One out of every 4 persons experiences a faint during his or her lifetime. In the US syncope is such a common complaint that each year as many as 1 million people seek medical treatment at a cost of $1 billion. It is estimated that as many as 6% of hospitalizations and 3% of emergency visits are prompted by transient loss of consciousness. In additional, 75% of patients with recurring syncope will alter their daily lives, nearly 40% will change jobs, and 75% will suffer from depression or anxiety, especially if not diagnosed and treated.
Syncope (Greek: synkope = cut-off) is a brief transient loss of consciousness (fainting) and postural tone (collapse) with rapid spontaneous recovery. Syncope is due to transient decrease in blood flow to the brain, an organ that cannot tolerate a brief deprivation of oxygen and blood-derived nutrients. The mechanisms of syncope range from nearly normal (physiological) to abnormal and life threatening. Management may extend from simple reassurance to life-saving emergency intervention. For some persons with heart disease and complicated by arrhythmias, syncope today may represent the potential for more serious complications.
Although individual differences in susceptibility to syncope exist, almost any healthy person can faint given the proper circumstances. The fact that simple faints are so common probably reflects incomplete evolutionary adaptation of humans to the upright body position. Standing upright requires special blood pressure regulation to drive blood against gravity up to the head. Most patients experience warning symptoms telling them they are about to pass out (pre-syncope or "gray-out"). Premonitory symptoms such as palpitations, weakness, confusion, and nausea allow an individual to "prepare" for collapse without bodily harm. However, elderly patients may be prone to serious injury such as hip fractures.
Vasodepressor syncope is one of the most common causes of syncope. It is caused by a reflex of the involuntary nervous system called a vasovagal reaction. The vasovagal reaction leads the heart to slow down (bradycardia) and, at the same time, it leads the nerves to the blood vessels in the legs to permit those vessels to dilate (widen). The result is that the heart puts out less blood, the blood pressure drops, and what blood is circulating tends to go into the legs rather than to the head. The brain is deprived of oxygen and the fainting episode occurs. This form of syncope is frequently recurrent and commonly precipitated by emotional stress, fear, extreme fatigue, injury or pain. Many episodes occur without antecedent cause. In the classic form it comprises constellation of symptoms including: low blood pressure (hypotension), slow heart rate (bradycardia), nausea, profuse sweating (diaphoresis), and the patient turning pale (pallor).
Evaluation of Syncope
It is important to determine whether syncopal spells occur only when patients are standing or sitting or whether they also occur when the individual is lying down. An orthostatic (relating to, or caused by erect posture/standing) mechanism suggests benign spells if the patient has no demonstrable heart disease. Likewise, syncope precipitated by straining may suggest a benign mechanism in persons without heart disease.
A history of syncope occurring during exercise or while lying down demands attention. In some persons, exercise may provoke atrial or ventricular arrhythmias. Rarely, obstructive mechanisms such as familial heart muscle disease (hypertrophic cardiomyopathy) and narrowing of the aortic valve (aortic valve stenosis) may limit cardiac output during exercise. Sometimes, reflex cardiac slowing immediately after abrupt termination of exercise can trigger a benign syncope. Syncope while lying down is highly suggestive of a pathologic cause.
Drugs taken by patients experiencing syncope should be carefully reviewed. Among the drugs that may precipitate syncope are agents commonly prescribed to treat high blood pressure, such as ACE inhibitors, calcium channel blockers, beta blockers, and alpha blockers. Paradoxically, medications used to treat arrhythmias may as a side effect provoke arrhythmias and syncope. Some drugs prescribed by psychiatrists may both lower arterial pressure and/or induce arrhythmias. "Recreational" drugs such as amphetamines and cocaine may trigger arrhythmias and syncope. Excessive treatment with diuretics may unduly decrease blood volume and invite syncopal spells.
Depending upon the historical features of the syncopal episode, one or both of two tests may be performed. Tilt table testing is useful to assess the possible contribution of venous pooling or orthostatic mechanisms. An electrophysiology study addresses arrhythmias as mechanisms for syncope. The recognition of ventricular tachyarrhythmias as a cause of syncope is of paramount importance, because such syncopes are associated with a high risk of sudden cardiac death; syncope due to ventricular tachyarrhythmias might be called "spontaneous recovery from sudden cardiac death". Tachyarrhythmias are usually easy to detect and characterize during electrophysiology studies. Bradyarrhythmias, including sinus node dysfunction and AV block, can be very difficult to detect or reproduce during electrophysiology studies. If patients experience warning symptoms such as dizziness or palpitations, they may be given an ECG event recorder to ascertain whether syncopal spells are associated with arrhythmias.
Treatment of Syncope
Treatment of syncope depends first on identifying the mechanisms and factors that cause or contribute to syncopal spells in an individual person. Since one of the most common forms of syncope is orthostatic syncope, measures that minimize the effects of gravity are usually recommended. If one can sit or lie down when symptoms begin, orthostatic or vasodepressor syncope can often be prevented. If one must maintain an upright posture, the person should avoid standing still. Walking increases venous return via the pumping action of the leg muscles on the leg veins. Standing and straining at the same time should be avoided whenever possible. If one must strain to urinate interruption of straining every few seconds is helpful. Men who experience "bathroom syncope" should sit to urinate. Also placing a carpet in the bathroom can avoid injuries. Treatment of the primary problem, such as prostate surgery for urinary obstruction or treatment of bronchitis to eliminate cough may eliminate the trigger for the syncopal episodes.
Maintenance of adequate hydration is also important in the prevention of orthostatic and vasodepressor syncope. Many healthy people follow very low sodium diets with the idea that salt restriction is a healthy way of eating. However, some of those people are actually chronically dehydrated and suffer syncopal episodes, especially if they engage in heavy exercise and sweat a lot. Diuretics given for the treatment of high blood pressure can also bring out a tendency for orthostatic syncope when the patient has not previously suffered an episode.
Medications are often involved in the cause of syncope, but they may also offer options for the management of syncope. Blood pressure medications which dilate the arteries and the veins (ACE inhibitors, calcium channel blockers, angiotensin receptor blockers) can override the body's mechanisms for preventing low blood pressure in response to changes in position. Changing medications may often be all that is necessary to prevent syncope, but in persons receiving drugs to lower blood pressure, some dizziness upon standing up may be the price to pay to protect oneself against the complications of high blood pressure. Because there are individual differences in the response to antihypertensive drugs, it may be possible to tailor drug regimens that minimize symptoms of low pressure when standing up. On the other hand, if the blood vessels are dilated inappropriately in the absence of medications, other medications (beta blockers or midodrine) may be used to constrict the vessels.
Syncopal spells related to arrhythmias require specific therapies. Diagnostic findings at electrophysiologic study often provide important therapeutic guidance. Supraventricular tachyarrhythmias may be cured by catheter-mediated (radiofrequency) ablation or treated with drugs. Bradyarrhythmias may require the implantion of a pacemaker. Ventricular tachyarrhythmias causing syncope are treated with implantable cardioverter defibrillators (ICD). These devices can also act as pacemakers and prevent syncope arising from slow heart rates (bradyarrhythmias).