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Syncope: Difference between revisions
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Syncope is a transient loss of consciousness (TLOC) due to global cerebral hypoperfusion characterized by rapid onset, short duration and spontaneous complete recovery. This excludes other causes of TLOC such as neurological, psychological and metabolic causes. | |||
Syncope is a transient loss of consciousness (TLOC) due to global cerebral hypoperfusion characterized by rapid onset, short duration and spontaneous complete recovery. This excludes other causes of TLOC such as neurological, psychological and metabolic causes. | |||
==Classification== | |||
Syncope can be classified into: | Syncope can be classified into: | ||
[[ | [[Image:Syncope_class.svg|center]] | ||
==Pathophysiology== | |||
( | Syncope can be caused by a low peripheral resistance (vasodepressor type), a low cardiac output (cardioinhibitory type) or a combination of both. | ||
A low peripheral resistance can be caused by an inappropriate reflex, or autonomic failure. A low cardiac output can be caused by reflex bradycardia, arrhythmias, or structural cardiac diseases or inadequate venous return. | |||
==Epidemiology== | ==Epidemiology== | ||
Syncope is common in the general population. The life-time cumulative incidence of | 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. | ||
==Clinical features== | ==Clinical features== | ||
History taking is the most important feature in syncope evaluation. | History taking is the most important feature in syncope evaluation. | ||
These clinical features suggestive of a specific cause of syncope: | These clinical features suggestive of a specific cause of syncope: | ||
{| class="wikitable" border="1" cellpadding="1" cellspacing="1" width="80%" | |||
{| class="wikitable" | |||
|- | |- | ||
!Reflex (neurally mediated) syncope | |||
|- | |- | ||
| | |||
*Absence of cardiac disease | |||
*Long history of syncope | |||
*After sudden, unexpected, unpleasant sight, sound, smell, or pain | |||
*Prolonged standing or crowded, hot places | |||
*Nausea, vomiting associated with syncope | |||
*During or in the absorptive state after a meal | |||
*With head rotation, pressure on carotid sinus (as in tumous, shaving, tight collars) | |||
*After exertion | |||
|- | |- | ||
!Syncope due to orthostatic hypotension | |||
|- | |- | ||
| | | | ||
*After standing up | |||
*Temporal relationship with start of medication leading to hypotension or changes of dosage | |||
*Prolonged standing especially in crowded, hot places | |||
*Presence of autonomic neuropathy or Parkinsonism | |||
*After exertion | |||
|- | |- | ||
!Cardiac syncope | |||
|- | |- | ||
| Family history of sudden death | | | ||
*Presence of severe structural heart disease | |||
*During exertion, or supine | |||
*Preceded by palpitation or accompanied by chest pain | |||
*Family history of sudden death | |||
|} | |} | ||
In all patients presenting to a physician with syncope an ECG is recommended to screen for a cardiac cause of syncope. Holter monitoring is indicated only in patients who have very frequent syncopes or presyncope. In-hospital monitoring (in bed or telemetric) is warranted only when the patient has important structural heart disease and is at high risk of life-threatening arrhythmias. | In all patients presenting to a physician with syncope an ECG is recommended to screen for a cardiac cause of syncope. Holter monitoring is indicated only in patients who have very frequent syncopes or presyncope. In-hospital monitoring (in bed or telemetric) is warranted only when the patient has important structural heart disease and is at high risk of life-threatening arrhythmias. | ||
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. | 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== | ==Reflex syncope== | ||
===Diagnostic evaluation=== | ===Diagnostic evaluation=== | ||
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 | 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 | 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). | ||
Head-up-tilt testing is used to examine the susceptibility to reflex syncope in patients who present with syncope of unknown cause. During head-up-tilt-testing a patient is passively changed from supine to upright position using a tilt-table. | Head-up-tilt testing is used to examine the susceptibility to reflex syncope in patients who present with syncope of unknown cause. During head-up-tilt-testing a patient is passively changed from supine to upright position using a tilt-table. | ||
===Treatment=== | ===Treatment=== | ||
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 | 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). | ||
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 | |||
==Orthostatic hypotension== | ==Orthostatic hypotension== | ||
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===Treatment=== | ===Treatment=== | ||
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. | 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. | ||
==Cardiac syncope== | ==Cardiac syncope== | ||
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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. | 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. | ||
If cardiac syncope is suspected cardiac evaluation (echocardiography, stress testing, electrophysiological study, and prolonged ECG monitoring including loop recorder) is recommended. | If cardiac syncope is suspected cardiac evaluation (echocardiography, stress testing, electrophysiological study, and prolonged ECG monitoring including loop recorder) is recommended. | ||
===Treatment=== | ===Treatment=== | ||
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==References== | ==References== | ||
#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\ | ||
# Hainsworth R. Pathophysiology of syncope. Clin Auton Res 2004; 14: Suppl 1:18-24 | #Hainsworth R. Pathophysiology of syncope. Clin Auton Res 2004; 14: Suppl 1:18-24 | ||
# | #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. | |||