Syncope is a sudden and transient loss of consciousness and postural tone, usually described as “fainting” or “passing out”. It is a common problem, accounting for 3% of emergency room visits. A history of an isolated episode of syncope will be found in as many as 25% of healthy young adults, especially in settings that precipitate fear, disgust or anxiety, and if not repeated does not warrant further work-up. Repeated episodes, however, may be caused by a wide variety of medical problems, and require diagnosis and treatment. It is important to distinguish syncope from “dizziness”, which generally refers to an alteration in balance, vision, or perception of the environment, without the loss of consciousness.
Neurally mediated syncope:
Neurally mediated syncope (NMS) is one of the most frequent forms of syncope. It has also been known as vasovagal syncope, neurocardiogenic syncope, common or emotional fainting, or reflex syncope. Neurally mediated syncope is characterized by peripheral vasodilation and a decrease in blood pressure, or hypotension, along with bradycardia, or a slow heart rate. This hypotension leads to loss of consciousness if sufficiently severe or to presyncope if less severe or if the patient is lying down. There is general agreement that these changes in heart rate and blood pressure are due to an increase in parasympathetic tone and concomitant inhibition of sympathetic outflow. The parasympathetic and sympathetic systems are part of the autonomic nervous system. Related terms and conditions include situational fainting such as cough, micturitional, defecation, diving, sneezing, and swallowing syncope, carotid sinus syncope (shaving syncope), and autonomic conditions including hyperadrenergic and hypoadrenergic states.
Initiating factors in postural NMS have not been entirely clarified. Early studies suggested an underlying abnormality in the peripheral veins that resulted in exaggerated orthostatic pooling during the upright position in these patients. Inferences from these studies suggest that venodilatation plays an important role by reducing cardiac filling, cardiac output, and blood pressure.
Causes of syncope can be differentiated into two major classifications, cardiac and noncardiac. Examples of cardiac syncope are heart rhythm disturbances or abnormalities in the structure of the heart. The list below presents a useful classification of noncardiac syncope:
In addition to characterizing the episode of loss of consciousness, an important initial objective in every case is differentiating those individuals with normal cardiovascular status from those with evident cardiac or cardiovascular disease. To accomplish these goals, the first step is to record a comprehensive medical history with particular emphasis on the description of the syncopal event, past history, family history and concomitant drug treatment.
The clinical history and physical is the most important component of the evaluation of a patient with syncope. Among cases in which a diagnosis can be made, the history and physical identify the cause in approximately 45% of cases. In an additional 8% of cases, the history and physical provide suggestive findings that are confirmed later on subsequent testing. The key points of the history should include the situation in which the event occurred, prodromal symptoms, witnessed appearance, postevent residua, past history and family history. Some causes of syncope have specific clinical presentations, such as syncope during arm exercise.
The physical examination should start with vital signs, including an assessment of orthostatic vitals. Orthostatic hypotension is defined as a fall in systolic blood pressure of at least 20 mmHg. Measuring the blood pressure on standing several times during a 3-minute period usually is sufficient to elicit this finding. Other important features of the physical examination include neurologic findings such as diplopia, dysarthria, nystagmus, ataxia and pupillary asymmetry, as well as cardiac findings such as carotid bruit, jugular venous distension, rales, a systolic murmur (of hypertrophic cardiomyopathy or aortic stenosis), pericardial rub or unequal blood pressure in the two arms.
The function of the autonomic nervous system can be determined by simple physiological and pharmacological tests. All these tests should be performed in a quiet environment after 15 minutes in the supine posture with blood pressure and heart rate monitoring.
Tilt table testing is a standard diagnostic test for evaluating patients with syncope. It is considered the gold standard for providing diagnostic evidence indicating susceptibility to neurally mediated syncope. Several observations suggest that symptomatic hypotension-bradycardia associated with a positive head-up tilt test is comparable to the spontaneous neurally mediated syncope. Unfortunately, tilt table testing is plagued by both false-positive and false-negative tests. Thus the tests MUST be interpreted carefully and within the clinical context.
The initial treatment for neurally mediated syncope is often an increase in dietary salt intake, an increase in fluid consumption and discontinuation of medications that potentiate vasodilation.
Nonpharmacologic therapies include sleeping with the head of the bed raised about 6 to 12 inches and elastic support hose (at least 30 to 40 mmHg ankle counterpressure). Although effective, the hose are difficult to put on and can be quite uncomfortable in hot climates. Biofeedback has proved useful in selected patients. Mild aerobic reconditioning is an important part of therapy, often best done using water activities. In some patients, building lower extremity strength and tilt training (spending progressively longer periods of time upright) can be helpful.
Pharmacotherapy in combination with education is often necessary. The medical treatment of neurally mediated syncope is complicated by the nearly complete lack of placebo controlled trials. The best method for assessing treatment is to evaluate the patient’s recurrence of symptoms and quality of life over time. The assessment of treatment efficacy must also include a careful evaluation of treatment side effects. Agents that have been used include beta-blockers, fludrocortisone, SSRIs, midodrine, disopyramide and yohimbine.
Severe neurally mediated syncope is characterized by severe symptoms (usually syncope), occurs without warning, occurs in any position, has no clear precipitating causes or occurs frequently. These patients are allowed to drive private vehicles after 3 months of documented control of the condition and commercial vehicles after they have been symptom free for 6 months.
Untreated patients with severe neurally mediated syncope are completely prohibited from driving.