APPROACH TO

SYNCOPE

PRESENTED BY:
PRAG G.K. SUBEDI
INTERN( DEPARTMENT OF MEDICINE)
INTRODUCTION:
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.

Other causes of transient loss of consciousness need to be distinguished from syncope

which includes:
i. Seizures
ii. Hypoxemia
iii. Hypoglycemia
iv. Vertebrobasilar ischemia

A syncopal prodrome(presyncope) is common, although loss of consciousness may

Typical presyncopal symptoms includes:
i. Dizziness
ii. Lightheadedness or faintness
iii. Weakness
iv. Fatigue
v. Visual and auditory disturbances

The causes of syncope can be divided into three general categories:

vi. Neurally mediated syncope aka reflex or vasovagal syncope
vii. Orthostatic hypotension
viii. Cardiac syncope
A. Neurally mediated syncope:
i. Vasovagal syncope:
Provoked fear, pain, anxiety, intense emotion, sight of blood,
unpleasant sights and odours.
ii. Situational reflex syncope:
a. Pulmonary:
Cough syncope, sneeze syncope, airway instrumentation,
b. Urogenital:
Postmicturition syncope, urogenital tract
instrumentation,prostatic massage
c. Gastrointestinal:
Swallow syncope, glossopharyngeal neuralgia, esophageal
stimulation, gastrointestinal tract instrumentation, rectal examination,
defecation syncope
 d. Cardiac:
Bezold-Jarisch reflex, cardiac outflow obstruction
e. Carotid sinus:
Carotid sinus sensitivity, carotid sinus massage
f. Ocular :
Ocular pressure, ocular examination, ocular surgery

B. Orthostatic hypotension:
i. Primary autonomic failure due to idiopathic central and peripheral
neurodegenerative diseases- the synucleopathies:
a. Lewy body diseases: Parkinsons disease, lewy body dementia,
pure autonomic failure
b. Multiple system atrophy( Shy dragger syndrome)
ii. Secondary autonomic failure due to autonomic peripheral neuropathies:
a. Diabetes
b. Hereditary and primary amyloidosis
c. Hereditary sensory and autonomic neuropathies(HSAN)
d. Idiopathic immune mediated autonomic neuropathy
e. Autoimmune autonomic gangliopathy
f. Sjorgens syndrome
g. Paraneoplastic autonomic neuropathy
h. HIV neuropathy
iii. Postprandial hypotension
iv. Iatrogenic( drug induced)
v. Volume depletion
C. Cardiac syncope:
i. Arrhythmias:
a. Sinus node dysfunction
b. Atrioventricular dysfunction
c. Supraventricular tachycardias
d. ventricular tachycardias
e. Inherited channelopathies
ii. Cardiac structural disease:
a. Valvular disease
b. Myocardial ischemia
c. Obstructive and other cardiomyopathies
d. Atrial myxoma
e. Pericardial effusions and tamponade
PATHOPHYSIOLOGY:
The upright posture imposes a unique physiologic stress upon humans; most,
although not all syncopal episodes occur from standing position.

Standing results in pooling of 500-1000 ml of blood in the lower extremities

and splanchnic circulation.

There is a decrease in venous return to the heart and reduced ventricular

filling that result in diminished cardiac output and blood pressure.

These hemodynamic changes provoke a compensatory reflex response,

initiated by the baroreceptors in the aortic arch and carotid sinus, resulting in
increased sympathetic outflow and decreased vagal nerve activity.
This reflex increases peripheral resistance, venous return to the heart, and
cardiac output and thus limits the fall in blood pressure.

If this response fails, as is the case chronically in orthostatic hypotension and

transiently in neurally mediated syncope, global cerebral hypoperfusion
occurs resulting in syncope.

Thus, syncope is a consequence of global cerebral hypoperfusion and thus

represents a failure of cerebral blood flow autoregulatory mechanisms.
Myogenic factors, local metabolites, and to a lesser extent autonomic
neurovascular control are responsible for the autoregulation of cerebral
blood flow. The latency of the autoregulatory response is 5-10 s.
Typically cerebral blood flow ranges from 50-60ml/min per 100gm brain
tissue and remains relatively constant over perfusion pressures ranging from
50 to 150 mmHg. Cessation of blood flow for 6-8 s will result in loss of
consciousness while impairment of consciousness ensues when blood flow
decreases to 25ml/min per 100 g brain tissue.

From the clinical standpoint, a fall in systolic blood pressure to ~ 50 mmHg

or lower will result in the syncope.

A decrease in the cardiac output and/or systemic vascular resistance[ the

determinants of blood pressure] underlies the pathophysiology of syncope.
Sequence of changes occurring in syncope after cerebral perfusion/
oxygenation cut off for 8 to 10 s,
i. Loss of consciousness and postural tone
ii. Pallor and swaeting
iii. Brief ( lasting few seconds) extensor stiffening or spasms
iv. Few irregular myoclonic jerks of limbs
Whole episode is brief, usually < 10 s.
APPROACH:
Careful history:
1. Full a description as possible of the first faint:
precipitating factors
posture
type of onset of the faint( abrupt or gradual)
the presence and duration of preceding and associated symptoms
duration of LOC
rate of recovery
and sequalae
2. Question an observer about:
 clonic movement
color changes
diaphoresis
pulse
respiration
urinary incontinence
nature of recovery

Clinical examination:
1. Valsalva maneuver
2. Orthosatic drop
3. Asses BP in both arms when suspecting cerebrovascular disease,
subclavian steal or Takayasu arteritis.
 4. Pulse rate and rhythm
5. Extra cardiac auscultation: cardiac, ophthalmic and supraclavicular bruits.
6. Carotid sinus massage in older patients suspected of having carotid sinus
syncope( the response to carotid massage is vasodepressor, cardioinhibitory
or mixed)

Investigations:
1. Doppler flow of cerebral blood vessels.
2. MR angiography
3. EEG has a low diagnostic yield( To do only when a seizure disorder is
suspected)
4. Tilt table testing in unexplained syncope in high risk settings or with
recurrent faints in the absence of heart disease.
5. ECG
6. Prolonged holter monitoring.
7. Radionuclide cardiac scanning
8. Echocardiography

D/D OF BLACKOUTS:
1. Syncope
2. Epilepsy
3. Psychogenic non epileptic seizures
4. Cataplexy
5. Drop attack
6. Transient csf obstruction
7. TIA of anterior and posterior circulation
8. Panic attack
9. Falls / trauma
10. Hypoglycaemia
11. Basilar migraine
12. Malingering
13. Intoxication
COMPARISON OF SYNCOPE AND SEIZURES
FEATURES SYNCOPE SEIZURES
Relation to posture Common No
Time of day Diurnal Diurnal or nocturnal

Precipitating factors Emotion, pain, crowds Sleep loss, alcohol/

,heat, exercise, fear, dehydration, drug withdrawl
coughing , micturition
Skin color Pallor Cyanosis or normal
Diaphoresis Common Rare
Aura or premonitory
symptoms Long Brief
Convulsion Rare Common
Other abnormal
movements Minor twitching Rhytmic jerks
Injury Rare Common with
convulsive jerks
Urinary incontinence Rare Common
Tongue biting No Can occur
Postictal confusion Rare common
Postictal headache No Common
Focal neurological signs No Occasional
Cardiovascular signs Common( in cardiac No
syncope)
Abnormal findings on EEG Rare( generalised slowing Common
may occur )
TREATMENT OF SYNCOPE:
• HIGH RISK FEATURES INDICATING HOSPITALIZATION OR INTENSIVE
EVALUATION OF SYNCOPE:
Chest pain suggesting coronary ischemia
Features of CHF
Moderate or severe valvular disease
Electrocardiographic features of ischemia
History of ventricular arrhythmias
Prolonged QT interval(> 500 ms)
Repetitive sinoatrial block or sinus pauses
 Persistent sinus bradycardia
Bi or trifascicular block or intraventricular conduction delay with QRS
duration >= 120ms
Atrial fibrillation
Nonsustained ventricular tachycardia
Family history of sudden death
Preexcitation syndromes
Brugada pattern on ECG
Palpitations at time of syncope
Syncope at rest or during exercise

• TREATMENT OF VASOVAGAL SYNCOPE:

Reassurance
Avoidance of provocative stimuli
 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.
Pharmacotherapy: fludrocortisone , vasoconstricting agents and beta-
adrenoreceptors antagonists.

• TREATMENT OF ORTHOSTATIC HYPOTENSION:

Remove the reversible causes( usually vasoactive medications)
Non-pharmacological interventions:
1. Education: staged move from supine to standing position
2. Warnings about the hypotensive effects of large meals
3. Isometric counterpressure maneuvers that increase intravascular pressure
4. Raising the head of the bed to reduce supine hypotension.
5. Intravascular volume expansion : fluid and salt
 Pharmacologic interventions:
1. Fludrocortisone acetate
2. Vasoconstricting agents: Midodrine, 1-dihydroxyphenylserine,
Pseudoephedrine
For intractable symptoms:
1. Pyridostigmine
2. Yohimbine
3. Desmopressin
4. Erythropoeitin
• TREATMENT OF CARDIAC SYNCOPE:
Cardiac pacing for sinus node disease and AV block
Ablation
Antiarrhythmic drugs and
Cardioverter-defibrillators
!!!THANK YOU!!!