P. ALBONI, M. DINELLI, F. PACCHIONI
Syncope is a symptom, defined as transient, self-limited loss of conscious- ness, usually leading to a fall. The onset of syncope is relatively rapid, and the subsequent recovery is spontaneous, complete, and usually prompt. The underlying mechanism is a transient global cerebral hypoperfusion. The subdivision of syncope is based on the pathophysiology as follows [1]:
- Neurally mediated reflex syncope - Orthostatic hypotension
- Cardiac arrhythmias as a primary cause
- Structural cardiac or cardiopulmonary disease and steal syndromes (when a blood vessel has to supply both parts of the brain)
Syncope must be differentiated from other ‘non-syncopal’ conditions (i.e.
those not secondary to global cerebral hypoperfusion) associated with real or apparent loss of consciousness, such as epilepsy, hypoglycaemia, hypoxia, vertebrobasilar transient ischaemic attack, fall, cataplexy, drop attack, and psychogenic pseudo-syncope.
It is commonly accepted that taking the history is an essential part of the work-up of patients with transient loss of consciousness. The historical find- ings per se may be diagnostic of the cause of syncope, or may suggest a strat- egy of evaluation. The clinical features of the presentation are most impor- tant, especially factors that might predispose to syncope and its sequelae.
Some attempts have been made to validate the diagnostic value of the history in prospective and case-control studies [2–6]. When taking a history, all the items listed in Table 1 should be carefully investigated [1]. Moreover, three key questions should be addressed during the initial evaluation: (1) Is the loss of consciousness attributable to syncope or not? (2) Is heart disease pre- sent or absent ? (3) Are there important clinical features in the history that suggest the diagnosis?
Division of Cardiology and Arrhythmologic Centre, Ospedale Civile, Cento (Ferrara), Italy
With regard to the first question, the most frequent cause of non-synco- pal loss of consciousness appears to be epilepsy. The diagnosis of the latter is generally easy if loss of consciousness is observed by an eyewitness. Clinical features suggesting epilepsy are as follows: tonic-clonic movements which are usually prolonged (> 15 s) and whose onset coincides with loss of con- sciousness, hemilateral clonic movements, tongue biting, blue face, typical aura, prolonged confusion, aching muscles, and ‘pins and needles’ before the event.
With regard to the second question, it is important to evaluate the pres- ence of heart disease, not only because of its prognostic significance, but because with few exceptions its absence excludes a cardiac cause of syncope.
Table 1.Important features in the history
Questions about circumstances just prior to attack Position (supine, sitting, or standing)
Activity (rest, change in posture, during or after exercise, during or immediately after urination, defecation, coughing, or swallowing)
Predisposing factors (e.g. crowded or warm places, prolonged standing, postprandial period)
Precipitating events (e.g. fear, intense pain, neck movements)
Questions about onset of attack
Nausea, vomiting, abdominal discomfort, feeling cold, sweating, aura, pain in neck or shoulders, blurred vision, chest pain, palpitations
Questions about the attack (eye witness)
Manner of fall (slumping or keeling over), skin colour (pallor, cyanosis, flushing), duration of loss of consciousness, breathing pattern (snoring), movements (tonic, clonic, tonic-clonic or minimal myoclonus, automatism) and their duration, onset of movement in relation to fall, tongue biting
Questions about the end of the attack
Nausea, vomiting, feeling cold, sweating, confusion, muscle aches, skin colour, injury, chest pain, palpitations, urinary or faecal incontinence
Questions about the background Family history of sudden death Previous cardiac disease
Neurological history (parkinsonism, epilepsy, narcolepsy) Metabolic disorders (diabetes, etc.)
Medication (antihypertensive, anti-anginal, antidepressant agent, anti-arrhythmic, diuretics, and QT prolonging agents)
(In the case of recurrent syncope:) Information on recurrences such as the time from the first syncopal episode and the number of spells
In fact, in a recent study [5], heart disease was an independent predictor of cardiac cause of syncope, with a sensitivity of 95% and a specificity of 45%;
by contrast, the absence of heart disease allowed exclusion of a cardiac cause of syncope in 97% of the patients.
Finally, accurate history taking alone may allow diagnosis of the cause of syncope or may suggest an evaluation strategy. The results of the initial eval- uation are diagnostic of the cause of syncope in the following situations [1]:
- Vasovagal syncope is diagnosed if precipitating events such as fear, severe pain, emotional distress, instrumentation, or prolonged standing are associated with typical prodromal symptoms.
- Situational syncope is diagnosed if syncope occurs during or immediate- ly after urination, defecation, cough, or swallowing.
- Orthostatic syncope is diagnosed when there is documentation of ortho- static hypotension associated with syncope or presyncope. Orthostatic blood pressure measurements are recommended after 5 min of lying supine, followed by measurements each minute, or more often, after standing for 3 min. Measurements may be continued for longer, if blood pressure is still falling at 3 min. If the patient does not tolerate standing for this period, the lowest systolic blood pressure during the upright pos- ture should be recorded. A decrease in systolic blood pressure ≥ 20 mmHg or a decrease of systolic blood pressure to < 90 mmHg is defined as orthostatic hypotension regardless of whether or not symptoms occur.
- Cardiac-ischaemia-related syncope is diagnosed when symptoms are pre- sent with electrocardiographic evidence of acute ischaemia with or with- out myocardial infarction, whatever its mechanism.
Under these circumstances, no further evaluation of the disease or disor- der may be needed and treatment, if any, can planned. More commonly, the initial evaluation leads to a suspected diagnosis, when one or more of the following features are present:
- Neurally mediated syncope: absence of cardiological disease; long history of syncope after sudden unpleasant sight, sound, smell, or pain; pro- longed standing or crowded, hot places; nausea, vomiting associated with syncope during the meal or in the absorptive state after a meal; with head rotation; pressure on carotid sinus; after exertion.
- Syncope due to orthostatic hypotension: after standing up, temporal rela- tionship with start of medication leading to hypotension, prolonged standing especially in crowded, hot places, presence of autonomic neu- ropathy or parkinsonism, after exertion.
- Cardiac syncope: presence of definite structural heart disease, during exertion or supine, preceded by palpitation, family history of sudden death.
- Cerebrovascular syncope: with arm exercise, differences in blood pressure or pulse in the two arms.
It should be underlined that neurally mediated syncopes (tilt-induced, carotid sinus) show very similar clinical features, apart from classical vaso- vagal syncope [7]. In the presence of clinical features suggesting a cardiac cause of syncope, the first examinations to be performed are the cardiologi- cal ones (echocardiography, prolonged electrocardiographic monitoring, etc.), whereas in the presence of features suggesting a neurally mediated syn- cope, the first examinations to be performed are the autonomic tests (tilt testing, carotid sinus massage). Therefore, a careful history can optimise the work-up of syncope, avoiding useless tests and reducing the high diagnostic costs in patients with syncope.
Data from seven population-based studies showed that the history and physical examination identified a potential cause of syncope in 726 of 1607 patients (45%) whose primary disorder can be diagnosed [1]. However, the diagnostic criteria for vasovagal syncope, which represents the most fre- quent cause of loss of consciousness, have been varied among studies and, probably, too extensive criteria have been used. In more recent studies [5, 8], history and physical examination identified a potential cause of syncope in 15–20% of patients.
History appears more useful in the younger than in the elderly (≥ 65 years); in fact a possible cause of syncope was suggested on the basis of the history in 32% of the former and in only 6% of the latter [8]. The clinical manifestations of syncope change significantly in elderly patients, since dur- ing the prodromal and recovery phase the frequency of symptoms (predomi- nantly the autonomic ones) decreases in older patients, thus reducing the utility of the history.
References
1. Brignole M, Alboni P, Benditt DG et al (2004) Guidelines on management (diag- nosis and treatment) of syncope. Update 2004. Europace 6:467–537
2. Kapoor WN, Karf M, Wieand S et al (1983) A prospective evaluation and follow- up of patients with syncope. N Engl J Med 309:197–204
3. Martin GJ, Adams SL, Martin HG et al (1984) Prospective evaluation of syncope.
Ann Emerg Med 3:499–504
4. Calkins H, Shyr Y, Frumin H et al (1995) The value of clinical history in the dif- ferentiation of syncope due to ventricular tachycardia, atrioventricular block and neurocardiogenic syncope. Am J Med 98:365–373
5. Alboni P, Brignole M, Menozzi C et al (2001) Diagnostic value of history in patients w ith sy ncope w ith or w ithout heart disease. J Am Coll Cardiol 37:1921–1928
6. Sheldon R, Rose S, Ritchie D et al (2002) Historical criteria that distinguish syn- cope from seizures. J Am Coll Cardiol 40:142–148
7. Alboni P, Brignole M, Menozzi C et al (2004) Clinical spectrum of neurally medi- ated reflex syncopes. Europace 6:52–56
8. Del Rosso A, Alboni P, Brignole M et al (2004) The clinical presentation of syn- cope depends on the age of the patients (submitted for publication)
