hypertension(redirected from orthostatic hypertension)
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hypertension or high blood pressure, elevated blood pressure resulting from an increase in the amount of blood pumped by the heart or from increased resistance to the flow of blood through the small arterial blood vessels (arterioles). Hypertension was generally defined as a blood pressure reading of 140 over 90 or higher, but new guidelines issued in 2017 define hypertension as 130 over 80 or higher. Presssures of 120–129 over less than 80 are considered elevated. When the cause is unknown, the hypertension is called primary, or essential, hypertension. When a cause can be identified (e.g., a disorder of the adrenal glands, kidneys, or arteries), the condition is known as secondary hypertension. Factors such as heredity, obesity, smoking, and emotional stress are thought to play a role; the usual immediate cause is an imbalance in the body's vasoconstriction/fluid retention systems, often involving a decrease in the kidney's secretion of the regulatory hormone, renin.
Known as the “silent killer,” hypertension often produces few overt symptoms; it may, however, result in damage to the heart, eyes, kidneys, or brain and ultimately lead to congestive heart failure, heart attack (see infarction), kidney failure, or stroke. African Americans and women are the most affected. Treatment of hypertension includes diets to reduce weight and salt and alcohol intake, increased exercise, quitting smoking, and various drugs, such as diuretics, ACE inhibitors, beta-blockers, calcium-channel blockers or angiotensin-receptor blockers, as well as biofeedback. Many patients require a combination of drugs to control their blood pressure. Treatment for persons with prehypertension includes dietary and other lifestyle changes. Recent research has questioned the importance of dietary salt as a major contributor to hypertension; some studies point to low calcium intake as a cause.
See also eclampsia.
a disease of the cardiovascular system, the principal manifestation of which is the elevation of blood pressure.
Hypertension was first described by the Soviet scientist G. F. Lang in 1922. The causes of its onset have not as yet been thoroughly elucidated. There are two points of view about the origin of hypertension. The first proceeds from the fundamental role played by the impairment of the nervous regulation of vascular tone together with a number of factors that predispose to the disease. These factors include hereditary deficiency in the hormonal mechanisms that regulate the state of the vascular system, previous kidney disease that has impaired circulation in them, changes in the blood vessels (especially of the brain and kidneys) through aging, and endocrine disturbances accompanying the climacteric.
Nervous and psychic tension and chronic overexhaustion, which with resistant humoral mechanisms cause no pathological changes, lead to spasm of the arterioles and elevation of blood pressure in the presence of predisposing factors. Increased tone in the muscles of the blood vessels (arterioles), with which the rise in blood pressure is associated, is connected with activation of the renin-angiotensin system (a group of biologically active substances whose interaction causes blood pressure elevation), with increased content in the blood of the hormone aldosterone, with a change in sodium metabolism, and with changes in blood circulation in the brain and kidney. All these changes are in turn associated with impairment of the nervous regulation of the processes described.
The second point of view proceeds from the role of the pressor (tending to increase blood pressure) and depressor factors of the kidney in the elevation of arterial blood pressure. The kidney contains the so-called juxtaglomerular apparatus, which stimulates formation of the pressor factor —renin. Renin, in turn, specifically stimulates formation by the adrenal cortex of a second factor—aldosterone— which regulates water metabolism and metabolism of potassium and sodium ions and influences the content of these elements in the smooth muscles of the blood vessels. Increase of sodium content in the smooth muscles of the vessels increases their tone, which in turn determines the elevation of blood pressure. Simultaneously, aldosterone blocks the paths of sodium elimination from the body. Thus, the renal factor may in itself induce blood pressure elevation. However, the kidney also possesses depressor properties, which lower blood pressure. Exhaustion of these properties may lead, in the opinion of advocates of the kidney theory, to the predominance of pressor activity and the development of hypertension.
The incidence of hypertension increases with age. Up to age 40, males are more frequently affected; after 40, morbidity among men and women is practically identical. Hypertension is one of the most common diseases of the cardiovascular system in the urban population, among which it is found at nearly three times the rate for the rural population. Persons most often affected are those whose work is to a large degree associated with nervous and psychic tension, such as engineering and technical personnel, workers in precision production, and workers in communications and transportation.
Hypertension is divided into three stages, according to the course and character of the clinical picture. Characteristic of the first, “transitory,” stage is short-term elevation of blood pressure, usually arising after overexhaustion or excessive nervous tension. The blood pressure quickly normalizes itself, without the use of special medications, under the influence of rest or of sedative preparations. During this period patients complain of increased nervous irritability, headaches, dizziness, and palpitations. Some enlargement of the heart and sometimes a systolic murmur at the apex may be noted; on the electrocardiogram there may be some indications of beginning myocardial hypertrophy. The second stage is divided into two phases. Characteristic of the first phase (labile hypertension) is vacillation of the blood pressure from minor elevation to rather high levels. In the second phase (stable hypertension) the blood pressure stands permanently at high levels. Illnesses in which blood pressure is lowered by rest and the use of ordinary sedatives are included in the first phase. In the second stage, in addition to the characteristic symptoms of hypertension, such as ringing in the ears, dizziness, headaches, and palpitations, signs may appear of cardiac insufficiency (dyspnea, edema, tachycardia, and arrhythmia) and coronary insufficiency (pain behind the sternum and in the region of the heart and development of myocardial infarction).
The third stage is characterized by the development of arteriolosclerosis, with renal impairment, cardiac failure, and cerebrovascular affection against a background of high and persistent hypertension. Development of renal failure, cicatricial changes in the myocardium, and disruption of blood supply to the brain are also possible in this stage.
Hypertensive crises, which represent brief exacerbations of the disease, may be distinguished in the course of hypertension; sudden, sharp elevation in blood pressure accompanied by headaches, dizziness, vomiting, tachycardia, chills, and, occasionally, impairment of vision are characteristic. Disruptions of coronary and brain circulation are also possible (myocardial infarction or cerebral apoplexy).
In the first stage of hypertension, treatment involves sufficient sleep, elimination of nervous, psychic, and physical overloads, prohibition of alcoholic beverages and smoking, and use of sedatives. In the later stages, medications that lower blood pressure, tranquilizers, and sleep-inducing drugs are prescribed, together with an appropriate diet. Surgical treatment has not been widely used. Elimination, where possible, of excessive emotional stress and psychic trauma, rational organization of the work and rest regime, and sufficient sleep are recommended for prevention.
REFERENCESLang, G. F. Gipertonieheskaia bolezn’. [Leningrad] 1950.
Miasnikov, A. L. Gipertonicheskaia bolezn’. Moscow, 1954.
Miasnikov, A. L., and K. N. Zamyslova. “Gipertonicheskaia bolezn’.” In Mnogotomnoe rukovodstvo po vnutrennim bolez-niam, vol. 2. Edited by E. M. Tareev. Moscow, 1964.
E. I. CHAZOV