Syncope Evaluation and Management

Syncope 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 syncope—either it's cardiac or it's not (Table I). There aren't 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.

TABLE I. Causes of Syncope

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 deple-tion, 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; they're 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, you're going to cause bradycardia. If you withdraw sympathetic tone, you're 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 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 patient's 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 in whom carotid sinus hypersensitivity is more common. There is an occasional incidence of stroke and TIA with carotid sinus massage—about 0.28%. Always listen for bruits before you press on the carotid sinus.

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. It's 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 patient's 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 we're 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 develop—in addition to their hypotension—significant 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. We're 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.