Cerebral AVMs have high flow, low resistance shunts that induce regional hemodynamic disturbances and possibly neural derangements. A better understanding of these mechanisms may help treatment planning and the management of complications after endovascular or surgical treatment.

Although the precise mechanisms of hemodynamic perturbation are still relatively unclear, the presence of chronic cerebral hypoperfusion is central and widely believed to be associated with both neurological deficits at presentation (‘steal‘) and ‘hyperemic’ complications following shunt obliteration. The ‘normal perfusion pressure breakthrough‘ (NPPB) theory states that chronic hypoperfusion around AVMs induces the loss of autoregulatory capability; following AVM shunt obliteration, perfusion pressure elevation induces an increase in flow, due to ‘vasomotor paralysis’, which can cause hemorrhage. The ‘dissociative vasoparalysis' theory suggests that vasodilation is preserved but not vasoconstriction. However, pharmacologic exploration of cerebral autoregulation with induced vasoconstriction (phenylephrine) and vasodilatation (acetazolamide) helps identify 3 patterns of autoregulatory behavior. The vast majority of AVM patients appear to retain autoregulatory capability, despite low arterial feeding pressures, consistent with a “shift to the left” of the autoregulation curve. Pronounced hypotension may “exhaust” cerebrovascular reserve in some patients, predisposing to hemorrhagic complications in the post-operative period. Lastly, “vasoparalysis” may coexist with a combination of vascular insult and marked hypotension.

Clinical presentation, AVM angioarchitecture and peri-operative physiologic data (especially feeding artery and venous outflow pressures) may assist patient management. Patients can be identified in whom staged treatment is recommended initially. Following AVM obliteration, the patient's hemodynamic response, which may range from a minimal increase in A-V pressure gradient to significant CBF increase may be predicted, and blood pressure, fluid and ICP management adjusted accordingly, as the monitoring of post-operative cerebral hemodynamics remains difficult. Extreme attention to endovascular and operative technique must be exercised, as technical problems can be devastating.

Although incompletely understood, hemodynamic derangements associated with cerebral AVMs increasingly appear to be associated with intact cerebral autoregulation in most patients. As cerebral hemodynamics monitoring remains challenging, clinical, angiographic and physiologic data from interventional/operative monitoring must be used to guide patient management.