Syncope is defi ned by a sudden loss of consciousness (seconds to 3 minutes) with breakdown of muscle tone resulting in a fall and then a rapid return of consciousness. The total amnesia of the fall can cause trauma.
Faintness generally refers to the symptoms présyncopaux combining a general ill feeling, dizziness, visual veil.
Often the syncopal phase does not occur when the patient lies down.
Faintness and syncope have the same etiology, but a cardiac faintness is exceptional.
This is a common cause of consultation with a general practitioner or an emergency department (nearly 10% of patients).
DIAGNOSIS OF SYNCOPE:
Syncope is a sudden loss of complete knowledge and brief in connection with a reduction in cerebral blood flow.
The questioning of the patient and potential witnesses, careful clinical examination (neurological examination, cardiac auscultation, pulse and management of lying and standing blood pressure), and the realization of an electrocardiogram (ECG) will establish a diagnosis immediate or predict later explorations.
We must quickly distinguish syncope from epileptic seizure. This exercise is not always easy in the absence of reliable witness, especially as hypertonic pseudoconvulsifs generalized movements may occur during syncope for more than a few seconds.
Epilepsy is characterized by a long period of unconsciousness (> 3 minutes), disorientation after the event, with a gradual return to consciousness.
The occurrence of context oriented towards the diagnosis of syncope: severe pain, violent efforts, urination or defecation, etc. Similarly, nausea and sweating are usually associated with syncope. The loss of urine during the event and tongue biting are not, for their specific epilepsy.
The most common causes are the vasovagal malaise, cardiac arrhythmias and orthostatic hypotension. However, in about one third of cases, syncope may not have immediate explanation.
The persistence of symptoms after the event (dyspnea, chest or abdominal pain, neurological disorders, infectious state, etc.) Out of this framework and should lead to etiological research guided by clinical history.
Vasovagal syncope or vasovagal:
This is the most frequent syncope. It is easily recognizable when all the symptoms are present.
This is often a subject young and anxious or tired without associated pathology.
There is often a precipitating factor: prolonged standing, heated atmosphere, emotion, severe pain, or competition or defecation. Then there are prodromal type of important sweating, pale skin, dizziness with tinnitus, blurred vision.
At this stage, the patient may eventually eliminate symptoms by lying on the ground.
Then, syncope can occur with bradycardia and hypotension. The duration of syncope is usually short with a very rapid return to full consciousness. Vagal equivalent can meet during the Valsalva-type efforts (micturition syncope or during defecation, laryngeal stroke chronic bronchitis, effort syncope during a violent sporting effort, hyperventilation syncope during the crisis spasmophilia).
When the vagal is typical there is no need to further explore, except by performing an ECG if there was a true syncopal phase.
However, many are syncope vasovagal origin, but diagnosis more difficult and less certain in the absence of prodromal symptoms.
The vagal origin can then be detected either by replicating the carotid sinus massage either on tilting table (Tilt test).
These maneuvers are only offered to repetitive unexplained syncope, socially or professionally embarrassing. In this context, the tilting table, which can be sensitized by the pharmaceutical adding isoproterenol (Isuprel) or nitroglycerin, has a good diagnostic yield (about 75 to 80% of positive test in case of vasovagal syncope with good specificity).
The medical management of vagal discomfort usually to reassure the patient about the benign origin of its symptoms. In case of repeated episodes, a mild sedative or beta-blocker treatment can be discussed. The placement of a pacemaker was proposed for severe and disabling vagal syncope. Its indication is very limited and the effectiveness of such a therapeutic proof.
Syncope in the elderly patient or suffering from atherosclerosis, occurring in evocative circumstances (cervical shaving, local shock carotid forced movement of the head, brain tumor compressive, etc.), Equivalent to a vasovagal syncope related to the sinocarotidienne hypersensitivity.
The knowledge cardiac losses should be suspected when the patient has a known heart disease detected during the clinical examination, and / or the basal electrocardiogram reveals anomalies.
Knowledge losses occurring in the effort may be a mode of revelation of aortic stenosis, especially in the elderly, or hypertrophic cardiomyopathy in younger subject. Other cardiac causes of syncope effort are rarer: obesity, congenital heart disease.
Syncope by arrhythmia or conduction are not specifically related to the effort syncope. Bradyarrhythmias by nodal abnormalities, ventricular tachycardia or supraventricular are diagnosed by ECG. The recognition of QT prolongation will seek torsade de pointes.
Recall the severity of cardiomyopathy amylose with arrhythmias and conduction sometimes causing syncope or sudden death.
The treatment of torsades de pointes based on stopping drugs that prolong the QT and / or correction of hypokalemia. In other cases, we discuss the pacemaker implantation, often after electrophysiological study.
Brugada syndrome is a condition involving severe ventricular rhythm, responsible for syncope and sudden death, and electrical anomalies. This syndrome is not associated with morphological abnormalities of the heart. It is genetic (causing abnormal sodium transport), and is transmitted in an autosomal dominant fashion. It turns out most often at maturity (40 years) with a male predominance (9 men to 1 woman). The diagnostic criteria based on the presence of a family history of sudden death, and compatible electrical anomalies:
– Recording potential of ventricular tachycardia or ventricular fibrillation polymorph;
– Basal ECG finding a block of appearance right branch with J point elevation, ST segment elevation from V1 to V3 or concave ST segment elevation in addition to previous bypass giving a “saddle” appearance.
Treatment: the very high excess mortality from sudden death in patients with Brugada syndrome requires the use of specialized explorations to recognize this syndrome and provide appropriate therapy (currently establishment of an implantable defibrillator challenge).
It is important to note that cardiac syncope are mainly found in patients with risk factors: heart failure, ischemic heart disease associated abnormal electrocardiogram.
Other causes of syncope:
Syncope associated with orthostatic hypotension should be routinely screened during the clinical examination by the decrease in the 3 minutes of the PAs orthostatic> 20 mmHg or PAd> 10 mmHg.
The causes acceleration of heart rate are usually: drugs, the presence of varicose veins, prolonged bed rest, an extracellular dehydration or pregnancy.
If the heart rate is not changed orthostatic, it should seek dysautonomia (diabetic neuropathy, Parkinson’s, Shy-Dragger, amylose, especially type AL [primary amyloidosis] or by mutation of the transthyretin).
Syncope occurring in a context of acute hypoxia and / or low cardiac output (pulmonary embolism, carbon monoxide poisoning) and original cerebrovascular syncope are detected by the persistence of symptoms after the malaise.
The dropp-attack (sudden fall on knees giving way lower limb) is not usually accompanied by a loss of consciousness.
Metabolic causes (hypoglycemia, severe hypocalcemia, acute alcohol poisoning) are easy to identify in young subjects. In elderly patients, the achievement of biology, possibly including the alcohol, can be helpful.
The psychosomatic origin, affecting young subjects during a violent emotional trauma, remains a difficult diagnosis of exclusion. But this diagnosis is yet to 5% syncopation for which no other cause was found.
Once the diagnosis of syncope established, three cases of major figures are presented to physicians:
– It is vagal syncope absolutely classic No further investigation is recommended.. Preventive measures are based predominantly on the information of the subject;
there is no evidence to affirm vagal syncope but were eliminated on questioning: the seizure and origin extracardiac syncope. The subject is young (<45 years). There is no known heart disease.
The ECG is normal. The only recommended further evaluation is the realization of a heart ultrasound that will stop the balance sheet if it proves normal. Only if these episodes are repeated frequent and severe manner appropriate to pursue a comprehensive etiological beginning with the completion of an EEG and by seeking hyperresponsiveness sinocarotidienne (or carotid massage table ‘better angle);
– This is a patient with cardiovascular risk factors or abnormalities in the electrical recording. A complete cardiac evaluation in search of a rhythm or conduction disorder must be achieved.
The need for hospitalization for syncope is dependent on the potential risk of occurrence of sudden death. This is essentially the prerogative of the patient with an arrhythmia intracardiac on preexisting heart disease.
Therefore, hospitalization with scope for 24 hours and cardiological explorations necessary.