Approach to a Patient with
-Dr. Sachin Adukia
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.
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.
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
decreased cardiac compliance,
attenuation of the vestibulosympathetic reflex
explained by the greater prevalence of
predisposing neurologic disorders,
and vasoactive medication use among institutionalized patients.
3 General Categories
Neurally mediated (also called reflex or vasovagal
transient change in the reflexes responsible for maintaining
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
most common form of neurally mediated syncope,
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.
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.
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
with partial autonomic failure, HR may increase but insufficient to
“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.
Upright posture- pooling of 500–1000 mL blood in LL and splanchnic
decrease in venous return and reduced ventricular filling – diminished CO and
compensatory reflex response, initiated by baroreceptors in carotid sinus, aortic
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.
Characteristic symptoms of
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
Angina - impaired myocardial perfusion
Symptoms exacerbated by exertion, prolonged standing, increased ambient
temperature, or meals.
Iatrogenic cause of Ortho. HypoTN
Drugs may lower peripheral resistance
antihypertensive agents of several classes
nitrates and other vasodilators;
Iatrogenic volume depletion due to diuresis
Volume depletion due to medical causes
decreased fluid intake
Patients with postural tachycardia syndrome (POTS)
frequently experience orthostatic symptoms without
orthostatic hypotension, but syncope can occur
Rarely, SACD, syringomyelia etc damage the
descending sympathetic pathways, producing
San Francisco Syncope rule
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
Syncope in Special situations
Syncope induced by Valsalva manoeuvre
increased intrathoracic pressure limits the venous return to the
increases vagal tone,
resulting in decreased cardiac outflow and syncope.
usually in men while standing for nighttime
Several mechanisms :
postural – standing on leaving a warm bed causing
straining – Valsalva manoeuvre increasing an
already high nocturnal vagal tone, causing
emptying bladder – abrupt decrease in stimulus to
bladder stretch receptors causing reflex
vasodilatation and hypotension.
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
transient or permanent neurological deficit,
stroke and sudden death.
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
face becomes flushed secondary to congestion, then pale.
loss of muscle tone
blockage of venous return by raised intrathoracic pressure.
weight-lifting syncope - similar mechanism
Hypoadrenalism - syncope orthostatic hypotension.
Disturbances of Ca, Mg, K metabolism: rare causes
Anoxic syncope- occurs d/t lack of oxygen or
production of vasodepressor
EEG changes in syncopal subjects
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.
is characterized by increasing and decreasing slow wave activity only
EEG flattening in the slow-flat-slow pattern denotes severe cerebral
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.
Seizure types that must be distinguished
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
Syncopal attacks provoking epileptic
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
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
Full a description as possible of the first faint
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,
question an observer about
nature of recovery.
Assess BP in both arms when suspecting
cerebrovascular disease, subclavian steal, or Takayasu
Pulse: rate and rhythm
Extra Cardiac Ascultation: carotid, ophthalmic, and
Carotid sinus massage in older patients suspected of
having carotid sinus syncope
The response to carotid massage is vasodepressor,
cardioinhibitory, or mixed
Doppler flow of cerebral vessels
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
False positives - 10% of healthy persons may faint,
Prolonged Holter monitoring
Implantable loop recordings
Radionuclide cardiac scanning,
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-
no consistent evidence from RCT any pharmacotherapy
Treatment of Orthostatic hypotension
REMOVE REVERSIBLE CAUSES—----------------usually vasoactive medications
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.
vasoconstricting agents -midodrine, l-dihydroxyphenylserine, pseudoephedrine
Treatment of cardiac syncope-
Treatment of underlying disorder.
cardiac pacing for sinus node disease and AV block,
antiarrhythmic drugs, and