Cerebral autoregulation testing after aneurysmal subarachnoid hemorrhage: The phase relationship between arterial blood pressure and cerebral blood flow velocity

Objective: Impairment of cerebral autoregulation (CA) appears to he an impo rtant cause for secondary ischemia after subarachnoid hemorrhage (SAH). It has been shown that graded CA impairment is predictive of outcome. Little i s known about whether such impairment is present, what causes GA impairment , whether it precedes vasospasm, and whether it is predictive of outcome in patients with severe aneurysmal SAH. Design: Prospective, controlled study. Setting: Neurosurgical intensive care unit. Patients: Twelve patients after aneurysmal subarachnoid hemorrhage, 40 cont rols. Interventions: Recording of cerebral blood flow Velocities and continuous m easurement of arterial blood pressure at a controlled ventilatory frequency of six per minute to standardize the influence of intrathoracic pressure c hanges on blood pressure. Measurements and Main Results: We calculated the phase shift angles (Delta phi degrees) between slow (0.1 Hz) arterial blood pressure and cerebral blo od flow velocity waves measured by transcranial Doppler ultrasound in the m iddle cerebral artery during a) posthemorrhage days (PHD) 1-6 (early or pre vasospasm phase), and b) during PHD 7-13 (late or vasospasm phase) using a 6/min ventilation protocol, and in 40 controls spontaneously ventilating at the same rate. Delta phi <30<degrees> indicated lost CA. Mean flow velocit ies >100 cm/sec were considered vasospasm. We combined early and late measu rements to assess the CA relationship with low cerebral perfusion pressure (cPP) and/or vasospasm. We assessed the Glasgow Outcome Scale (GOS) score a t discharge (1 = worst, 5 = best). The admission Hunt and Hess score was 3.6 +/- 0.7. GOS scores were n = 3 (G OS 1), n = 2 (GOS 2), n = 5 (GOS 3), n = 1 (GOS 4), and n = 1 (GOS 5). In t he early phase, Delta phi was 40.4 +/- 19.8 degrees (left), and 40.4 +/- 19 .2 degrees (right). CPP was 69.4 +/- 10.9, intracranial pressure (ICP) was 6.7 +/- 2.8 mm Hg. In the late phase, Delta phi worsened in six patients an d none improved: 32.1 +/- 21 degrees (left), and 26.9 +/- 17.2 degrees (rig ht); CPP was 68.1 +/- 12.1, ICP was 7.5 +/- 3.7 mm Hg. GA was significantly impaired in both phases when compared with normal subjects (Delta phi: 65. 7 +/- 24.5 degrees; p <.01 for early, p <.001 for late phase). In the early phase, seven of eight patients in whom autoregulation was intact had a GOS >2 at discharge and disturbed GA on at least one side was predictive of ei ther vegetative condition at discharge or death (p <.01). In the late phase , <Delta>phi was no longer predictive of outcome. Spasm was present in 8 of 17 vessels (47%) in which GA was lost; no spasm was found in 25 of 28 vess els (89%) in which CA was intact (p <.01). A low CPP was present in 6 of 17 Vessels (35%) in which CA was lost; a normal CPP was found in 21 of 27 ves sels (78%) in which CA was intact (p >.05, NS). However, 14 of 17 vessels ( 82%) with lost GA showed spasm and/or low CPP while only 8 of 27 Gases (30% ) with intact CA had either spasm or low CPP (p <.001). Conclusions: CA can he assessed in a graded fashion in SAH patients. GA imp airment precedes vasospasm; ongoing vasospasm worsens CA. CA assessment ear ly after subarachnoid hemorrhage, within PHD 1-6, is predictive of outcome whereas late assessment is not. GA impairment is associated with cerebral v asospasm and low CPP.