The Nurse Expects To Find Which Pathologic Change In A Patient With Pulmonary Arterial Hypertension?

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Arterial hypertension

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Arterial hypertension - an increase in blood force per unit area at residual systolic (upwards to 140 mm Hg. Fine art. And to a higher place), diastolic (upward to xc mm Hg. Art. And to a higher place), or both.

Arterial hypertension, the cause of which is unknown (primary, essential), occurs most ofttimes; hypertension with a known cause of occurrence (secondary arterial hypertension) is about often the result kidney disease. Usually the patient does not feel the presence of hypertension until it becomes pronounced or permanent. The diagnosis is established past measuring blood pressure. Other studies are used to determine the crusade, assess the risk and place other cardiovascular risk factors. Handling of arterial hypertension involves lifestyle changes and medications such every bit diuretics, b-blockers, ACE inhibitors, angiotensin Two receptor blockers, calcium channel blockers.

trusted-source [one], [ii], [3], [4], [v], [6], [7], [viii], [ix], [10], [11], [12]

Epidemiology

In the United states of america, arterial hypertension is nowadays in near l one thousand thousand people. But 70% of them know that they have arterial hypertension, 59% are treated and but 34% have adequate claret pressure command (BP). Amid adults, arterial hypertension is more mutual in African Americans (32%) than in Caucasians with white skin (23%) or Mexicans (23%). Morbidity and mortality are also higher among African Americans.

Blood pressure rises with age. About 2 thirds of people over 65 suffer from arterial hypertension. People over 55 years of age with normal claret pressure take a 90% risk of developing hypertension over fourth dimension. Since an increase in blood pressure is common in the elderly, such "age-related" hypertension may seem natural, simply increased blood force per unit area increases the risk of complications and death. Hypertension can develop during pregnancy.

According to the criteria for the diagnosis of arterial hypertension, adopted by the Globe Health Arrangement in conjunction with the International Order of Hypertension (WHO-ISH), and the Starting time Written report of Experts of the Scientific Social club for the Report of Arterial Hypertension of the All-Russian Scientific Gild of Cardiology and the Interagency Quango on Cardiovascular Diseases (DAG-ane), arterial Hypertension is a condition in which the level of systolic blood pressure level is equal to or greater than 140 mm Hg. And / or the level of diastolic claret pressure is equal to or greater than ninety mm Hg. With 3 different blood pressure measurements.

According to the modern classification of arterial hypertension, renal arterial hypertension is understood equally arterial hypertension pathogenetically associated with kidney disease. This is the largest group of diseases of secondary arterial hypertension, which is about 5% of the number of all patients suffering from arterial hypertension. Even with normal renal function, renal arterial hypertension is observed two-four times more often than in the full general population. With a subtract in renal function, the frequency of its development increases, reaching 85-90% in the stage of last renal failure. With normal blood pressure, but those patients who endure from salt-losing kidney diseases remain.

trusted-source [13], [fourteen], [fifteen], [16], [17], [18], [19]

Causes of hypertension

Arterial hypertension can be main (85-95% of all cases) or secondary.

trusted-source [20], [21], [22], [23]

Primary arterial hypertension

Hemodynamic and physiological components (such as plasma volume, plasma plasma renin activity) change, which confirms the assumption that principal arterial hypertension is unlikely to have i cause of development. Fifty-fifty if at the commencement one factor is predominant, so many factors are likely to accept part in maintaining high claret force per unit area all the time (mosaic theory). In systemic arterioles, dysfunction of ion pumps of sarcolemma of smooth musculus cells tin can lead to a chronic increase in vascular tone. Heredity is a predisposing cistron, but the exact mechanism is unclear. Ecology factors (for example, the amount of sodium supplied with food, obesity, stress) are probably important only in people with hereditary predisposition.

trusted-source [24], [25]

Secondary arterial hypertension

Causes of arterial hypertension include renal parenchymal diseases (for example, chronic glomerulonephritis or pyelonephritis, polycystic kidney disease, connective tissue diseases, obstructive uropathy), renovascular diseases, pheochromocytoma, Cushing syndrome, main hyperdialodenalonism, cardiovascular dysfunction, fever, fever, cholangiosis Excessive alcohol employ and the use of oral contraceptives are frequent causes of curable hypertension. Often, the employ of sympathomimetics, glucocorticoids, cocaine or licorice contributes to an increase in blood force per unit area.

The connectedness between the kidneys and arterial hypertension has attracted the attention of researchers for more than 150 years. The first among the researchers who made a pregnant contribution to this problem are the names R. Bright (1831) and F. Volhard (1914), who pointed out the role of primary lesion of the renal vessels in the evolution of hypertension and presented a link between the kidneys and an increment in claret pressure in in the grade of a vicious circle where the kidneys were both the cause of hypertension and the target organ. In the middle of the 20th century, the provision of the primary office of the kidneys in the evolution of arterial hypertension was confirmed and further developed in the studies of Russian (EM Tareev, GF Lang, AL Myasnikov, etc.) and foreign scientists (Due north. Goldblatt, Air conditioning Guyton et al.). The discovery of renin, produced by the kidney during its ischemia, and the renal prostaglandins: vasodilators and natriuretics - formed the footing for the development of knowledge about the renal endocrine system, which is able to regulate blood pressure. Sodium retentiveness by the kidneys, leading to an increment in circulating blood book, determined the mechanism for increasing claret pressure level in acute nephritis and chronic renal failure.

A great contribution to the report of arterial hypertension was fabricated by A.S. Guyton et al. (1970-1980). In a series of experiments, the authors proved the role of master renal sodium retention in the genesis of essential arterial hypertension and postulated that the cause of any arterial hypertension is the inability of the kidneys to provide sodium homeostasis at normal blood pressure, including in NaCl elimination. The maintenance of sodium homeostasis is achieved by "switching" the kidney to the manner of operation under atmospheric condition of higher blood pressure values, the level of which is then fixed.

Farther, in the experiment and in the clinic, straight evidence of the office of the kidneys in the development of arterial hypertension was obtained. They were based on the feel of kidney transplantation. Both in the experiment and in the clinic, transplantation of a kidney from a donor with arterial hypertension caused its evolution in the recipient, and, conversely, during transplantation of "normotensive" kidneys, previously high arterial pressure became normal.

A significant milestone in the study of the bug of the kidneys and hypertension were the piece of work of V. Brenner et al., Which appeared in the mid-1980s. Keeping the main retention of sodium by the kidneys as the principal mechanism of arterial hypertension pathogenesis, the authors attributed the crusade of this disorder to a decrease in the number of renal glomeruli and a respective decrease in the filtering surface of the renal capillaries. This leads to a decrease in kidney excretion of sodium (renal hypotrophy at nativity, chief kidney disease, the land after nephrectomy, including kidney donors). At the same fourth dimension, the authors thoroughly developed the mechanism of the damaging effect of arterial hypertension on the kidneys equally a target organ. Arterial hypertension affects the kidneys (primary wrinkled kidney as the event of arterial hypertension or arterial hypertension accelerates the stride of evolution of renal failure) due to violations of intrarenal hemodynamics - increasing pressure within the renal capillaries (intraglacial hypertension) and the development of hyperfiltration. Currently, the latter two factors are considered as leading in non-immune hemodynamic progression of renal failure.

Thus, it was confirmed that the kidneys can be both the cause of hypertension and the target organ.

The main group of diseases that pb to the evolution of renal arterial hypertension, are renal parenchymal diseases. Separately distinguish renovascular arterial hypertension resulting from renal avenue stenosis.

Parenchymal kidney diseases include astute and chronic glomerulonephritis, chronic pyelonephritis, obstructive nephropathy, polycystic kidney disease, diabetic nephropathy, hydronephrosis, congenital renal hypoplasia, kidney injuries, renal-secreting tumors, renopodomy.

The frequency of detection of arterial hypertension in renal parenchymal diseases depends on the nosological course of renal pathology and the country of renal office. In almost 100% of cases, hypertension syndrome accompanies renin-secreting kidney tumor (renin) and lesions of the main renal vessels (renovascular hypertension).

trusted-source [26], [27], [28], [29], [xxx], [31], [32],

Pathophysiology of arterial hypertension

Since arterial pressure level depends on cardiac output (SV) and total peripheral vascular resistance (OPS), the pathogenetic mechanisms must include an increase in EF, an increase in OSS, or both of these changes.

In most patients, CB is normal or slightly increased, and OPSS is increased. Such changes are characteristic of main arterial hypertension and hypertension acquired by pheochromocytoma, primary aldosteronism, renovascular pathology and renal parenchymal diseases.

In other patients, the SV is elevated (possibly due to the constriction of the large veins), and OPSS remains relatively normal for the corresponding SV; as the disease progresses, OPSS increases, and the SV returns to normal, probably due to self-regulation. In some diseases that increase SV (thyrotoxicosis, arteriovenous shunts, aortic regurgitation), peculiarly when the stroke book increases, isolated systolic arterial hypertension is formed. In some elderly patients, isolated systolic hypertension with normal or decreased CB is present, probably due to a decrease in the elasticity of the aorta and its main branches. Patients with persistent loftier diastolic pressure ever have a reduced CB.

With an increase in blood pressure there is a tendency to a subtract in plasma book; sometimes the plasma volume remains the aforementioned or increases. Plasma volume in arterial hypertension increases due to master hyper aldosteronism or renal parenchymal diseases and tin significantly decrease with arterial hypertension associated with pheochromocytoma. With an increase in diastolic blood force per unit area and the development of sclerosis of arterioles, there is a gradual decrease in renal blood flow. Until the late stages of the evolution of the disease, OPSS remains normal; as a result, the filtration fraction increases. Coronary, cerebral and muscular claret flow is maintained until such fourth dimension as the astringent atherosclerotic lesion of the vascular bed joins.

trusted-source [33], [34]

Sodium transport change

In some embodiments of arterial hypertension, sodium transport through the cell wall is dumb due to the bibelot or inhibition of Na, M-ATPase, or due to the increased permeability of the wall to Na. The consequence is an increased content of intracellular sodium, which makes the cell more sensitive to sympathetic stimulation. Ca ions follow Na ions, therefore the accumulation of intracellular calcium may likewise exist responsible for increased sensitivity. Since Na, K-ATPase can return norepinephrine back to sympathetic neurons (thus inactivating this neurotransmitter), the inhibition of this mechanism may besides enhance the furnishings of norepinephrine, contributing to an increment in blood pressure. Defects in the send of sodium ions tin can occur in healthy children if their parents endure from arterial hypertension.

trusted-source [35], [36], [37], [38], [39], [40], [41], [42], [43], [44], [45], [46], [47]

Sympathetic nervous system

Sympathetic stimulation leads to an increment in blood pressure level, usually to a greater extent in patients with borderline claret pressure level (120-139 / 80-89 mm Hg. Art.) Or with arterial hypertension (systolic blood pressure level 140 mm Hg., Diastolic xc mm Hg. Or both changes) than in patients with normal blood pressure. This hyperreactivity occurs in sympathetic nerves or in the myocardium and the muscular sheath of claret vessels - is unknown. High resting middle rate, which may be the result of increased sympathetic activity, is a well-known predictor of arterial hypertension. In some patients with arterial hypertension, the content of catecholamines circulating in plasma alone is in a higher place normal.

trusted-source [48], [49], [l], [51], [52], [53], [54], [55], [56], [57], [58], [59], [60], [61], [62]

Renin-angiotensin-aldosterone system

This system is involved in the regulation of blood volume and, appropriately, blood pressure. Renin, an enzyme synthesized in the juxtaglomerular apparatus, catalyzes the conversion of angiotensinogen to angiotensin I. Information technology is an inactive substance that is converted by ACE, mainly in the lungs, but as well in the kidneys and brain, into angiotensin Ii - a powerful vaso-constrictor that also stimulates democratic centers in encephalon, increasing sympathetic activity, and stimulates the release of aldosterone and ADH. Both of these substances contribute to the memory of sodium and water, increasing blood pressure. Aldosterone also contributes to the removal of K ⁺; low potassium content in blood plasma (<three.5 mmol / l) increases vasoconstriction due to the closure of potassium channels. Angiotensin III, circulating in the blood, stimulates the synthesis of aldosterone equally intensely as angiotensin 2, just has a much lower force per unit area activity. Since they also convert angiotensin I to angiotensin II, ACE inhibiting drugs do non completely block the formation of angiotensin II.

Renin secretion is controlled by at least four non-specific mechanisms:

renal vascular receptors that reply to changes in pressure in the afflicted arteriole wall;
dumbo macula receptors {macula densa) that respond to changes in the concentration of NaCI in the distal tubule;
circulating angiotensin, renin secretion;
the sympathetic nervous arrangement, like the kidney nerves, stimulates renin secretion indirectly through b-adrenoreceptors.

In general, information technology is proved that angiotensin is responsible for the development of renovascular hypertension, at to the lowest degree in the early on stages, but the office of the renin-angiotensin-aldosterone arrangement in the development of main hypertension has not been established. It is known that in African Americans and elderly patients with arterial hypertension, renin content tends to decrease. The elderly also have a trend to reduce the amount of angiotensin 2.

Arterial hypertension associated with damage to the renal parenchyma (renal hypertension) is the issue of a combination of renin-dependent and volume-dependent mechanisms. In most cases, there is no increase in renin activity in the peripheral claret. Hypertension is often moderate and sensitive to the residue of sodium and water.

trusted-source [63], [64], [65], [66], [67]

Insufficiency of vazodilatator

Insufficiency of vasodilators (for case, bradykinin, nitric oxide), as well as an backlog of vasoconstrictors (such as angiotensin, noradrenaline), tin can lead to the development of arterial hypertension. If the kidneys do not secrete vasodilators in the required amount (due to impairment to the kidney parenchyma or bilateral nephrectomy), blood pressure may increase. Vasodilators and vasoconstrictors (mainly endothelium) are also synthesized in endothelial cells, therefore endothelial dysfunction is a powerful factor in arterial hypertension.

trusted-source [68], [69], [70], [71]

Pathological changes and complications

There are no pathological changes in the early stages of hypertension. Astringent or prolonged arterial hypertension affects target organs (primarily the cardiovascular system, brain and kidneys), increasing the chance of coronary vascular disease (PVA), MI, stroke (mainly hemorrhagic), and renal failure. The mechanism includes the development of generalized atherosclerosis and increased atherogenesis. Atherosclerosis leads to hypertrophy, hyperplasia of the centre choroid and its hyalinization. Mostly these changes develop in pocket-sized arterioles, which is noticeable in the kidneys and the eyeball. In the kidney, changes lead to a narrowing of the lumen of the arterioles, increasing the round neck. Thus, hypertension leads to a further increment in claret force per unit area. Since arterioles are narrowed, any slight narrowing against the groundwork of an already hypertrophied muscle layer leads to a reduction in the lumen to a much greater degree than in unaffected arteries. This mechanism explains why the longer there is arterial hypertension, the less likely that specific handling (for example, surgery on the renal arteries) in secondary hypertension will pb to normalization of blood pressure.

Due to increased afterload, left ventricular hypertrophy gradually occurs, resulting in diastolic dysfunction. Every bit a result, the ventricle expands, leading to dilated cardiomyopathy and heart failure (HF) due to systolic dysfunction. The dissection of the thoracic aorta is a typical complication of hypertension. Almost all patients with intestinal aortic aneurysms exhibit arterial hypertension.

trusted-source [72], [73], [74], [75], [76], [77], [78], [79], [80], [81], [82]

Symptoms of arterial hypertension

There are no symptoms of arterial hypertension until complications develop in the target organs. Excessive sweating, facial flushing, headache, angst, nosebleeds and irritability are not signs of uncomplicated hypertension. Severe arterial hypertension tin can occur with severe cardiovascular, neurological, renal symptoms or lesions of the retina (for instance, clinically manifested atherosclerosis of the coronary vessels, middle failure, hypertensive encephalopathy, renal failure).

Early on symptom of high blood force per unit area - IV center tone. Changes in the retina may include narrowing of the arterioles, hemorrhages, exudation and, in the presence of encephalopathy, swelling of the nipple of the optic nervus. Changes are divided into 4 groups co-ordinate to the increased likelihood of a poor prognosis (there are Kiss, Wegener and Barker classifications):

Stage I - constriction of arterioles;
Stage II - constriction and sclerosis of arterioles;
Stage Iii - hemorrhages and exudation in improver to changes in claret vessels;
Phase IV - swelling of the nipple of the optic nerve.

trusted-source [83], [84], [85], [86], [87], [88], [89]

What'south bothering you?

Diagnosis of arterial hypertension

Diagnosis of arterial hypertension is based on the results of changes in blood pressure. Anamnesis, concrete examination and other methods of enquiry help to identify the crusade and clarify the damage to target organs.

Blood pressure should exist measured twice (for the first time in the patient's position lying or sitting, again - after the patient stands at least 2 minutes) on 3 different days. The results of these measurements are used for diagnosis. BP is regarded every bit normal, prehypertension (borderline hypertension), stage I and stage II hypertension. Normal blood pressure is much lower in children.

Ideally, BP should be measured after a patient'south more than 5-infinitesimal residuum at unlike times of the mean solar day. Tonometer cuff impose on the shoulder. The correct cuff covers two thirds of the biceps muscle of the shoulder; covers more than 80% (but not less than 40%) of the arm. Thus, obese patients need a large cuff. A specialist measuring blood pressure, injects air above the level of systolic pressure and so slowly releases it, producing auscultation of the brachial artery. The pressure at which the first eye sound is heard during the descent of the cuff is systolic blood pressure. The disappearance of the sound indicates diastolic claret force per unit area. The same principle is used to measure blood pressure on the wrist (radial artery) and thigh (popliteal artery). The nearly accurate measurement of blood pressure is mercury tonometers. Mechanical tonometers need to exist calibrated regularly; Automatic blood pressure monitors often have a big error.

Claret pressure is measured on both hands; if the pressure on one hand is significantly higher than on the other, higher numbers are taken into account. Blood pressure is as well measured on the legs (using a larger cuff) to detect aortic coarctation, especially in patients with a reduced or poorly maintained femoral pulse; with coarctation, blood pressure level in the legs is significantly lower. If the blood force per unit area numbers are within the borderline hypertension or vary significantly, it is advisable to perform more than blood pressure level measurements. Figures of pressure level tin exist raised only from fourth dimension to time until the moment when arterial hypertension becomes stable; This phenomenon is often referred to as "white coat hypertension," in which claret pressure rises when measured by a md in a medical institution and remains normal when measured at habitation and monitoring blood pressure daily. At the aforementioned time, pronounced precipitous increases in claret pressure confronting the groundwork of normal normal numbers are not usual and may indicate pheochromocytoma or unrecognized use of narcotic substances.

trusted-source [90], [91], [92], [93], [94], [95], [96]

Anamnesis

When collecting anamnesis, the duration of arterial hypertension and the highest figures of claret pressure, which were previously registered, are specified; any indication of the presence or manifestation of PVA, HF, or other comorbidities (for example, stroke, renal failure, peripheral arterial disease, dyslipidemia, diabetes mellitus, gout), and a family history of these diseases. The history of life includes the level of physical activity, smoking, alcohol and stimulants (prescribed past a doctor and taken independently). Nutrition specifies in terms of the amount of common salt consumed and stimulants (for case, tea, coffee).

trusted-source [97], [98], [99], [100], [101], [102], [103]

Objective examination

An objective test involves measuring height, body weight and waist circumference; examination of the fundus to find retinopathy; auscultation of noises in the neck and over the abdominal aorta, too as a consummate cardiological, neurological test and study of the respiratory system. Abdominal palpation is performed to detect an increment in the kidneys and tumors of the intestinal cavity. Determine the peripheral pulse; a weakened or poorly conducted femoral pulse may betoken aortic coarctation, especially in patients younger than thirty years.

trusted-source [104], [105], [106], [107], [108], [109], [110], [111]

Instrumental diagnosis of arterial hypertension

With more severe hypertension and in younger patients, instrumental diagnosis is more likely to lead to findings. In general, if arterial hypertension is diagnosed for the first time, routine tests are performed to place target organ damage and gamble factors for cardiovascular affliction. Studies include urinalysis, the ratio of urine albumin fraction to creatinine; blood tests (amount of creatinine, potassium, sodium, serum glucose, lipid profile) and ECG. The concentration of thyroid stimulating hormone is oft examined. In normal cases, outpatient monitoring of blood pressure level, radioisotope renography, chest X-ray, screening for pheochromocytoma and interdependent renin-Na are non needed. The report of plasma renin concentration is not important for the diagnosis or pick of drugs.

Depending on the results of the initial examination and examination, additional utilize of various research methods is possible. If microalbuminuria, albuminuria or proteinuria, cylindruria or microhematuria are detected in the urine analysis, and if the serum creatinine content is elevated (123.6 μmol / l in men, 106.0 μmol / l in women), ultrasound of the kidneys is used to make up one's mind their size, which tin make a large difference. In patients with hypokalemia, not associated with the appointment of diuretics, should be suspected primary hyperaldosteronism or excessive consumption of salt.

On the electrocardiogram, one of the earliest symptoms of "heart hypertension" is an extended pointed P wave, reflecting atrial hypertrophy (but this is a not-specific sign). The hypertrophy of the left ventricle, accompanied by the appearance of a pronounced apical impulse and a alter in the QRS voltage with or without signs of ischemia, may announced later. In the upshot that whatever of these symptoms are detected, an echocardiographic exam is often performed. Patients with an altered lipid profile or signs of PVA are prescribed studies to identify other cardiovascular risk factors (for example, determine the content of C-reactive protein).

If aortic coarctation is suspected, chest x-rays, echocardiography, CT or MRI are performed, which allows to confirm the diagnosis.

Patients with labile blood pressure, characterized by significant increases, with clinical symptoms in the class of headache, palpitations, tachycardia, increased breathing, tremor and pallor, should be examined for the possible presence of pheochromocytoma (for example, a study of costless plasma metanephrine).

Patients with symptoms suggestive of Cushing'south syndrome, connective tissue diseases, eclampsia, acute porphyria, hyperthyroidism, myxedema, acromegaly, or CNS disorders should exist examined (meet other sections of the transmission).

trusted-source [112], [113], [114]

What do need to examine?

How to examine?

What tests are needed?

Who to contact?

Treatment of hypertension

Primary arterial hypertension has no crusade, only in some variants of secondary arterial hypertension, the crusade can exist affected. In all cases, blood pressure control can significantly reduce the number of complications. Despite the treatment of hypertension, blood pressure is reduced to the target numbers in only one third of patients with arterial hypertension in the United states.

More information of the treatment

Drugs

Prognosis for hypertension

The higher the blood force per unit area and the more pronounced changes in retinal vessels or other manifestations of target organ impairment, the worse the prognosis. Systolic blood pressure is the all-time predictor of fatal and not-fatal complications than diastolic. Without arterial hypertension treatment, the 1-yr survival of patients with retinosclerosis, cloud-like exudates, narrowing of arterioles and hemorrhages (Three stage of retinopathy) is less than 10%, and in patients with the same changes and edema of the optic nerve (Iv stage of retinopathy) - beneath v%. PVA is becoming the virtually frequent cause of death in treated patients with arterial hypertension. Ischemic and hemorrhagic strokes are frequent complications of arterial hypertension in patients who have not properly called treatment. In general, effective command of blood force per unit area prevents the evolution of about complications and increases life expectancy.

trusted-source [115], [116], [117], [118], [119]

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