definition, classification, evaluation and clinical differentiation of syncope

1. Approach to a Patient with
Syncope
-Dr. Sachin Adukia

2.  Syncope is a transient, self-limited loss of
consciousness due to acute global impairment of
cerebral blood flow.
 The onset is rapid, duration brief, and recovery
spontaneous and complete.
 A syncopal prodrome (presyncope) is common,
although LOC may occur without warning.
 Typical presyncopal symptoms
 include dizziness, lightheadedness or faintness,
weakness, fatigue, and visual, auditory disturbances.

3. Pathophysiological basis
 Gradual failure of cerebral perfusion, with a reduction
in cerebral oxygen availability.
 Cerebral perfusion/oxygenation cut off for 8–10 s,
 then loss of consciousness and postural tone,
 pallor and sweating,
 brief (lasting seconds) extensor stiffening or spasms,
 few irregular myoclonic jerks of limbs
 The whole episode is brief, usually <10 s.

4. Syncope and age groups
 Neurally mediated syncope – MC cause of syncope.
 slightly higher in females than males.
 In young subjects- family history in first-degree relatives.
 Cardiovascular - in emergency room settings and in older patients.
 Syncope due to basilar migraine - more common in young females.
 Orthostatic hypotension –
 increases in prevalence with age because of reduced baroreflex
responsiveness,
 decreased cardiac compliance,
 attenuation of the vestibulosympathetic reflex
 explained by the greater prevalence of
 predisposing neurologic disorders,
 physiologic impairment,
 and vasoactive medication use among institutionalized patients.

5. 3 General Categories
 Neurally mediated (also called reflex or vasovagal
syncope)
 transient change in the reflexes responsible for maintaining
cardiovascular homeostasis.
 Episodic vasodilation (or loss of vasoconstrictor tone) and
bradycardia occur in varying combinations, resulting in
temporary failure of blood pressure control.
 Orthostatic hypotension due to autonomic failure:
 cardiovascular homeostatic reflexes are chronically impaired.
 Cardiac syncope: arrhythmias or structural cardiac
diseases

6. Vasovagal syncope
 most common form of neurally mediated syncope,
 Results from
 excessive vagal tone,
 Abnormal catecholamine response to stress,
 venous pooling during an upright stance
 and impaired cardiac filling.
 The frequency of vasovagal syncopes varies
considerably from one to two during a lifetime to as
common as more than once a day.

9. C/F of Vasovagal syncope
 Symptoms of orthostatic intolerance
 dizziness, lightheadedness, and fatigue,
 premonitory features of autonomic activation
 diaphoresis, pallor, palpitations, nausea, hyperventilation, and yawning.
 During the syncopal event, proximal and distal myoclonus (typically arrhythmic and
multifocal) may occur, raising the possibility of epilepsy.
 The eyes typically remain open and usually deviate upward. Pupils are usually dilated.
Roving eye movements may occur.
 Grunting, moaning, snorting, and stertorous breathing may be present.
 Urinary incontinence may occur. Fecal incontinence is very rare.
 Postictal confusion is also rare
 Although visual and auditory hallucinations and
 near death and out-of-body experiences are sometimes reported.

10. ORTHOSTATIC HYPOTENSION
 Defined As: systolic drop at least 20 mmHg or diastolic drop at least
10 mmHg within 3 min of standing or head-up tilt on a tilt table,
 Is a manifestation of sympathetic vasoconstrictor (autonomic) failure
 In most cases, there is no compensatory increase in HR despite
hypotension;
 with partial autonomic failure, HR may increase but insufficient to
maintain CO
 “delayed” orthostatic hypotension, occurs beyond 3 min of
standing; reflects mild or early sympathetic adrenergic dysfunction.
 “initial” orthostatic hypotension occurs within 15 s of standing:
reflects a transient mismatch between CO and PVR, and does not
represent autonomic failure.

12.  Upright posture- pooling of 500–1000 mL blood in LL and splanchnic
circulation.
 decrease in venous return and reduced ventricular filling – diminished CO and
BP.
 compensatory reflex response, initiated by baroreceptors in carotid sinus, aortic
arch:
 resulting in increased sympathetic outflow
 decreased vagal nerve activity
 This increases peripheral resistance, venous return, and CO and limits the fall in BP.
 If this response fails, as in orthostatic hypotension and transiently in neurally
mediated syncope, cerebral hypoperfusion occurs.
 Cessation of blood flow for 6–8 s will result in LOC,
 impairment of consciousness -if blood flow < 25 mL/min per 100 g brain tissue.
 Clinically fall in systemic SBP to ~50 mmHg or lower will result in syncope.

13. Characteristic symptoms of
Orthostatic hypotension
 lightheadedness, dizziness, and presyncope
 nonspecific, such as generalized weakness, fatigue, cognitive slowing, leg
buckling, or headache.
 Visual blurring - due to retinal or occipital lobe ischemia.
 Neck pain, suboccipital, posterior cervical, and shoulder region (the “coat-
hanger headache”), - neck muscle ischemia
 Orthostatic Dyspnea – VQ mismatch due to inadequate perfusion of ventilated
lung apices)
 Angina - impaired myocardial perfusion
 Symptoms exacerbated by exertion, prolonged standing, increased ambient
temperature, or meals.

14. Iatrogenic cause of Ortho. HypoTN
 Drugs may lower peripheral resistance
 Alpha-adrenoreceptor antagonists
 antihypertensive agents of several classes
 nitrates and other vasodilators;
 Tricyclic agents
 phenothiazines
 Iatrogenic volume depletion due to diuresis
 Volume depletion due to medical causes
 hemorrhage,
 vomiting,
 diarrhea,
 decreased fluid intake

15. Rare causes
 Patients with postural tachycardia syndrome (POTS)
frequently experience orthostatic symptoms without
orthostatic hypotension, but syncope can occur
occasionally.
 Rarely, SACD, syringomyelia etc damage the
descending sympathetic pathways, producing
orthostatic hypotension

18. San Francisco Syncope rule
 CHESS
 C - CHF
 H – Hematocrit <30%
 E – ECG Abnormal
 S – Shortness of breath
 S – SBP in triage area <90
 should only be applied to patients whom no cause of syncope
is identified

19. Other causes of Syncope

20. Syncope in Special situations
Syncope induced by Valsalva manoeuvre
 increased intrathoracic pressure limits the venous return to the
heart
 increases vagal tone,
 resulting in decreased cardiac outflow and syncope.

21. Micturition syncope
 usually in men while standing for nighttime
micturition.
 Several mechanisms :
 postural – standing on leaving a warm bed causing
hypotension
 straining – Valsalva manoeuvre increasing an
already high nocturnal vagal tone, causing
bradycardia
 emptying bladder – abrupt decrease in stimulus to
bladder stretch receptors causing reflex
vasodilatation and hypotension.

22. Carotid sinus syncope
 Common cause of unexplained falls in elderly>50
years, increses with age
 Activation of one or both carotid sinuses causes
peripheral vasodilation, hypotension and syncope in
carotid sinus hypersensitivity.
 Clinical attacks of are attributed to carotid sinus
pressure by head turning or tight collars.
 Diagnostic carotid sinus massage may be positive in
asymptomatic elderly patients but carries a risk of
 prolonged asystole,
 transient or permanent neurological deficit,
 stroke and sudden death.

23. Cough (tussive) syncope
 LOC occurs after a paroxysm of severe coughing, most likely
in obese men (smokers or chronic bronchitis)
 Before losing consciousness, the patient may feel
lightheaded.
 face becomes flushed secondary to congestion, then pale.
 Diaphoresis
 loss of muscle tone
 Several factors
 blockage of venous return by raised intrathoracic pressure.
 weight-lifting syncope - similar mechanism

24.  Hypoglycemic syncope
 Hypoadrenalism - syncope orthostatic hypotension.
 Disturbances of Ca, Mg, K metabolism: rare causes
 Anoxic syncope- occurs d/t lack of oxygen or
production of vasodepressor

25. EEG changes in syncopal subjects
(2 patterns)
 “Slow-flat-slow” pattern
 normal background activity is replaced with high-amplitude slow delta.
This is followed by sudden flattening of the EEG—a cessation or
attenuation of cortical activity—followed by the return of slow waves, and
then normal activity.
 “Slow pattern,”
 is characterized by increasing and decreasing slow wave activity only
 EEG flattening in the slow-flat-slow pattern denotes severe cerebral
hypoperfusion.
 Despite the presence of myoclonic movements and other motor activity
during some syncopal events, EEG seizure discharges are not detected.
 Convulsive syncope is a term used for any type of syncope
manifesting with convulsive movements.

31. Seizure types that must be distinguished
from syncope
 Orbitofrontal
 complex partial seizures, associated with autonomic changes
 Temporal lobe syncope
 complex partial seizures with sudden falls and altered awareness,
followed by confusion and gradual recovery

32. Syncopal attacks provoking epileptic
seizures
 Anoxic epileptic seizures
 Occasionally, true epileptic seizures are triggered by nonepileptic
syncopes in children and adults.
 This combination of syncope and epileptic seizure is called an
anoxic epileptic seizure

33. Epileptic seizures imitating syncope
 Epileptic seizures may manifest with syncopal like
attacks – “ictal syncope” in Panayiotopoulos syndrome
 ‘Ictal syncope’ is used to describe this state, because
‘unresponsiveness with loss of postural tone’ is the
defining clinical symptom of syncope.
 She complained of ‘dizziness’ and then her eyes
deviated to the left, she fell on the floor and she
became totally flaccid and unresponsive for 5 minutes

34. Differential diagnosis of Blackouts
• Syncope
• Epilepsy
• Psychogenic non-epileptic seizures
•Cataplexy
 Drop attack
• Transient CSF obstruction
• Transient ischaemic attack - anterior and posterior circulation
• Panic attack,
• Falls / trauma
• Hypoglycaemia
• Basilar migraine
 Malingeering
 Intoxication

35. APPROACH
Careful history
 Full a description as possible of the first faint
 Precipitating factors,
 posture,
 type of onset of the faint (abrupt or gradual),
 position of head and neck,
 the presence and duration of preceding and associated symptoms,
 duration of loss of consciousness,
 rate of recovery,
 and sequelae.
 question an observer about
 clonic movements,
 color changes,
 diaphoresis,
 pulse,
 respiration,
 urinary incontinence,
 nature of recovery.

36. Clinical examination
 Valsalva maneuver
 Orthostatic drop
 Assess BP in both arms when suspecting
cerebrovascular disease, subclavian steal, or Takayasu
arteritis.
 Pulse: rate and rhythm
 Extra Cardiac Ascultation: carotid, ophthalmic, and
supraclavicular bruits
 Carotid sinus massage in older patients suspected of
having carotid sinus syncope
 The response to carotid massage is vasodepressor,
cardioinhibitory, or mixed

37. Investigations
 Doppler flow of cerebral vessels
 MRA
 EEG has a low diagnostic yield
 To do only when a seizure disorder is suspected
 Tilt-table testing in unexplained syncope in high-risk
settings or with recurrent faints in the absence of heart
disease
 False positives - 10% of healthy persons may faint,
 specificity -90%
 ECG
 Prolonged Holter monitoring
 Implantable loop recordings
 Radionuclide cardiac scanning,
 Echocardiography

38. Treatment of Vasovagal syncope
 Reassurance, avoidance of provocative stimuli, and
plasma volume expansion with fluid
 Isometric counterpressure maneuvers of the limbs
(leg crossing or handgrip and arm tensing) to
maintain pressure in the autoregulatory zone,
 Fludrocortisone, vasoconstricting agents, and beta-
adrenoreceptor antagonists
 no consistent evidence from RCT any pharmacotherapy

39. Treatment of Orthostatic hypotension
 REMOVE REVERSIBLE CAUSES—----------------usually vasoactive medications
 NONPHARMACOLOGIC INTERVENTIONS
 education : staged moves from supine to upright;
 Warnings about the hypotensive effects of large meals;
 isometric counterpressure maneuvers that increase intravascular pressure
 raising the head of the bed to reduce supine hypertension.
 Intravascular volume expansion : fluid and salt.
 PHARMACOLOGIC INTERVENTION
 fludrocortisone acetate
vasoconstricting agents -midodrine, l-dihydroxyphenylserine, pseudoephedrine
 INTRACTABLE SYMPTOMS
 pyridostigmine,
 yohimbine,
 desmopressin
 erythropoietin

40. Treatment of cardiac syncope-
 Treatment of underlying disorder.
 cardiac pacing for sinus node disease and AV block,
 ablation,
 antiarrhythmic drugs, and
 cardioverter-defibrillators

41. References
 Bradley 7th edtn
 Harrison 19th edtn
 Panayiotopoulos 2nd edtn
 Essential Neurology 4th edtn
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