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Adequate cerebral blood flow (CBF) must be maintained at all times in order to ensure the delivery of sufficient O2 and glucose to the brain. Fortunately we have automatic regulating systems which ensure adequate flow. The cerebral arterial vasculature is in a normal state of partial constriction and the CBF can be increased by vasodilation, which decreases cerebrovascular resistance. Likewise, increased vasoconstriction causes the cerebrovascular resistance to increase, producing a corresponding decrease in cerebral blood flow. Changes in cerebrovascular resistance and hence cerebral blood flow are caused by (1) fluctuations in perfusion pressure and (2) variations in circulating Po2, and Pco2.

bullet Changes in Perfusion Pressure

If we subtract intracranial pressure (ICP) from the mean arterial pressure (MAP), we obtain the effective perfusion pressure (PP) in the brain. Within physiological limits, changes in PP feed back negatively to change cerebrovascular resistance, thus maintaining a constant CBF. If the PP decreases, the expected drop in CBF is not realized because the automatic compensatory decrease in cerebrovascular resistance maintains blood flow near normal limits. Similarly, an increase in PP doesn't produce an increase in CBF because com­pensatory increases in cerebrovascular resistance again maintain the CBF at normal levels.

This auto regulating compensatory mechanism operates within the PP range of 50 to 180 mmHg. Since the cerebral vessels have presumably dilated maximally when the PP drops to 50 mmHg, further drops in pressure can't be compensated for, and CBF begins to fall accordingly (Fig. 17-4). Likewise, once the PP increases to around 180 mmHg, the vessels are maximally vaso­constricted and cannot compensate for further increases in pressure. Thus be­yond 180 mmHg the cerebral blood flow rises directly with the perfusion pressure.


bullet Changes in PO2 and PCO2

Decreases in arterial P02 produce no change in cerebrovascular resistance until the level falls to approximately 50 mmHg. Below this level we see vasodilation and an increase in CBF. When the P02 drops to 30 mmHg, the CBF reaches a level about 50 percent greater than normal. Increases in P02 above the normal level of 96 mmHg cause a slight increase in cerebrovascular resistance and a subsequent drop in CBF. It is interesting to note that the compensatory rise in CBF caused by falling O2 levels is greater than the drop in CBF caused by higher than normal O2 levels, once again stressing the importance the body puts on supplying adequate O2 to the brain.

Increases in arterial Pco, profoundly increase the CBF. Blood flow to the brain can be almost doubled by breathing 7 percent CO2, Conversely, hyper­ventilating can reduce the arterial Pco, sufficiently to drop the CBF from its normal 55 mL per 100 g per minute to 34 mL per 100 g per minute. It is not surprising to find that dizziness often occurs at this level when you consider that unconsciousness appears at 30 mL per 100 g per minute.

Because pH is profoundly influenced by Pco., through the reaction of CO2 with H20 to form H2C03 in the presence of the enzyme carbonic anhydrase, there has been some question as to whether the changes in vasomotor tone are due to CO2 or Hrions. Studies in which carbonic anhydrase has been poisoned by acetazolamide show that the normal effects of altered Pco, on vasomotor tone are eliminated. This would suggest that CO2 plays only an indirect role while it is actually the change in H + -ion concentration which is the directly act­ing agent. Further, since the application of acid to the cortex causes no vascular change nor do H+ ions freely enter cells while CO2 does, it is likely that in­tracellular rather than extracellular H+ ions are involved.


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Copyright [2007] [CNS Clinic-Jordan]. All rights reserved