Syncope: Difference between revisions

Syncope is common in the general population. The life-time cumulative incidence of ≥1 syncopal episodes in teenagers in the general population is high, with about 40 % by the age of 21 years. Reflex syncope is by far the most common cause. The majority have experienced reflex-mediated syncope episodes as teenagers and adolescents. The frequency of orhtostatic hypotension and cardiac syncope increases with age. Approximately 10-30% of the syncope episodes in patients above 60 years visiting a hospital for their syncope episodes are of cardiac origin.

History taking is the most important feature in syncope evaluation. After that the following clinical features are suggestive of a specific cause of syncope:

When the mechanism of syncope remains unclear after full evaluation, an implantable loop recorder is indicated in patients who have clinical or ECG features suggesting arrhythmic syncope.  

Reflex syncope refers to a heterogeneous group of conditions in which there is a relatively sudden change in autonomic nervous system activity (decreased sympathic tonus causing less vasoconstriction and increased parasympathic (vagal) tonus causing bradycardia), triggered by a central (e.g. emotions, pain, blood phobia) or peripheral (e.g. prolonged orthostasis or increased carotid sinus afferent activity). It leads to a fall in blood pressure and cerebral perfusion. The range of bradycardia varies widely in reflex syncope, from a small reduction in peak heart rate to several seconds of asystole. As reflex syncope requires a reversal of the normal autonomic outflow, it usually occurs in people with a functional autonomic nervous system and should therefore be distinguished from syncope due to neurogenic orthostatic hypotension in patients with chronic autonomic failure.  

Adequate history taking reveals the clinical features associated with a syncopal event that are important to differentiate the different causes of syncope. Vasovagal syncope, a specific form of reflex syncope, is diagnosed if syncope is precipitated by emotional distress or orthostatic stress and is associated with typical prodromes (such as nausea, warmth, pallor, light-headedness, and/or diaphoresis).  

The prognosis of reflex syncope is excellent. However, syncope episodes can have a considerable impact on quality of life, because of its unexpected nature and fear for recurrences. Initial treatment of reflex syncope consists of non-pharmacological treatment measures, including reassurance regarding the benign nature of the condition, increasing the dietary salt and fluid intake, moderate exercise training, and physical counterpressure maneuvres (muscle tensing).  

Delayed orthostatic hypotension is a sustained reduction of systolic BP beyond 3 minutes of standing. These delayed falls in BP may be a mild or early form of sympathetic adrenergic failure. It can be detected with an extended lying-to-standing test or during head-up-tilt test.

Initial treatment is educating regarding awareness and possible avoidance of triggers (e.g. hot crowded environments, volume depletion), early recognition of premonitory symptoms and performing manoeuvres to abort the episode (e.g. supine posture, muscle tensing). Drug-induced autonomic failure is probably the most frequent cause of orthostatic hypotension; in these cases elimination of the offending agents, mainly diuretics and vasodilators, is the main strategy. Alcohol is also commonly associated with orthostatic intolerance. Additionally, in some patients expanding intravascular volume by encouraging a higher than normal salt- and fluid intake can be helpful.  

Higher age, an abnormal ECG (rhythm abnormalities, conduction disorders, hypertrophy, old myocardial infarction, possible acute ischaemia, and AV block), a history of cardiovascular disease, especially ventricular arrhythmia, heart failure, syncope occurring without prodrome or during effort or supine, were found to be predictors of arrhythmia and/or 1-year mortality.  

#The ESC Textbook of Cardiovascular Medicine. Second edition. Editors: Camm AJ, Luscher TF, Serruys PW. 2009. Oxford university press.

#Freeman R et al. Consensus statement on the definition of orthostatic hypotension, neurally mediated syncope and the postural tachycardia syndrome. Clin Auton Res 2011; 21:69-72

#Moya A et al. Guidelines for the diagnosis and management of syncope. Eur Heart J 2009; 30:2631-71

#Wieling W et al. Symptoms and signs of syncope: a review of the link between physiology and clinical clues. Brain 2009; 132:2630-42.