Causes range from non-serious to potentially fatal. There are three broad categories of causes: heart or blood vessel related; reflex, also known as neurally mediated; and orthostatic hypotension. Issues with the heart and blood vessels are the cause in about 10% and typically the most serious while neurally mediated is the most common. There also seems to be a genetic component to syncope. A recent genetic study has identified first risk locus for syncope and collapse. The lead genetic variant, residing at chromosome 2q31.1, is an intergenic variant approximately 250 kb downstream of the ZNF804A gene. The variant effected the expression of ZNF804A, making this gene the strongest driver of the association. Neurally mediated syncope Reflex syncope or neurally mediated syncope occurs when blood vessels expand and heart rate decreases inappropriately leading to poor blood flow to the brain. This may occur from either a triggering event such as exposure to blood, pain, strong feelings, or a specific activity such as urination, vomiting, or coughing. Vasovagal syncope Vasovagal (situational) syncope is one of the most common types which may occur in response to any of a variety of triggers, such as scary, embarrassing or uneasy situations, during blood drawing, or moments of sudden unusually high stress. There are many different syncope syndromes which all fall under the umbrella of vasovagal syncope related by the same central mechanism. First, the person is usually predisposed to decreased blood pressure by various environmental factors. A lower than expected blood volume, for instance, from taking a low-salt diet in the absence of any salt-retaining tendency. Or heat causing vaso-dilation and worsening the effect of the relatively insufficient blood volume. The next stage is the adrenergic response. If there is underlying fear or anxiety (e.g., social circumstances), or acute fear (e.g., acute threat, needle phobia), the vaso-motor centre demands an increased pumping action by the heart (flight or fight response). This is set in motion via the adrenergic (sympathetic) outflow from the brain, but the heart is unable to meet requirements because of the low blood volume, or decreased return. A feedback response to the medulla is triggered via the afferent vagus nerve. The high (ineffective) sympathetic activity is thereby modulated by vagal (parasympathetic) outflow leading to excessive slowing of heart rate. The abnormality lies in this excessive vagal response causing loss of blood flow to the brain. The tilt-table test typically evokes the attack. Avoiding what brings on the syncope and possibly greater salt intake is often all that is needed. Associated symptoms may be felt in the minutes leading up to a vasovagal episode and are referred to as the prodrome. These consist of light-headedness, confusion, pallor, nausea, salivation, sweating, tachycardia, blurred vision, and sudden urge to defecate among other symptoms. Vasovagal syncope can be considered in two forms: *Isolated episodes of loss of consciousness, unheralded by any warning symptoms for more than a few moments. These tend to occur in the adolescent age group and may be associated with fasting, exercise, abdominal straining, or circumstances promoting vaso-dilation (e.g., heat, alcohol). The subject is invariably upright. The tilt-table test, if performed, is generally negative. *Recurrent syncope with complex associated symptoms. This is neurally mediated syncope (NMS). It is associated with any of the following: preceding or succeeding sleepiness, preceding visual disturbance ("spots before the eyes"), sweating, lightheadedness. The subject is usually but not always upright. The tilt-table test, if performed, is generally positive. It is relatively uncommon. Syncope has been linked with psychological triggers. This includes fainting in response to the sight or thought of blood, needles, pain, and other emotionally stressful situations. One theory in evolutionary psychology is that fainting at the sight of blood might have evolved as a form of playing dead which increased survival from attackers and might have slowed blood loss in a primitive environment. "Blood-injury phobia", as this is called, is experienced by about 15% of people. It is often possible to manage these symptoms with specific behavioral techniques. Another evolutionary psychology view is that some forms of fainting are non-verbal signals that developed in response to increased inter-group aggression during the paleolithic. A non-combatant who has fainted signals that she or he is not a threat. This would explain the association between fainting and stimuli such as bloodletting and injuries seen in blood-injection-injury type phobias such as needle phobia as well as the gender differences. Much of this pathway was discovered in animal experiments by Bezold (Vienna) in the 1860s. In animals, it may represent a defence mechanism when confronted by danger ("playing possum"). Situational syncope Syncope may be caused by specific behaviors including coughing, urination, defecation, vomiting, swallowing (deglutition), and following exercise. Manisty et al. note: "Deglutition syncope is characterised by loss of consciousness on swallowing; it has been associated not only with ingestion of solid food, but also with carbonated and ice-cold beverages, and even belching." Fainting can occur in "cough syncope" following severe fits of coughing, such as that associated with pertussis or "whooping cough." Neurally mediated syncope may also occur when an area in the neck known as the carotid sinus is pressed. A normal response to carotid sinus massage is reduction in blood pressure and slowing of the heart rate. Especially in people with hypersensitive carotid sinus syndrome this response can cause syncope or presyncope. Cardiac Heart-related causes may include an abnormal heart rhythm, problems with the heart valves or heart muscle, or blockages of blood vessels from a pulmonary embolism or aortic dissection, among others.Syncope from bradycardia Cardiac arrhythmias The most common cause of cardiac syncope is cardiac arrhythmia (abnormal heart rhythm) wherein the heart beats too slowly, too rapidly, or too irregularly to pump enough blood to the brain. Some arrhythmias can be life-threatening. Two major groups of arrhythmias are bradycardia and tachycardia. Bradycardia can be caused by heart blocks. Tachycardias include SVT (supraventricular tachycardia) and VT (ventricular tachycardia). SVT does not cause syncope except in Wolff-Parkinson-White syndrome. Ventricular tachycardia originate in the ventricles. VT causes syncope and can result in sudden death. Ventricular tachycardia, which describes a heart rate of over 100 beats per minute with at least three irregular heartbeats as a sequence of consecutive premature beats, can degenerate into ventricular fibrillation, which is rapidly fatal without cardiopulmonary resuscitation (CPR) and defibrillation. Long QT syndrome can cause syncope when it sets off ventricular tachycardia or torsades de pointes. The degree of QT prolongation determines the risk of syncope. Brugada syndrome also commonly presents with syncope secondary to arrhythmia. Typically, tachycardic-generated syncope is caused by a cessation of beats following a tachycardic episode. This condition, called tachycardia-bradycardia syndrome, is usually caused by sinoatrial node dysfunction or block or atrioventricular block. Obstructive cardiac lesion Blockages in major vessels or within the heart can also impede blood flow to the brain. Aortic stenosis and mitral stenosis are the most common examples. Major valves of the heart become stiffened and reduce the efficiency of the hearts pumping action. This may not cause symptoms at rest but with exertion, the heart is unable to keep up with increased demands leading to syncope. Aortic stenosis presents with repeated episodes of syncope. Rarely, cardiac tumors such as atrial myxomas can also lead to syncope. Structural cardiopulmonary disease Diseases involving the shape and strength of the heart can be a cause of reduced blood flow to the brain, which increases risk for syncope. The most common cause in this category is fainting associated with an acute myocardial infarction or ischemic event. The faint in this case is primarily caused by an abnormal nervous system reaction similar to the reflex faints. Women are significantly more likely to experience syncope as a presenting symptom of a myocardial infarction. In general, faints caused by structural disease of the heart or blood vessels are particularly important to recognize, as they are warning of potentially life-threatening conditions. Among other conditions prone to trigger syncope (by either hemodynamic compromise or by a neural reflex mechanism, or both), some of the most important are hypertrophic cardiomyopathy, acute aortic dissection, pericardial tamponade, pulmonary embolism, aortic stenosis, and pulmonary hypertension. Other cardiac causes Sick sinus syndrome, a sinus node dysfunction, causing alternating bradycardia and tachycardia. Often there is a long pause (asystole) between heartbeats. Adams-Stokes syndrome is a cardiac syncope that occurs with seizures caused by complete or incomplete heart block. Symptoms include deep and fast respiration, weak and slow pulse, and respiratory pauses that may last for 60 seconds. Subclavian steal syndrome arises from retrograde (reversed) flow of blood in the vertebral artery or the internal thoracic artery, due to a proximal stenosis (narrowing) and/or occlusion of the subclavian artery. Symptoms such as syncope, lightheadedness, and paresthesias occur while exercising the arm on the affected side (most commonly the left). Aortic dissection (a tear in the aorta) and cardiomyopathy can also result in syncope. Various medications, such as beta blockers, may cause bradycardia induced syncope. A pulmonary embolism can cause obstructed blood vessels and is the cause of syncope in less than 1%
symptom of Arrhythmia
symptom of Myocardial infarction
symptom of Heart failure
symptom of Hypotension
symptoms of Arrhythmia
symptom of Cardiovascular disease
symptom of Ventricular fibrillation
symptom of Coronary artery disease