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Syncope Evaluation
and Management

John J. Seger, MD

From: The Texas Heart

Institute at St. Lukes
Episcopal Hospital,
Houston, Texas 77030
Presented at the Texas
Heart Institute Sixth
Symposium on Cardiac
Arrhythmias: New
Pharmacologic and
Interventional Strategies;
held at the Houstonian
Hotel, Club & Spa; 19
February 2005; Houston
2005 by the Texas Heart
Institute, Houston


yncope is defined as the abrupt and transient loss of consciousness associated with loss of postural tone, typically followed by rapid recovery. There
are about a half a million new cases every year; in the Framingham cohort,
about 11% of people fainted over 17 years. About 30% of people will faint over
the course of their lives. Twenty-five percent of those episodes of fainting recur. In
the Framingham study, as subjects get over the age of 60, the incidence of fainting
becomes quite significant, with no real difference between women and men. The
cost of syncope is significant: $750 million a year. About 3% to 5% of emergency
room visits and 1% of hospital admissions are because of syncope. About 20% of
what I see in my office is syncope.
My approach as a cardiologist is simple: there are 2 categories of syncopeeither
its cardiac or its not (Table I). There arent that many noncardiac causes. Neurologic causes include seizure disorders (probably the most common), narcolepsy, hydrocephalus, migraine headaches, etc. People whose blood pressure drops can also
have pseudoseizure-like movements, and deciding which came first can be confusing.
Cerebrovascular disease is an uncommon cause of noncardiac syncope. This includes vertebrobasilar disease, subclavian steal, and bilateral carotid disease. Metabolic and endocrine abnormalities include hypoglycemia, hypoxia, volume depletion, and hypocapnia. Then there are psychiatric disturbances.
What about cardiac causes? I subdivide cardiac causes into mechanical and electrical. Mechanical causes abruptly impede blood flow and lead to systemic hypoperfusion and syncope; aortic stenosis, hypertrophic cardiomyopathy, cardiac
tumors, pulmonary hypertension, and pulmonary embolus are all mechanical
causes. Electrical causes manifest in the form of arrhythmias. Electrical abnormalities can be subdivided into fast or slow and ischemic or nonischemic.
Perhaps the most common causes of syncope are the neurally mediated syndromes. There are cardiac and neurocardiac reflexes that lead to a combination of
bradycardia and hypotension; theyre normal reflexes that are exaggerated in some
people and under some situations. They can occur out of the blue, like vasovagal or
neurocardiogenic syncope. They can occur in reaction to visual stimuli (like seeing
blood) or in reaction to the stimulation of various organ systems in the body (in response to post-micturition, deglutition, defecation, or tussis, for example). All of
these are basically triggers that stimulate afferent pathways to the brain and then efferent pathways from the brain, enhancing parasympathetic tone and withdrawing
sympathetic tone. If you enhance parasympathetic tone, youre going to cause
bradycardia. If you withdraw sympathetic tone, youre going to cause both bradycardia and hypotension. Then there are the dysautonomias like orthostatic hypotension. These can be from primary autonomic failure, multisystem atrophy, or
secondary causes (like diabetic neuropathy, amyloidosis, and drug-induced orthostatic syncope).
In pooled data from 5 population-based studies of syncope, 34% of all patients
ended up not having a diagnosis. Twenty-five percent of them had neurally mediated syndromes. About 18% to 20% of this cohort had a cardiac origin for their
syncope and 10% had neurologic causes; psychiatric causes were very rare. In the
Framingham study, men had significantly higher risk of having a cardiac cause of
syncope than did women.
What is the prognosis? The probability of survival following vasovagal or the
neurally mediated syncope is no different from that of a control population without syncope. Patients who have a cardiac cause for their syncope have a significant
Volume 32, Number 2, 2005

TABLE I. Causes of Syncope

Seizure disorder
Subarachnoid hemorrhage
Cerebrovascular Disease
Vertebrobasilar disease/subclavian steal
Carotid artery disease
Metabolic/Endocrine Abnormality
Volume depletion
Systemic mastocytosis, carcinoid
Psychiatric Disturbances
Panic attacks
Structural Cardiovascular Abnormality
Myocardial disease/ischemia
Pericardial disease valvular disease
Hypertrophic obstructive cardiomyopathy
Cardiac tumors
Pulmonary hypertension/embolus
Primary Cardiac Rhythm Disturbance
Neurally Mediated Disturbances of
Blood Pressure/Heart Rate Control
Vasovagal syncope
Respiratory-tussive syncope
Airway stimulation
Defecation syncope
Urologic-micturition syncope
Carotid sinus hypersensitivity
Dysautonomic/Orthostatic Disturbances
of Blood Pressure Control
Primary antonomic failure
Diabetic neuropathy/amyloidosis
Drug induced orthostasis

increase in mortality. On the other hand, 1 study showed

a 24% incidence at about 2 years of sudden death in a
subset of patients who had known or identified structural heart disease as part of their syncope evaluation.
The history is extremely important in patients who
have fainted. On the basis of history alone, you should
have a diagnosis or a very good idea of the diagnosis in
about 50% of patients. The situation surrounding the
event, the duration of the event, the patients position
at the time of the event, and family history are all important points to consider. On physical examination,
vital signs need to be documented: orthostasis and irregular pulse may be present. A cardiac exam may give
you some clues on the presence or absence of an underlying cardiac or pulmonary pathology. Carotid
sinus massage is a useful tool, particularly in patients
Texas Heart Institute Journal

in whom carotid sinus hypersensitivity is more common. There is an occasional incidence of stroke and
TIA with carotid sinus massageabout 0.28%. Always listen for bruits before you press on the carotid
The workup also includes chest x-ray and EKG. An
echocardiogram is another extremely important part
of the evaluation for organic heart disease.
A word about tilt table testing: When you tilt a person from supine to 70, blood pools in the legs and
there is a sympathetic response, which causes the heart
to vigorously contract. The vigorous contraction stimulates mechanoreceptors in the aorta and the heart and
elsewhere, which leads to the withdrawal of peripheral
sympathetic tone and enhancement of vagal tone. Its a
common provocative test. It does have a high sensitivity, but up to 45% of normal people will also be able to
generate the provocative reflexes as measured by heart
rate and blood pressure. What is really necessary is to
be able to reproduce a patients clinical symptoms with
tilt testing. It is an inexpensive, very low-risk test that
can be helpful in confirming your diagnosis.
Patients who have evidence of organic heart disease
are at much higher risk for bad outcomes associated
with syncope, and were much more aggressive about
investigating them with an electrophysiology study.
Other options include Holter monitors, long-term
loop recorders (for up to a month)in some patients
we even use an implantable loop recorder, which is
basically a 2-year Holter monitor. In a 12-month study
of patients with undiagnosed syncope, 65% of them
got a diagnosis with this kind of device.
For the more benign neurocardiogenic syndromes,
patients need an education about situation avoidance:
lying down, putting their legs up as soon as they feel
the onset of the symptoms, volume expansion, keeping their salt intake up, and possibly wearing compression stockings. There are some exercises that might
help abort the spells when they are occurring, or actual
tilt training exercises in which the patients lean up
against a wall and keep their legs steady for a certain
period of time each day, in an attempt to diminish the
frequency of the episodes. There are also lots of drugs
that we can prescribe to help prevent and decrease the
frequency of the events.
Placement of permanent pacemakers is an issue that
has come up, of course, because a lot of these patients
developin addition to their hypotensionsignificant bradycardias. Several studies have shown the significant benefit from pacemakers, over both placebo
and beta-blocker therapy in syncope patients. Pacemakers should be considered in people who have recurrent, refractory symptoms with a documented
bradyarrhythmia. There are lifestyle issues that become important when considering a pacemaker: people who drive cars for a living and want to continue to

work, or people who have episodes with minimal

warning and injure themselves. Were a little bit more
aggressive about pacing people like that.
In summary, syncope is a common clinical entity
with a variety of causes, some of which are life-threatening. Assessment for structural heart disease is very
important in identifying patients who may be particularly at risk for subsequent adverse events.


Volume 32, Number 2, 2005