Systemic hemodynamics and cerebral blood flow

A detailed discussion of cerebral circulation is given by Menon (1995). The cranial vault is a closed cavity, and intracranial pressure (ICP) has a major influence on cerebral blood flow (CBF). Consequently, unlike many other organs, the pressure driving cerebral perfusion is not the mean arterial pressure (MAP) but the cerebral perfusion pressure (CPP), which is defined as follows:

The cerebrovascular bed is capable of pressure autoregulation: changes in cerebral perfusion pressure are matched by changes in cerebrovascular resistance, so that cerebral blood flow remains constant (Fig 1(a)). When the capacity for autoregulatory changes in cerebrovascular resistance are exhausted, cerebral blood flow follows cerebral perfusion pressure and is said to be pressure passive. Even within autoregulatory limits, cerebral blood flow is closely coupled to neuronal activity, is exquisitely sensitive to changes in PaCO2 within the physiological range, and increases with severe hypoxemia (below a PaO2 of about 6.5 kPa).

Fig. 1 Schematic representation of the effect of changes in cerebral perfusion pressure (CPP) on cerebral blood flow (CBF), cerebrovascular resistance (CVR), and cerebral blood volume (CBV) within the limits of autoregulation (cerebrovascular resistance and cerebral blood volume curves are non-quantitative). (a) Cerebral blood flow is maintained when cerebral perfusion pressure changes by compensatory changes in cerebrovascular resistance. The changes in cerebrovascular resistance are caused by changes in cerebral vasomotor tone and hence are accompanied by changes in cerebral blood volume, which may have significant effects on intracranial pressure when intracranial compliance is reduced. These dynamic compensatory mechanisms do not operate effectively outside the limits of autoregulation, and reduction of cerebral perfusion pressure below the lower autoregulatory threshold will result in cerebral blood flow reductions and cerebral ischemia. In acute head injury this autoregulatory threshold may be elevated to 70 mmHg. (b) Reductions in cerebral perfusion pressure result in reductions in cerebrovascular resistance. The accompanying increases in cerebral blood volume cause elevation of intracranial pressure and further reduction in cerebral perfusion pressure. (c) Increases in cerebral perfusion pressure initiate vasoconstriction and hence reductions in cerebral blood volume and intracranial pressure.

These physiological relationships between cerebral perfusion pressure and cerebral blood flow may be seriously disrupted in disease. Experimental data suggest that while cardiac output may only be a minor determinant of cerebral blood flow in health, it may have a marked effect, independent of changes in cerebral perfusion pressure, on cerebral perfusion in disease. The response of the cerebral circulation to systemic hemodynamic changes may also be affected by drugs, including volatile anesthetic agents and systemic vasodilators (nitrates, nitroprusside). Regional flow may be affected by focal ischemia, intra- or extracranial occlusive vascular disease, or large-vessel spasm after subarachnoid hemorrhage. Clearly, many of these effects are focal or regional, and result in heterogeneity in cerebrovascular physiology. Under these circumstances assumptions about uniformity of the cerebrovascular effects of systemic hemodynamic changes may no longer hold true.

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