Arterial Hypertension – Etiology and Pathogenesis, Classifications, Diagnosis and Treatment

Arterial hypertension (Arterial hypertension) is a condition in which systolic blood pressure is 140 mm Hg. and more and / or diastolic blood pressure 90 mm Hg. and more, provided that these values ​​were obtained as a result of at least three measurements made at different times in a calm environment, and the patient on that day did not take drugs that change blood pressure.

If it is possible to identify the causes of hypertension, then it is considered secondary (symptomatic).

In the absence of an obvious cause of hypertension, it is called primary, essential, idiopathic, and in Russia it is called hypertension.

Isolated systolic hypertension is characterized by systolic blood pressure above 140 mm Hg. and diastolic blood pressure less than 90 mm Hg.

Arterial hypertension is considered to be malignant when the level of diastolic blood pressure is more than 110 mm Hg. and the presence of pronounced changes in the fundus (retinal hemorrhage, edema of the optic nipple).

 

Prevalence

In Arterial hypertension, Arterial hypertension affects 30-40% of the adult population. With age, the prevalence increases and reaches 60-70% in people over 65 years old, and in old age, isolated systolic hypertension is more common, which is found in less than 5% of the population under the age of 50. Up to 50 years of age hypertension is more common in men, and after 50 years – in women. Among all forms of Arterial hypertension, the share of mild and moderate accounts for about 70-80%, in other cases, pronounced Arterial hypertension is observed.

Secondary Arterial hypertension accounts for 5-10% of all hypertension cases. At the same time, according to the data of specialized clinics, where patients with high and persistent hypertension are concentrated, using complex and expensive research methods, secondary hypertension can be detected in 30-35% of cases.

 

ETIOLOGY OF ARTERIAL HYPERTENSION

In Arterial hypertension, Cardiac output and total peripheral vascular resistance are the main determinants of blood pressure. An increase in one of these factors leads to an increase in blood pressure and vice versa. In the development of hypertension, both internal humoral and neurogenic (renin-angiotensin system, sympathetic nervous system, baroreceptors and chemoreceptors) and external factors (excessive consumption of table salt, alcohol, obesity) are important.

  • Vasopressor hormones include renin, angiotensin II, vasopressin, endothelin.
  • Vasodepressors are natriuretic peptides, kallikrein-kinin system, adrenomedullin, nitric oxide, prostaglandins (prostacyclin).

In Arterial hypertension, In recent years, the genetic mechanisms of hypertension have been actively studied. Reliably established genetic abnormalities contributing to the development of hypertension are presented below.

  • Mutations in the angiotensin gene.
  • Mutations leading to the expression of an enzyme that synthesizes aldosterone.
  • Mutations of β-subunits of amiloride-sensitive sodium channels of the renal epithelium.


PATHOGENESIS OF ARTERIAL HYPERTENSION

In Arterial hypertension, One of the consequences of a prolonged increase in blood pressure is damage to internal organs, the so-called target organs. These include:

  • heart;
  • brain;
  • kidneys;
  • vessels.

In Arterial hypertension, Heart failure in hypertension may manifest as left ventricular hypertrophy, angina pectoris, myocardial infarction, heart failure, and sudden cardiac death; brain damage – thrombosis and hemorrhage, hypertensive encephalopathy and damage to perforating arteries; kidney – microalbuminuria, proteinuria, chronic renal failure; vessels – involvement in the process of vessels of the retina of the eyes, carotid arteries, aorta (aneurysm). In untreated patients with hypertension, 80% of deaths are caused by pathology of the cardiovascular system (CVS): in 43% – CHF, in 36% – coronary artery insufficiency. Cerebrovascular and renal causes are less common – 14% and 7%, respectively.

 

Heart with arterial hypertension

In Arterial hypertension, Due to the severity and high frequency of heart changes in hypertension (in 50% of patients), the terms “hypertensive heart disease” and “hypertensive heart” have recently begun to be used, which mean the entire complex of morphological and functional changes. E. D. Frolikh (1987) identified four stages of hypertensive heart disease.

  • Stage I – there are no obvious changes in the heart, but, according to the echocardiography, there are signs of impaired diastolic function (see chapter 11 “Heart failure”). Violation of left ventricular diastolic function in hypertension can develop before systolic disorders and be an independent risk factor for the development of heart failure.
  • Stage II – an increase in the left atrium (according to EchoCG and ECG).
  • Stage III – the presence of left ventricular hypertrophy (according to ECG, EchoCG, X-ray). Left ventricular hypertrophy is the most frequent complication of hypertension, and this complication serves as an extremely unfavorable prognostic sign: the risk of developing vascular accidents (myocardial infarction, stroke) increases 4 times, and the risk of death from cardiovascular diseases 3 times compared with patients with hypertension without left ventricular hypertrophy. In untreated patients with severe hypertension and left ventricular hypertrophy, the two-year mortality rate is 20%.
    • Echocardiography is the most accurate method for detecting left ventricular hypertrophy. According to EchoCG data, left ventricular hypertrophy develops in more than 50% of patients with hypertension.
    • The information content of the X-ray examination is low, since it reveals only significant hypertrophy with dilatation of the left ventricular cavity.
  • Stage IV – the development of CHF, possibly the addition of CHD. CHF is a “classic” outcome of hypertension, i.e. a condition that inevitably arises in hypertension (if the patient does not die earlier) and ultimately leads to death. In this regard, it is necessary to know the clinical manifestations of heart failure and methods of its timely detection (see chapter 11 “Heart failure”).

IHD can occur not only due to damage to the coronary arteries (their epicardial parts), but also due to microvasculopathy.

 

Kidneys with arterial hypertension

In Arterial hypertension, The kidneys occupy one of the central places in the regulation of blood pressure, as they produce vasoactive substances. The state of the kidneys is summarized by the glomerular filtration rate (GFR). In uncomplicated hypertension, it is usually normal. With pronounced or malignant hypertension, GFR is significantly reduced. Since constant overpressure in the glomeruli leads to dysfunction of the glomerular membranes, it is believed that GFR with long-term hypertension depends on the level of blood pressure: the higher the blood pressure, the lower it is. In addition, while maintaining elevated blood pressure, constriction of the renal artery occurs, which leads to early ischemia of the proximal convoluted tubules and impairment of their functions, and then to damage to the entire nephron.

Hypertensive nephrosclerosis is a characteristic complication of hypertension, which is manifested by a decrease in renal excretory function. The main predisposing factors for the development of nephrosclerosis:

  • elderly age;
  • male gender;
  • decreased glucose tolerance.

In Arterial hypertension, The main indicators of the involvement of the kidneys in the pathological process in hypertension are the content of creatinine in the blood and the concentration of protein in the urine.

  • The concentration of creatinine in the blood correlates with the level of blood pressure, as well as with the risk of developing cardiovascular diseases in the future. High creatinine clearance, reflecting glomerular hyperfiltration, can be regarded as a clinical marker of the early stage of hypertensive renal disease.
  • With microalbuminuria, the amount of excreted protein reaches 300 mg / day. Protein secretion of more than 300 mg / day is considered proteinuria.

 

Vessels with arterial hypertension

In Arterial hypertension, Increased total peripheral vascular resistance plays a leading role in maintaining high blood pressure. At the same time, the vessels simultaneously serve as one of the target organs. Damage to small arteries of the brain (occlusion or microaneurysms) can lead to strokes, renal arteries – to impairment of their functions.

The presence of hypertensive retinopathy, diagnosed by examination of the fundus (ophthalmoscopy), is of great importance for the prognosis of the disease. There are four stages of hypertensive retinopathy.

  • Stage I – slight narrowing of arterioles, angiosclerosis.
  • Stage II – more pronounced narrowing of arterioles, arteriovenous intersections, no retinopathy.
  • Stage III – angiospastic retinopathy (“cotton tricks”), hemorrhages, retinal edema.
  • Stage IV – edema of the optic nerve head and significant vasoconstriction.

With ophthalmoscopy, the arteries and arterioles of the retina have a more rectilinear course than usual; numerous arteriovenous intersections are revealed. The wall of the artery is compacted, presses on the underlying vein, causing a narrowing of its lumen at the intersection. In some cases, especially in the elderly, the arterioles become severely narrowed and pale (the “silver wire” symptom), tortuosity and enlargement of the veins appear (the Gvist symptom).

In Arterial hypertension, The developed hypertension is indicated by stagnation in the vein distal to the arteriovenous junction. In the later stages, retinal changes are complicated by retinopathy with the appearance of hemorrhages and exudates. Hemorrhages often occur in the macular region. With a sudden increase in diastolic blood pressure, a true retinal infarction can develop, which looks like a ball of cotton wool (cotton exudate). The appearance of neovascularization of the retina and optic nerve is possible. In case of malignant hypertension, edema of the optic nerve develops, in the area of ​​the macula, deposits of solid exudate in the form of a star may occur.

Metabolic syndrome is understood as various combinations of risk factors for CVD diseases. See chapter 61, Metabolic Syndrome, for details.

 

CLASSIFICATIONS OF ARTERIAL HYPERTENSION

Currently, several classifications of hypertension are used. First of all, the degree of increase in blood pressure is established (Table 4-1). In cases where the values ​​of systolic and diastolic blood pressure fall into different categories, then a higher degree of hypertension is taken into the diagnosis. It should be emphasized that the degree of hypertension is established only in cases when a patient is diagnosed with hypertension for the first time or when he does not receive antihypertensive therapy.

Table 4-1. Hypertension classification

Category

Systolic blood pressure ,

mm Hg . Art .

Diastolic blood pressure ,

mm Hg . Art .

Optimal

‹120

‹80

Normal

‹130

‹85

High normal

130-139

85-89

1 degree (soft)

140-159

90-99

Grade 2 (moderate)

160-179

100-109

3 degree (severe)

> 180

> 110

Isolated systolic

> 140

‹90

Note. When determining the degree, the highest blood pressure value should be used, for example, 140/100 mm Hg. – II degree of hypertension.

Table 4-2. Classification of hypertension

Stage I

Stage II

III stage

Increase in blood pressure more than 140/90 mm Hg. in the absence of organic changes in target organs

Increase in blood pressure more than 140/90 mm Hg. in combination with changes in target organs (heart, kidneys, brain, fundus vessels) caused by hypertension

Hypertension combined with damage to target organs and the presence of associated clinical conditions (brain damage, heart disease, kidney disease, peripheral arterial disease, severe retinopathy)

 

Risk stratification In Arterial hypertension

In Arterial hypertension, With the accumulation of epidemiological data on the natural course of the disease, it became apparent that the risk of cardiovascular morbidity and mortality is constantly increasing as blood pressure rises. However, it was impossible to clearly distinguish between normal and pathological blood pressure levels. The risk of complications increases with an increase in blood pressure, even within the normal range of blood pressure. Moreover, the vast majority of cardiovascular complications are recorded in persons with a slight increase in blood pressure.

In patients with hypertension, the prognosis depends not only on the level of blood pressure. The presence of concomitant risk factors, the degree of involvement of target organs in the process, as well as the presence of associated clinical conditions are of no less importance than the degree of increase in blood pressure, and therefore stratification of patients has been introduced into the modern classification depending on the degree of risk.

Patient risk stratification is based on traditional assessment of target organ damage and cardiovascular complications. Dividing patients according to the degree of risk allows for a qualitative assessment of the individual prognosis (the higher the risk, the worse the prognosis) and identifying groups for preferential social and medical support.

In Arterial hypertension, Methods for calculating the risk of coronary heart disease over 10 years, proposed by the European Society of Cardiology, the European Society for Atherosclerosis and the European Society for Hypertension, are used for quantitative risk assessment, which were described in the report of Russian experts on the study of hypertension. The overall risk of cardiovascular complications is calculated taking into account the risk of coronary artery disease: the risk of coronary artery disease is multiplied by a factor of 4/3. For example, if the risk of CHD is 30%, then the risk of cardiovascular complications is 40%.

Clinical manifestations of cardiovascular disease and target organ damage are considered more significant prognostic factors than traditional risk factors. This approach provides physicians with a simplified method for determining the level of risk for each individual patient, gives a clear idea of ​​the long-term prognosis, and facilitates decisions about the timing and nature of antihypertensive therapy, as well as the target blood pressure level. The particular value of the described approach lies in the fact that the blood pressure level is losing its dominant role in the choice of treatment tactics. This seems to be extremely important, given the significant variability in blood pressure, especially in patients who have not received regular treatment, and the inevitable difficulties in attributing a patient to a particular risk group based on blood pressure values ​​alone.

 

Risk stratification criteria are given below.

  • Low risk group. This group includes men and women under 55 years of age with grade 1 hypertension in the absence of risk factors, target organ damage and concomitant cardiovascular diseases. The risk of developing cardiovascular complications in the next 10 years is less than 15%.
  • Medium risk group. This group includes patients with a wide range of blood pressure. A fundamental sign of belonging to this group is the presence of risk factors (men over 55 years old, women over 65 years old, smoking, blood cholesterol concentration of more than 6.5 mmol / L, family history of early cardiovascular diseases) in the absence of target organ damage and / or concomitant diseases. In other words, this group includes patients with a slight increase in blood pressure and numerous risk factors and patients with a pronounced increase in blood pressure. The risk of developing cardiovascular complications in the next 10 years is 15-20%.
  • High risk group. This category includes patients with damage to target organs (left ventricular hypertrophy according to ECG, echocardiography, proteinuria or an increase in the concentration of creatinine in the blood up to 175 μmol / L, generalized or focal narrowing of the retinal arteries), regardless of the degree of hypertension and the presence of associated risk factors … The risk of developing cardiovascular complications in the next 10 years exceeds 20%.
  • Very high risk group. This group includes patients who have associated diseases (angina pectoris and / or myocardial infarction, revascularization surgery, heart failure, previous cerebral stroke or transient ischemic attack, nephropathy, chronic renal failure, peripheral vascular disease, grade III-IV retinopathy), regardless of degree of Arterial hypertension. This group also includes patients with high normal blood pressure in the presence of diabetes mellitus. The risk of developing cardiovascular complications in the next 10 years exceeds 30%.


 

CLINICAL PICTURE AND DIAGNOSTICS OF ARTERIAL HYPERTENSION

In Arterial hypertension, The clinical picture of hypertension is nonspecific and is determined by damage to target organs. When examining patients with hypertension, it is necessary to adhere to the well-known clinical principles of diagnosing any disease: go from a simple study to a complex one and the examination for a patient should not be more difficult than the disease itself.

 

The goals of diagnostic measures for arterial hypertension

In Arterial hypertension, Diagnostic measures for hypertension are carried out for the following purposes.

  • Determination of the possible cause of hypertension (the tactics of patient management depends on the correct diagnosis).
  • Diagnosis of concomitant diseases (may affect the course of hypertension, and the prescribed treatment may affect the course of concomitant diseases).
  • Identification of risk factors for the development of coronary artery disease (see chapter 3 “Prevention of coronary heart disease”). Since hypertension itself is one of the risk factors for the development of coronary artery disease, the presence of another risk factor further increases the likelihood of developing coronary artery disease. In addition, the treatment prescribed can seriously affect risk factors (for example, diuretics and β-blockers in the presence of dyslipidemia and insulin resistance can exacerbate these disorders).
  • Determination of the involvement of target organs in the pathological process, since their defeat in the most serious way affects the prognosis of the disease and approaches to the treatment of hypertension.

 

COMPLAINTS AND ANAMNESIS OF ARTERIAL HYPERTENSION

In Arterial hypertension, Despite high BP values, there may be no complaints. In some patients, with an increase in blood pressure, headaches, dizziness, nausea, flashing “flies” before the eyes, pain in the heart, palpitations, fatigue, nosebleeds are possible. Questioning the patient should include clarification of the following important circumstances.

  • Family history of hypertension, diabetes mellitus, lipid metabolism disorders, coronary heart disease, stroke, kidney disease.
  • Duration of hypertension, previous blood pressure, results and side effects of previously used antihypertensive drugs. Detailed questioning about the use of drugs that increase blood pressure [oral contraceptives, non-steroidal anti-inflammatory drugs (NSAIDs), amphetamines, erythropoietin, cyclosporins, GC].
  • The presence and course of ischemic heart disease, heart failure, stroke, other pathological processes in this patient (gout, dyslipidemia, sexual dysfunction, kidney pathology, diseases with bronchospastic syndrome).
  • Identification of symptoms of secondary hypertension.
  • Assessment of lifestyle (the amount of table salt, fat, alcohol, smoking, physical activity), personal, psychosocial and external factors affecting blood pressure (family, work).

 

INSPECTION AND PHYSICAL EXAMINATION OF ARTERIAL HYPERTENSION

In Arterial hypertension, Physical examination and physical examination usually do not show any specific symptoms, but it is possible to identify signs of secondary hypertension and damage to target organs.

  • During the examination, it is possible to identify the manifestations of some endocrine diseases accompanied by hypertension: hypothyroidism, thyrotoxicosis, Cushing’s syndrome, pheochromocytoma, acromegaly.
  • Palpation of peripheral arteries, auscultation of blood vessels, heart, chest, abdomen suggest vascular lesions as a cause of hypertension, suspect aortic disease, renovascular hypertension (auscultation of the renal arteries is performed slightly higher and lateral to the navel).

However, blood pressure measurement remains the main method of research and diagnosis of hypertension.

 

Conditions and rules for measuring blood pressure In Arterial hypertension

  • The measurement must be carried out after a period of complete rest (at least 5 minutes). At least 30 minutes before the procedure, it is not recommended to eat, drink coffee, alcohol, exercise, or smoke. When measuring, the legs should not be crossed, the feet should be on the floor, the back should rest on the back of the chair. The arm needs support; the bladder must be emptied before measurement. Failure to comply with these conditions can lead to overestimation of blood pressure values:
  • after taking coffee at 11 mm Hg. systolic blood pressure and 5 mm Hg. diastolic blood pressure;
  • after drinking alcohol by 8 mm Hg;
  • after smoking by 6 mm Hg. systolic blood pressure and 5 mm Hg. diastolic blood pressure;
  • with an overflowing bladder by 15 mm Hg. systolic blood pressure and 10 mm Hg. diastolic blood pressure;
  • in the absence of a back support of 6-10 mm Hg. systolic blood pressure;
  • in the absence of a 7 mm Hg arm support. systolic blood pressure and 11 mm Hg. diastolic blood pressure.
  • The shoulder should be at the level of the fourth or fifth intercostal space (low elbow position overestimates systolic blood pressure by an average of 6 mm Hg, high – underestimates blood pressure by 5/5 mm Hg). When measuring blood pressure in the patient’s lying position, his arm should be slightly raised (but not suspended) and be at the level of the middle of the chest. The shoulder should not be squeezed by clothing (all the more, measurement through clothing is unacceptable), since the systolic pressure can be overestimated by 5-50 mm Hg. The lower edge of the cuff should be 2 cm above the elbow (misalignment of the cuff can lead to an overestimation of blood pressure by 4 mm Hg systolic blood pressure and 3 mm Hg diastolic blood pressure), and it should fit snugly against the shoulder. The air in the cuff should be injected to a level of 30 mm Hg. above the pressure at which the pulse on the radial artery disappears. The stethoscope should be placed in the antecubital fossa. The rate of decrease in pressure in the cuff is 2 mm / s (with slow decompression, systolic blood pressure is overestimated by 2 mm Hg and diastolic blood pressure by 6 mm Hg, and diastolic blood pressure during rapid decompression). The moment of appearance of the first sounds corresponds to phase I of Korotkoff tones and shows systolic blood pressure. The moment of disappearance of the last sounds will correspond to the V phase of Korotkoff’s tones – diastolic blood pressure.
  • The measured values ​​should be indicated with an accuracy of 2 mm Hg. When measuring, it is necessary to listen to the area of ​​the ulnar fossa until the pressure in the cuff drops to zero (one should remember about the possible insufficiency of the aortic valve, other pathological conditions with high pulse pressure, large stroke volume of the heart). During each examination of the patient, blood pressure is measured at least twice on the same arm and the average values ​​are recorded. During the first examination, the pressure is measured on both arms, and subsequently on the arm where it was higher. The difference in blood pressure on the left and right hand normally does not exceed 5 mm Hg. More significant differences should be alarming regarding the pathology of the vessels of the upper extremities.
  • Repeat measurements should be carried out under the same conditions. It is necessary to measure blood pressure in two positions (lying and sitting) in the elderly, with diabetes mellitus, in patients taking peripheral vasodilators (to identify possible orthostatic arterial hypotension).

 

LABORATORY AND INSTRUMENTAL METHODS OF RESEARCH OF ARTERIAL HYPERTENSION

In uncomplicated cases, it is enough to conduct a small number of studies to exclude symptomatic hypertension, to identify risk factors and the degree of damage to target organs. It is necessary to carry out the following laboratory research methods.

  • General blood analysis. Anemia, erythrocytosis, leukocytosis, accelerated ESR are signs of secondary hypertension.
  • A general urinalysis is performed to detect leukocyturia, erythrocyturia, proteinuria (symptomatic hypertension), glucosuria (diabetes mellitus).
  • In a biochemical blood test to exclude secondary hypertension and assess risk factors, the concentration of potassium, creatinine, glucose, cholesterol is determined. It should be remembered that a rapid decrease in blood pressure with long-term hypertension of any etiology can lead to an increase in creatinine in the blood.

In Arterial hypertension, Instrumental research methods are presented below.

  • ECG allows detecting left ventricular hypertrophy, rhythm and conduction disturbances, signs of concomitant ischemic heart disease, suspect electrolyte disturbances.
  • Echocardiography is performed to diagnose left ventricular hypertrophy, assess myocardial contractility, and identify valvular defects as a cause of hypertension.
  • Ultrasound of vessels, kidneys, adrenal glands, renal arteries should be performed to exclude secondary hypertension.
  • Study of the fundus.

WHO and the International Society of Hypertension consider it necessary to introduce additional methods of examination of patients with hypertension.

  • Determination of lipid spectrum (HDL, LDL, triglycerides), concentration of uric acid, hormones (aldosterone, urine catecholamines).
  • Conducting an in-depth examination in specialized hospitals with complicated hypertension or in order to identify secondary hypertension.

 

DIFFERENTIAL DIAGNOSTICS OF ARTERIAL HYPERTENSION

HYPERTONIC DISEASE OF ARTERIAL HYPERTENSION

The diagnosis of hypertension (essential, primary hypertension) is made only by excluding secondary hypertension.

RENOPARENCHYMATOUS ARTERIAL HYPERTENSION

In Arterial hypertension, Renoparenchymal hypertension accounts for 2-3% (according to specialized clinics, 4-5%) of all cases of high blood pressure.

The causes of renoparenchymal hypertension can be bilateral (glomerulonephritis, diabetic nephropathy, tubulointerstitial nephritis, polycystic) and unilateral renal lesions (pyelonephritis, tumor, trauma, single renal cyst, hypoplasia, tuberculosis). The most common cause of renoparenchymal hypertension is glomerulonephritis (for more details see chapter 30 “Acute glomerulonephritis”, chapter 31 “Rapidly progressive glomerulonephritis”, chapter 33 “Chronic glomerulonephritis”).

In the pathogenesis of renoparenchymal hypertension, hypervolemia, hypernatremia due to a decrease in the number of functioning nephrons and activation of the renin-angiotensin system, an increase in total peripheral resistance with normal or decreased cardiac output are important.

The main signs of this form of hypertension are considered:

  • a history of kidney disease;
  • changes in urinalysis (proteinuria more than 2 g / day, cylindruria, hematuria, leukocyturia, high concentration of blood creatinine);
  • signs of kidney damage on ultrasound.

Usually, changes in urinalysis precede an increase in blood pressure.

 

VASORENAL ARTERIAL HYPERTENSION

Renal hypertension is symptomatic hypertension caused by renal (renal) ischemia due to impaired renal artery patency. The prevalence of this form of the disease is 1-2% (up to 4-16%, according to specialized clinics) among all types of hypertension.

In the structure of the causes of vasorenal hypertension, 60-70% of cases are caused by atherosclerosis of the renal arteries, 30-40% by fibromuscular dysplasia, less than 1% by rare causes (renal artery aneurysm, renal artery thrombosis, renal arteriovenous fistulas, renal vein thrombosis).

In the pathogenesis of vasorenal hypertension, activation of the renin-angiotensin system due to hypoperfusion of the kidney (kidneys) is of greatest importance, which leads to vasospasm, increased synthesis of renin and aldosterone, retention of sodium and water ions, an increase in intravascular volume and stimulation of the sympathetic nervous system.

 

Clinical presentation and diagnosis in Arterial hypertension, 

In vasorenal hypertension, the disease usually occurs before the age of 30 or in individuals over 50 years of age, there is no family history of hypertension. Characterized by rapid progression of the disease, high blood pressure with the addition of retinopathy, resistance to treatment, vascular complications, often an increase in blood creatinine during treatment with ACE inhibitors. The following symptoms are often identified: noise in the projection of the renal artery (in about 50% of cases), hypokalemia (against the background of excessive secretion of aldosterone), kidney asymmetry on ultrasound (reduction of one kidney). To confirm the diagnosis, it is necessary to carry out the following research methods.

  • Determination of plasma renin activity is one of the most reliable diagnostic methods, especially in combination with the captopril test (100% sensitivity and 95% specificity). An increase in plasma renin activity after taking captopril by more than 100% of the initial value indicates pathologically high renin secretion and is a sign of vasorenal hypertension.
  • Doppler ultrasound of the renal arteries detects acceleration and turbulence in blood flow.
  • Renal scintigraphy reveals a decrease in the supply of the isotope to the affected kidney. It is optimal to combine renal scintigraphy with captopril intake at a dose of 25-50 mg orally, since in the case of a disease, captopril intake decreases the intake of the isotope into the renal tissue. A normal renal scintigram after taking captopril excludes hemodynamically significant renal artery stenosis.
  • Renal arteriography – the “gold standard” in the diagnosis of renal artery stenosis.


 

ENDOCRINE ARTERIAL HYPERTENSION

Endocrine hypertension accounts for approximately 0.1-1% of all hypertension (up to 12%, according to specialized clinics).

 

Pheochromocytoma In Arterial hypertension

Arterial hypertension is caused by pheochromocytoma in less than 0.1-0.2% of all Arterial hypertension cases. Pheochromocytoma is a catecholamine-producing tumor, in most cases localized in the adrenal glands (85-90%). To characterize it, you can use the “rule of ten”: in 10% of cases it is familial, in 10% – bilateral, in 10% – malignant, in 10% – multiple, in 10% – extra-adrenal, in 10% it develops in children.

The clinical manifestations of pheochromocytoma are very numerous, varied, but nonspecific (Table 4-3).

Table 4-3. Clinical manifestations of pheochromocytoma

Clinical manifestation

Frequency

AG

90%

Headache

80%

Orthostatic arterial hypotension, palpitations and tachycardia

60%

Sweating

65%

Paleness, fear

45%

Limb tremor

35%

Abdominal pain

15%

Visual impairment

15%

In 50% of cases, hypertension can be permanent, and in 50% it can be combined with crises. A crisis usually arises out of connection with external factors. Hyperglycemia is common. It should be remembered that pheochromocytoma can occur during pregnancy and that it can be accompanied by other endocrine pathologies.

The following research methods are used to confirm the diagnosis.

  • An ultrasound scan of the adrenal glands usually detects a tumor that is larger than 2 cm.
  • Determination of the content of catecholamines in blood plasma is informative only during a hypertensive crisis. Of greater diagnostic value is the determination of the level of urine catecholamines during the day. In the presence of pheochromocytoma, the concentration of adrenaline and norepinephrine is more than 200 μg / day. In case of doubtful values ​​(concentration 51-200 μg / day), a test is performed with suppression of clonidine. Its essence lies in the fact that at night there is a decrease in the production of catecholamines, and the use of clonidine further reduces the physiological, but not autonomous (produced by the tumor) secretion of catecholamines. The patient is given 0.15 mg or 0.3 mg of clonidine at bedtime, and in the morning, night urine is collected (from 9 pm to 7 am), provided the subject is completely at rest. In the absence of pheochromocytoma, the content of catecholamines will be significantly reduced,

 

Primary hyperaldosteronism In Arterial hypertension,

Arterial hypertension is caused by primary hyperaldosteronism in 0.5% of all cases of Arterial hypertension (up to 12%, according to specialized clinics).

There are several etiological forms of primary hyperaldosteronism: Conn’s syndrome (aldosterone-producing adenoma), adrenocortical carcinoma, primary adrenal hyperplasia, idiopathic bilateral adrenal hyperplasia. In the pathogenesis of hypertension, excessive production of aldosterone is of primary importance.

The main clinical signs: Arterial hypertension, ECG changes in the form of T wave flattening (in 80% of cases), muscle weakness (in 80% of cases), polyuria (in 70% of cases), headache (in 65% of cases), polydipsia (in 45% of cases), paresthesia (in 25% of cases), visual impairment (in 20% of cases), fatigue (in 20% of cases), transient convulsions (in 20% of cases), myalgia (in 15% of cases). As you can see, these symptoms are not specific and are of little use for differential diagnosis.

The leading clinical and pathogenetic sign of primary hyperaldosteronism is hypokalemia (in 90% of cases). It is necessary to differentiate primary hyperaldosteronism with other causes of hypokalemia: taking diuretics and laxatives, diarrhea and vomiting.

 

Hypothyroidism , hyperthyroidism In Arterial hypertension

In Arterial hypertension, A characteristic sign of hypothyroidism is high diastolic blood pressure. Other manifestations of hypothyroidism on the part of CVS are a decrease in heart rate and cardiac output.

In Arterial hypertension, The characteristic signs of hyperthyroidism are an increase in heart rate and cardiac output, predominantly isolated systolic hypertension with low (normal) diastolic blood pressure. It is believed that an increase in diastolic blood pressure in hyperthyroidism is a sign of another disease, accompanied by hypertension, or a sign of hypertension.

In both cases, in order to clarify the diagnosis, in addition to the usual clinical examination, it is necessary to examine the state of the thyroid gland.

 

 

DRUG ARTERIAL HYPERTENSION

In the pathogenesis of hypertension caused by drugs, the following factors may be important.

  • Vasoconstriction caused by sympathetic stimulation or direct action on vascular smooth muscle cells.
  • Increased blood viscosity.
  • Stimulation of the renin-angiotensin system, retention of sodium and water ions.
  • Interaction with central regulatory mechanisms.

Hypertension can cause the following drugs.

  • Medicines containing adrenomimetic or sympathomimetic agents (eg ephedrine, pseudoephedrine, phenylephrine) and used to treat diseases of the nasal cavity can increase blood pressure.
  • Oral contraceptives. A possible mechanism of the hypertensive action of drugs containing estrogens is the stimulation of the renin-angiotensin system and fluid retention. According to some reports, about 5% of women develop hypertension while taking contraceptives.
  • NSAIDs cause hypertension as a result of suppression of the synthesis of prostaglandins, which have a vasodilating effect, and also due to fluid retention.
  • Carbenoxolone, licorice preparations increase blood pressure due to fluid retention (hypokalemic hypertension, pseudohyperaldosteronism due to mineralocorticoid activity).
  • Tricyclic antidepressants can raise blood pressure by stimulating the sympathetic nervous system.
  • HA causes an increase in blood pressure due to an increase in vascular reactivity to angiotensin II and norepinephrine, as well as as a result of fluid retention.

 

ALCOHOL AND ARTERIAL HYPERTENSION

In 5-25% of cases, chronic alcohol consumption is the cause of hypertension.

In Arterial hypertension, The exact mechanism of the hypertensive effect of alcohol is not known. Perhaps the stimulation of the sympathetic nervous system, an increase in the production of hormones of the adrenal cortex, hyperinsulinemia, an increase in the uptake of calcium ions by cells and an increase in total peripheral resistance under the influence of alcohol are important.

Revealing the connection between hypertension and alcohol consumption in practice is often an insoluble problem, since the anamnestic information is not very reliable, and there are no specific clinical signs. At the same time, one should pay attention to the indicative signs of excessive alcohol consumption (Table 4-4). The exact correlation between the increase in blood pressure and the amount of alcohol consumed has not yet been identified.

Table 4-4. Signs of alcohol abuse

Early signs

Late signs

High activity of transaminases (ALT, AST) in the blood

Cushingoid signs

Increased average erythrocyte volume

Signs of liver damage

The smell of alcohol

Hepatic encephalopathy, Wernicke’s encephalopathy

Telangiectasia on the face

Peripheral neuropathy

Laboratory tests confirming the effect of alcohol on the body include increased activity of the hepatic enzyme γ-glutamyl transpeptidase. It should be remembered about other clinical manifestations of alcohol abuse: chronic gastritis, chronic pancreatitis, chronic bronchitis, frequent pneumonia, kidney damage.

 

 

ARTERIAL HYPERTENSION IN THE ELDERLY

In Arterial hypertension, The elderly include persons over 65 years of age. Currently, this category is about 15% of the total population both in our country and in many industrially developed countries. The criterion for hypertension for the elderly is considered to be blood pressure more than 160/90 mm Hg. The prevalence of hypertension in this age group reaches 50%. Hypertension in the elderly can be isolated systolic or both systolic and diastolic.

In the pathogenesis, in addition to other factors affecting the increase in blood pressure, in the elderly, it is important to reduce the elasticity of the aortic walls, which is manifested by an increase in systolic blood pressure and a decrease in diastolic blood pressure.

 

Clinical features In Arterial hypertension

The elderly are characterized by a tendency to orthostatic arterial hypotension (due to a decrease in cerebral blood flow due to sclerosis of the arteries of the brain), a decrease in renal excretory function, a decrease in the elasticity of the arteries (and, accordingly, an increase in total peripheral resistance) and a decrease in cardiac output. When examining elderly patients with hypertension, it is necessary to pay attention to the risk factors for coronary heart disease (smoking, diabetes mellitus, left ventricular hypertrophy and others) and take them into account when prescribing therapy. Epidemiological studies have shown that an increase in systolic blood pressure compared with an increase in diastolic blood pressure is more important for predicting the risk of cardiovascular complications.

 

Pseudohypertension In Arterial hypertension

It should be remembered about the possible pseudohypertension in the elderly – an overestimation of systolic blood pressure by 98 mm Hg. and diastolic blood pressure at 49 mm Hg. Pseudohypertension is associated with severe wall rigidity (up to sclerosis) of the brachial arteries. In the elderly, the prevalence of pseudohypertension is about 2%. Pseudohypertension can be suspected in elderly people with a positive Osler symptom: despite the clamping of the brachial artery with a finger or a cuff, the pulse on the radial artery remains palpable due to the rigidity of the vessel wall.

 

Atherosclerosis of the renal arteries , aortic aneurysm

In Arterial hypertension, Common causes of hypertension in old age are atherosclerosis of the renal arteries or an aneurysm of the abdominal aorta, which narrows the lumen of the renal artery (one or both). These pathological conditions should be excluded with the rapid progression of hypertension or a sudden increase in blood pressure, especially when hypertension is resistant to therapy.

 

ISOLATED OFFICE ARTERIAL HYPERTENSION

The isolated office AG is also called the “White Coat AG.” It is characterized by an increase in blood pressure in a medical institution (office), while in out-of-hospital conditions, blood pressure is normal. Isolated office hypertension is diagnosed only in a minority of patients. When carrying out daily monitoring of blood pressure, normal values ​​of the average daily blood pressure are found – less than 125/80 mm Hg.



 

TREATMENT OF ARTERIAL HYPERTENSION

In Arterial hypertension, WHO and the International Society for Hypertension (1999) believe that in young and middle-aged people, as well as in patients with diabetes mellitus, it is necessary to maintain blood pressure at a level not higher than 130/85 mm Hg. In the elderly, blood pressure should be reduced below 140/90 mm Hg. At the same time, it must be remembered that an excessive decrease in blood pressure with a significant duration and severity of the disease can lead to hypoperfusion of vital organs – the brain (hypoxia, stroke), heart (exacerbation of angina pectoris, myocardial infarction), kidneys (renal failure). The goal of treating hypertension is not only to reduce high blood pressure, but also to protect target organs, eliminate risk factors (quitting smoking, compensating for diabetes mellitus, reducing blood cholesterol concentration and overweight) and, as an ultimate goal,

Plan the treatment of arterial hypertension

  • Control of blood pressure and risk factors.
  • Changing your lifestyle (see chapter 3 “Prevention of coronary heart disease”).
  • Drug therapy.

 

 

NON-MEDICINAL TREATMENT OF ARTERIAL HYPERTENSION

In Arterial hypertension, Non-drug treatment is indicated for all patients. Without the use of drugs, blood pressure is normalized in 40-60% of patients with an initial stage of hypertension with low blood pressure values. With severe hypertension, non-drug therapy in combination with drug treatment helps to reduce the dose of drugs taken and thereby reduces the risk of their side effects.

The main measures of non-drug exposure in hypertension are diet, reduction of excess body weight, sufficient physical activity.

 

Diet In Arterial hypertension

  • Limiting the consumption of table salt to less than 6 g / day (but not less than 1-2 g / day, since in this case a compensatory activation of the renin-angiotensin system may occur).
  • Restriction of carbohydrates and fats, which is very important for the prevention of ischemic heart disease, the likelihood of which increases with hypertension. It is believed that a decrease in excess body weight by 1 kg leads to a decrease in blood pressure by an average of 2 mm Hg.
  • An increased amount of potassium ions (possibly calcium and magnesium) in the diet can help lower blood pressure.
  • Refusal or significant restriction of alcohol intake (especially if abused) can help lower blood pressure.

 

Physical activity In Arterial hypertension

Sufficient physical activity of a cyclic type (walking, light jogging, skiing) in the absence of contraindications from the heart (the presence of coronary artery disease), leg vessels (obliterating atherosclerosis), the central nervous system (cerebrovascular accident) reduces blood pressure, and at low levels it can normalize it. At the same time, it is recommended to carry out moderate and gradual dosing of physical activity. Physical activity with a high level of emotional stress (competition, gymnastic exercises), as well as isometric efforts (lifting weights) are undesirable. The mechanisms leading to a decrease in blood pressure are considered to be a decrease in cardiac output, a decrease in total peripheral resistance, or a combination of both.

 

Other methods In Arterial hypertension

Other methods of treating hypertension also retain their importance: psychological (psychotherapy, autogenous training, relaxation), acupuncture, massage, physiotherapeutic methods (electrosleep, diadynamic currents, hyperbaric oxygenation), water procedures (swimming, shower, including contrast), herbal medicine ( black chokeberry fruits, hawthorn fruits, motherwort herb, marsh creeper grass, sandy immortelle flowers).

For the effectiveness of treatment, the patient is explained the features of the disease (the disease cannot be cured, but blood pressure can be effectively reduced), the duration of the course (chronic in most patients), the nature of target organ damage, possible complications in the absence of proper blood pressure control. The patient should be informed about effective modern antihypertensive drugs that allow to achieve normalization or decrease in blood pressure in 90-95% of patients who are resorted to in the absence of the effect of non-drug therapy.

 

 

MEDICAL THERAPY

In Arterial hypertension, The basic principles of drug therapy can be formulated in three theses.

  • Treatment of mild hypertension should be started with low doses of drugs.
  • A combination of drugs should be used to increase their effectiveness and reduce side effects.
  • It is necessary to use long-acting drugs (acting for 12-24 hours with a single dose).

Currently, six main groups of drugs are used to treat hypertension: slow calcium channel blockers, diuretics, β-blockers, ACE inhibitors, angiotensin II antagonists (receptor blockers), α-adrenergic blockers. In addition, in practice, centrally acting drugs (for example, clonidine), combined agents (reserpine + dihydralazine + hydrochlorothiazide) are widely used. Details of the most commonly used drugs are presented in table. 4-5.

Table 4-5. The main drugs for the treatment of hypertension

International non-proprietary name

Dose , mg

Duration of action , hours

Multiplicity of reception

Diuretics

Chlorthalidone

Hydrochlorothiazide

Indapamide

Furosemide

Spironolactone

Triamteren

12.5-50

12.5-50

2.5

40-240

25-100

50-100

6-12

12-18

18-24

3-6

3-6

3-6

one

one

one

one

one

one

β- adrenergic blockers

Atenolol

Betaxolol

Bisoprolol

Metoprolol

Nadolol

Pindolol

Propranolol

Timolol

Carvedilol

50-100

5-20

2.5-20

100-300

40-320

10-60

40-320

20-60

25-50

12-24

24

24

12

24

6-12

6-12

6-12

8-12

1-2

one

one

2

one

2-3

3

2

1-2

Drug of central action

Clonidine

Guanfatsin

Methyldopa

0.225-0.9

1-3

500-2000

6-12

12-24

6-12

3

1-2

2-3

α – and β -adrenergic blockers

Carvedilol

12.5-100

12

2

α- adrenergic blockers

Doxazosin

Prazosin

1-16

0.5-20

24

3-6

one

2-3

Sympatholytics

Guanethidine

Reserpine

10-75

0.05-0.5

24

6-8

one

2-3

inhibitors ACE

Benazepril

Captopril

Hinapril

Lisinopril

Moexipril

Perindopril

Ramipril

Spirapril

Fosinopril

Enalapril

10-40

25-150

5-80

5-40

3.75-30

2-8

2.5-10

3-6

10-40

5-40

12-24

4-8

12-24

12

ten

12

1-2

3

1-2

2

1-2

one

1-2

one

1-2

1-2

Blockers receptors of angiotensin II

Valsartan

Irbesartan

Losartan

80-160

150-300

25-100

24

24

12-24

one

one

1-2

Blockers of slow calcium channels

Verapamil

Diltiazem

Amlodipine

Felodipine

Isradipin

Nifedipine (long-acting form)

480

60-360

5-10

5-20

5-20

30-180

12

12-24

24

24

12

24

2

2

one

one

1-2

one

Direct vasodilators

Hydralazine

Minoxidil

50-300

5-100

6

up to 72

2-4

1-2

Slow calcium channel blockers

The main drugs in this group are given in table. 4-6.

Table 4-6. Slow calcium channel blockers

Short- acting dihydropyridines

Dihydropyridines

long acting

Phenylalkyl mines

Benzodiaze pins

Nifedipine

Amlodipine, isradipine, felodipine, nifedipine (long-acting forms), nitrendipine, lacidipine

Verapamil

Diltiazem

In Arterial hypertension, Blockers of slow calcium channels inhibit the entry of calcium ions into the cell during the depolarization of the membranes of cardiomyocytes and smooth muscle cells, which leads to a negative inotropic effect, a decrease in heart rate, a decrease in the automatism of the sinus node, a slowdown in atrioventricular conduction, prolonged relaxation of smooth muscle cells (mainly vessels, especially arterioles).

Preference for slow calcium channel blockers in the treatment of hypertension should be given when hypertension is combined with angina pectoris (especially vasospastic), dyslipidemia, hyperglycemia, broncho-obstructive diseases, hyperuricemia, supraventricular arrhythmias (verapamil, diltiazem), diastolic dysfunction of the left ventricular syndrome.

Before prescribing drugs of this class, the state of the basic functions of the myocardium should be assessed. With bradycardia or predisposition to it, decreased myocardial contractility, impaired conduction, verapamil or diltiazem, which have pronounced negative inotropic, chronotropic and dromotropic effects, should not be prescribed, and, conversely, the use of dihydropyridine derivatives is indicated. Due to the different sensitivity of patients to slow calcium channel blockers, treatment is started with small doses. You should also take into account the features of the pharmacokinetics of drugs.

  • Verapamil, isradipine, felodipine have a pronounced effect of the first passage through the liver, therefore they are prescribed with extreme caution in case of dysfunctions of this organ.
  • Almost all drugs bind to a large extent with blood plasma proteins, which should be taken into account when prescribing blockers of slow calcium channels in patients with hypoproteinemia.
  • Verapamil, diltiazem, isradipine are used in patients with chronic renal failure in lower doses.

Contraindications to the use of slow calcium channel blockers.

  • Myocardial infarction, unstable angina pectoris.
  • Sick sinus syndrome and heart block (verapamil, diltiazem).
  • Aortic stenosis (nifedipines).
  • Hypertrophic cardiomyopathy with obstruction (dihydropyridines).
  • Heart failure (verapamil and diltiazem).
  • Hepatic and renal failure.

The following are the side effects of slow calcium channel blockers.

  • Associated with peripheral vasodilation: tachycardia, flushing of the face, peripheral edema (more typical for dihydropyridines).
  • Associated with effects on the heart: negative effects on conduction, cardiac contractility (bradycardia, slowing AV conduction, decreased left ventricular ejection fraction, the appearance or aggravation of symptoms of heart failure [more typical for verapamil and diltiazem]).
  • Associated with effects on the gastrointestinal tract (GIT): constipation, diarrhea, nausea.

 

β- adrenergic blockers

The main groups of β-blockers are listed in table. 4-7.

Table 4-7. The main groups of β-blockers

Drug groups

Without adrenomimetic activity

With adrenomimetic activity

With a vasodilating effect

Non-selective

Propranolol,

nadolol

Pindolol

Carvedilol

Selective

Atenolol, Betaxolol, Bisoprolol, Metoprolol

Celiprolol,

nebivolol

The antihypertensive effect of β-blockers is associated with the blockade of β 1 -adrenoreceptors of the heart, as well as with a decrease in renin secretion, an increase in the synthesis of vasodilating prostaglandins and an increase in the secretion of atrial natriuretic factor. There are non-selective β 1 and β 2 -adrenergic blockers, selective β 1-adrenergic blockers (cardioselective). In each of these groups, drugs with internal adrenomimetic activity are also isolated (to a lesser extent, they reduce heart rate and inhibit myocardial contractility). It should be borne in mind that at a high dosage of drugs, cardioselectivity is lost, therefore, in the presence of concomitant diseases, the course of which may worsen with the appointment of β-blockers (diabetes mellitus, bronchial asthma, peripheral arterial disease), β-blockers are not recommended. Recently, β-blockers with vasodilating properties have been synthesized. The clinical significance of this effect is that vasodilation leads to an additional antihypertensive effect and less pronounced bradycardia.

Preference for β-blockers should be given:

  • when Arterial hypertension is combined with IHD (exertional angina and unstable angina, postinfarction cardiosclerosis with preserved heart function);
  • with tachyarrhythmias and extrasystoles.

There are the following contraindications to the use of β-blockers.

  • Blockade of the cardiac conduction system.
  • Diseases accompanied by broncho-obstructive syndrome.
  • Insulin therapy with a tendency to hypoglycemia.
  • Dyslipidemia.
  • Intermittent claudication.
  • Raynaud’s syndrome.
  • Psychogenic depression.
  • Erectile disfunction.
  • Vasospastic angina.

β-blockers have a number of side effects: bronchospasm, sinus bradycardia, heart failure, blockages of the cardiac conduction system, coldness of the lower extremities, dizziness, sleep disturbances, asthenia, increased gastrointestinal motility, sexual dysfunction, hypersensitivity, hypoglycemia (especially in patients with a labile flow of sugar diabetes when combined with insulin or oral antidiabetic drugs), dyslipidemia, hyperuricemia, hyperkalemia.

After abrupt withdrawal of β-blockers, withdrawal syndrome may develop, manifested by tachycardia, arrhythmias, increased blood pressure, exacerbation of angina pectoris, the development of myocardial infarction, and in some cases even sudden cardiac death. For the prevention of withdrawal syndrome, it is recommended to gradually reduce the dose of β-blocker for at least 2 weeks. A high-risk group for the development of withdrawal syndrome is distinguished: persons with hypertension in combination with exertional angina, as well as with ventricular arrhythmias.

 

Diuretic drugs means In Arterial hypertension

The main groups of diuretics used in the treatment of hypertension.

  • Thiazides and thiazide-like diuretics (most often used in the treatment of hypertension) are diuretics of medium strength that suppress the reabsorption of 5-10% of sodium ions. This group includes hydrochlorothiazide, chlorthalidone, indapamide, clopamide.
  • Loop diuretics (characterized by a rapid onset of action when administered parenterally) are powerful diuretics that suppress the reabsorption of 15-25% of sodium ions. Loop diuretics are considered furosemide, bumetanide.
  • Potassium-sparing diuretics – weak diuretics causing additional excretion of no more than 5% sodium ions. The representatives of this group of diuretics are spironolactone and triamterene.

Natriuresis leads to a decrease in plasma volume, venous return of blood to the heart, cardiac output, and total peripheral resistance, which leads to a decrease in blood pressure. In addition to the effects of diuretics on systemic circulation, a decrease in CVS reactivity to catecholamines is also important. At the same time, it should be remembered that during treatment with diuretics, reflex activation of the renin-angiotensin system is possible with all the ensuing consequences (increased blood pressure, tachycardia and other manifestations), which may require discontinuation of the drug.

When treating hypertension, diuretics should be used:

  • with a tendency to edema;
  • in elderly patients.

In Arterial hypertension, There are separate contraindications for each group of diuretics. Thiazides and thiazide-like diuretics are contraindicated in severe forms of gout and diabetes mellitus, severe hypokalemia, loop diuretics – in case of allergy to sulfa drugs, potassium-sparing diuretics – in chronic renal failure, hyperkalemia and acidosis. When taken together with ACE inhibitors, potassium-sparing diuretics can be used only in small doses in the presence of heart failure.

Diuretic drugs have a number of side effects.

  • Side effects common to all antihypertensive drugs: headache, dizziness.
  • Metabolic disorders: hyponatremia, hypomagnesemia, hypokalemia or hyperkalemia, hypocalcemia or hypercalcemia, hyperuricemia, hyperglycemia, dyslipidemia.
  • Violations of the genitourinary system: hypovolemia, urinary retention (loop diuretics), menstrual irregularities (spironolactone), decreased libido (thiazides, spironolactone), gynecomastia (spironolactone).
  • Rare side effects: pancreatitis, cholecystitis (thiazides), ototoxicity (furosemide, ethacrynic acid), interstitial nephritis (thiazides, loop diuretics, triamterene), necrotizing vasculitis (thiazides), thrombocytopenia (thiazides), hemolytic anemia (thiazides).

 

Angiotensin Converting Enzyme Inhibitors

According to the pharmacokinetic classification, there are two groups of drugs.

  • Medicines in active form: captopril, lisinopril.
  • Prodrugs that are converted in the liver into active substances: benazepril, moexipril, perindopril, ramipril, trandolapril, fosinopril, cilazapril, enalapril.

ACE inhibitors block the conversion of angiotensin I to angiotensin II, which leads to a weakening of the vasoconstrictor effect, inhibition of aldosterone secretion. Blocking ACE leads to inactivation of bradykinin, vasodilating prostaglandins. There is a decrease in vascular tone, mainly of arterioles, a decrease in blood pressure, total peripheral resistance (and, accordingly, a decrease in afterload, which contributes to an increase in cardiac output, an increase in the release of sodium ions and a delay of potassium ions). Nevertheless, clinical experience with the use of ACE inhibitors shows that in some patients with hypertension, drugs in this group are ineffective. In addition, quite often, after a certain period of lowering blood pressure while taking ACE inhibitors, its increase is again noted, despite an increase in the dose of the drug.

ACE inhibitors should be used when hypertension is combined with the following concomitant conditions (diseases).

  • Left ventricular hypertrophy (ACE inhibitors are most effective in promoting its regression).
  • Hyperglycemia, hyperuricemia, hyperlipidemia (ACE inhibitors do not exacerbate these disorders).
  • History of myocardial infarction, heart failure (ACE inhibitors are among the most effective drugs for the treatment of heart failure, since they not only weaken its clinical manifestations, but also increase the life expectancy of patients).
  • Elderly age.

Below are the contraindications for the appointment of ACE inhibitors.

  • Pregnancy (teratogenic effect), breastfeeding.
  • Mitral stenosis or stenosis of the aortic mouth with hemodynamic disturbances (vasodilation at a fixed minute blood volume can lead to severe arterial hypotension).
  • Excessive diuresis (vasodilation with reduced blood volume can lead to a sharp and prolonged decrease in blood pressure).
  • Severe renal dysfunction, azotemia, renal artery stenosis of a single kidney.
  • Hyperkalemia.
  • Broncho-obstructive diseases (cases of status asthmaticus are described when taking ACE inhibitors).

With caution, drugs of this group should be prescribed for bilateral stenosis of the renal arteries, autoimmune diseases, impaired liver or kidney function, the presence of a dry cough (the appearance of side effects will be hidden by an existing cough). ACE inhibitors are not effective in primary hyperaldosteronism.

ACE inhibitors are generally well tolerated. Side effects such as headache, dizziness, nausea, loss of appetite, and fatigue are usually mild. More serious side effects are also possible, especially when high doses of drugs are used (for captopril more than 150 mg / day): arterial hypotension up to collapse (especially when combined with diuretics), worsening renal failure, neurological disorders, hyperkalemia, dry cough (in 1 -30% of patients, and 2% need to discontinue the drug), allergic reactions (including angioedema), neutropenia, proteinuria.

 

Blockers receptors of angiotensin II

The main blockers of angiotensin II receptors are presented in table. 4-8.

Table 4-8. Angiotensin II receptor blockers

Group of drugs

Drugs

Biphenyltetrazoles

Losartan, irbesartan, candesartan

Nonbiphenyltetrazoles

Eprosartan

Non-heterocyclic blockers

Valsartan

Angiotensin II receptor blockers are preferably used when dry cough occurs during treatment with ACE inhibitors.

Contraindications for the use of this group of drugs are similar to those for the appointment of ACE inhibitors.

Side effects of therapy with angiotensin II receptor blockers – headache, dizziness, nausea, loss of appetite, fatigue, cough.

 

α- adrenergic blockers In Arterial hypertension

α-blockers prevent the action of catecholamines on α-adrenergic receptors, which leads to vasodilation and a decrease in blood pressure. For long-term treatment of hypertension, mainly selective α 1 -adrenoceptor blockers (prazosin, doxazosin, terazosin) are used. Despite the many positive effects, drugs in this group are rarely used as monotherapy. Apparently, this is due to the disadvantages and side effects of these drugs, although the danger of most of them is likely exaggerated.

Preference for drugs of this group as monotherapy should be given when:

  • high total peripheral resistance;
  • dyslipidemias;
  • diabetes mellitus;
  • benign prostatic hyperplasia.

Contraindications to the appointment of α-blockers are listed below.

  • History of orthostatic arterial hypotension.
  • Tendency to swelling.
  • Tachycardia.
  • Hemodynamically significant stenosis of the aortic orifice or mitral foramen (due to the presence of a fixed minute volume, vasodilation can lead to significant arterial hypotension).
  • Myocardial infarction and cerebrovascular accident (due to a possible sharp decrease in blood pressure and hypoperfusion of the myocardium and brain).
  • Elderly age (with age, the mechanisms of regulation of blood circulation are disturbed, syncope are not uncommon).

The disadvantages of α-adrenergic blockers include the “first dose phenomenon” (a marked decrease in blood pressure after the first dose), orthostatic arterial hypotension, long-term selection of the drug dose, the development of tolerance (decrease in the effectiveness of drugs), withdrawal syndrome. To prevent the “first dose phenomenon”, it is recommended to take the drug while lying down, followed by staying in this position for several hours (it is better to prescribe it at night).

Side effects of α-blockers: dizziness, palpitations, nausea, edema, orthostatic arterial hypotension. Less common are rashes, polyarthritis, dry mouth, nasal congestion, depression, priapism, and urinary incontinence.

 

Formulations central action In Arterial hypertension

The drugs in this group include reserpine and combined preparations containing it, methyldopa, clonidine, moxonidine, guanfacine.

Centrally acting drugs cause a decrease in blood pressure due to inhibition of the deposition of catecholamines in central and peripheral neurons (reserpine), stimulation of central α 2 -adrenoceptors (clonidine, guanfacine, methyldopa, moxonidine) and I 1 -imidazoline receptors (clonidine and especially the specific agonist moxonist), which ultimately weakens the sympathetic effect and leads to a decrease in total peripheral resistance, a decrease in heart rate and cardiac output.

Drugs in this group are mainly used internally. Imidazoline receptor agonists should be preferred as first-line agents when:

  • diabetes mellitus and hyperlipidemia (do not aggravate metabolic disorders);
  • obstructive pulmonary diseases (drugs do not affect bronchial patency);
  • severe hypersympathicotonia;
  • left ventricular hypertrophy (causing its regression).

Methyldopa is most commonly used in the treatment of hypertension in pregnant women.

All centrally acting drugs are contraindicated in severe bradycardia, heart block (suppression of the sympathetic nervous system leads to the predominance of the influence of the parasympathetic nervous system), unstable angina pectoris and myocardial infarction, severe liver and kidney damage, pregnancy and breastfeeding, depression. Methyldopa and reserpine are contraindicated in parkinsonism, and moxonidine in Raynaud’s syndrome, epilepsy, and glaucoma.

When using centrally acting drugs, side effects often arise from the central nervous system (depression, drowsiness, decreased attention, fatigue, dizziness, decreased libido), but dry mouth, nasal congestion, and bradycardia may develop.

  • Reserpine-containing drugs have a large number of side effects, the severity of which depends on the drug dose (depression, fatigue, drowsiness, nasal congestion, stomach ulcers), and therefore should not be used for long-term treatment of hypertension.
  • Despite its effectiveness, methyldopa is not recommended for long-term treatment of hypertension due to serious side effects: pronounced sedation (up to 60% of patients), weakness, fatigue, decreased attention, nasal congestion, impotence.
  • Clonidine and, to a lesser extent, guanfacine, moxonidine and methyldopa, upon sudden discontinuation of the drug, cause a withdrawal syndrome, clinically manifested by a sharp increase in blood pressure, tachycardia, sweating, tremors of the extremities, agitation, headache. To prevent this syndrome, the dose of the drug should be reduced gradually over 7-10 days.


Combination therapy In Arterial hypertension

According to international studies, the need for combination therapy occurs in 54-70% of patients. The indications for combination therapy are as follows.

  • Ineffectiveness of monotherapy.
  • Monotherapy is effective in about 50% of patients with hypertension (better results can be achieved, but the risk of side effects increases).
  • For the treatment of the rest of the patients, it is necessary to use a combination of 2 or more antihypertensive drugs.
  • The need for additional protection of target organs, primarily the heart and brain.

Rational drug combinations are presented below.

  • Diuretic + β-blocker. This combination has approximately the same additive effect as the combination of a diuretic + ACE inhibitor. However, this combination is not the most successful, since both a diuretic and a β-blocker affect glucose and lipid metabolism.
  • Diuretic + ACE inhibitor – the most effective combination (possibly a fixed combination, for example, captopril + hydrochlorothiazide).
  • Diuretic + angiotensin II receptor blocker.
  • Diuretic + blocker of slow calcium channels (combination, the appropriateness of which is controversial).
  • ACE inhibitor + blocker of slow calcium channels.
  • β-blocker + blocker of slow calcium channels (dihydropyridines).
  • β-blocker + α-blocker.
  • Angiotensin II receptor blocker + slow calcium channel blocker.
  • Verapamil (or diltiazem) + amlodipine (or felodipine) (combination, the appropriateness of which is controversial).

The most commonly used combination of a diuretic and a drug of another class. In some countries, combination therapy with a diuretic is considered a mandatory step in the treatment of hypertension.

Irrational combinations of antihypertensive drugs (Tables 4-9) can lead to both increased side effects and an increase in the cost of treatment in the absence of an effect. A striking example of an irrational combination is the combination of β-blockers and slow calcium channel blockers, since both groups of drugs worsen both myocardial contractility and AV conduction (increased side effects).

Table 4-9. Inappropriate combinations of antihypertensive drugs

Combination

Disadvantage

Slow calcium channel blocker + diuretic

Lack of additivity

β-blocker + slow calcium channel blocker (verapamil, diltiazem)

Strengthening side effects

β-blocker + centrally acting drug

Strengthening side effects

Slow calcium channel blocker + α-blocker

Strengthening side effects

 

Drug interactions In Arterial hypertension

  • NSAIDs reduce the antihypertensive effects of ACE inhibitors, angiotensin II receptor blockers, diuretics, β-blockers.
  • Antacids reduce the antihypertensive effects of ACE inhibitors, angiotensin II receptor blockers.
  • Rifampicin, barbiturates reduce the antihypertensive effects of β-blockers and slow calcium channel blockers such as verapamil.
  • Cimetidine enhances the antihypertensive effects of β-blockers and slow calcium channel blockers.
  • Concomitant administration of opioids and ACE inhibitors or angiotensin II receptor blockers can lead to increased analgesia and depression of the respiratory center.
  • Concomitant administration of glucocorticosteroids and diuretics (not potassium-sparing) can cause hypokalemia.
  • Digoxin, carbamazepine, quinidine, theophylline can increase the concentration of verapamil in the blood, which can lead to the phenomenon of an overdose of the latter.
  • Theophylline, chlorpromazine, lidocaine can increase the concentration of β-blockers in the blood, provoking an overdose phenomenon.

 

GENERAL RECOMMENDATIONS ON THE USE OF ANTIHYPERTENSIVE DRUGS

General recommendations for the use of antihypertensive drugs are presented in table. 4-10 and 4-11.

Table 4-10. Influence of comorbidities on the choice of antihypertensive agent

Diseases and conditions

Diuretics

β- adrenergic blockers

Blockers of slow calcium channels

inhibitors ACE

α- adrenergic blockers

Formulations central action

Aortic stenosis

!

0

!

0

Obstructive pulmonary disease

++

0

+

!

Heart failure

++

!

0

++

Depression

!

0

Diabetes

!

0

+

++

Gout

0

+

+

+

Dyslipidemia

!

!

Vascular disease

+

0

++

!

Pregnancy

!

!

!

0

!

Angina pectoris

!

++

++

+

Renal artery stenosis

0

Note. ! – caution when applying; 0 – should be avoided, + – application is possible; ++ is the drug of choice.

Table 4-11. WHO and International Society for Hypertension Guidelines on the Choice of Medicines for the Treatment of Hypertension (1999)

Group of drugs

Shown

maybe

application

Contraindicated

Maybe,

contraindicated

Diuretics

CHF, advanced age, systolic hypertension

Diabetes

Gout

Dyslipidemia, sexually active men

β-blockers

Angina pectoris, condition after myocardial infarction, tachyarrhythmias

CHF, pregnancy, diabetes mellitus

Bronchial asthma and chronic lung diseases, AV block II-

III degree

Dyslipidemia, physically active patients, vascular disease

ACE inhibitors

CHF, left ventricular dysfunction, condition after myocardial infarction, diabetic nephropathy

Pregnancy, bilateral renal artery stenosis, hyperkalemia

Slow calcium channel blockers

Angina pectoris, advanced age, systolic hypertension

Vascular disease

AV blockade (verapamil, diltiazem)

CHF (verapamil, diltiazem)

α-blockers

Benign prostatic hyperplasia

Decreased glucose tolerance, dyslipidemia

Orthostatic arterial hypotension

Angiotensin II receptor blockers

Cough when taking ACE inhibitors

CHF

Pregnancy, bilateral renal artery stenosis, hyperkalemia

TREATMENT OF SEPARATE TYPES OF ARTERIAL HYPERTENSION

Refractory and malignant arterial hypertension

In Arterial hypertension, The criterion for the refractoriness of hypertension is a decrease in systolic blood pressure by less than 15% and in diastolic blood pressure by less than 10% from the initial level against the background of rational therapy using adequate doses of 3 or more antihypertensive drugs.

  • The lack of adequate blood pressure control in more than 60% of patients is due to non-adherence to the treatment regimen (pseudo-refractoriness). The other most common and easily treatable cause of this phenomenon is excessive consumption of table salt.
  • True refractoriness to treatment is often caused by volume overload associated with inadequate diuretic therapy. True refractory hypertension is more often observed in parenchymal kidney diseases, less often in hypertension. The absence of the desired antihypertensive effect in some patients with renovascular hypertension and tumors of the cortical or medullary layer of the adrenal glands should not be regarded as a true refractoriness to treatment, since surgical intervention improves the ability to control blood pressure, and in some cases leads to its complete normalization.

The term “malignant hypertension” (primary or any form of secondary) means an increase in blood pressure to 220/130 mm Hg. and more in combination with grade III-IV retinopathy, as well as fibrinoid arteriolonecrosis detected by microscopy of kidney biopsies. A kidney biopsy is not considered a mandatory study, given its traumatic nature and the lack of full correspondence between morphological changes in the kidneys, retina and brain.

  • Of all cases of malignant hypertension, 40% are among patients with pheochromocytoma, 30% – with renovascular hypertension, 12% – with primary hyperaldosteronism, 10% – with parenchymal kidney diseases, 2% – with hypertension, 6% – with other forms of secondary hypertension (systemic scleroderma , polyarteritis nodosa, kidney tumors, etc.).
  • Especially often malignant hypertension is detected in patients with combined forms of hypertension and in multiple embolism of small branches of the renal arteries with cholesterol particles (in 50% of such patients).

In patients with malignant hypertension, in most cases, myocardial hypertrophy, cardiac arrhythmias, predisposition to ventricular fibrillation, myocardial infarction and cerebrovascular accident in history, heart failure, proteinuria, renal failure are detected. However, these clinical manifestations are not considered decisive in the diagnosis of malignant hypertension.

The tactics of treating patients with refractory and malignant hypertension are largely similar.

  • required simultaneously administered combination of 3-5 antihypertensive drugs in high enough doses: ACE inhibitors, calcium antagonists, β-blockers, diuretics, and in some cases also agonists α 2 -adrenoceptor or imidazoline receptor blockers, angiotensin II receptor α 1 adrenoblokatorov …
  • In the absence of an adequate antihypertensive effect against the background of combination therapy, intravenous sodium nitroprusside (3-5 infusions), prostaglandin E 2 (2-3 infusions) are used or extracorporeal methods of treatment are carried out: plasmapheresis, hemosorption, ultrafiltration (in the presence of CHF), immunosorption (in the presence of severe hypercholesterolemia), hemofiltration (with an increase in the level of creatinine in the blood to 150-180 μmol / l).
  • In order to prevent cerebral and cardiac complications and rapid progression of renal failure at the first stage in patients with refractory and malignant hypertension, one should strive to reduce blood pressure by 20-25% of the initial level. In the future, also with caution, you should try to achieve a lower blood pressure (preferably 140/90 mm Hg). A gradual decrease in blood pressure is necessary for the adaptation of vital organs to the new conditions of blood supply.

 

Arterial hypertension in the elderly

In Arterial hypertension, Treatment should begin with non-pharmacological measures that often reduce blood pressure to acceptable values. Limiting the consumption of table salt and increasing the content of potassium and magnesium salts in the diet are of great importance. Drug therapy is based on the pathogenetic characteristics of hypertension at a given age. In addition, it should be remembered that the elderly often have various comorbidities.

  • It is necessary to start treatment with smaller doses (often half of the standard). The dose should be increased gradually over several weeks.
  • It is necessary to use a simple treatment regimen (1 tablet once a day).
  • The dose is selected under constant monitoring of blood pressure, and it is better to measure blood pressure in a standing position to identify possible orthostatic arterial hypotension. Care should be taken to use drugs that can cause orthostatic arterial hypotension (methyldopa, prazosin), and centrally acting drugs (clonidine, methyldopa, reserpine), the use of which in old age is often complicated by depression or pseudodementia. When treating with diuretics and / or ACE inhibitors, it is desirable to monitor renal function and blood electrolyte composition.


Renoparenchymal arterial hypertension

The general principles of treatment and the selection of drugs in general do not differ from those in other types of hypertension. However, it must be remembered that due to impaired renal excretory function, it is possible to slow down the elimination and accumulation of drugs. In addition, drugs themselves can impair renal excretory function, which sometimes makes it necessary to determine GFR.

  • Diuretics can be used for renoparenchymal hypertension. Thiazide diuretics are believed to be effective up to a creatinine concentration of 176.6 μmol / L; at higher values, additional use of loop diuretics is recommended. Potassium-sparing diuretics are inappropriate to use, since they contribute to the aggravation of hyperkalemia, to one degree or another, noted in chronic kidney disease.
  • β-blockers can reduce GFR. In addition, the accumulation of water-soluble β-blockers (atenolol, nadolol) in the body is possible as a result of slowing down their excretion by the kidneys, which can lead to overdose.
  • ACE inhibitors are the drugs of choice for renoparenchymal hypertension, because by reducing the constriction of the efferent arterioles of the renal glomerulus and intraglomerular pressure, they improve renal hemodynamics and reduce the severity of proteinuria.

 

Renovascular arterial hypertension

First of all, it is necessary to consider the possibility of radical treatment – percutaneous transluminal renal angioplasty or radical surgical treatment. If such treatment is impossible or if there are contraindications to it, antihypertensive drugs can be prescribed.

Pathogenetically, ACE inhibitors are most substantiated due to the fact that in this pathology the concentration of renin in the blood is high. Nevertheless, when prescribing them, some caution is necessary: ​​the expansion of efferent arterioles and blockade of the renin-angiotensin system with ACE inhibitors can lead to impaired autoregulation of renal blood flow and a decrease in GFR with subsequent impairment of renal excretory function (one of the simple methods of monitoring renal function is monitoring creatinine ). As a result, progressive deterioration of renal function and prolonged uncontrolled arterial hypotension are possible. In this regard, treatment should be started with a minimum dose of short-acting ACE inhibitors – captopril at a dose of 6.25 mg (quickly acting and quickly excreted). In the absence of side effects, you can increase the dose of captopril or prescribe long-acting drugs. However, in bilateral renal artery stenosis, ACE inhibitors are best avoided.

Endocrine arterial hypertension

Treatment of hypertension with endocrine system damage is different.

  • For pheochromocytoma and primary hyperaldosteronism caused by adrenal adenoma or carcinoma, surgical treatment should be considered first. If surgical treatment for pheochromocytoma is impossible for one reason or another, α-adrenergic blockers (doxazosin, prazosin) are usually used. It should be remembered about the possibility of developing orthostatic arterial hypotension when using drugs of this group. The appointment of β-blockers (especially non-selective ones) is not recommended, since they can increase blood pressure, since these drugs block β 2 -adrenergic receptors. Indications for the appointment of β-blockers are various arrhythmias complicating the course of pheochromocytoma (preference should be given to selective β 1 -adrenergic blockers).
  • In case of primary hyperaldosteronism caused by adrenal hyperplasia, spironolactone is often used at a dose of 100-400 mg / day. If it is necessary to enhance the antihypertensive effect, hydrochlorothiazide or α-blockers can be added. There is evidence of the effectiveness of amlodipine.
  • In hypothyroidism, drugs of all groups are prescribed, with the exception of β-blockers.

 

Arterial hypertension when abuse of alcohol

First of all, it is necessary to stop drinking alcohol (complete exception). In some cases, only this measure (not always easily feasible) can lead to normalization of blood pressure or its decrease. Persons who are unable to completely give up alcohol are recommended to limit their intake to 21 doses per week for men and up to 14 doses for women (1 dose of alcohol corresponds to 8-10 g of pure alcohol, i.e. 0.5 liters of beer or 1 glass wine). One of the methods for controlling the cessation of alcohol intake is considered to be the determination in the dynamics of the content of γ-glutamyl transpeptidase (GGTP) and the average volume of erythrocytes.

The drugs of choice for the treatment of this form of hypertension are clonidine, ACE inhibitors, β-blockers and, possibly, blockers of slow calcium channels of the dihydropyridine series. When taking drugs and alcohol, one should remember about their interactions (for example, a combination of clonidine + alcohol) and withdrawal symptoms of drugs (both drugs and alcohol), which must be warned about the patient. With the development of post-alcohol withdrawal syndrome accompanied by hypertension, β-blockers are considered one of the effective means (in the absence of contraindications).

 

COMPLICATIONS

Complications of In Arterial hypertension:

  • myocardial infarction;
  • stroke;
  • heart failure;
  • renal failure;
  • hypertensive encephalopathy;
  • retinopathy;
  • hypertensive crisis;
  • dissecting aortic aneurysm.

 

FORECAST

In Arterial hypertension, The prognosis depends on the adequacy of the prescribed therapy and the patient’s compliance with medical recommendations.

 

HYPERTENSIVE CRISIS

In Arterial hypertension, a Hypertensive crisis is a sudden increase in systolic and / or diastolic blood pressure, accompanied by signs of deterioration of cerebral, cardiac or renal blood circulation, as well as severe autonomic symptoms. A hypertensive crisis, as a rule, develops in untreated patients, with a sharp discontinuation of antihypertensive drugs, but may be the first manifestation of hypertension or symptomatic hypertension.

 

CLINICAL PICTURE AND DIAGNOSTICS

In Arterial hypertension, The clinical picture of a hypertensive crisis is manifested by an increase in blood pressure, encephalopathy, subarachnoid hemorrhage, stroke, myocardial infarction, acute left ventricular failure in the form of pulmonary edema, aortic dissection, acute renal failure (ARF) may occur. With a hypertensive crisis, patients may be disturbed by severe headache, severe dizziness, visual impairment in the form of a decrease in acuity and loss of visual fields, chest pain (due to myocardial ischemia, aorthalgia), palpitations, shortness of breath.

When examining a patient, signs of damage to target organs should be detected.

  • Changes in the fundus (narrowing of arterioles, hemorrhages, exudates, edema of the optic nipple).
  • Dysfunction of the left ventricle (tachycardia, gallop rhythm, pulmonary edema, dilated neck veins).
  • Disorders of cerebral circulation (neurological signs).

In a clinical setting, in addition to measuring blood pressure, the following studies should be prescribed.

  • Chest X-ray.
  • ECG.
  • Study of the fundus.
  • General analysis of blood and urine.

If possible, it is recommended to monitor blood pressure (preferably intra-arterial).

 

Treatment In Arterial hypertension, 

From a clinical point of view, it is advisable to highlight emergency conditions in which it is necessary to reduce high blood pressure within 1 hour, and conditions when it is possible to reduce blood pressure within a few hours (Table 4-12).

Table 4-12. Types of hypertensive crisis

State , at which the need to reduce blood pressure in within h

State , at which blood pressure can decrease in for several hours (12-24 h)

Aortic dissection (dissecting aortic aneurysm)

Systolic blood pressure 240 mm Hg

and / or diastolic blood pressure 130 mm Hg. and more without complications

Acute heart failure

Malignant hypertension without complications

Myocardial infarction

Hypertension in the preoperative and postoperative period

Unstable angina

Severe withdrawal of antihypertensive drugs

Heavy nosebleeds

Severe burns

Encephalopathy

Renal crisis in scleroderma (see chapter 47 “Systemic scleroderma”)

Hemorrhagic stroke

Subarachnoid hemorrhage

Skull trauma

Eclampsia

Catecholamine crisis with pheochromocytoma

Postoperative bleeding from the area of ​​vascular sutures

There are some features of lowering blood pressure in various conditions. So, in case of impaired cerebral circulation, the mean blood pressure should be reduced by no more than 20-25% of the initial level or diastolic blood pressure should not be lower than 105-110 mm Hg. This blood pressure level is recommended to be maintained for several days from the moment of its increase. It should be remembered that in the elderly, even small doses of antihypertensive drugs when taken orally can significantly reduce blood pressure and lead to arterial hypotension.

The algorithm for managing patients with hypertensive crisis is shown in Fig. 4-4. Recommendations for the treatment of conditions requiring a decrease in blood pressure within 1 hour are set out in table. 4-13.

 

Medicines used in emergency conditions are presented in table. 4-14.

Table 4-13. Recommendations for the treatment of conditions requiring a decrease in blood pressure within 1 hour

Emergency state

Recommended

Not recommended

Hypertensive encephalopathy

Sodium nitroprusside

β-blockers *, clonidine, methyldopa, reserpine

Subarachnoid hemorrhage

Nimodipine, sodium nitroprusside

β-blockers *, clonidine, methyldopa, reserpine, hydralazine

Ischemic stroke

Sodium nitroprusside

β-blockers *, clonidine, methyldopa, reserpine, hydralazine

Myocardial infarction

Nitroglycerin, sodium nitroprusside

Hydralazine

Acute left ventricular failure

Sodium nitroprusside, nitroglycerin

β-blockers, hydralazine

Aortic dissection

β-blockers, sodium nitroprusside

Hydralazine

Surge arrester

Sodium nitroprusside

β-blockers

Eclampsia

Magnesium sulfate, hydralazine, slow calcium channel blockers

ACE inhibitors, diuretics, sodium nitroprusside

Hyperadrenergic conditions (pheochromocytoma, withdrawal of clonidine, use of cocaine, amphetamines)

Phentolamine, sodium nitroprusside, clonidine (for clonidine withdrawal)

β-blockers

Hypertensive crisis in the postoperative period

Nitroglycerin, sodium nitroprusside

Note. * – the appropriateness of the appointment is debatable.

Table 4-14. Drugs used to relieve hypertensive crisis

LS

Dose

Start

actions

Duration

actions

Sodium nitroprusside

0.25-8 μg (kg min) IV drip

Immediately

1-2 minutes

Nitroglycerine

5-100 mcg / min IV drip

2-5 minutes

3-5 minutes

Enalaprilat

1.25 mg i.v.

15-30 minutes

6 h

Esmolol

250-500 μg (kg min)

for 1 min, then

50-100 μg (kg min)

in 4 minutes

1-2 minutes

10-20 minutes

Bendazole

30-40 mg IV bolus

10-15 minutes

1 hour or more

Clonidine

0.075-0.150 mg IV slowly

10-20 minutes

4-8 h

Captopril

6.25-50 mg orally

15 minutes

6-8

Furosemide

20-120 mg IV bolus

5 minutes

2 h