Pathofisiology of hypertension can cause intracranial bleed?

i want to know the pathofisiology of hypertension can cause intra cranial bleed

For neurosurgical patient collectives, the impact of induced hypertension and CPP and ICP management on physiological variables and outcome has only been insufficiently evaluated. However, for stroke patients, relevant data are almost nonexistent. Because of the different pathophysiology, the results from patients with head trauma can hardly be used to guide the management of stroke patients.

In theory, the rationale for inducing hypertension is that the ischemic infarct core may be surrounded by areas perfused by collateral vessels where the blood flow is pressure dependent because of impaired autoregulation, constituting a "chronic penumbra." If a chronic penumbra exists, the extent of reversible tissue damage can be reduced by increasing the blood flow in the penumbra. It has been shown in positron emission tomography and MRI studies that the penumbra is unstable over time and space; substantial volumes of potentially viable brain tissue have been demonstrated up to 17 hours after stroke, giving justification for a prolonged treatment with induced arterial hypertension.

There are no recommendations available regarding the levels to which the BP should be increased. It seems to be obvious that the optimal BP depends heavily on the underlying pathophysiology and individual factors. In chronically hypertensive patients, the plot of CBF versus MAP is shifted toward higher BP. The same is true for patients with diabetes. In hypertensive patients, cerebral autoregulation may therefore be impaired at "normotensive" levels of MAP. In persons with chronic, inadequately managed arterial hypertension, CBF may therefore passively change with the MAP at normotensive levels and decrease rapidly as the MAP decreases to even lower levels.

Induced hypertension may also carry some risks for the patient. If an occluded vessel is reperfused, the ischemic infarct changes into a hyperemic infarct where blood flow is severely increased, because in the area of severe focal ischemia, maximum arteriolar vasodilatation occurs and the capacity for vasoconstriction is lost. In patients treated with fibrinolysis, arterial hypertension represents a strong risk for bleeding complications. In healthy subjects, systemic hypertension would not be expected to increase CBF. However, in areas of ischemia, if autoregulation of the CBF is lost, arterial hypertension would severely augment CBF, potentially increasing the likelihood of blood-brain barrier disruption and the risk of worsening edema formation or hemorrhage. Thus, induced hypertension could exert opposite effects, depending on the underlying pathophysiology and time point: it could be beneficial in the very early phase of stroke before recanalization has occurred and a large penumbra exists, but it could also be hazardous when applied during longer periods or when initiated after too much time has elapsed.