2000•Cerebrovascular DiseasesRequires access

A Case of Arrhythmia-Induced Transient Cerebral Hyperaemia

Brian J. Carey, Penelope J. Eames, Ronney Bernardes Panerai, John F. Potter

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Abstract

Transient cerebral hyperaemia following an arrhythmia has not been previously demonstrated in humans. We report the effects of head-up tilt on a 78-year-old man with neurocardiogenic syncope. During tilt, an asymptomatic arrhythmia caused arterial blood pressure and transcranial Doppler-recorded cerebral blood flow velocity to fall markedly. Upon spontaneous resumption of sinus rhythm, cerebral blood flow velocity increased to values greater than those prior to the arrhythmia. This occurred prior to a full recovery of arterial blood pressure, indicating spontaneous transisent hyperaemia. Pressure-flow velocity graphs support current methods of measuring critical closing pressure and demonstrate a rise in critical closing and a fall in resistance-area product after the arrhythmia.

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Transient cerebral hyperaemia following an arrhythmia has not been previously demonstrated in humans. We report the effects of head-up tilt on a 78-year-old man with neurocardiogenic syncope. During tilt, an asymptomatic arrhythmia caused arterial blood pressure and transcranial Doppler-recorded cerebral blood flow velocity to fall markedly. Upon spontaneous resumption of sinus rhythm, cerebral blood flow velocity increased to values greater than those prior to the arrhythmia. This occurred prior to a full recovery of arterial blood pressure, indicating spontaneous transisent hyperaemia. Pressure-flow velocity graphs support current methods of measuring critical closing pressure and demonstrate a rise in critical closing and a fall in resistance-area product after the arrhythmia.

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Available abstract

Transient cerebral hyperaemia following an arrhythmia has not been previously demonstrated in humans. We report the effects of head-up tilt on a 78-year-old man with neurocardiogenic syncope. During tilt, an asymptomatic arrhythmia caused arterial blood pressure and transcranial Doppler-recorded cerebral blood flow velocity to fall markedly. Upon spontaneous resumption of sinus rhythm, cerebral blood flow velocity increased to values greater than those prior to the arrhythmia. This occurred prior to a full recovery of arterial blood pressure, indicating spontaneous transisent hyperaemia. Pressure-flow velocity graphs support current methods of measuring critical closing pressure and demonstrate a rise in critical closing and a fall in resistance-area product after the arrhythmia.

Key concepts: Hyperaemia, Medicine, Cardiology, Critical closing pressure, Cerebral blood flow, Asymptomatic, Blood pressure, Internal medicine

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