CO2 reactivity of cerebral vasospasm after aneurysmal subarachnoid haemorrhage.
CO2 reactivity of the brain vessels was investigated in 33 patients (Grade I-III after Hunt and Hess) with cerebral vasospasm after an aneurysmal subarachnoid haemorrhage (SAH) and after early operation within 72 hours. In all cases, transcranial Doppler sonography was used to measure flow velocities in the middle cerebral artery (MCA) and internal carotid artery (ICA) and vasomotor reactivity to CO2 changes. Vasospastic conditions lead to higher flow velocities through the narrow segment, lower peripheral stream resistance due to the post-stenotic pressure drop and lower vasodilating capacities of arterioles under hypercapnia. In severe vasospastic conditions, the peripheral stream bed is already maximally dilated and the hypercapnic response is weak. On the other hand, the peripheral vascular bed reacts normally to hypocapnia in all vasospastic situations. Our results point out two dangerous conditions of vasospastic disease: 1) exhaustion of peripheral vasodilating capacities, and 2) hyperventilatory therapy. Both of these situations can result in a reduction of CBF to brain tissue, mainly for two reasons: 1) In the former, a further increase in vasospasm cannot be compensated for anymore when the peripheral arterioles are maximally dilated, and 2) in the latter, hypocapnia produces a strong peripheral vasoconstrictor response with further reduction of CBF.
Hassler
W
W
Department of Neurosurgery, University of Tübingen, Federal Republic of Germany.
Chioffi
F
F
D001783:Blood Flow Velocity; D002245:Carbon Dioxide; D006801:Humans; D002532:Intracranial Aneurysm / Q000150:complications; D002546:Ischemic Attack, Transient / Q000175:diagnosis / Q000209:etiology / Q000503:physiopathology*; D013345:Subarachnoid Hemorrhage / Q000150:complications* / Q000209:etiology; D014465:Ultrasonics; D014655:Vascular Resistance
D002245:Carbon Dioxide