Autoregulation is the maintenance of constant cerebral blood flow (CBF) over a range of cerebral perfusion pressure (CPP). Cerebral perfusion pressure is defined as mean arterial pressure (MAP)−central venous pressure (CVP) or intracranial pressure (ICP) or cerebral venous pressure (cVP), whichever is greatest. Because ICP, CVP, and cVP are usually less than 10 mm Hg in the healthy brain, MAP is the main driving force for CPP. In light of this, autoregulation is often depicted as maintenance of constant CBF over range of MAP usually 50-150 mm Hg (Figure 118-1).
Relationship between CBF and MAP. (Reproduced with permission from Butterworth JF, Mackey DC, Wasnick JD, Morgan and Mikhail’s Clinical Anesthesiology, 5th ed. McGraw-Hill; 2013.)
To keep CBF constant, compensatory changes in vasomotor tone are made in response to changes in CPP or MAP. When CPP increases, cerebral vascular resistance increases. Likewise, when CPP decreases, cerebral vascular resistance decreases. It may take up to a minute for these compensatory changes to initiate. Hence, for brief periods there may be changes in CBF with swings in blood pressure even within the limits where there is usually autoregulation.
For individuals who are chronically hypertensive, the autoregulatory curve is shifted to the right for both the upper and lower limits. These individuals are at risk of experiencing cerebral hypoperfusion and ischemia with blood pressures that would be considered acceptable for individuals without hypertension.
Autoregulation may be impaired or nonexistent in or around areas of the brain with relative ischemia, surrounding mass lesions, following brain injury, during the postictal state, or during periods of hypoxemia, or hypercarbia. Patients are susceptible to new or worsening injuries from swings in blood pressure.
EFFECTS OF ANESTHETIC AGENTS
The degree to which the cerebral vasculature tone can be altered to facilitate autoregulation while under anesthesia is influenced by background factors that also alter vascular tone. Such factors include hypercapnea, hypocapnea, temperature, cerebral metabolic rate, and neuronal activation. All of these factors must be taken into consideration when assessing the effect of anesthesia on cerebral autoregulation. For example, when administered alone, volatile anesthetics impair cerebral autoregulation in a dose-dependent manner such that as the dose of the anesthetic is increased the level of impairment increases. Autoregulation may be completely abolished at very high doses. The effect is different for each agent. Nitrous oxide causes significant cerebral vasodilation and increase in CBF. This effect can be attenuated by other anesthetic agents or by hyperventilation. Cerebral autoregulation is preserved with intravenous induction agents. Opioids generally do not affect cerebral autoregulation