History and exam
Other diagnostic factors
common
history of recurrent faints
Patients with NMRS often have a many-year history of recurrent faints, especially beginning before the age of 40 years.[2]
absence of structural heart disease
The presence of heart disease is an independent predictor of a cardiac cause for syncope (i.e., a primary arrhythmic cause or a cause based on a structural cardiac abnormality leading to a transient haemodynamic disturbance), with a sensitivity of 95% and a specificity of 45%; by contrast, the absence of heart disease excludes a cardiac cause of syncope in 97% of the patients.[23]
provocative factor
In vasovagal syncope, provocative factors include: unpleasant sights, pain from physical injury, fatigue, palpitations or bradycardia (consistent with but not diagnostic of vasovagal syncope), emotional stress, prolonged standing, dehydration, vigorous exercise (if syncope occurs post exercise).
In carotid sinus syndrome, there is a history of accidental manipulation of the neck that results in external pressure on the carotid sinus baroreceptors. Accidental manipulation of the neck can be as simple as a tight shirt collar or tie.
Situational syncope can be triggered by acute haemorrhage, a cough, a sneeze, gastrointestinal stimulation (swallow, defecation, visceral pain), micturition, post exercise, or other situations including brass instrument playing, weightlifting, or eating a meal (post-prandial).
nausea
A common premonitory symptom possibly of central nervous system origin, but may also be due to splanchnic bed venous dilation.
low risk for adverse outcomes
Patients with symptoms strongly suggestive of vasovagal, situational, or orthostatic faints (excluding perhaps older people with excessive injury risk) are considered low risk. After initial accident and emergency department assessment for syncope in the absence of evidence for structural heart disease, they can be referred for outpatient evaluation (preferably to a syncope clinic).
lightheadedness
A non-specific complaint suggesting a foggy sensation in the head. This may reflect some diminution of cerebral blood flow but not sufficient to cause a syncope. It is also a complaint that may have no relevance to syncope, being a common symptom particularly in older people. Lightheadedness occurs in many conditions and may not prove helpful. In addition, it tends to mean different things to different people.
pallor
This finding is characteristic of vasovagal faints; its absence should therefore make one question the diagnosis. However, the finding tends to be more apparent in white people and is less helpful in people with dark skin.
diaphoresis
The sensation of feeling sweaty and experiencing a coldness and/or clammy sensation is characteristic of vasovagal and closely related situational faints.
diminished vision or hearing
These are often early symptoms and although not diagnostic of vasovagal syncope per se, they are essential in order to consider that the patient's spell was indeed a true faint.
Typically, these symptoms occur immediately preceding (prodromal) or during a syncopal episode and are transient in nature.
physical injury
Pain of an injury may induce a vasovagal faint. In addition, signs of a traumatic injury (e.g., head laceration) may indicate true syncope rather than near syncope.
fatigue after episode
The presence of fatigue or tiredness after recovery from the event is an important clue to a vasovagal cause.
palpitations
Although slow (or relatively slow) heart rates are thought to be most characteristic of vasovagal events, the episodes typically begin with an early phase of sinus tachycardia. Consequently, palpitations at an early stage before collapse are common. Palpitations may occur before collapse in patients with tachyarrhythmia-induced faints as well. Thus, palpitations are consistent with, but not diagnostic of, vasovagal syncope.
bradycardia
Slow heart rates are a common finding at the time of vasovagal syncope. At times, the bradycardia may be dramatic (e.g., pauses of 5 to 25 seconds or longer), whereas at other times the heart rate may seem reasonable but is, in fact, much slower than appropriate for the degree of hypotension (i.e., predominantly vasodepressor form of vasovagal syncope). Bradycardia is common in neurally mediated reflex vasovagal syncope but may also indicate conduction system disease or excess drug effects.
absence of family history of sudden death
Vasovagal syncope is not usually associated with sudden death. Family history of sudden death should trigger concern about other diagnoses (e.g., structural heart disease, long QT syndrome, Brugada syndrome).
uncommon
neuralgia
Glossopharyngeal neuralgia is an unusual pain syndrome associated with syncope. The hallmarks of this syndrome are episodic sensations of usually left-sided pharyngeal pain that frequently result in syncope.[40]
Trigeminal neuralgia is a somewhat more common facial pain syndrome presenting with pain at one of the divisions of the trigeminal nerve. However, syncope resulting from trigeminal neuralgia is unusual and the pathogenesis is unclear.[41]
Risk factors
strong
prior syncope
Patients with NMRS often have a many-year history of recurrent faints, especially beginning before the age of 40 years.[2]
prior history of arrhythmias, myocardial infarction, heart failure, or cardiomyopathy
Patients with a known history of symptomatic bradycardiac and ventricular tachyarrhythmias, myocardial infarction, heart failure, or cardiomyopathy are at elevated risk for syncope.
severe aortic stenosis
Patients with severe aortic stenosis (with a large pressure gradient) are likely to be at an increased risk of syncope.
weak
prolonged standing
Associated with neurally mediated types of syncope.
emotional stress (especially in a warm, crowded environment)
Associated with neurally mediated types of syncope.
dehydration/hypovolaemia
Associated with neurally mediated types and orthostatic syncope.
preceding episode of nausea and/or vomiting
Associated with neurally mediated types of syncope.
preceding episode of severe pain
Associated with neurally mediated types of syncope.
Use of this content is subject to our disclaimer