Gradually progressive hypertension: Symptom identification and prevention of cerebrovascular complications

Slow-onset hypertension: Early stages are often asymptomatic, but some patients may experience headaches, dizziness, palpitations, insomnia, memory loss, poor concentration, fatigue, irritability, tension, and anger. Later stages may lead to organic damage and functional impairment of organs such as the brain, heart, and kidneys.

1. Cerebral manifestations: Headache, head distension, dizziness, neck stiffness, and blurred vision are common cerebral symptoms. If there is temporary or intermittent spasm of cerebral arteries, temporary aphasia, blindness, limb weakness, or even hemiplegia may occur, lasting from several minutes to several days, with the vast majority recovering within 24 hours. Severe and persistent spasm of cerebral blood vessels or a significant increase in blood pressure can cause a rapid disruption of cerebral blood circulation, leading to cerebral edema and a series of symptoms of increased intracranial pressure, known as hypertensive encephalopathy.

(1) Increased water content in brain tissue, resulting in increased volume and weight, is called cerebral edema. Cerebral edema, due to the increased brain volume, often leads to increased intracranial pressure, manifesting as headache, vomiting, or papilledema. It is often accompanied by neurological dysfunction, slowed reflexes, and memory loss; in severe cases, it can induce brain herniation.

(2) Increased intracranial pressure can be caused by various diseases of the nervous system, resulting from an increase in the volume of intracranial contents (brain tissue, cerebrospinal fluid, and cerebral blood volume) or intracranial space-occupying lesions. Headache, vomiting, and papilledema are the three main symptoms of increased intracranial pressure.

Headache: This is the most common and earliest symptom, mostly located in the frontotemporal region, but can also radiate to the occipital region or back of the neck. It may be caused by traction on the meninges, blood vessels, or nerves. It presents as a throbbing or pulsating pain, is persistent, and may have paroxysmal exacerbations; it is characterized by worsening in the morning or waking the patient in the middle of the night. Neck flexion, coughing, and straining during bowel movements can all worsen the headache. In acute intracranial hypertension, such as in meningitis or subarachnoid hemorrhage, headache is often severe.

Vomiting: This often occurs in the morning on an empty stomach, or accompanies severe headache, and is unrelated to food intake. Vomiting is usually preceded by nausea; typically, it is projectile vomiting, sometimes induced by changes in head position. In children, headache may be less pronounced, with only vomiting present.

Papilledema: This is the most important and reliable objective sign of intracranial hypertension. Its occurrence is related to the speed and duration of the development of intracranial hypertension. Papilledema may be subtle in acute intracranial hypertension, but in rapidly developing, widespread cerebral edema can appear within minutes. Chronic cases may present with typical fundus changes, but papilledema usually develops several weeks after the onset of the disease. Early stages may be visually impaired, but continued progression can lead to central scotoma, paroxysmal amaurosis, and eventually optic atrophy and blindness.

2. Cardiac manifestations: Left ventricular hypertrophy and dilation, known as hypertensive heart disease, can gradually lead to left ventricular failure in later stages.

Hypertensive heart disease is an organic heart disease caused by long-term elevated blood pressure, which gradually increases the load on the left ventricle. The left ventricle gradually thickens and dilates as a compensatory mechanism. Hypertensive heart disease generally appears several to more than ten years after the onset of hypertension. Based on changes in cardiac function, it can be divided into the compensated stage and the decompensated stage. In the compensated stage, patients may have no obvious symptoms. However, in the decompensated stage, symptoms of left ventricular failure gradually appear. Initially, palpitations, shortness of breath, and coughing only occur with exertion, after a large meal, or excessive talking. Later, the symptoms gradually worsen, and these symptoms occur paroxysmically, often manifesting as paroxysmal nocturnal dyspnea with hemoptysis. In severe cases, acute pulmonary edema may occur.