Cerebral hemorrhage is often unpreventable and has resulted in many irreparable situations, which are physically and mentally devastating for patients and their families. In fact, it is possible to prevent and treat cerebral hemorrhage with a scientific management approach. Treatment of the acute phase of cerebral hemorrhage includes: general treatment: monitoring and stabilization of neurological status and vital signs (blood pressure, pulse, oxygen concentration and body temperature); prevention and treatment of neurological complications (such as the occupying effect of edema or seizures) and medical complications (such as aspiration, infection, decubitus ulcer, DVT or PE); early secondary prevention to reduce the early recurrence rate of cerebral hemorrhage; early rehabilitation; and surgical procedures. Monitoring and management of blood pressure Monitoring and management of blood pressure is a key issue in the acute treatment of cerebral hemorrhage, and in primary cerebral hemorrhage (ICH), there is little prospective evidence that a threshold value for blood pressure should be established. Controversy therefore remains. Previously recommended principles for blood pressure management were to maintain systolic blood pressure below 180 mmHg and mean arterial pressure below 130 mmHg, supported by evidence that a systolic blood pressure ≤210 mmHg alone is less significantly associated with hematoma enlargement or neurological deterioration.PET monitoring found that when arterial pressure decreased by 15% did not result in a decrease in cerebral CBF. Prospective studies have shown that when blood pressure was brought down below 160/90 mmHg within 60 hours of onset in patients with ICH, 7% of these patients had worsening neurological function and 9% had hematoma enlargement, yet there was a trend toward improved prognosis. The largest prospective study and the rFVIIa trial for ICH demonstrated no relationship between baseline blood pressure and hematoma enlargement. Patients with elevated systolic blood pressure are more likely to have hematoma enlargement, but it is unclear whether the effect of hematoma enlargement is associated with high cranial pressure or whether it is the primary cause of hematoma enlargement. Experience in traumatic brain injury, as in spontaneous ICH, supports the maintenance of cerebral perfusion pressure above 60 mmHg. Blood pressure lowering given in the acute phase of cerebral hemorrhage may prevent or stop hematoma expansion and may reduce the risk of rebleeding, but cerebral perfusion pressure (CPP) decreases and intracranial pressure increases leaving cerebral blood flow inadequate. Stroke patients usually have a history of chronic hypertension and their intracranial pressure autoregulation curve is shifted to the right. This means that cerebral blood flow remains stable at a mean arterial pressure (MAP) of approximately 50 to 150 mmHg in normal subjects, however, patients with hypertensive stroke are adapted to higher MAP levels, so for MAP levels tolerated by normal subjects, patients with hypertensive stroke are at risk of hypoperfusion. In patients with chronic hypertension, their MAP should be controlled to less than 120 mmHg, but a reduction of >20% should be avoided and MAP should not be <84 mmhg.< span=""> Based on the limited data available, the recommended high limit of blood pressure control for patients with a previous history of hypertension or signs of chronic hypertension (ECG, retinal) is systolic blood pressure If treatment is required, the target blood pressure is 160/100 mmHg (or 120 mmHg MAP); for patients without a known history of hypertension, the recommended upper limit of blood pressure control is 160/95 mmHg. If treatment is required, the target blood pressure is 150/90 mmHg (or 110 mmHg MAP); for intracranial pressure (ICP), the recommended upper limit of blood pressure control is 180 mmHg systolic and 105 mmHg diastolic. ); for patients with elevated intracranial pressure (ICP), the upper blood pressure limit and control target should be increased accordingly to ensure at least cerebral perfusion pressure; CPP=MAP-ICP) between 60 and 70 mmHg to ensure adequate cerebral perfusion, all from patients with traumatic brain injury. Indications for the need for immediate hypotensive therapy Immediate hypotension is appropriate when accompanied by the following conditions, such as acute myocardial ischemia (although extreme hypotension is also harmful in patients with myocardial infarction), cardiac insufficiency, acute renal failure, acute hypertensive encephalopathy, or aortic arch entrapment. Intravenous antihypertensive drugs with a short half-life are the ideal first-line treatment option. Intravenous labetalol is recommended in the United States and Canada, which is not commonly used in Europe, or esmolol hydrochloride, nicardipine, or enalapril. Intravenous uradil is also being used increasingly. Finally, sodium nitroprusside is applied when necessary, but in addition to its major adverse effects such as reflex tachycardia, coronary ischemia, antiplatelet activity and increased intracranial pressure, it decreases cerebral perfusion pressure. Oral, sublingual, and intravenous calcium channel blockers should be used with caution because of their rapid and dramatic lowering of blood pressure. Subcutaneous colistin also needs to be used with caution.