The blood pressure and baroreceptor changes following acute stroke

This thesis examines aspects of blood pressure (BP) and its control in clinical studies during the acute and subacute phases of stroke.;Casual and 24-hour BP levels fall spontaneously during the first week following acute stroke. Higher 24-hour systolic BP (SBP) levels within the first 24 hours of ictus are associated with an increased likelihood of poor short-term outcome, whether assessed by death, dependency in activities of daily living or neurological outcome.;Following acute stroke, not only are BP levels raised, but there is an increase in short-term SBP variability. This may reflect an impairment in cardiac baroreceptor sensitivity, as assessed by time and frequency domain analysis techniques. There is no evidence of increased sympathetic nervous system activity (SNSA) in acute stroke patients compared to control subjects as reflected by the ratio of low-to-high frequency pulse interval variability (a surrogate market of SNSA), though this ratio was altered in favour of sympathetic predominance in right compared to left hemisphere strokes. Changes in autonomic control of BP variability are seen in the high frequency region following acute stroke, probably reflecting the mechanical effects of respiration.;However, an impairment in baroreceptor-mediated vasomotor control also appears to be present in the acute stroke period, as demonstrated by impaired forearm vascular resistance (FVR), responses to hypotensive lower body negative pressure. Furthermore, BP falls significantly in response to orthostatic, but not postprandial, stress in stroke patients, with no significant change in FVR.;Acute stroke is associated with increased BP levels which convey an adverse prognosis. This and the increased short-term BP variability after acute stroke may be related to changes in both cardiac baroreceptor sensitivity and control of vasomotor tone in the post-ictal period.