This document discusses syncope, dizziness, and vertigo. It defines syncope as a transient loss of consciousness due to reduced cerebral blood flow. The pathophysiology involves a reduction in cardiac output leading to hypotension and cerebral hypoperfusion. Common causes include neurocardiogenic reflexes, orthostatic hypotension, and cardiac arrhythmias. Evaluation involves taking a history and performing tests like ECG, tilt table testing, and echocardiogram. Treatment focuses on addressing the underlying cause and may include medications. Dizziness encompasses sensations like lightheadedness and vertigo, which is a hallucination of movement. Vertigo is often due to disturbances in the vestibular system within

1. SYNCOPE,DIZZINESS AND VERTIGO
EVALUATION
SANJAY CHOUDHARY
ASSAM MEDICAL COLLEGE
DIBRUGARH

2. SYNCOPE
• DEFINITION-Syncope,a transient loss of
consciousness and postural tone due to
reduced cerebral flow,is associated with
spontaneous recovery.It may occur suddenly
without warning,or may be preceded by
symptoms of faintness (“Presyncope”).These
symptoms include lightheadness,dizziness,a
feeling of warmth,diaphoresis,nausea and
visual blurring occasionaly proceeding to
transient blindness.

3. PATHOPHYSIOLOGY
• Approximately three-fourth of the systemic
blood volume is contained in the venous bed
and any interference in venous return may lead
to a reduction in cardiac output.
• Cerebral blood flow can be maintained if
cardiac output and systemic arterial
vasoconstriction compensate,but when these
adjustments fail,hypotension with resultant
cerebral underperfusion to less than half of
normal results in syncope

4. PATHOPHYSIOLOGY CONTD….
• Normally the pooling of the blood in the lower
parts of the body is prevented by
• (1) pressor reflexes that induce constriction of
peripheral arterioles and venules
• (2) reflex acceleration of the heart by means
of aortic and carotid reflexes, and
• (3) improvement of venous return to the heart
by activity of the muscles of limbs.

5. CAUSES OF SYNCOPE
• I.Disorders of vascular tone or blood volume
A.Reflex syncopes
1.Neurocardiogenic
2.Situational- Cough, Micturition, Defecation,
Valsalva, Deglutition
3. Carotid sinus hypersensitivity
B. Orthostatic hypotension
1.Drug induced (Anti HTN, Vasodilators)
2. Pure autonomic failure(idiopathic
orthostatic hypotension)

6. Contd…
3.Multisystem atrophies
4. Peripheral neuropathy
5. Physical deconditioning
6. Sympathectomy
7. Decreased blood volume
II. Cardiovascular disorders
A. Structural and obstructive cause
1. Pulmonary embolism
2. Pulmonary hypertension

7. Contd…..
3. Atrial myxoma
4. Mitral stenosis
5. Myocardial disease
6. Left ventricular myocardial constriction
7. Pericardial constriction
8. Aortic outflow tract obstruction
9. Aortic valvular stenosis
10. Hypertrophic obstructive cardiomyopathy

8. Contd…
B. Cardiac arrhythmias
1. Bradyarrhythmias-
a.sinus bradycardia, sinoatrial block, sinus arrest
b. Atrioventricular block
2. Tachyarrhythmias
a. Supraventricular tachycardia
b. Atrial fibrillation
c. Atrial flutter
d. Ventricular tachycardia

9. Contd…
III. Cerebrovascular disease
A. Vertebrobasilar insufficiency
B. Basilar artery migraine
IV. Other disorder may resemble syncope
A. Metabolic-eg. Hypoxia, Anemia, Diminished
CO2 due to hyperventilation, Hypoglycaemia
B. Psychogenic- eg. Anxiety attacks, Hysterical
fainting
C. Seizures

10. NEUROCARDIOGENIC SYNCOPE
• The term neurocardiogenic is generally used to
encompass both vagovagal and vaso depressor
syncope.
-Vagovagal syncope is associated with both sympathetic
withdrawal(vasodilation) and increased
parasympathetic activity(bradycardia),whereas
vasodepressor syncope is associated with sympathetic
withdrawal alone.

11. NEUROCARDIOGENIC SYNCOPE cont…
• It is frequently recurrent and commonly
precipitate by a hot or crowded
environment,alchohol,extreme fatigue,severe
pain,hunger,prolonged standing and
emotional or stressful situation. It is often
preceded by presyncopal proderm lasting
seconds to minutes, and rarely occur in supine
position.

12. NEUROCARDIOGENIC SYNCOPE cont…
• Neurocardiogenic syncope often occur in the
setting of increased peripheral sympathetic
activity and venous pooling. Under these
condition vigorous myocardial contraction of a
relatively empty left ventricle is thought to
activate myocardial mechanoreceptors and vagal
afferent nerve fibres that inhibits sympathetic
activity and increase parasympathetic activity.
The resultant vasodilation and bradycardia induce
hypotension and syncope.

13. SITUATIONAL SYNCOPE
• A variety of activities including
cough,deglutition,micturation and defecation are
associated with syncope in susceptible
individuals.
• Like Neurocardiogenic syncope these syndrome
may involve a cardioinhibitory response, a
vasodepressor response or both.
• Cough,micturation and defecation are associated
with maneuvers (such as valsalva’s, straining,and
coughing) that may contribute to hypotension
and syncope by decreasing venous return.

14. SITUATIONAL SYNCOPE cont…
• Increased intra cranial pressure secondry to the
increase intrathoracic pressure may also
contribute by decreasing cerebral blood flow.
• Cough syncope typically occur in men with
chronic bronchitis or COPD or after prolong
coughing fits.
• Micturation syncope occur usually in middle aged
and older men particularly those with prostatic
hypertrophy and obstruction of bladder neck.
• Deglutition syncope may be associated with
oesophageal disorder particularly spasm.

15. CAROTID SINUS HYPERSENSITIVITY
• It is precipitated by pressure on the carotid sinus
baroreceptors.
• This typically occur in the setting of shaving,a tight
collar,turning the head to one side.
• This type hypersensitivity occurs predominantly in men>50
yrs old.
• Activation of baroreceptors give rise to impulses carried via
the nerve of hering, branch of glossopharyngeal nerve to
the medulla in the brain stem.
• These afferent impulse activate efferent sympathetic nerve
fibre to the heart and blood vessels,cardiac vagal efferent
nerve fibres or both.

16. POSTURAL(ORTHOSTATIC)
HYPOTENSION
• Orthostatic hypotension may be the cause of syncope
upto 30% of the elderly;polypharmacy with anti HTN or
antidepressants drugs is often contributor in these
patients.
• Orthostatic intolrance can result from hypovolemia or
from disturbance in vascular control.
• Sudden rising from a recumbent position or standing
quietly are precipitating circumstances.
• Postural syncope may occur in otherwise normal
persons with defective postural reflexes, it is more
common in men than women and typically begins
between 50 and 75 years.

17. CARDIAC SYNCOPE
• In normal individuals heart rate between 30 and
180 beats/min do not reduce cerebral blood flow,
specially in the supine position.
• At rate less than 30 beats/min, stroke volume can
no longer increase to compensate adequately for
the decrease heart rate.
• If greater than 180 beats/min, ventricular filling
time is inadequate to maintain adequate stroke
volume in either case, cerebral hypoperfusion
and syncope may occur.

18. CEREBROVASCULAR DISEASE
• Rarely causes syncope but may lower the
threshold for syncope in patients with other
causes.
• The vertebrobasilar arteries, which supply
brainstem structures responsible for
maintaining consciousness, are usually
involved when cerebrovascular disease causes
or contribute to syncope.

19. DIFFERENTIAL DIAGNOSIS OF SYNCOPE
• (1) Anxiety attacks and Hyperventilation
syndrome
• (2) Seizures
• (3) Hypoglycemia
• (4) Hysterical fainting

20. APPROACH TO THE PATIENTS WITH
SYNCOPE

21. DIAGNOSTIC TEST
• The choice of the diagnostic test should be
guided by history and the physical examination.
• (1) Measurement of serum electrolyte,glucose
and haematocrit.
• (2) Cardiac enzyme if Myocardial ischaemia
suspected.
• (3) Blood and urine toxicology screen.
• (4) Adrenocortical insufficiency patients-
aldosterone and mineralocorticoid level should
be evaluated.

22. DIAGNOSTIC TEST cotd…
• (5) ECG almost all patients.
• (6) Invasive cardiac physiological testing
• (7) Upright tilt table testing (indicated in
recurrent syncope)
• (8) Echocardiogram
• (9) Cerebral syncope- Neuroimaging test(
Doppler ultrasound,MRI)

23. TREATMENT
• The treatment of syncope is directed at the
underlying cause.
• Patient should lower their head to the extent
possible and preferably should lie down. But
lowering the head by bending at the waist should
be avoided because it may further compromise
venous return to the heart.
• The patient should be place supine with the head
turn to the side to prevent aspiration and the
tongue from blocking the airway.
• Monitor vitals of the patient should be regularly.

24. Contd….
• Clothing around the neck and waist should be
loosened.
• Patient should not be given anything by
mouth or be permitted to rise until the sense
of weakness has passed.
• Drug therapy may be necessary when
vagovagal syncope is resistant to the above
measures.

25. DRUG THERAPY-
• Beta adrenergic receptor antagonist- eg.
Metoprolol, Atenolol
• Serotonin reuptake inhibitors- eg. Paroxetine,
Sertraline
• Hydrofludrocortisone is useful for patients with
intravascular volume depletion and for those who
also have postural hypotension.
• Alpha agonist in some patients.
• Vagolytic antiarrhythmic drug eg. Disopyramide
,Transdermal scopolamine treat vagovagal
syncope.

26. Contd…
• Patient with orthostatic hypotension should
be instructed to rise slowly and systematically
from the bed or chair.
• Patient should hospitalized when there is a
possibility that the episode may have resulted
from a life threatening abnormality or if
recurrence with significant injury seems likely.

27. DIZZINESS AND VERTIGO
• DIZZINESS- Dizziness is a common and often
vexing symptom, patients use the term to
encompass a variety of sensations, including
those that seen semantically appropriate(eg.
Lightheadedness, faintness, spinning, giddiness)
and those that are misleadingly in appropriate,
such as mental confusion, blurred vision,
headache, or tingling.
• Dizziness may be classified into three categories-
(1) faintness (2) vertigo (3) miscellaneous head
sensations

28. Contd….
(1)Faintness:- Prior to an actual faint(syncope), there
are often prodromal presyncopal symptoms (faintness)
reflecting ischaemia to a degree insufficient to impair
consciousness.
(2)Vertigo:- An illosory or hallucinatory sense of
movement of the body or environment most often a
felling spinning.
- Vertigo is usually due to a disturbance in the vestibular
system. The end organ of this system, situated in the
bony labyrinths of the inner ears, consist of the free
semicircular canals and the otolithics apparatus(utricle
and saccule) on each side.

29. Contd...
- The canals transduce angular acceleration, while the
otoliths transduce linear acceleration and the static
gravitational forces that provide a sense of head
position in space.
- Vertigo may represent either physiological stimulation
or pathological dysfunction in this system.
- Physiological vertigo- this occur in normal individuals
when-
(1) the brain is confronted with an intersensory
mismatch among the three stabilizing sensory systems

30. Contd….
(2) The vestibular system is subjected to
unfamiliar head movements to which it is
unadapted, such as in seasickness.
(3) Unusual head /neck positions, such as the
extreme extension when painting a ceiling
(4) Following a spin

31. Contd….
- Pathologic vertigo- this results from lesions of the
visual, somatosensory, or vestibular systems.
visual vertigo is caused by new or incorrect eyeglasses
or by the sudden onset of an extraocular muscle
paresis with diplopia ; in either instance , CNS
compensation rapidly counteracts the vertigo.
somatosensory vertigo, rare in isolation , is usually due
to a peripheral neuropathy or myelopathy that reduce
the sensory input necessary for central compensation
when there is dysfunction of the vestibular systems.

32. Contd….
Most common cause of pathological vertigo is
vestibular dysfunction. It may be
central(brainstem or cerebellum) or
peripheral(labyrinth).

33. Features of central and peripheral
vertigo
Signs or symptom Peripheral Central
Direction of associated
nystagmus
Unidirectional;fast phase
opposite lesion
Bidirectional or
unidirectional
Purely horizontal
nystagmus without
torsional component
Uncommon Common
Vertical or purely torsional
nystagmus
Never present May be present
Visual fixation Inhibits nystagmus and
vertigo
No inhibition
Severity of vertigo Marked Often mild
Direction of spin Toward fast phase variable
Direction of fall Towards slow phase variable

34. Signs or symptoms Peripheral Central
Duration of symptoms Finite(minutes,days,weeks)
but recurrent
May be chronic
Tinnitus and/or deafness Often present Usually absent
Associate CNS
abnormalities
None Extremely common(eg.
Diplopia, hiccups, cranial
neuropathies, dysarthria)
Common causes BPPV( Benign proxysmal
positional vertigo),
infection( ladyrinthitis),
meniere’s , neuronitis,
ischaemia, trauma, toxins
Vascular, demyelinating,
neoplasm

35. Contd….
(3). Miscellaneous head sensations- In this
classification describe dizziness that is neither
faintness nor vertigo. For eg. Small decrease in
blood pressure or a slight vestibular imbalance
may cause sensations different from distinct
faintness or vertigo.
- Other cause in this category are hyperventilation
syndrome, hypoglycaemia, and the somatic
symptoms of a clinical depressions ;these
patients should all have normal neurological
examinations and vestibular function tests.

36. APPROACH TO THE PATIENT:
Dizziness and Vertigo
• Most common diagnostic tool is detailed history focus on
the meaning of dizziness to the patient, is it
faintness(presyncope)? is there sensations of spinning?
• If meaning of dizziness is uncertain provocative test may be
helpful.
• The simplest provocative test for vestibular dysfunction is
rapid rotation and abrupt cessation of movement in a
swivel chair.
• A final provocative and diagnostic vestibular test, requiring
the use of frenzel eye glasses(self illuminated goggles with
convex lenses that blur out the patient vision, but allow the
examiner to see the eye greatly magnified), is vigorous
head shaking in the horizontal for about 10 seconds.

37. • If central etiology suspected MRI of the head
is mandatory.
• A neurological examination is always required
even if the history or provocative test suggest
a cardio, peripheral vestibular, or psychogenic
etiology.
• Any abnormality in the neurological
examination should prompt appropriate
neurodiagnostic studies.

38. TREATMENT OF VERTIGO
• Bed rest (1-2 days maximum)
• Vestibular suppresents drugs such as
• (1) antihistaminics
(maclizin,dimenhydrinate,promethazine)
• (2) tranquilizers with gabba – ergic
effects(diazepam, clonazepam)
(3) phenothiazines (prochlorperazine)
• (4) glucocorticoids

39. Contd…
• Chronic vertigo of labyrinthine origin may be
treated with a systematized vestibular
rehabilitation programme to facilitate central
compensation.
• Prophylactic mesures to prevent recurrent vertigo
are variably effective. Antihistamine are
commonly utalized but are of limited value.
• Psychogenic vertigo is best treated with cognitive
behavioral therapy.

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