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A recurrent concern is that of acceptable levels of blood pressure reduction in chronically hypertensive patients. Firm guidelines have not been established. However, from the vantage of cerebral well-being, limiting elective MAP reduction to 30% to 35% of resting mean levels seems appropriate for both hypertensive and normotensive patients. It is reasonable that the same guidelines might apply in both populations because in chronic hypertension, both the upper and lower limits of autoregulation are shifted to the right with apparently little distortion.[54]
The rationale for a limit of 30% to 35% is as follows. It has been demonstrated that MAP reductions of 50% in nonanesthetized patients, both normotensive and hypertensive, will commonly produce reversible symptoms of cerebral hypoperfusion. [54] [585] [586] Although even greater reductions will probably be tolerated, provided that exposure is brief, the hematocrit is reasonable, and the cerebral vasculature is patent, we counsel against it. A reduction in MAP of this magnitude will result in the patient, normal or hypertensive, "falling off" the lower end of the autoregulatory plateau. It has been demonstrated that a reduction in MAP of 25% will bring both normotensive and hypertensive patients to the LLA.[54] As the reduction in MAP exceeds 25% of baseline, CBF values will be below normal, albeit in subjects free of occlusive vascular disease, but above the threshold for neurophysiologic dysfunction or injury (see Fig. 21-4 ). However, physiologic reserve is being encroached on, with little margin left for error or for other causes of impaired cerebral oxygen delivery (low hematocrit, unrecognized cerebrovascular disease).
It has been demonstrated in animals that treatment of chronic hypertension can restore the LLA to normal.[587] [588] A similar phenomenon has been observed in humans by Strandgaard, although restoration was incomplete and failed to occur after as long as 12 months of treatment in some subjects.[54] It is an unexplored possibility that the extent of restoration of the LLA with antihypertensive therapy is agent dependent. Some may restore the LLA more effectively than others do. In particular, angiotensin-converting enzyme inhibitors have been shown to decrease the LLA acutely in both normotensive and hypertensive subjects.[55] [589]
Control of intracranial hypertension is discussed in detail in Chapter 53 .
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