
Bilateral carotid stenosis
(Takayasu’s arteritis)
Syncope with Upper Limb
exercise
Subclavian steal syndrome
Syncope with cough Cough syncope
Syncope with micturition Micturition syncope
Syncope with neck turning Carotid sinus hypersensitivity
a) Important aspects in history

60. b) Important aspects in physical examination
Features Could indicate
Drowsiness / altered sensorium Hypoglycemia
Central nervous disorder
Pulse rate Vasovagal
Arrhythmia
Blood pressure Postural hypotension
Hypertension
Reactive hypertension following a fall
Tongue (bruise, bleeding) Epilepsy
Head injury Subdural hematoma
Carotid bruit TIA
Heart
S4, murmurs
Non-ejection click
Irregular rhythm
Pericardial rub
Aortic stenosis or other valvular lesions
Mitral valve prolapse
Arrhythmia
Cardiac tamponade
Leg veins / calf muscles DVT with pulmonary embolism
Rectal examination / stool heme test Occult GI bleeding
Neurological examination Neurological cause
Provocative maneuvers
Carotid sinus massage
Hyperventilation
Valsalva maneuver
Ocular compression
Tests to bring out vagal instability

61. c) Diagnostic testing in syncope
Test Mechanism
Blood sugar Hypoglycemia
Hemoglobin, PCV Low level indicates bleeding
Serum potassium Arrhythymias due to high or low levels
Serum bicarbonate Low level suggests seizure occurred
Blood gases Hypoxia indicates pulmonary embolism
Cardiac enzymes Myocardial infarction
ECG (2-8 % yield) Arrhythymia
MI
Unstable angina
Vasospastic angina
Hyperkalemia
Hypokalemia
Pre-excitation
Prolong QT interval
Cardiac tamponade
Acute pulmonary embolism

62. c) Diagnostic testing in syncope
Test Mechanism
Holter monitoring (2% yield)
(syncopal episodes >1/week)
Arrhythmia
Echocardiogram (1.3% yield) Valvular disease
Pulmonary hypertension
Intracardiac tumors
Hypertropic cardiomyopathy
Cardiac tamponade
Ventricular aneurysm
LV dysfunction
Wall motion abnormalities
Tilt test Indicated to confirm diagnosis of
vasovagal syncope
Electrophysiological study Low yield if done in all patients
VT, VF, Syncopal SVT or AF may be
induced
Useful in assessing sinus node function
and conduction system
Neurologic testing (EEG, CT, MRI) Low yield

63. AUTONOMIC NERVOUS SYSTEM
TESTING
• This is done by TILT TABLE TESTING.
• This includes assessment of
• A) Parasympathetic ANS (eg :- heart rate in
response to deep respiration and valsalva
manoeuver)
• B) Sympathetic cholinergic functions ( eg:-
thermoregulatory sweat response and quantitative
pseudomotor axon reflex test)
• C) Sympathetic adrenergic function (eg :- blood
pressure response to a valsalva maneuver and tilt
table test with beat to beat blood pressure
measurement)

66. - Dr. Meghana