In this case, the second compensatory mechanism should work, which consists in increasing the tone of the venous vessels. It provides an acceleration of the outflow of excess blood from the cranial cavity. If a sufficient increase in the tone of the venous system does not occur, then an angiohypotonic hypertensive cerebral crisis develops. It is based on congestion occurring in the venous system of the brain, accompanied by the accumulation of an excess amount of celebrex in a limited space of the cranium (hydrocephalus), which leads to an increase in intracranial pressure.
An excessive increase in the tone of the cerebral arteries in response to a jump in blood pressure leads to a violation of the blood supply to the brain tissues with the development of hypoxia (oxygen starvation) in them and the occurrence of an ischemic variant of a hypertensive cerebral crisis. In this case, the brain structures most sensitive to hypoxia (cerebral cortex) suffer first of all. The irregularity of the architectonics of the cerebral vessels, as well as the possible attachment of local angiospasm, lead to the appearance of foci with more pronounced ischemia, which are associated with clinically observed focal symptoms.
The pathogenesis of a complex hypertensive cerebral crisis includes hypotension of cerebral vessels with blood deposition in the venous system and ischemia of certain parts of the brain due to deterioration of capillary blood flow due to shunt discharge of blood from arteries to veins, bypassing the capillary network. Symptoms of a hypertensive cerebral crisis.
Angiohypotensive hypertensive cerebral crisis usually develops against the background of a typical and habitual headache for hypertensive patients, which is localized in the occipital region or occurs as a feeling of heaviness in the head. A characteristic sign of such a headache is its intensification in the position of the body, which makes it difficult for venous outflow from the cranial cavity (straining, tilting, lying down, coughing). By itself, a headache of this nature is already a sign of angiodystonia of cerebral vessels, but it often disappears in an upright position of the body and when taking caffeinated drinks.
The onset of a hypertensive cerebral crisis is indicated by the spread of headache in the retroorbital region. At the same time, patients complain of the appearance of pressure on the eyes and behind the eyeballs. A distinctive feature of the angiohypotensive hypertensive cerebral crisis is its occurrence with a moderate rise in blood pressure (170/100 mm Hg). Then there is a rapid (within an hour) intensification of the headache and its diffuse spread throughout the head. There is nausea, repeated vomiting, bringing some temporary relief.
Angiohypotensive hypertensive cerebral crisis, as a rule, is accompanied by vegetative reactions. increased sweating, tachycardia, undulating breathing, sometimes cyanosis of the face. The late phase of the crisis is characterized by increasing lethargy, nystagmus, dissociation of tendon reflexes. During this period, blood pressure may be at the level of 220/120 mm Hg. Art. and more, but in some cases it does not rise above 200/100 mm Hg. Art.
Ischemic hypertensive cerebral crisis is observed much less often than angiohypotensive crisis and is typical mainly for hypertensive patients who do not suffer from headaches and tolerate high blood pressure well. Often, an ischemic hypertensive cerebral crisis develops against the background of very high blood pressure numbers, sometimes going beyond the limits of the tonometer scale. The clinical manifestations of such a crisis in the initial period may go unnoticed.
They relate mainly to disorders of the mental sphere in the form of increased energy, excessive emotionality or external efficiency. Then irritability appears, replaced by depression and tearfulness, possibly aggressive behavior. At the same time, due to the lack of criticism, the patients themselves cannot adequately assess their condition.
A complex hypertensive cerebral crisis begins with clinical manifestations characteristic of the angiohypotensive variant of a cerebral crisis, but often occurs against the background of a significantly elevated blood pressure. As the crisis develops, during the period of pronounced clinical manifestations, focal symptoms appear, typical of the ischemic variant of the cerebral crisis. In this case, the nature of the emerging focal symptoms depends on the location of the ischemic areas of the brain tissue.
BeforeAdditional instrumental studies are usually carried out after the provision of emergency care to the patient and are aimed at in-depth diagnosis of the state of cerebral circulation and the cardiovascular system. They may include ECG, 24-hour blood pressure monitoring, rheoencephalography, EchoEG, EEG, ultrasound of the head vessels, consultation with an ophthalmologist, ophthalmoscopy, perimetry, MRI of the brain. It is necessary to differentiate a hypertensive cerebral crisis from hemorrhagic stroke, TIA, ischemic stroke, acutely developing hydrocephalus in brain tumors and liquorodynamic disorders of another etiology. Treatment of hypertensive cerebral crisis.
A hypertensive cerebral crisis is diagnosed by a general practitioner, neurologist or cardiologist on the basis of a typical clinical picture, data on the development of existing symptoms and blood pressure measurements. Ischemic and mixed hypertensive cerebral crisis are indications for hospitalization of the patient. The need for inpatient treatment in an uncomplicated angiohypotensive variant of the crisis depends on its severity. In any case, a hypertensive cerebral crisis requires complex treatment, including antihypertensive and tranquilizing therapy common to all types of hypertensive crisis, the appointment of vasoactive drugs, the choice of which depends on the type of cerebral crisis, and symptomatic treatment. The patient must comply with bed rest until the stabilization of blood pressure and regression of the neurological symptoms that have arisen.
