Cerebrovascular and cardiovascular responses associated with orthostatic intolerance and tachycardia.

Idiopathic orthostatic intolerance syndrome is characterized by postural symptoms of cerebral hypoperfusion without arterial hypotension. Abnormal baroreceptor responses with deranged cerebral autoregulation leading to cerebral vasoconstriction have been proposed as a causative mechanism. The authors report the cerebrovascular and cardiovascular responses in a patient who recovered from orthostatic intolerance and tachycardia. Changes in the orthostatic responses of mean arterial pressure (MAP), heart rate (HR), cardiac output (CO), and transcranial Doppler middle cerebral artery (MCA) mean blood flow velocity (Vmean) were assessed at admission and again 6 months after recovery. Normal cardiovascular responses to forced breathing and to standing indicated intact overall baroreflex integrity with normal baroreflex sensitivity (10.2 msec.mm Hg(-1)). After the patient stood for 8 minutes, presyncopal symptoms developed, with unchanged MAP but increased HR (+41 beats/min) and reduced stroke volume (SV) (-69%), CO (-50%), and MCA Vmean (-46%; 57 to 31 cm. s(-1)). After a reconditioning program and recovery, the patient was reexamined. The supine MCA Vmean was larger (79 cm. s(-1)), as were MAP (76 versus 70 mm Hg) and CO (+15%). The orthostatic HR increase was smaller (+5 beats/min), as was the reduction in SV (-44%) and CO (-30%), with an increase in MAP to 93 mm Hg. The orthostatic reduction in MCA Vmean was smaller (-13 versus -26 cm.s(-1)) and standing cerebrovascular resistance decreased (1.41 versus 2.39 mm Hg.cm. s(-1)). In this patient who had intact baroreflex control and no postural decrease in blood pressure, the reduction in MCA Vmean, concomitant with a large decrease in CO, seemed reversible. The result suggests that a symptomatic reduction in cerebrovascular conductance during standing is to be interpreted as being an adaptive response to a critically limited systemic blood flow, rather than to derangement of cerebral autoregulation.