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Emphasizes cerebral perfusion in syncope evaluation; leaves open targeted interventions pending prospective validation.
Syncope is a transient loss of consciousness secondary to inadequate cerebral perfusion with oxygenated blood. It is a common medical problem, accounting for around 5% of acute medical admissions and 3% of emergency department visits.1 Syncope secondary to cardiac causes carries the worst prognosis, with a one year mortality rate of 20–30%.2 An understanding of the events preceding syncope is essential if the correct diagnostic strategy is to be implemented. A state of consciousness is maintained by adequate cerebral blood flow. Cerebral vascular autoregulation ensures that the cerebral blood flow is kept within a narrow range, independent of the underlying systemic blood pressure. In a young healthy adult the systolic blood pressure may fall to 70 mm Hg without significant cerebral ischaemia.3 Elderly people and those with chronic hypertension are susceptible to relatively small falls in systemic blood pressure, leading to an increased incidence of syncope in this population.4 #### Box 1: Neurally mediated reflex syncopal syndromes The term “vasovagal” as applied to syncope has been used since the early 1900s and has become synonymous with the common “faint”.5 Early studies found that vasovagal syncope was the most common cause of fainting, being found in 58% of patients who had experienced this symptom.6 As our understanding of human neuroautonomic regulation has evolved it has become apparent that the vasovagal episode, although the most common, is one of a number of neurally …
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W Arthur (2000) studied this question.
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