What is syncope? Syncope (SINK-a-pee) is another word for fainting or passing out. Someone is considered to have syncope if they become unconscious and go limp, then soon recover. For most people, syncope occurs once in a great while, if ever, and is not a sign of serious illness.

1. Lecture for classes in internal medicine
for the foreign 6-year students
Syncope and Arterial Hypotension

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. 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. Other causes of Syncope

19. 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.

20. 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.

21. 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.

22. 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

23. • 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

24. 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.

30. 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

31. 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

32. 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

33. 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.

34. 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

35. 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

36. 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

37. 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

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