• Syncope is a sudden loss of consciousness and postural tone resulting from a
decrease in cerebral blood flow. The loss of consciousness is brief, and
recovery is rapid and spontaneous.
• Syncope itself is not a diagnosis but rather a symptom of an underlying
• The incidence of syncope increases dramatically with advancing age.
• The incidence of syncope per 1000 person-years increases from 6 in the
sixth decade of life to 11 in the seventh decade. The incidence is 17 and 20
for men and women, respectively, in the eighth decade.
• Almost 50% of emergency room visits for syncope are made by persons 65
years of age or older.
• Subjects with cardiac, neurologic, or unknown causes of syncope have a
worse prognosis than subjects without syncope. Interestingly, subjects with
vasovagal, orthostatic, or medications as a cause of their syncope did not
have a decreased survival compared with subjects without syncope.
• The underlying pathophysiology leading to syncope is inadequate
oxygenation of the cerebral cortex and reticular activating system, resulting
in loss of consciousness.
Risk factors for increased syncope in elderly:
• Having more underlying chronic conditions and being on more medications
than younger adults.
• age-related physiological changes that increase their syncope risk:
1. Atherosclerosis (impairing dilation of cerebral blood vessels in the
face of reduced blood flow)
2. Increased endothelin production (increasing vasoconstriction of
3. Left ventricular dysfunction, due to long standing hypertension and/or
heart disease (causing decreased cardiac output)
4. Cardiac valvular disease (increasing the likelihood of arrhythmias
and heart block)
5. Blunting of autonomic responses, baroreceptor reflex (predisposing
the person to orthostatic hypotension)
• They fall into these general categories: neurally mediated (reflex) causes,
orthostatic hypotension, cardiac causes, central nervous system diseases, and
• History from the patient and an eyewitness, if present, is needed to
distinguish syncope from other entities such as dizziness, vertigo, drop
attacks, coma, and seizure.
• Historical features are often sufficient to distinguish syncope from seizures.
Seizures are associated with blue face (or not pale), frothing at the mouth,
tongue biting, disorientation, aching muscles, sleepiness after the event, and
duration of unconsciousness of more than 5 minutes. On the other hand,
symptoms associated with syncope are sweating or nausea before the event
and being oriented after the event. The best discriminatory symptom is
disorientation after the episode, which often signifies a seizure.
• Vasovagal or neurocardiogenic syncope is the most common type of neurally
mediated syncope; it includes the common faint. Typically, a situation
involving prolonged standing, emotional distress, or exertion in a warm
environment causes peripheral venous pooling and a drop in blood return to
the heart. As the heart recognizes a sudden decrease in preload, it tries to
compensate by contracting harder. The quick increase in contraction
activates mechanoreceptors in the ventricles that start a reflex mechanism
causing the central nervous system to stimulate vasodilation and
bradycardia. As the drop in cardiac output becomes more profound, syncope
may occur.When suspecting a neurally mediated syncope, look for
associated symptoms of nausea and/or vomiting, prolonged standing, hot
environments, and unpleasant situations. You should be cautious to not
assume this diagnosis in patients with known heart disease or repetitive
episodes of syncope.
• Carotid sinus syndrome: when manual stimulation of the carotid sinus can,
in susceptible individuals, stimulate neurally mediated syncope.
• Orthostatic hypotension: is a drop in arterial pressure that occurs when an
individual moves to an upright position. Typically, the autonomic nervous
system rapidly compensates for this by increasing the venous tone in the
legs; when this system fails, syncope may occur. When the circulating blood
volume is depleted, as in dehydration, orthostatic hypotension, and syncope
may occur even with appropriate autonomic compensation. This diagnosis
should be considered in individuals who are on medications that can
predispose to hypotension, who have reason due to illness or blood loss to be
dehydrated, or have autonomic insufficiency from a neurological disorder
such as Parkinsonism. A typical case occurs soon after standing up
• Cardiac syncope occurs when reduction in cardiac functioning by
arrhythmia, death of myocardium, or outflow obstruction leads to decreased
blood flow to the brain. Several studies have shown an increase in overall
mortality and sudden death among patients with cardiac syncope compared
to patients with syncope from other causes. A cardiac cause should be
considered when syncope is preceded by palpitations or chest pain, or when
it occurs during exertion. Patients with known severe structural heart disease
should be considered to have cardiac syncope until proven otherwise.
• Cerebrovascular disease is a rare but plausible cause of syncope. Most
transient ischemic attacks or strokes do not cause loss of consciousness, but
occasionally this can occur. There is a low yield to use of neurological
testing in the evaluation of individuals with syncope unless it is directed at
those with neurological findings on initial evaluation.
• Psychiatric causes should be considered in patients with repetitive syncope
of unknown origin after cardiac causes have been effectively ruled out. They
are more common in younger patients. Prodromal symptoms, such as
dizziness, are common. Several hypotheses exist regarding the connection
between psychiatric disorders and syncope. Hyperventilation can increase
susceptibility to neurally mediated syncope. There is also a term called
pseudo- syncope, which has been used to describe patients with syncope of
unknown but presumed psychiatric origin, who have no pathological
findings on exam and documented syncope without any change in blood
pressure or pulse.
The history can identify symptoms and situations surrounding
syncope that can help diagnose three common etiologies, neurally
mediated (vasovagal), orthostasis, and drug related syncope.
B) PHYSICAL EXAMINATION:
• .In detection of orthostatic hypotension, supine blood pressure and heart rate
should be measured after the patient has been lying down for at least 5
minutes. Standing measurements should be obtained immediately and for at
least 3 minutes. Sitting blood pressures are not reliable for detection of
• Several cardiovascular findings are crucial diagnostically. Differences in the
pulse intensity and blood pressure (generally >20 mmHg) in the two arms
are suggestive of aortic dissection or subclavian steal syndrome.
• Special focus on cardiovascular examination for aortic stenosis,
• Carotid Bruits, carotid massage.
• Neurological examination.
The evaluation of the patient with syncope involves the parallel process of
seeking a specific diagnosis and ruling out cardiac causes. The initial history,
examination, and electrocardiogram are sufficient in most cases to rule in or out
C) Further evaluation: Should focus on the following issues:
(1) arrhythmia detection, (2) tilt testing, and (3) multiple abnormalities
Electrocardiogram or a rhythm strip
Ambulatory holter monitoring
External loop recorders
Implantable loop recorders.
Cardiac stress testing is rarely diagnostic in the evaluation of syncope. It should be
considered in patients who have syncope during exertion or experience chest pain
associated with syncope.
Tilt table testing:
Can be useful as confirmatory tests for neurally mediated syncope.
The procedure involves baseline measurement of blood pressure and heart rate
while supine, then quickly bringing the patient to an upright position by tilting to
approximately 60 degrees. A foot board is in place for support. The patient is then
kept in the tilted position for 45 minutes to observe for syncope or presyncopal
symptoms while continuing to monitor heart rate and blood pressure. Some protocols
include giving isoproterenol or nitroglycerin after the patient has been asymptomatic
in the tilted position for 10 to 15 minutes followed by further monitoring. If syncope
symptoms occur during testing and correlate with a quick drop in blood pressure or
pulse rate, it is considered a positive test. Likewise, if syncope occurs without a
change in vital signs, a neurally mediated syncope is less likely and other etiologies
should be reconsidered
CSM is performed as follows:
1. Confirm that no carotid bruits are present and that there is no known significant cerebral
vascular disease. If bruits are present, or the patient is at high risk for atherosclerotic
disease, consider carotid Doppler ultrasound to evaluate for significant plaque.
2. Have the patient supine, on continuous ECG monitoring and beat-to-beat blood pressure
monitoring. An IV line should be in place, and atropine and transcutaneous pacing available.
3. Turn the patient’s head to the left in the supine position and find the maximum impulse in
the right carotid artery at the level of the thyroid cartilage. Use two fingers, firmly press
down,and massage longitudinally for 5 to 10 seconds. Wait a few minutes and repeat on the
left carotid sinus. Repeat in the head-up tilt position if symptoms do not occur in the supine
A positive cardioinhibitory result is present if a cardiac pause (asystole) of 3 seconds or
longer occurs during or immediately after CSM; a positive vasopressor result is present if the
systolic blood pressure drops 50 mmHg or more, and is accompanied by symptoms.
Multiple abnormalities causing symptoms:
According to the published recommendations for syncope evaluation, neuroimaging and
EEG can be limited to patients with symptoms or signs of acute stroke or seizure.
Initial laboratory blood tests rarely yield diagnostically helpful information. Hypoglycemia,
hyponatremia, hypocalcemia, or renal failure is found in 2% to 3% of patients, but in most
cases appears to result in seizures rather than syncope .
o Management issues include hospitalization decision, treatment selection, and patient
instructions and education.
o the treatment largely depends on the cause of syncope.
o First-time syncope in patients without known or suspected heart disease usually
warrants the reduction of risk factors for further syncope. This includes reducing
polypharmacy and medication misuse, treating underlying illness, and education
regarding avoidance of triggers.
o Individuals with cardiac disease deserve a more aggressive effort in establishing an
etiology of syncope and treatment of cardiac causes. Identifying and treating
structural heart disease will help reduce the risk of recurrent syncope.
When to Hospitalize
o Consider hospitalization of older patients with multiple comorbidities when the etiology seems
multifactorial and a monitored environment is needed to sort it out.
o Hospitalize patients with known or suspected potentially fatal arrhythmias.
o Hospitalize patients with unknown etiology of syncope when cardiac disease is known or
suspected by initial evaluation.
o Hospitalize when the cause is identified and requires admission (e.g., myocardial infarction or
the treatment according to the cause of syncope
Neurally Mediated Syncope
o Because of potential side effects, treatment should be reserved for elderly patients with
frequent or disabling symptoms. Because psychiatric illnesses (especially depression and
anxiety) probably lead to vasovagal reactions, screening for the psychiatric illnesses
noted above should be performed. Treatment of the psychiatric illness often results in
resolution of recurrent syncope.
o The most commonly used drugs are beta-blockers (e.g., metoprolol 50–200 mg/day,
atenolol 25–200 mg/day, and propranolol 40–160 mg/day), which may inhibit the
activation of cardiac mechanoreceptors by decreasing cardiac contractility. Other drugs
include anticholinergic drugs, such as transdermal scopolamine one patch every 2 to 3
days, disopyramide (200 –600 mg/day), paroxetine (20–40 mg/day) theophylline (6–12
mg/ kg/day), and measures to expand volume (increased salt intake, custom fitted
counter pressure support garments from ankle to waist, and fludrocortisone acetate at
0.1–1 mg per day).
o The initial approach to treatment of orthostatic hypotension is to ensure adequate salt
and volume intake and to discontinue drugs that cause orthostatic hypotension. Patients
with orthostatic hypotension should be advised to raise the head of the bed at night, to
rise from bed or chair slowly, and avoid prolonged standing. Compressive stockings
applied up to thigh level may help decrease venous pooling. Frequent small feedings
may be helpful for patients with marked postprandial hypotension.
o Pharmacologic agents of potential benefit include fludrocortisone (0.1–1 mg/day), in
conjunction with increased salt intake. Various agents have been used including
midodrine, ephedrine, phenylephrine, and others.
Patient Instructions and Education
o Issues in patient education include instructions in prevention of syncope,
nonpharmacologic treatment, and restriction of activities. Many patients with vasovagal
syncope have precipitating factors or situations that should be identified, and the patient
instructed to avoid these situations. Common triggers include prolonged standing,
venipuncture, large meals, and heat (such as hot baths or sunbathing). Additionally,
fasting, lack of sleep, and alcohol intake may predispose to vasovagal syncope and
should be avoided.
o Post exercise vasovagal syncope may occasionally be related to chronic inadequate salt
and fluid replacement. Syncope may be prevented with the use of electrolyte containing
solutions and water in such instances. In other patients exercise may have to be
Finally, do not forget to think of safety issues such as driving, flying, operating heavy
machinery, and risk of injury from falls.