The human body is like a complex clockwork mechanism. If any “part” fails, a disease occurs, which affects the functioning of other organs and systems. Hypertension is extremely common among the population. Hypertension should be understood as a stable increase in blood pressure above 140/90 mmHg. with two consecutive visits to the doctor and provided that the patient does not take any drugs that lower or increase blood pressure. A condition characterized by increased blood pressure is dangerous due to the development of complications from of cardio-vascular system, blood vessels of the brain, eyes and kidneys.
Why does this disease occur? How is hypertension formed? Answers to many questions about the origin and mechanism of development hypertension will be given in this article.
1 Etiology of hypertension
Heredity, stressful situations, excessive consumption table salt, insufficient intake of magnesium and calcium from food and water, smoking, alcohol, obesity, low physical activity - all these factors contribute to increased blood pressure and the development of essential hypertension (HD) or arterial hypertension (AH). The risk of developing hypertension has been noted to be higher among people with lower socioeconomic status.
This is explained by the fact that people with low incomes pay less attention balanced diet, proper active rest due to lack of material resources, and also smoke and drink more alcohol. Worth highlighting separate form hypertension - “white coat” hypertension, which occurs in people only when visiting a doctor due to anxiety and psycho-emotional stress, at home, in a familiar environment, the blood pressure of such persons is within normal limits.
If the cause of hypertension cannot be clearly established, there is a connection with heredity, it is more common in men and the incidence increases with age, we are talking about primary (essential) hypertension. It accounts for about 80% of all hypertension. The etiology of arterial hypertension of secondary origin (the incidence of the secondary form is about 20% of all identified cases of high blood pressure) is directly related to the disease that caused it.
The following types of secondary (essential) hypertension are distinguished:
- Renal hypertension. The cause of such hypertension is diseases of the kidneys and renal vessels: congenital anomalies development, infection, anomalies and disorders of the kidney vessels, diseases of the kidney tissue (glomerulonephritis, pyelonephritis, amyloidosis);
- Endocrine hypertension. The reason for the increase in blood pressure lies in disorders of the endocrine organs: pathology of the adrenal glands, excessive thyroid function, acromegaly, hormonal imbalances during menopause;
- Hemodynamic hypertension. When large vessels and the heart are damaged, symptomatic hypertension may occur: coarctation of the aorta, ischemia, circulatory congestion, valvular insufficiency, arrhythmias and other disorders;
- Neurogenic hypertension. Hypertension caused by pathological activity nervous system and brain diseases: brain tumors, inflammation (meningitis, encephalitis), trauma, vascular disorders.
In addition to the main causes of symptomatic hypertension, there are also special causes of pathologically high blood pressure:
- Salt or food hypertension: develops as a result of excess salt intake in food, or excessive consumption of foods that contain tyramine - cheese, red wine;
- Drug-induced secondary hypertension - develops when taking certain medications that can cause hypertension.
2 Pathogenesis of hypertension
Many systems and factors regulate blood pressure in the human body. Here are the most significant of them:
- higher centers of the nervous system (hypothalamic),
- renin-angiotensinII-aldosterone system,
- sympathoadrenal system,
- factors produced by the vascular endothelium.
Under the influence of provoking factors, activation of the sympathoadrenal system may occur, this leads to the release of adrenaline and norepinephrine in the human body. These substances have a vasoconstrictor effect and increase blood pressure by constricting blood vessels.
The RAAS system has a more complex mechanism - the renin-angiotensin-aldosterone system. A simplified scheme of the RAAS can be represented as follows: renin is produced in specialized cells of the kidney vessels, entering the blood, it promotes the formation of a substance - angiotensinogen II, in turn, angiotensinogen II contributes to the fact that the adrenal glands begin to produce the hormone aldosterone.
Aldosterone retains sodium, which promotes the attraction and retention of water and increases the volume of intracellular fluid; excess aldosterone increases blood pressure. In addition to stimulating aldosterone production, angiotensinogen II has the following effects: it has the ability to constrict arterial vessels, activates the sympathetic nervous system, increases sodium absorption, and creates a feeling of thirst. All these factors together lead to hypertension.
To understand how vascular endothelial factors act, you need to understand the anatomy of a vessel, in particular an artery. The anatomy of an artery is quite complex: the artery consists of three membranes: internal (it is represented by endothelium), middle (contains muscle fibers) and external (includes elements connective tissue). The inner lining, or endothelium, is of greatest interest in the mechanism of development of hypertension.
The endothelium is a regulator of vascular tone, as it produces both vasoconstrictor and vasodilator factors. The balance between these factors ensures normal vascular tone. Nitric oxide, endothelial factor, prostacyclin, natriuretic peptide-C, bradykinin are substances produced by the inner lining of the arteries that promote vasodilation.
The following factors produced by the endothelium are responsible for vasoconstriction: endothelins, angiotensinogen II, thromboxane, endoperoxin, superoxide ion. If pathological activity occurs and increased release into bloodstream vasoconstrictors, vascular tone and blood pressure increases.
The mechanism of development of hypertension is quite complex. It should be noted that the pathogenesis of hypertension is inextricably linked with etiology, i.e. causal factors diseases. Hypertension develops through the interaction of genetic factors, environmental factors and the inclusion of the main mechanisms of pathogenesis - activation of the sympathetic-adrenal system, RAAS, dysfunction of the endothelium.
3 Pathological anatomy of blood vessels and organs in hypertension
With hypertension, all blood vessels in the human body are affected and, accordingly, the work and function of the organs that these vessels supply with blood are disrupted. The heart, kidney vessels, brain vessels, retina of the eyes, and peripheral arteries of the body suffer from hypertension. A heart with arterial hypertension is called “hypertensive” in medicine. Pathological changes in a “hypertensive” heart are characterized by an increase muscle tissue left ventricle - hypertrophy.
There is an increase in the size of cardiomyocytes - myocardial cells, fibrosis and ischemia develop, the structure and function of the heart muscle is disrupted, which ultimately leads to the development of heart failure. Kidney damage or “hypertensive nephropathy” develops gradually: first, vascular changes occur in the form of spasm, wall thickening, capillary wrinkling, then sclerosis of the kidney tissue develops, tubular atrophy develops, the size of the kidneys decreases, and renal failure.
The vessels of the retina undergo changes in the form of narrowing of the arteries, tortuosity and dilation of veins, thickening of the walls of blood vessels, and hemorrhages in the retina may be observed. All these changes lead to deterioration of vision, retinal detachment is possible with the threat of vision loss. The vessels of the brain are most sensitive to high blood pressure, since arterial spasm leads to oxygen “starvation” of brain tissue, impaired vascular tone leads to impaired blood circulation in the brain.
It has Negative consequences for the body, cerebral infarctions and strokes may develop, which leads to disability of the patient or to fatal outcome. Understanding pathological anatomy, occurring in the vessels, it becomes clear that hypertension “hits” all systems and organs of the human body. And it’s not so much its high numbers that are scary, but the consequences.
4 Prevention of hypertension
Having an idea of the etiology of hypertension and pathogenesis, it becomes obvious: in order to prevent the development of hypertension, the person himself can influence certain factors in its development. If it is impossible to fight genetics, then control can be found on environmental factors.
For prevention of this disease you need to quit smoking, drink alcohol, stop adding salt to your food, and ideally give up salt altogether, watch your diet, avoid overeating and obesity, lead an active lifestyle, take walks before bed. Perhaps, following these simple rules will be the key to your health, and your blood pressure will invariably be 120/80.
Arterial hypertension (AH) (from Greek hyper - excessive, Latin tensio - tension) - a persistent increase in blood pressure - an important symptom of pathological conditions and diseases accompanied by either an increase in resistance to arterial blood flow, or an increase in cardiac output, or a combination of these factors. Normal blood pressure = 110-140 / 65-90 mm Hg. Art., and 150/94 is a transition zone, not yet hypertension.
SDC plays a major role in neurohumoral regulation blood circulation, it can be divided into 3 interconnected sections:
a) a group of neurons located in the lateral parts of the medulla oblongata - their constant activity through pre- and postganglionic sympathetic neurons has a tonic activating effect on the function of the heart and vascular smooth muscles;
b) medially located neurons, which have the opposite (inhibitory) effect on pre- and postganglionic sympathetic neurons and reduce the effect of adrenergic innervation on blood circulation;
c) dorsally located nucleus vagus nerve which has an inhibitory effect on the heart.
Efferent mechanisms (peripheral link functional system) are realized through the sympathetic nervous system and the endocrine system (pituitary gland, adrenal glands, thyroid- increased blood pressure). But there are also feedback mechanisms - a depressor mechanism - when the aortic arch and sinocarotid zone are stretched (when the wall of the common carotid artery is stretched), the depressor effect on the SDC increases and inhibits it Long-term or significant arterial hypertension in itself forms a pathological condition, which is manifested by overload and hypertrophy of the heart, tension of the adaptation mechanisms of regional circulation. Hypertension- systemic increase in pressure in the arteries great circle blood circulation, and hypertension- increased muscle tone - vasospasm.
Relevance: high frequency, the leading place is hypertension - in 5-6% of the population, high danger atherosclerosis, stroke, vascular thrombosis, etc. Arterial hypertension is one of the forms of vascular insufficiency, as well as arterial hypotension - vascular insufficiency in the form of hypotension (there is also heart failure - but more often mixed forms - cardiovascular failure).
Types, causes and mechanisms of arterial hypertension:
1. Hypertonic disease- an independent nosological form, the leading and primary symptom is increased blood pressure (90-95% of arterial hypertension)
2. Secondary- symptomatic arterial hypertension - in connection with any disease, not primarily associated with an increase in blood pressure, but it increases during the course of the disease as a symptom of the disease:
a) nephrogenic (renal - 7-8%),
b) renoprival (when both kidneys are removed),
c) endocrinopathic (adrenal),
d) neurogenic,
e) hemodynamic,
e) congestive (with heart defects complicated by heart failure).
Based on the nature of the increase in blood pressure, there are:
a) systolic hypertension (an increase in systolic blood pressure with normal or reduced diastolic blood pressure develops due to an increase in SV,
b) systole - diastolic with an increase in stroke volume and resistance to blood flow and
c) diastolic with an increase in peripheral resistance to blood flow with a decrease in the propulsive function of the left ventricle of the heart.
There are 5 variants of AG along the flow:
A) transometric arterial hypertension - rare, short-term and slight increases in blood pressure, normalizes without treatment,
b) labile(moderate and unstable frequent increase in blood pressure, normalizing under influence of treatment),
V) stable Hypertension is a persistent and often significant increase in blood pressure, the reduction of which is possible only with active antihypertensive therapy,
G) malignant Hypertension - with very high blood pressure, especially diastolic (above 120 mm), with rapid progression, significant tolerance to treatment + renopathy and rapidly developing renal failure,
e) AG with a crisis course, and paroxysmal increases in blood pressure can occur against the background of any initial values - low, normal or high blood pressure.
Pathogenesis of secondary arterial hypertension. In the emergence and maintenance of many forms of symptomatic hypertension great importance has a humoral system renin – angiotensin – aldosterone. Enzyme renin produced by granular cells of the juxtaglomerular apparatus of the kidneys. When interacting with the α 2 -globulin fraction of blood plasma - angiotensinogen (produced by the liver), is formed angiotensin-I (also has no effect on the tone of the vascular wall. But under the influence convertinenzyme turns into angiotensin-II , having a powerful vasopressor action. There is a direct connection between the content angiotensin-II And aldosterone. Aldosterone (adrenal cortex hormone - mineralocorticoid) increases sodium reabsorption in the kidneys and its retention in the muscular elements of the arterioles, which is accompanied by their swelling and increased sensitivity of the vascular wall receptors to pressor influences (for example, norepinephrine). There is normally an inverse relationship between the blood level of aldosterone and renin activity. Under physiological conditions, a decrease in renal blood flow in the cells of the juxtaglomerular apparatus causes abundant granulation and increased synthesis renina. These cells play a role volume receptors and participate in the regulation of blood pressure levels, responding to changes in the amount of blood flowing to the glomerulus. Emerging angiotensin increases blood pressure, improves renal perfusion and reduces the intensity of renin synthesis. However inverse relationship between renin production and blood pressure is violated in many pathological conditions- primarily with nephrogenic and especially with renovascular hypertension.
1. Renal arterial hypertension:
a) arterial hypertension can occur with nephropathy in pregnant women; for autoimmune-allergic kidney diseases, both inflammatory (diffuse glomerulonephritis, collagenosis) and dystrophic (amyloidosis, diabetic glomerulosclerosis).
For example, in patients with chronic diffuse glomerulonephritis, there is a proliferative-sclerosing process in the renal tissue with desolation of some of the glomeruli, compression of the afferent vessels and, ultimately, an increase in blood pressure.
b) in infectious interstitial kidney diseases - in chronic pyelonephritis, hypertrophy and hyperplasia of the juxtaglomerular apparatus and persistent increased secretion are observed renina. The nephrogenic nature of arterial hypertension in chronic unilateral pyelonephritis is confirmed by the results of surgical treatment - if the second kidney is without pathology, then after removal of the diseased kidney the blood pressure normalizes.
c) renovascular or vasorenal - in case of impaired blood supply to the kidneys and with congenital narrowing of the arteries, or their hypoplasia, aneurysms, with acquired lesions of the arteries due to atherosclerosis, thrombosis, calcenosis, compression by scars, hemotoms, neoplasms (in the experiment - a screw clamp, a rubber capsule).
In this case, the leading role in stimulating secretion renina belongs to a decrease in blood flow in the renal arteries. The resulting angiotensin-II has a direct pressor effect and stimulates synthesis aldosterone, which in turn increases the accumulation of Na + in the vascular walls and enhances pressor reactions.
d) for urological kidney diseases and urinary tract(congenital - renal hypoplasia, polycystic disease) or acquired (renal stone disease, tumors of the urinary tract structure), with kidney injuries, with the formation of hematomas in the perinephric tissue.
e) renoprivative arterial hypertension develops after removal of both kidneys. Normally, the kidneys produce antihypertensive factors - kinins And prostaglandins and with their deficiency, blood pressure rises. Of particular importance in this hypertension is an imbalance in the content of Na + and K + in tissues and tissue fluids. Renoprial hypertension is accompanied by edema, and the edema disappears and blood pressure normalizes if the “artificial kidney” device is used during treatment with an appropriate selection of electrolytes in the perfusion fluid.
2. Neurogenic symptomatic arterial hypertension:
a) centrogenic - associated with brain damage - encephalitis, tumors, hemorrhages, ischemia, trauma (in experiment - by creating negative emotions in animals - fear, rage, inability to avoid danger; overexertion of VND - development of complex differentiation reflexes, restructuring of stereotypes, perversion circadian rhythms, ligation of blood vessels, compression of brain tissue).
b) peripheral - associated with damage to the peripheral NS - with poliomyelitis, polyneuritis; reflexogenic (disinhibition) in patients with atherosclerosis, the vascular wall is low-extensible → decrease in irritation of baroreceptors and increase in blood pressure (in an experiment when cutting depressor nerves from the aorta or carotid sinuses).
3. Endocrinopathic arterial hypertension:
a) when hormonal tumors pituitary gland – acromegaly + increased blood pressure, Itsenko-Cushing’s disease + increased cortisol levels;
b) for tumors of the adrenal cortex - increased levels of glucocorticoids, mineralocorticoids → hyperaldosteronism, pheochromocytoma → increased levels of norepinephrine;
c) with diffuse toxic goiter – increased thyroxine levels → hyperkinesia;
d) with discrimination during menopause.
4. Hemodynamic arterial hypertension:
a) when the elasticity of the walls of the aorta and large vessels decreases, adequate stretching of the vascular wall does not occur pulse wave, passing through the vessels;
b) hypertension in aortic valve insufficiency is caused by an increase in the end-diastolic volume of blood in the left ventricle as a result of regurgitation of blood from the aorta during diastole;
c) hypertension during coarctation of the aorta is associated, on the one hand, with a sharp increase in resistance to blood flow in the area of narrowing of the aorta, and on the other hand, with impaired blood supply to the kidneys, since the renal arteries extend below the site of coarctation;
d) narrowing of the carotid, vertebral or basilar arteries leads to cerebral ischemia - cerebroischemic arterial hypertension;
e) purely diastolic arterial hypertension develops with an increase in peripheral resistance to arterial blood flow due to a decrease in the propulsive function of the left ventricle in myocarditis or its insufficiency due to overstrain or impaired venous return of blood to the heart.
Hypertonic disease(GB) - essential, primary - the main manifestations of which are:
1. elevated blood pressure with frequent cerebral disorders of vascular tone;
2. stages in the development of symptoms;
3. pronounced dependence on functional state neural mechanisms of blood pressure regulation;
4. absence of a visible causal connection of the disease with primary organic damage to any organs or systems. This distinguishes hypertension from secondary (symptomatic arterial hypertension), which is based on damage internal organs or systems that regulate blood pressure. The leading, triggering factor of hypertension is arterial spasm as a result of disinhibition of the SDC and the emergence of a pathological dominant in it (stagnant, prolonged, inert excitation, reinforced by nonspecific stimuli and having no biological expediency for the body). The main cause of headache is acute or prolonged emotional stress, leading to the development of neurosis and disruption of the nervous mechanisms of blood pressure regulation against the background of weakness of the main cortical processes.
Obviously, there are also some acquired or congenital characteristics of the body (including personality traits). It is possible that genetically determined metabolic characteristics predispose to the development of hypertension - it has been noted that in relatives of patients with hypertension, the frequency of this disease is higher than among the general population.
A high incidence of headache in identical twins has been noted.
Excessive salt intake is important
And there is another theory - the role of a hereditary defect cell membranes, changing the permeability of membranes for electrolytes and as a consequence of this:
1. the concentration of Na + in the cell increases and the concentration of K + decreases and
2. the concentration of free Ca 2+ increases, which increases cell contractility and releases agents of sympathoadrenal action.
According to this theory, this is the cause of headache, and emotional stress- as a condition for identifying pathology.
Already in initial period HD pathogenesis includes changes in the humoral pressor and depressor systems. Their activation is compensatory in nature and occurs as a reaction to overexertion and trophic disturbances nerve cells brain. Forms quickly hyperkinetic type of blood circulation - increased cardiac output and little change in total peripheral vascular resistance. But very often vascular resistance in the kidneys increases early - ischemia develops and the activity of the renin-angiotensin system increases.
During this period, while the distensibility and elasticity of the aorta are still preserved, baroreceptor reconfiguration sinocarotid zone and aortic arch, which is expressed in the preservation of normal activity of the aortic nerve at elevated blood pressure (and normally a depressor effect). Perhaps this “reconfiguration” of baroreceptors ensures the tasks of regulating blood supply, shifting its parameters to a level optimal for new conditions. But then thickening of the aortic walls and carotid arteries and a decrease in their elasticity in the later stages of headache leads to a decrease in the sensitivity of baroreceptors and a decrease in depressor reactions.
The influence of the central nervous system on the tone of arteries and especially arterioles, as well as on myocardial function, is mediated through sympathoadrenal system, including the vasomotor centers of the hypothalamus, the sympathetic nerve, the adrenal glands, α- and β-adrenergic receptors of the heart and blood vessels, which ultimately leads to cardiac hyperkinesia and vascular constriction. IN initial stages Due to increased cardiac output, renal blood flow may be increased and this leads to increased urine output and Na + excretion. Loss of sodium stimulates secretion aldosterone, which retains sodium in the tissues and walls of arterioles, which increases their sensitivity to pressor influences. Thus, they are formed vicious circles:
1) increased secretion of catecholamines + renal factor → renin-angiotensin mechanism → SDC → increased levels of catecholamines;
2) the renin-angiotensin and aldosterone mechanisms potentiate each other;
3) weakening of the depressor mechanism contributes to the disinhibition of the SDC → an increase in blood pressure and a decrease in the excitability of depressor baroreceptors.
The stability and severity of arterial hypertension in hypertension is determined not only by the activity of the body’s pressor systems, but also by the state of a number of depressor systems, including the kinin system of the kidneys and blood, the activity of angiotensinase and renal prostaglandins.
Increased activity of depressor mechanisms on early stages hypertension should be considered as a reaction to arterial hypertension. Under physiological conditions, depressor systems neutralize the effect of factors that cause an increase in blood pressure, since there is a clear interaction between the pressor and depressor systems.
The period of stabilization of hypertension is characterized by new hemodynamic changes: a gradual decrease in cardiac output and an increase in total peripheral vascular resistance. A major role during this period is played by the decrease in compensatory reserves of depressor nervous and humoral mechanisms(humoral depressor systems, sensitivity of baroreceptors of the aortic arch and sinocarotid zone). The constant tension of the hypothalamic structures responsible for the regulation of blood pressure leads to the fact that the initially unstable and short-term increase in the tone of the arterioles (and especially the arterioles of the kidneys) becomes permanent. Therefore, in the pathogenesis of hypertension during the period of stabilization, humoral factors play an increasingly important role. Functional (vasoconstriction) and then organic (arteriohyalinosis) narrowing of the renal arterioles causes hyperfunction and hypertrophy of the juxtaglomerular apparatus and increased secretion renina.
New links are often included in the pathogenesis - in particular, an increase in the pressor activity of hypothalamic structures under the influence of ischemia associated with vasoconstriction and angiopathy of cerebral vessels. A significant proportion of patients develop atherosclerosis of the aorta, leading to loss of its elasticity, which contributes to a further increase in systolic pressure and destruction of baroreceptor zones. Atherosclerosis of the cerebral arteries and renal arteries creates the prerequisites for the stabilization of high blood pressure due to constant ischemia of the brain and kidneys.
Early cardiac overload occurs and heart failure develops.
All arterial hypertension is divided by origin into two groups: essential (primary) arterial hypertension, previously called hypertension, and symptomatic (secondary) arterial hypertension.
Essential (primary) arterial hypertension is a disease of unknown etiology with a hereditary predisposition, resulting from the interaction of genetic and environmental factors, characterized by a stable increase in blood pressure (BP) in the absence of organic damage to the organs and systems that regulate it.
Etiology of arterial hypertension
Remains unknown. It is assumed that the interaction of genetic and environmental factors is of key importance. Environmental factors: excess salt consumption, smoking, alcohol, obesity, low physical activity, physical inactivity, psycho-emotional stressful situations.
Risk factors for the development of arterial hypertension (AH): age, gender (under the age of 40 years - male), smoking, obesity, physical inactivity.
Pathogenesis of arterial hypertension
The pathogenesis of hypertension is based on a violation of regulatory mechanisms, then functional and organic disorders are added.
The following mechanisms of regulation are distinguished: hyperadrenergic, sodium-volume-dependent, hyperrenin, calcium-dependent.
1. Hyperadrenergic: increased sympathetic tone, increased density and sensitivity of adrenergic receptors, activation of the sympathoadrenal system: increased heart rate, increased cardiac output, increased renal vascular resistance, total peripheral resistance is normal.
2. Sodium-volume-dependent mechanism: sodium and fluid retention associated with increased salt intake. As a result, an increase in circulating blood volume, cardiac output, and total peripheral resistance.
3. Hyperrenin: due to an increase in the level of renin in plasma, an increase in angiotensin 2 occurs, followed by an increase in aldosterone.
4. Calcium-dependent: excessive accumulation of cytosolic calcium occurs in vascular smooth muscle due to impaired transmembrane transport of calcium and sodium.
Classification of arterial hypertension
Several classifications of essential arterial hypertension have been proposed.
According to the degree of blood pressure increase:
I degree: blood pressure levels 140-159/90-99 mmHg;
II degree: 160-179/100-109 mmHg;
III degree: more than 180/110 mm Hg.
According to the risk of development cardiovascular complications for the forecast scene:
1) low risk: no risk factors, grade I increase in blood pressure - the risk of complications is less than 15% in the next 10 years;
2) average risk: 1-2 risk factors, except diabetes mellitus, I or II degree of increase in blood pressure - 15-20%;
3) high risk: 3 or more factors, or target organ damage, or diabetes, I, II, III degree of increase in blood pressure - the risk of complications is 20-30%.
4) very high risk: concomitant diseases (stroke, myocardial infarction, chronic heart failure, angina pectoris, chronic renal failure, dissecting aortic aneurysm, fundus hemorrhage), especially with grade III increase in blood pressure - the risk is more than 30% in the next 10 years.
Risk factors: males over 50 years of age: females over 65 years of age; smoking; obesity; cholesterol (more than 6.5 mmol/l); diabetes; family history of early cardiovascular disease; increase in blood pressure over 140/90 mm Hg.
Target organ damage. Heart: left ventricular myocardial hypertrophy, retina: generalized narrowing of the retinal arteries; kidneys: proteinuria or a slight increase in blood creatinine levels (up to 200 µmol/l); vessels: atherosclerotic plaques in the aorta or other large arteries.
By stage (depending on target organ damage):
Stage I. There are no objective signs of target organ damage;
Stage II. Damage to target organs, without disrupting their function.
Heart: left ventricular myocardial hypertrophy; retina: narrowing of the retinal arteries; kidneys: proteinuria or a slight increase in blood creatinine levels (up to 200 µmol/l); vessels: atherosclerotic plaques in the aorta, carotid, femoral or iliac arteries- Stage III. Damage to target organs with disruption of their function.
Heart: angina pectoris, myocardial infarction, heart failure; brain: transient cerebrovascular accident, stroke, hypertensive encephalopathy, vascular dementia; kidneys: increased creatine levels in the blood (more than 200 µmol/l), renal failure; retina: hemorrhages, degenerative changes, edema, atrophy optic nerve; vessels: dissecting aortic aneurysm, arterial occlusion with clinical manifestations.
Symptoms of arterial hypertension
Complaints: headache more often occurs at night or early in the morning after waking up, in the back of the head, forehead or throughout the head, dizziness, noise in the head, flashing spots before the eyes or other signs of visual impairment, pain in the heart. There was a previous history of elevated blood pressure or a family history.
When examining the patient: obesity is often observed, hyperemia of the face and upper half of the body is noted, sometimes in combination with cyanosis.
Auscultation reveals an emphasis on the 2nd heart sound on the aorta.
Laboratory and instrumental diagnostics
Laboratory methods research:
General blood analysis;
Biochemical blood test: cholesterol, glucose, triglycerides, HDL, LDL, creatinine, urea, potassium, sodium, calcium;
General urine analysis;
Urinalysis according to Nechiporenko;
Urinalysis according to Zimnitsky;
Rehberg's test.
Instrumental methods research.
EchoCG: this method The study allows you to identify signs of hypertrophy, determine the size of the heart chambers, evaluate the systolic and diastolic functions of the LV, and identify impaired myocardial contractility.
Ultrasound of the kidneys and adrenal glands.
RG chest: allows you to assess the degree of LV dilatation.
Daily blood pressure monitoring.
Consultation with an ophthalmologist. Fundus ophthalmoscopy is performed to assess the degree of changes in the retinal vessels. The following changes are detected:
1) narrowing of the retinal arterioles (silver wire symptom, copper wire symptom);
2) expansion of the retinal veins;
3) characteristic changes in the veins at the place of their intersection with the artery: the following degrees of such changes are distinguished: Salus symptom 1 - dilation of the vein is observed on both sides of its intersection with the artery;
Salus symptom 2: the vein forms an arch at the intersection;
Salus symptom 3: an arched bend of the vein is formed at the point of crossover, resulting in the impression of a “break” of the vein at the point of crossover;
4) hypertensive retinopathy.
Consultation with a neurologist.
The most significant complications of hypertension are: hypertensive crises, hemorrhagic or ischemic strokes, myocardial infarction, nephrosclerosis, heart failure.
Symptomatic arterial hypertension
This is an increase in blood pressure, etiologically associated with a specific disease of the organs or systems involved in its regulation. They account for about 10% of all arterial hypertension.
Classification
Renal.
Diseases of the kidney parenchyma: acute and chronic glomerulonephritis(high value in differential diagnosis has a urine test: proteinuria, erythrocyturia; pain in the lumbar region; history streptococcal infection), chronic pyelonephritis (in urine analysis: proteinuria, leukocyturia, bacteriuria; dysuric disorders; fever; pain in the lumbar region; normalization of blood pressure against antibacterial therapy), polycystic kidney disease, kidney damage in systemic connective tissue diseases and systemic vasculitis, hydronephrosis, Goodpasture's syndrome.
Renovascular: atherosclerosis of the renal arteries, thrombosis of the renal arteries and veins, aneurysms of the renal arteries. These antigens are resistant to drug treatment, rare occurrence of hypertensive crises. Aortography is of decisive importance for the diagnosis of renovascular hypertension.
Renin-producing kidney tumors.
Nephroptosis.
Endocrine.
Primary hyperaldosteronism (Conn syndrome): features of clinical manifestations are associated with hypokalemia. Oliguria, nocturia, muscle weakness, and transient paresis occur.
Pheochromocytoma. Sudden hypertensive crises with severe autonomic symptoms, rapid development of fundus changes, cardiomegaly, tachycardia, weight loss, diabetes mellitus, or decreased glucose tolerance occur. Diagnosis requires detection of catecholamines or their metabolites in urine.
Itsenko-Cushing syndrome and disease: to diagnose the disease, it is necessary to determine the content of 17 ketosteroids and 17 oxyketosteroids in the urine; if they increase, the concentration of cortisol in the blood should be determined.
Thyrotoxicosis.
Acromegaly.
Hemodynamic hypertension: coarctation of the aorta (diagnosis is helped by measuring blood pressure: increased in the shoulder, decreased in the thigh); atherosclerosis of the aorta.
Hypertension during pregnancy.
Hypertension associated with damage to the nervous system: meningitis, encephalitis, abscesses, brain tumors, lead intoxication, acute porphyria.
Acute stress, including operating stress.
Admission-induced hypertension medicines.
Alcohol abuse.
Systolic hypertension with increased cardiac output: aortic valve insufficiency, thyrotoxicosis syndrome, Paget's disease; sclerotic rigid aorta.
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Arterial hypertension is far from rare disease. The older a person gets, the more likely he or she is to have hypertension. This pathology also occurs in young people. No one is immune from the development of serious complications, therefore, at any age it is necessary to carry out adequate and timely treatment.
There is primary, or essential, arterial hypertension - doctors call it “hypertension.” It occurs much more often and is characterized by a persistent increase in the level of pressure in the vessels in the absence of any reason. This disease is also called idiopathic. There is also secondary hypertension, which occurs as a result of the pathology of any organ or system.
Description of the disease
Secondary, or symptomatic arterial hypertension is a pathology in which an increase in blood pressure (BP) is recorded, caused by another disease and of a secondary nature. For example, with damage to the kidneys, blood vessels, endocrine system. It is registered in 5-10% of cases among people with high blood pressure. However, if we take into account the malignant course of hypertension, the incidence reaches 20%. It is often registered in young people - in 25% of cases under the age of 35 years.
It is important to identify and begin treatment for this condition as early as possible, since a constant increase in blood pressure leads to irreversible consequences for the heart and blood vessels.
The likelihood of developing severe complications, such as heart attack or stroke, even in young people, increases. Therapeutic effects involve treatment of the primary disease causing increased blood pressure. Correcting blood pressure levels with medications for an untreated primary disease most often does not have an effect.
Classification by etiological factor
Depending on the cause of secondary hypertension, the following types of disease are distinguished.
IN in this case The development of hypertension is provoked by kidney diseases:
- Renal artery disease is one of the most common causes. It is also called renovascular hypertension. The kidneys are very important in regulating blood pressure, therefore, when their blood supply is insufficient, substances that increase systemic blood pressure begin to be released into the blood to ensure renal blood flow. We are talking about the renin-angiotensin system. The reasons for poor blood supply can be very different: congenital pathology renal arteries, atherosclerosis, thrombosis, compression from the outside by a space-occupying formation.
- Polycystic kidney disease is a hereditary disease that causes gross changes in the form of the appearance of a large number of cysts and, as a result, dysfunction of the organ up to the development of terminal renal failure.
- Inflammatory processes in the kidneys - chronic pyelonephritis, glomerulonephritis. Much less frequently, but still can cause secondary changes in the form of increased blood pressure.
Diagram of renal artery lesions Endocrine arterial hypertension
An increase in blood pressure is provoked by a disease of the endocrine system, namely:
- Itsenko-Cushing syndrome. The pathogenesis of this disease is based on damage to the adrenal cortex, resulting in increased production of glucocorticosteroids. Such processes lead to an increase in blood pressure and also cause characteristic external changes in the patient.
- Pheochromocytoma is a disease that affects the adrenal medulla. Occurs infrequently, however, leads to a malignant form arterial hypertension. Due to compression of the inner layer of the adrenal glands by the tumor, adrenaline and norepinephrine are released into the blood, which causes a constant or crisis increase in pressure.
- Conn's syndrome (primary hyperaldosteronism) is a tumor of the adrenal gland that leads to increased aldosterone levels. As a result, hypokalemia and increased blood pressure develop, which is difficult to correct with medication.
- Diseases thyroid gland– hyperparathyroidism, hyper- and hypothyroidism.
Hemodynamic or cardiovascular arterial hypertension
Occurs as a result of involvement in pathological process great vessels, namely:
- Coarctation, or narrowing of the aorta, is a congenital disease in which high blood pressure in the arteries arising from the aorta above the site of narrowing and low blood pressure below the site of narrowing. For example, a large difference is recorded between blood pressure in the arms and legs.
- Late stages of chronic heart failure.
Types of arterial hypertension Arterial hypertension of central origin
Increased blood pressure is caused by a primary brain disease with a secondary disturbance of central regulation. Such diseases include stroke, encephalitis, and head injuries.
Hypertension of drug etiology
We are talking about taking drugs of certain groups that can cause hypertension, for example, oral contraceptives, non-steroidal anti-inflammatory drugs, glucocorticosteroids.
Other reasons:
- alcohol abuse;
- vertebral artery syndrome;
- allergies.
Symptoms and detection methods
The symptoms of both primary and secondary hypertension are generally similar. The difference is that secondary hypertension is accompanied by manifestations of the underlying disease. Increased blood pressure may occur without symptoms. Sometimes there are complaints such as headache, a feeling of tightness in the temples, dizziness, tinnitus, spots before the eyes, redness of the face, general weakness, nausea. Diagnosis is based on analysis of complaints, physical examination and instrumental methods, which may vary depending on the patient’s condition.
Diagnosis of the described type of hypertension is difficult due to the large list of diseases that can cause it. There are several signs that are not typical for hypertension. If these symptoms are present, you can suspect the secondary nature of the disease and continue the examination:
- Increased blood pressure in young people.
- Sudden acute onset of the disease immediately with high blood pressure numbers. Hypertension is characterized by a slowly progressive course with a gradual increase in blood pressure numbers.
- Malignant course - from the very beginning, elevated blood pressure numbers respond poorly to treatment, and are characterized by resistance to standard antihypertensive therapy.
- Sympathoadrenal crises.
The presence of these signs should prompt the doctor to think about the secondary nature of the disease. In such cases, it is necessary to continue the diagnostic search to identify the primary pathology. The suspected diagnosis and accompanying symptoms determine the examination methods that will be used in a given patient.
If the renal nature of hypertension is suspected, the diagnosis will include a general urinalysis according to Nechiporenko, urine culture to determine the pathogen, determination of the amount of protein in the urine, ultrasound of the kidneys, and intravenous urography. To exclude narrowing of the lumen of the renal arteries, ultrasound of the renal arteries, magnetic resonance angiography, CT scan with vascular contrast.
If the endocrine genesis of arterial hypertension is suspected, then the hormonal sphere is analyzed - catecholamines in the blood and urine and thyroid hormones are determined. Instrumental methods include ultrasound, MRI of the adrenal glands, thyroid gland.
In addition, by the degree of change in systolic and diastolic blood pressure, one or another genesis of the disease can be suspected. With kidney pathology, diastolic pressure most often increases predominantly; hemodynamic hypertension is characterized by an isolated increase in systolic blood pressure. With endocrine genesis, systolic-diastolic arterial hypertension is more often observed.
Treatment options
Standard treatment with conventional antihypertensive drugs for the secondary nature of the disease usually has no effect or helps only slightly. If during the diagnostic search a primary disease causing an increase in blood pressure was identified, it is necessary to treat the primary pathology:
- If there is a tumor or other mass formation in the kidneys or adrenal glands, surgical treatment is performed whenever possible.
- At inflammatory diseases in the kidneys (pyelonephritis), a course of antibacterial and anti-inflammatory therapy is carried out.
- For diseases of the thyroid gland, drug correction of hormonal levels is carried out.
- With the hemodynamic etiology of hypertension, severe narrowing of the aorta or heart disease, cardiac surgery is necessary, as well as drug correction of heart failure.
- If medication is the cause, the patient should stop taking such medications.
- In case of hypertension of central origin, the primary disease is compensated whenever possible, conservative treatment is carried out (for stroke) or surgical treatment(for example, with a brain tumor).
- Abnormalities in the vessels of the kidneys, if possible, require surgical correction.
In parallel with the treatment of the primary disease, antihypertensive therapy is also carried out, that is, drug reduction of blood pressure. It includes the use of antihypertensive drugs of the main groups: ACE inhibitors, calcium channel antagonists, β-blockers, diuretics, antihypertensive drugs central action. Selected for each patient individual scheme treatment depending on the primary disease, the presence of contraindications, individual characteristics, concomitant pathology.
Secondary hypertension is a complex disease that requires special attention doctors, thorough examination, selection effective method treatment. The problem is relevant in modern medicine, since this disease does not respond well to standard drug correction and often has a malignant course, young people are often susceptible to the disease.
Timely detection, correct diagnosis and adequate treatment will help stop the unfavorable course of the disease in time and prevent possible unpleasant complications.
