Sanjay personnel

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

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IT WILL HELP U TO STUDY THE DIZZINESS VERTIGO AND SYNCOPE

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SYNCOPE,DIZZINESS AND VERTIGO

EVALUATION

SANJAY CHOUDHARY

ASSAM MEDICAL COLLEGE

DIBRUGARH

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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,afeeling of warmth,diaphoresis,nausea and visual blurring occasionaly proceeding to transient blindness.

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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

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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.

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CAUSES OF SYNCOPE

• I.Disorders of vascular tone or blood volume A.Reflex syncopes

1.Neurocardiogenic2.Situational- Cough, Micturition, Defecation,

Valsalva, Deglutition3. Carotid sinus hypersensitivity

B. Orthostatic hypotension1.Drug induced (Anti HTN, Vasodilators)2. Pure autonomic failure(idiopathic

orthostatic hypotension)

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Contd…

3.Multisystem atrophies4. Peripheral neuropathy5. Physical deconditioning6. Sympathectomy7. Decreased blood volume

II. Cardiovascular disordersA. Structural and obstructive cause

1. Pulmonary embolism2. Pulmonary hypertension

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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

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Contd…

B. Cardiac arrhythmias1. Bradyarrhythmias-

a.sinus bradycardia, sinoatrial block, sinus arrestb. Atrioventricular block

2. Tachyarrhythmiasa. Supraventricular tachycardiab. Atrial fibrillationc. Atrial flutterd. Ventricular tachycardia

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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

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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.

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NEUROCARDIOGENIC SYNCOPE cont…

• It is frequently recurrent and commonly precipitate by a hot or crowded environment,alchohol,extreme fatigue,severepain,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.

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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 vagalafferent nerve fibres that inhibits sympathetic activity and increase parasympathetic activity. The resultant vasodilation and bradycardia induce hypotension and syncope.

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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,andcoughing) that may contribute to hypotension and syncope by decreasing venous return.

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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.

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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.

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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.

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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 hypoperfusionand syncope may occur.

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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.

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DIFFERENTIAL DIAGNOSIS OF SYNCOPE

• (1) Anxiety attacks and Hyperventilation syndrome

• (2) Seizures

• (3) Hypoglycemia

• (4) Hysterical fainting

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APPROACH TO THE PATIENTS WITH SYNCOPE

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DIAGNOSTIC TEST

• The choice of the diagnostic test should be guided by history and the physical examination.

• (1) Measurement of serum electrolyte,glucoseand haematocrit.

• (2) Cardiac enzyme if Myocardial ischaemiasuspected.

• (3) Blood and urine toxicology screen.• (4) Adrenocortical insufficiency patients-

aldosterone and mineralocorticoid level should be evaluated.

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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)

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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.

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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.

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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 vagovagalsyncope.

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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.

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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

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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.

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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 intersensorymismatch among the three stabilizing sensory systems

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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

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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.

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Contd….

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

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Features of central and peripheral vertigo

Signs or symptom Peripheral Central

Direction of associatednystagmus

Unidirectional;fast phase opposite lesion

Bidirectional or unidirectional

Purely horizontal nystagmus without torsional component

Uncommon Common

Vertical or purely torsionalnystagmus

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

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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 CNSabnormalities

None Extremely common(eg. Diplopia, hiccups, cranial neuropathies, dysarthria)

Common causes BPPV( Benign proxysmalpositional vertigo), infection( ladyrinthitis), meniere’s , neuronitis, ischaemia, trauma, toxins

Vascular, demyelinating, neoplasm

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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.

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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.

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• 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.

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TREATMENT OF VERTIGO

• Bed rest (1-2 days maximum)

• Vestibular suppresents drugs such as

• (1) antihistaminics(maclizin,dimenhydrinate,promethazine)

• (2) tranquilizers with gabba – ergiceffects(diazepam, clonazepam)(3) phenothiazines (prochlorperazine)

• (4) glucocorticoids

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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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