Syncope (medicine)
Classification according to ICD-10 | |
---|---|
R55 | Syncope and collapse
Blackout |
I95.1 | Orthostatic hypotension |
R57.9 | Shock, unspecified
Circulatory collapse |
ICD-10 online (WHO version 2019) |
In medicine, syncope (from ancient Greek συνκοπή synkopé , German ' colliding ' , ' pushing out'; late Latin syncope ), also known in German as fainting , is a sudden onset of short-term unconsciousness that is accompanied by a loss of posture control and without special treatment stops spontaneously.
term
Syncope, also known as (general) collapse , is characterized by a temporary reduced blood supply to the brain and, depending on its cause, is divided into neural (vasovagal), circulatory ( orthostatic ), cardiogenic (cardiogenic) or cerebrovascular disorders caused by the heart ) Syncopation classified. The circulatory or orthostatic syncope is a temporary circulatory weakness or a short-lasting state of shock and is referred to as (orthostatic) collapse or circulatory collapse .
Syncope can be confused with impaired consciousness of a neurological ( seizure ) or psychogenic cause as well as metabolic imbalances (e.g. hypoglycaemia ). The various causes usually make a broad diagnosis necessary. Therapy depends on the cause.
Colloquially, syncope is also referred to as powerlessness (from Middle High German ā power 'weakness, lack of strength, unconsciousness'; in the Middle Ages also referred to as sincope ) or blackout , the latter being particularly common in Great Britain, while in Germany the term blackout is used in medical- psychological area rather for temporary memory loss e.g. B. is common during an exam.
physiology
The permanent adequate supply of blood to the brain in any posture, even with a sudden change of position, is guaranteed by several mechanisms. On the one hand, the vessels, especially those of the legs, adapt in that their muscles contract and their capacity is reduced. In this way, the body prevents the blood from sinking into the legs, the so-called preload of the heart increases, which enables it to keep the blood pressure constant or increase it slightly and adapt it to the changed conditions. Another regulatory mechanism is the increase in heart rate in order to maintain the blood flow through this increased work.
A small area in the carotid artery , the carotid sinus , represents an important control point. The blood pressure is continuously measured here as a measure of the cerebral blood flow. The body then regulates blood pressure via the autonomic nervous system via the vascular resistance and the heart rate.
Causes and classification
Circulatory causes
Orthostatic syncope
As part of the change from a lying, sitting or kneeling position to an upright position ( orthostasis ), the blood shifts to the deeper parts of the body. If the counter-regulation of the autonomic nervous system is inadequate , up to a quarter of the blood sinks into the veins in the lower half of the body (venous pooling). Jointly responsible for insufficient counter-regulation can e.g. B. dehydrated or overdosed blood pressure medication. There are often varicose veins ( varicosis ). In diabetics , diabetic neuropathy can affect the autonomic nerves and, in addition to other complaints, dysregulation of the vessels during orthostatic stress .
Neurally mediated syncope
In neurocardiogenic or vasovagal syncope (from Latin vas 'vessel' and nervus vagus ) , the blood vessels expand ( vasodilation ) and the heart rate decreased ( bradycardia ), mediated by a reflex . The respective share of these two factors in the resulting drop in blood pressure and the reduced blood flow to the brain is very different from patient to patient. The triggering factors are emotional or circulatory (orthostatic) stress (long, motionless standing), but also fright, pain, noise, cold, and banal bleeding.
A subgroup are pressor syncope during urine or stool evacuation (see micturition syncope ), cough or Valsalva attempt (especially after hyperventilation ).
A special form is an overly sensitive carotid sinus as part of a carotid sinus syndrome . Mechanical pressure or even just turning the head can lead to a drop in heart rate and / or blood pressure. If a sustained pause of at least three seconds in the electrocardiogram (ECG) is detected as part of a carotid pressure test , an AAI pacemaker can be implanted.
Other circulatory causes
- In terms of drugs , syncope can be triggered by drugs that lower the heart rate and blood pressure.
- Vena cava compression syndrome in pregnant women may reduce the return flow of blood to the heart when lying down. Insufficient filling of the heart can lead to unconsciousness.
- In older people, venous pooling in the intestinal vessels after a large meal can lead to postprandial syncope .
Cardiac syncope
The syncope originating from the heart can be subdivided again. This includes those attacks that are caused by a disturbed rhythm of the heartbeat ( arrhythmia ). Both too low and too high a pumping frequency can lead to a reduction in the ejection volume of the heart.
The second subset is the inability of the heart based eject blood sufficiently (about when due to low cardiac output , oliguria marked, peripheral vascular constriction and anxiety or confusion low output syndrome ). If the pulmonary circulation is narrowed or blocked ( pulmonary embolism , pulmonary stenosis ), the right ventricle cannot pump blood into the lungs and if the left ventricular outflow path is narrowed ( hypertrophic cardiomyopathy , aortic stenosis ), the left heart cannot eject blood into the body. Both halves of the heart can be affected as part of a heart attack in the sense of a pump failure. This is also the case if the heart can not expand in the pericardium due to an effusion ( pericardial tamponade ).
Cerebrovascular syncope
In rare cases, reduced blood flow to the brain can also be caused by a so-called tap phenomenon . Particularly with increased muscle work, there is a redistribution of blood from the brain to an arm if there is a narrowing ( stenosis ) of the arm artery ( subclavian artery ) before the vertebral artery emerges ( subclavian steal syndrome ).
Electrical current
An electrical accident can also be triggering.
Epidemiology
With up to a fifth of affected children and adolescents up to the age of 18, syncope is a very common symptom even in childhood. Every year, 6% of all older people suffer from syncope. Of these, neural syncope is by far the most common with around two-thirds, followed by cardiovascular (10%) and cardiac arrhythmias (11%) caused fainting. In contrast, structural heart muscle changes are roughly as rare (around 5%) as non-syncopal seizure-like disorders of consciousness (6%).
diagnosis
Taking the medical history ( anamnesis ) is of particular importance in the clarification of syncope. The examiner must inquire about the accompanying circumstances of the fainting (prolonged standing, change of position), possible triggers and possible precursor symptoms ( prodromi ) such as dizziness, eye flickering, sweating or nausea. Other important information, such as the duration of the unconsciousness, possible twitching of the patient during this time or possibly a prolonged confusion after regaining consciousness can only be obtained from witnesses of the event (external anamnesis). An increased urge to urinate after the event indicates a rhythmogenic event (release of atrial natriuretic peptide (ANP) through atrial distension).
In addition to the physical examination , basic technical diagnostics include blood pressure measurement while lying down and standing, long-term blood pressure measurement and a tilt table examination if possible, alternatively a Schellong test . A resting and long-term ECG and possibly also a stress ECG are necessary to clarify arrhythmias . A heart ultrasound should also be performed. Laboratory examinations serve primarily to prove metabolic imbalances or anemia ( anemia ).
If carotid sinus syndrome is suspected , a Doppler ultrasound scan of the carotid artery should be performed. A cardiac catheter examination is only necessary if a structural heart disease is suspected in the previous examinations. Possible non-syncopal disorders of consciousness can be found by taking an electroencephalogram and tomography examinations of the brain using computed tomography or magnetic resonance imaging .
Differential diagnosis
Attack-like, temporary disturbances of consciousness, which are not caused by a temporary reduced blood supply to the brain, must be distinguished from the actual syncope. Among the neurological causes, these include epileptic seizures , cerebral haemorrhages or acute vascular occlusions in the central nervous system ( stroke ). The psychological causes include hyperventilation, for example in the context of panic attacks or conversion symptoms . Metabolic derailments are, for example, hypoglycaemia or derailments in the salt concentration in the blood as well as poisoning . Even simple falls or a cataplexy , which are not accompanied by a loss of consciousness, can be misinterpreted as syncope.
Therapy and prophylaxis
In the acute situation, the patient should be positioned with the upper body low and the legs raised. This facilitates the return of blood to the heart and the patient should clear up again quickly. Further treatment is usually unnecessary.
As a prophylaxis for the frequent vasovagal syncope, general measures such as alternating showers, regular endurance sports and adequate fluid intake are primarily recommended. The effectiveness of standing training, if possible standardized as a so-called tilting table training, has also been proven . In the long term, however, patient cooperation is often insufficient.
If the patient notices warning symptoms of impending syncope, various isometric exercises such as clasping hands and pulling arms or crossing legs and tensing the muscles can prevent or at least delay unconsciousness. If necessary, the patient should sit on the floor on the spot. Wearing compression stockings makes sense, especially if you have varicose veins at the same time. In contrast, drugs have not been able to prove their effectiveness in placebo-controlled studies. This applies to both beta blockers and the frequently used vasoconstricting α-agonists .
If syncope is more caused by orthostatic stress, other medications that reduce blood pressure should be discontinued if possible. In these patients, in addition to increasing the filling volume of the blood vessels through increased salt and fluid intake, drug treatment with the mineralocorticoid fludrocortisone can also be considered. Compression stockings also reduce the drop in blood pressure in the upright position.
Finally, if the cause is a disorder of the heart function, this must of course be treated. Depending on the underlying rhythm disturbance, artificial pacemakers , an implantable cardioverter defibrillator (ICD) or catheter ablation can be used. Surgery for aortic valve stenosis after syncope is also urgently indicated, as is catheter ablation for hypertrophic obstructive cardiomyopathy ( HOCM ).
literature
- Angel Moya et al .: Guidelines for the diagnosis and management of syncope (version 2009): The Task Force for the Diagnosis and Management of Syncope of the European Society of Cardiology (ESC) . In: European Heart Journal . tape 30 , no. 21 , August 27, 2009, p. 2631–2671 , doi : 10.1093 / eurheartj / ehp298 (English, Syncope (Guidelines on Diagnosis and Management of). ESC Clinical Practice Guidelines).
- S1 guideline syncope of the German Society for Neurology (DGN). In: AWMF online (as of 2012)
- Herbert Reindell , Helmut Klepzig: diseases of the heart and blood vessels. In: Ludwig Heilmeyer (ed.): Textbook of internal medicine. Springer-Verlag, Berlin / Göttingen / Heidelberg 1955; 2nd edition ibid. 1961, pp. 450-598, here: pp. 480-484: The acute peripheral circulatory failure (fainting, shock, collapse).
Web links
Individual evidence
- ↑ Alphabetical directory for the ICD-10-WHO Version 2019, Volume 3. German Institute for Medical Documentation and Information (DIMDI), Cologne, 2019, p. 484
- ↑ Wolfgang Pfeifer [Head] (Ed.): Etymological Dictionary of German . 2nd revised and expanded edition. Deutscher Taschenbuch Verlag, Munich 1997, ISBN 3-423-03358-4 , keyword “Synkope” .
- ↑ a b c d e Robert Dalla Pozza: Syncope in childhood and adolescence . In: Monthly Pediatrics . tape 154 , no. 6 , 2006, ISSN 0026-9298 , p. 583-593 , doi : 10.1007 / s00112-006-1339-y .
- ^ F. Weissinger, T. Lempert: Powerlessness . In: Bettina Schmitz, Barbara Tettenborn (Hrsg.): Paroxysmal disorders in neurology . Springer, Berlin 2005, ISBN 3-540-40789-8 , pp. 6 .
- ↑ www.gesundheits-lexikon.com: Syncope and Collapse .
- ↑ a b c d e f g Michele Brignole: Diagnosis and treatment of syncope . In: Heart . tape 93 , no. 1 , 2007, p. 130–136 , doi : 10.1136 / hrt.2005.080713 , PMID 17170354 , PMC 1861366 (free full text) - (English).
- ↑ flexicon.doccheck: Syncope .
- ↑ Wolfgang Pfeifer : Etymological Dictionary of German. Academy, Berlin 1989 (and other editions), s. v .; Middle High German Dictionary, Volume 1. Hirzel, Stuttgart 2013, Sp. 192 f.
- ↑ Michele Brignole et al .: Practical Instructions for the 2018 ESC Guidelines for the diagnosis and management of syncope . In: European Heart Journal . tape 00 , 2018, p. e1-e38 , doi : 10.1093 / eurheartj / ehy071 (English).
- ↑ Reinhard Larsen: Anesthesia and intensive medicine in cardiac, thoracic and vascular surgery. (1st edition 1986) 5th edition. Springer, Berlin / Heidelberg / New York et al. 1999, ISBN 3-540-65024-5 , p. 234.
- ↑ Gerd Herold (Ed.): Internal Medicine . Herold, Cologne 1999, OCLC 174381635 .
- ↑ Johannes-Martin Hahn: Checklist internal medicine . 7th edition. Thieme, Stuttgart 2013, ISBN 978-3-13-107247-4 , doi : 10.1055 / b-003-104359 ( limited preview in Google Book Search [accessed June 7, 2016]).
- ↑ Electricity accident. (PDF) DGUV. First Aid Department, September 2016, accessed January 30, 2017 .