Mechanisms of Syncope
Transient reductions in brain blood flow may be due to a generalized failure of the circulatory system or a regional circulatory problem selectively affecting the brain. Syncope most commonly results from a transient generalized or systemic breakdown of the circulation. Blood flow to the brain may be transiently insufficient due to failure of the heart to pump blood (cardiogenic syncope), blood collecting or pooling in veins of the legs or abdomen "upstream" of the heart and never reaching the heart to be pumped to the body (orthostatic syncope), and mismatch of blood flow to body tissues other than the brain with insufficient distribution to the brain. Chronic disease of the arteries (atherosclerosis) may also reduce blood supply to the brain. In some persons, moving the neck or upper body may transiently aggravate the reduced flow through narrowed arteries of the neck. Regional disturbances in blood flow to the brain, especially the lower brain (brain stem), are a rare cause of syncope.
What makes an understanding of events contributing to syncope difficult is that the mechanisms are complex, operate in combination, and influence each other. It is often difficult to analyze the sequence of events to determine whether an event is primary or secondary. Three major mechanisms may contribute to a breakdown in systemic circulation:
Sudden failure of the heart as a pump ("cardiogenic syncope")
The amount of blood pumped by the heart per minute (cardiac output) may transiently drop during episodes of rapid heart rates (tachycardia), very slow heart rates (bradycardia), or true failure of the heart to beat (asystole). During abnormal tachycardias, the heart often pumps inefficiently, either due to a change in the pattern of muscle contraction or to the lack of time for the heart to fill completely. In ventricular fibrillation, for example, the heart lacks any organized pattern of contraction and effective pumping motion does not occur.
A rare mechanism of cardiogenic syncope can occur due to sudden transient obstruction to flow within the heart. Mobile tumors (myxomas) at the level of the mitral valve may intermittently position themselves at the valve opening and prevent blood from entering the ventricle. In some unusual types of cardiac enlargement (hypertrophic cardiomyopathy), the thickened-walls of ventricles may obstruct the outlet of the ventricle, impeding ventricular emptying.
Sudden excessive reduction of "venous return" - Orthostatic syncope
The veins are thin-walled elastic vessels that bring back oxygen depleted blood from the "peripheral circulation" (organs outside of the chest) to the "central circulation" (heart and lungs). An important feature of the venous system is that it can substantially expand or reduce its capacity. Two forces, gravity and voluntary compression of the chest and abdomen (straining) can suddenly distend the peripheral venous system and increase its capacity. The venous system then retains blood that would otherwise return to the heart to be recirculated. However, veins are muscular and can counteract distending forces by contracting and narrowing their diameter (venoconstriction) which decreases the capacity of the venous system and enhances blood return to the heart upon command of the autonomic nervous system. Large veins also contain valves, which prevent backward flow in the veins and force blood to flow in the direction of the heart.
Venous pooling in the upright (orthostatic - Greek = standing straight) position is the major mechanism of common faint of benign syncope. Retention of blood in the venous system reduces the circulating blood volume available to the heart (effective blood volume). During excessive venous pooling, cardiac output and arterial pressure fall (orthostatic hypotension) and these events may critically reduce blood flow to the brain and precipitate syncope. As a person changes posture from recumbent to an erect standing position, the veins are suddenly pressurized by gravity. Upon assuming a standing position, as much as 20% (one liter) of the blood volume may be retained in the venous system of the lower body. Venous pooling upon standing up is normal, but it may be excessive under certain situations. Motionless standing of military guards or singers in choirs during lengthy ceremonies may cause orthostatic syncope due to venous pooling. Years ago fashionable women wore tight corsets that would impede venous return from the lower body, and it was commonplace and even elegant for high society ladies to swoon at least once a day. Standing immobile and straining with coughing or difficulty urinating in elderly men enhances venous pooling.
Standing up is poorly tolerated in persons with reduced absolute blood volume due to bleeding or a deficit in body fluids (water). Dehydration may occur when a person does not drink enough or loses excessive fluid through the lungs, skin (sweat), or kidney (urine). For instance, a marathon runner who sweats a lot and does not drink may lose an excessive amount of fluid and pass out, even though he/she may be completely healthy. In some patients, fluid losses may result from treatment with water pills or diuretics.
Orthostatic syncope is mediated primarily by a disturbance in venous regulation with the heart being a victim rather than a faulty actor. The heart cannot perform its job as a pump if not enough blood comes to it. However, when the circulation is challenged because of insufficient return to the heart, complex neural and hormonal regulatory events are always elicited. In some persons a decrease in circulating volume triggers a reflex slowing of the heart, which may secondarily aggravate circulatory failure.
Interventions that inhibit venoconstrictor responses (surgical interruption of nerves, selected drugs, diabetic neuropathy, and varicose veins) markedly increase the susceptibility to orthostatic syncope. Venodilation, a widening of the skin veins to dispose of heat in response to a hot environment such as a "Hot tub" or sauna, also results in a substantial increase in the venous capacity and a fall in the venous pressure. This lower venous pressure decreases venous return. Deprived of circulating blood volume, a drop in arterial pressure and loss of consciousness may even result in drowning ("Jacuzzi syncope").
Straining increases the pressure inside of the chest and/or abdomen, which hinders venous blood from entering these body cavities and returning to the heart. Straining occurs during a variety of activities including weightlifting, breath holding (referred to in medicine as the Valsalva maneuver), prolonged exhalation (trumpet blowing) or coughing (tussive syncope), difficulty in swallowing (deglutition syncope), bowel movement, and urination (micturation syncope). Straining also induces complex neurological adjustments (reflexes) which are sometimes thought to be the involved in causing syncope.
Sudden abnormal distribution of cardiac output (inappropriate arterial vasodilation)
Generalized arterial vasodilation (widening of the arteries) may produce a distribution problem in which the brain suddenly does not get its fair share of blood. During exercise the arteries of the muscles expand, thus diverting a large fraction of the cardiac output from the organs to the working musculature. Concomitantly, multiple circulatory adjustments help to maintain arterial pressure despite the increased blood flow to skeletal muscle. One adjustment promoting venous return to the heart is the intermittent compression of the veins caused by body movements. Another is the limitation of blood flow to selected organs making a greater fraction of cardiac output available to the muscles. If atherosclerosis involves the arteries to the brain, the blood flow may be marginal from the start and may decline even further.
Under special situations when stress is unanticipated a fright signal may trigger the lower brain to evoke a sudden muscular arterial vasodilation. When this occurs, the blood pressure falls, thus depriving the brain of blood flow. Seemingly inappropriate arterial vasodilation may play an important role when syncope occurs immediately after receipt of frightening or threatening sensory inputs, such as seeing blood or hearing bad news. In animal physiology, such signals may be viewed as "playing dead" to avoid harm.