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michigan hypertension core curriculum - State of Michigan

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Clinical Implications: In the setting <strong>of</strong> chronic, poorly controlled <strong>hypertension</strong> rapid reductions in<br />

BP can lead to cerebral ischemia attributable to reductions in cerebral blood flow at BP levels that<br />

are within the hypertensive range.<br />

A. Reductions in MAP below the Lower Limit <strong>of</strong> CBF Autoregulation<br />

As systemic perfusion pressure falls below the lower limits <strong>of</strong> CBF autoregulation, cerebral<br />

resistance vessels have dilated maximally but are no longer able to maintain cerebral blood flow.<br />

As CBF falls, cerebral oxidative metabolism is supported by augmentation <strong>of</strong> oxygen extraction<br />

from the declining cerebral blood flow. At this point symptoms <strong>of</strong> cerebral hypoperfusion such as<br />

lethargy, confusion, somnolence, etc. can appear. When CBF falls below ~10 ml/100g/min, the<br />

ionic gradient across neuronal cell membranes becomes disrupted leading to calcium influx and<br />

potassium efflux and neuronal cell injury/death occur. Unlike the heart where oxygen extraction<br />

is maximal at rest, the brain can extract greater amounts <strong>of</strong> oxygen from blood traversing it<br />

when cerebral blood flow falls. This provides at least some measure <strong>of</strong> cushion against cerebral<br />

ischemia.<br />

B. Increases in MAP above the Upper Limit <strong>of</strong> CBF Autoregulation<br />

As systemic perfusion pressure rises cerebral resistance vessels normally constrict.<br />

When systemic perfusion pressure rises above the upper limits <strong>of</strong> CBF autoregulation then CBF<br />

increases dramatically and there is increased permeability <strong>of</strong> the cerebral vasculature leading<br />

to cerebral edema and increased intracranial pressure. Raised intracranial pressure has two<br />

important physiological effects. First, systemic BP increases further. Secondly CBF may fall<br />

though this tendency is counterbalanced by the reflex rise in systemic perfusion pressure.<br />

Symptoms <strong>of</strong> CNS dysfunction again can occur such as seizures, lethargy, stupor, coma, etc.<br />

The clinical term for this life-threatening clinical situation is hypertensive encephalopathy. Table<br />

6 displays clinical symptoms that characterize hypertensive encephalopathy.<br />

Table 6<br />

9. Blood Pressure and Cerebral Blood Flow Regulation during Acute Brain Ischemia<br />

Hypertension is the major risk factor for stroke. Approximately 80% <strong>of</strong> patients with acute<br />

stroke have elevated BP at the time <strong>of</strong> hospital admission. The observation <strong>of</strong> elevated BP at the<br />

time <strong>of</strong> admission has also been made in persons without antecedent <strong>hypertension</strong>.<br />

Blood pressure reflexively rises during acute cerebral ischemia and brain trauma. During<br />

acute cerebral ischemia, cerebral blood flow autoregulation is disrupted in the ischemic areas<br />

<strong>of</strong> the brain surrounding the already infarcted area. Disruption <strong>of</strong> CBF autoregulation is greater<br />

for brainstem ischemic lesions than for hemispheric lesions; severe hemispheric lesions cause<br />

greater disruption <strong>of</strong> autoregulation than minor hemispheric lesions; and subcoritcal lesions<br />

NKFM & MDCH 35

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