This document provides an overview of syncope (transient loss of consciousness). It discusses the pathophysiology, typical presentations, differential diagnoses, evaluation and treatment of different syncope types. The main causes discussed are neurally-mediated syncope (the most common), orthostatic hypotension, and cardiac syncope. For evaluation, the document recommends a thorough history, physical exam including orthostatic vital signs and carotid sinus massage in older patients, and tests like ECG, tilt table testing and cardiac monitoring. Treatment depends on the underlying cause, including fluid supplementation, compression stockings and pharmacotherapy for orthostatic hypotension, and pacing for cardiac 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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