It is based on a careful history and physical examination including orthostatic blood pressure measurements. Apart from young patients without heart disease, a 12-lead ECG should usually be part of the general evaluation of patients.
Three key questions should be addressed during the initial evaluation :
1. Is loss of consciousness attributable to syncope or not? Differentiating true syncope from ‘non-syncopal’ conditions associated with real or apparent transient loss of consciousness is generally the first diagnostic challenge and influences the subsequent diagnostic strategy.
2. Are there features in the history of the patient that suggest the diagnosis? Accurate history taking alone is a key stage and often leads to the diagnosis or may suggest the strategy for evaluation.
3. Is heart disease present or absent ? The absence of signs of suspected or overt heart disease virtually excludes a cardiac cause of syncope with the exception of syncope accompanied by palpitations which could be due to paroxysmal tachycardia (especially paroxysmal supraventricular tachycardia). Conversely, the presence of heart disease at the initial evaluation is a strong predictor of a cardiac cause of syncope, but its specificity is low - about half of patients with heart disease have a non-cardiac cause of syncope.
Differentiating syncope from non-syncopal loss of consciousness
Causes of syncope are: Neurally-mediated (reflex) syncopal syndromes, Orthostatic, Cardiac arrhythmias as primary cause and Structural cardiac or cardiopulmonary disease.
Whatever the mechanism of syncope is in a any given clinical circumstance, it is a transient global cerebral hypoperfusion (most often due to diminished systemic arterial pressure) that is the principal factor leading to loss of consciousness.
It is the global cerebral hypoperfusion that differentiates syncope from the non-syncopal causes of transient loss of consciousness in which the disorder of consciousness is not associated with decreased cerebral blood.
Several disorders may resemble syncope in two different ways. In some, consciousness is truly lost, but the mechanism is not related to cerebral hypoperfusion: epilepsy, metabolic disorders (including hypoxia and, hypoglycaemia), intoxications and transient ischemic vertebro-basilar attacks.
In several other disorders, consciousness is only apparently lost; this is the case in 'psychogenic pseudo-syncope', cataplexy and drop attacks.
Certain diagnosis at initial evaluation
Initial evaluation may lead to a certain diagnosis (no further evaluation may be needed and treatment can be planned), in the following situations:
• Vasovagal syncope: if precipitating events such as fear, severe pain, emotional distress, instrumentation or prolonged standing are associated with typical prodromal symptoms.
• Situational syncope: if syncope occurs during or immediately after urination, defaecation, cough or swallowing.
• Orthostatic syncope: when there is documentation of orthostatic hypotension associated with syncope or pre-syncope. A decrease in systolic blood pressure >20 mmHg or a decrease of systolic blood pressure to <90 mmHg measured after 1 or 3 min of standing is defined as orthostatic hypotension regardless of whether or not symptoms occur.
• Cardiac ischaemia-related syncope: when symptoms are present with ECG evidence of acute ischaemia with or without myocardial infarction, independently of its mechanism.
• Arrhythmia-related syncope in presence of the following ECG abnormalities:
- Sinus bradycardia <40 beats/min or repetitive sinoatrial blocks or sinus pauses >3 s in the absence of negatively chronotropic medications
- Mobitz II 2nd or 3rd degree atrioventricular block
- Alternating left and right bundle branch block
- Rapid paroxysmal supraventricular tachycardia or ventricular tachycardia
- Pacemaker malfunction with cardiac pauses
Suspected diagnosis at initial evaluation
Commonly, initial evaluation leads to a suspected diagnosis which needs to be confirmed by other investigations.
The presence of suspected or certain heart disease is associated with a higher risk of arrhythmias and mortality at one year. In these patients, cardiac evaluation (echocardiography, stress testing, electrophysiological study and prolonged ECG monitoring including loop recorder) is recommended.
If cardiac evaluation does not show evidence of arrhythmia as a cause of syncope, evaluation for neurally-mediated syndromes is recommended only in those with recurrent or severe syncope. It includes tilt testing, carotid sinus massage, ECG monitoring, and often further necessitates of implantation of an Implantable Loop Recorder (ILR).
The majority of patients with single or rare episodes in this setting have a high likelihood of neurally-mediated syncope and tests for confirmation are usually not necessary.
If the diagnosis is confirmed, treatment may be initiated; if not, a reappraisal process may be useful.
The cause of syncope may remain unexplained after the initial evaluation.
The strategy varies according to the severity and frequency of the episodes.
For patients with unexplained syncope the most likely diagnosis is neurally-mediated for which the appropriate tests are described above. The majority of patients with single or rare episodes in this category probably have neurally-mediated syncope and tests for confirmation are usually not necessary.
Once the evaluation is completed and the cause of syncope is undetermined, re-appraisal of the work-up is needed since subtle findings or new historical information may change the strategy.
Re-appraisal may consist of obtaining additional details of history and re-examining the patient, placement of an ILR if not previously undertaken, as well as review of the entire work-up.
If new clues to possible cardiac or neurological disease are yielded, further cardiac and neurological assessment are recommended. In these circumstances, consultation with appropriate specialists may be useful.
Psychiatric assessment is recommended in patients with frequent recurrent syncope who have multiple other somatic complaints and when initial evaluation raises concerns about stress, anxiety and possible other psychiatric disorders.
The content of this article reflects the personal opinion of the author/s and is not necessarily the official position of the European Society of Cardiology.