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==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 | 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 only 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. | ||
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 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). | 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). | ||
==Orthostatic hypotension== | ==Orthostatic hypotension== | ||
===Diagnostic evaluation=== | ===Diagnostic evaluation=== | ||
[[Image:Orthostatic.JPG|right|400px]] | [[Image:Orthostatic.JPG|right|400px]] | ||
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. | Orthostatic hypotension can be divided into 3 variants depending on the time interval between rising from supine position to complaints of light-headedness and/or fainting. | ||
1. Initial orthostatic hypotension is defined as a transient blood pressure decrease (>40 mmHg systolic blood pressure (BP) and/or >20 mmHg diastolic BP) within 15 seconds of standing. It can only be present during active standing, because the initial drop in BP is not seen during head-up-tilt test in which both BP and heart rate (HR) gradually increases until stabilization is reached. Because of the rapid initial changes, it can only be detected by continuous beat-to-beat BP measuring of finger arterial. | |||
2. Classical orthostatic hypotension is defined as a sustained reduction of systolic blood pressure of at least 20 mmHg or diastolic blood pressure of 10 mmHg within 3 min of standing or head-up tilt to at least 60 degree on a tilt table. Because the fall of BP is dependent on the baseline BP, a reduction in systolic BP of 30 mmHg may be a more appropriate criterion for OH in patients with supine hypertension. Orthostatic hypotension is a clinical sign and may be symptomatic or asymptomatic and can be a result of primary or secondary autonomic failure. Classical orthostatic hypotension can be detected during bedside evaluation with an active lying-to-standing test using the manual cuff. | |||
3. 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. | |||
===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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Cardiac arrhythmias, both brady- and tachyarrhythmias can cause syncope, due to a decrease in cardiac output. Additional factors which determine the susceptibility to syncope due to arrhythmias are the type of arrhythmia (atrial or ventricular), the status of left ventricular function, posture and the adequacy of vascular compensation are important. Structural heart disease can cause syncope when circulatory demands outweigh the impaired ability of the heart rate to increase its output. | Cardiac arrhythmias, both brady- and tachyarrhythmias can cause syncope, due to a decrease in cardiac output. Additional factors which determine the susceptibility to syncope due to arrhythmias are the type of arrhythmia (atrial or ventricular), the status of left ventricular function, posture and the adequacy of vascular compensation are important. Structural heart disease can cause syncope when circulatory demands outweigh the impaired ability of the heart rate to increase its output. | ||
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 | 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 mortality within 1 year. | ||
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. | ||
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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. | <biblio> | ||
# | #ESC The ESC Textbook of Cardiovascular Medicine. Second edition. Editors: Camm AJ, Luscher TF, Serruys PW. 2009. Oxford university press. | ||
#Moya pmid=19713422 | |||
#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 | ||
# | #Wieling pmid=19587129 | ||
# | #Wieling2 pmid=21431947 | ||
#Colman pmid=15480928 | |||
</biblio> | |||