Alberto J. Muniagurria
It occurs because the hemodynamic pressure of the blood within the arteries is increased. Hypertension is the pathology that most damages all the structures of the cardiovascular system.
It has a high morbidity and mortality rate and a high social and economic cost for global public health.
It affects the entire arterial tree, but especially the heart, brain and kidneys. These anatomical structures, due to the importance of their homeostatic functions, are known as white and noble organs.
This disease is one of the most investigated with universal population studies trying to know its pathophysiology and the therapeutic approaches that can stop structural damage.
It is the most important cardiovascular risk factor, but it does not always act alone since it is usually accompanied by other cardiovascular risk factors, causing joint damage.
It has a high percentage of global prevalence and affects almost equally all races, sexes and ages. In the black race its prevalence and incidence is higher than in the white race. Until menopause, the number of hypertensive women is less than that of men, but after this period the figures are equal. According to the latest population studies, the number of hypertensive women is greater due to the change in the lifestyle adopted by the female sex.
The number of affected reaches 30% of the young population, 45% in adults and 75% from 70 years.
Only 20% treat it well and permanently, 25% regularly or badly and 55% abandon the treatment. 60% are unaware that they have it and do not carry out any study to detect it.
Diastolic arterial hypertension is more frequent between 25 and 45 years, systodiastolic between 45 and 60 years and pure systolic from that age. Multiple factors intervene in its pathogenesis (multifactorial), it damages many vital organs (multisystemic) and produces serious alterations in the homeostatic balance (high risk factor). Its symptoms are scarce or null (silent) and it occurs over time in a watery or chronic form.
The most common causes for its appearance are related to genetic factors, socio-environmental factors and negative changes in lifestyle. An exaggerated consumption of salt, alcohol, tobacco, narcotics, drugs that raise blood pressure, foods high in carbohydrates and animal fats accompanied by being overweight, sedentary and a high degree of mental stress.
It is a disease that causes permanent functional and structural changes inside the arterial walls, preventing them from complying with the normal transport of blood and its nutrients.
An inflammatory and morbid state occurs known as endothelial dysfunction (ED).
It presents hormonal, metabolic and changes in the renin-angiotensin-aldosterone system (RAAS). The production of vasoactive substances, hydrosaline retention and peripheral resistance are increased. Vascular tone and systolic discharge are altered.
It is a very frequent reason for medical consultation and its demand is very high in home, hospital or sanatorium emergency services.
The recommendations of the seventh report of the Joint National Committee of Prevention, Detention, Evaluation and Treatement og High Blood Pressute (JNC 7) for individuals older than 18 years thus classify the stages with figures in mm Hg.
NORMAL: systolic less than 120 mmHg. and diastolic less than 80 mmHg.
PREHYPERTENSION: systolic 120 to 139 mmHg. and diastolic DE 80 to 89 mmHg.
STAGE 1: systolic 140 to 159 mmHg. and diastolic 90 to 99 mmHg.
STAGE 2: systolic 160 mmHg. or more and diastolic 100 mmHg. or more.
The normality or abnormality figures also arise from guidelines or consensus of the European Society of Cardiology and the European Society of Arterial Hypertension. Others come from the World Health Organization (WHO) or the Framingham risk guidelines.
They are elaborated based on the results of multicenter population studies trying to elaborate a classification stratified by levels and accompanied by updated pharmacological treatments.
There are other types of hypertensions known as white coat, malignant hypertension, and gravidarum hypertension. The first occurs in 10% of patients with high levels of both systolic and diastolic at the time of taking blood pressure by doctors, nurses or pharmacists and not in other circumstances. It must be controlled by ambulatory blood pressure monitoring (ABPM) and if the figures found are lower than those found, it is classified as reactive hypertension.
The second is a very seriously evolving pathology with occlusive damage to the microcirculation, mainly at the renal and cerebral level. It does not respond to any of the instituted therapeutics and reaches figures of more than 200 mmHg for systolic and 120 mmHg for diastolic.
It presents innumerable arteriolopathies with great endothelial damage due to exaggerated cell proliferation in the intima of the vessels. These layers thicken leading to arteriolar occlusion. He presents retinal hemorrhages, cottony exudates, micro aneurysms and papilledema. It is deadly in the short term.
The third is the one that dangerously increases its numbers after 30 weeks of pregnancy. Some evolve to pre-eclampsia or eclampsia. There is elevated preteinuria, high cretinemia, significant hemolysis, increased liver enzymes, and low platelet counts. It is serious if systolic numbers exceed 160 mmHg, or diastolic numbers exceed 110 mmHg. it occurs in 6 to 8% of pregnant women.
Arterial hypertension produces ischemic or hemorrhagic pictures.
In the central nervous system, stroke, transient ischemic attacks, cerebral and cerebellar hemorrhage, as well as thrombosis or lacunar infarcts. Retinal and conjunctival hemorrhages in the eye.
Blockage of the central retinal artery. In the abdomen, mesenteric thrombosis and acute and chronic obliterations in the peripheral arterial circulation.
In the cardiovascular system, HTN produces acute coronary events with cardiac tamponade, arrhythmias and sudden death. In the nose epistaxis and in the aorta dissecting aneurysms and their rupture.
At first, HT increases cardiac output, decreasing or keeping peripheral resistance stable. With the progression of the disease, cardiac output falls and peripheral resistance increases permanently.
The alterations in cardiac output are due to a high consumption of sodium and minerals or corticosteroids. In addition, decreased kidney function is added. The increased viscosity, hemodynamic force or tension of
the blood exerted on the arterial wall, the greater pulse wave, the change in blood flow and the increase in speed affecting the blood volume are always present in the pathogenesis of arterial hypertension.
Alterations in peripheral resistance depend on humoral changes, the autonomic nervous system and the loss of local self-regulation. The peripheral nervous system has an alpha vasoconstrictor effect and beta vasodilator effect. In peripheral resistance, vasoconstrictor substances such as endothelin, angiotensins and catecholamines and vasodilator substances such as nitric oxide, prostaglandins and kinins act.
Cell growth increases the thickness of the walls, decreasing the elasticity and caliber of the arterial vessels. There is a vasoreactivity with greater growth of arteriolar smooth muscle causing its remodeling.
Normal blood pressure is the hemodynamic force that keeps blood circulating in the cardiovascular circuit. It produces a continuous flow that reaches to cross the capillary barrier allowing oxygen and nutrients to reach within the intracellular space (cellular perfusion).
This force makes it possible to maintain a constant balance between supply and demand. Vasoconstriction, vasodilation and blood flow velocity are regulated by the pre and post capillary sphincters, constituting protective barriers in the target organs.
The arterial pressure formula is formed on the one hand by the volume of blood expelled in one minute (minute volume or cardiac output) and on the other hand by peripheral vasoconstriction (peripheral resistance).
BLOOD PRESSURE: MINUTE VOLUME X PERIPHERAL RESISTANCE.
Systolic blood pressure (SBP) is regulated by the cardiac ejection volume in one minute in addition to the regulation of aortic pressure. Diastolic blood pressure (DBP) is regulated by peripheral resistance and the tone of the arterioles. The higher systolic blood pressure produces a volume HT and the higher diastolic blood pressure produces a resistance-dependent HT.
The growth of the thickness of the vascular walls increases the peripheral resistance producing a retrograde reflux of the poulsatile waves in the aortic wall increasing to systolic arterial pressure.
According to its cause of production, it is classified as essential, idiopathic, primary or of unknown cause. It is present in 95% of hypertensive patients. It cannot be proved where it came from. Secondary or known causes are known from where they come and are only present in 5% of patients.
The known ones come from kidney diseases such as acute and chronic glomerulonephritis, acute and chronic pyelnephritis, renal artery stenosis, polycystic kidney and diabetic kidney, vascular diseases such as periarteritis nodosa, hemangiomas and coarctation of the aorta, adrenal diseases such as Cushing's Syndrome , Cohn's syndrome or pheochromocytoma.
In all cases, both primary and secondary hypertension, its damage is related to the elevation of systolic and diastolic pressures or both at the same time.
At first, high blood pressure is occasional, but over time it becomes permanent. It begins with prehypertension figures at an early age and is almost asymptomatic. Then it is established in stages 1 or 2, it is asymptomatic and the manifestations of damage to the frame and micro vasculature, in the heart, in the kidneys, in the brain and in the retina begin to appear.
It is an extensive gland of internal secretion that is located in the entire inner layer of the arteries. It separates the intravascular space from the rest of the tissues of the vessels. Avoid contact of blood with arterial walls. Modulates the input of macromolecules.
It produces nitric oxide (NO), regulates platelet aggregation and coagulation by modulating arterial tone. Autocrine and paracrine elements act within the endothelium. They produce growth and remodeling of the wall. They favor angiogenesis by the formation of growth factors. They regulate blood pressure and stimulate the proliferation of vascular smooth muscle.
It modulates the vasomotor activity by the action on the RAAS and the conversion enzyme (ACE) regulating the amount of angiotensin II.
The endothelium acts on the tone through the synthesis of vasodilator substances such as nitric oxide and platelet aggregation by the synthesis of Von Willebrand factor, plasminogen inhibitors and prostaglandins.
Hypertension, dyslipidemias with elevated LDL levels, diabetes 1 and 2, smoking, obesity, sedentary lifestyle, estrogen deficiency, infectious agents, and metabolic syndrome produce great endothelial injury.
Changes occur in endothelial cells, smooth muscle cells, and platelets. It begins with an intense inflammatory state and an increase in cell fibroproliferation. Neutrophils inside the wall and acting as macrophages incorporate the oxidized LDL, beginning to form and increase the size of atheromatous plaques.
The walls thicken, their elasticity is lost and the arterial lumen is diminished. Smooth muscle cells proliferate in the cell matrix and areas of necrosis are formed in the innermost part of the plaque.
It can reach the vascular middle layer by erosion of the internal elastic lamina.
When the atheromatous plaque becomes unstable, it ulcerates and an intraluminal thrombus forms. The atheromatous matrix metalloproteinases contribute to these. Plaque rupture or clot detachment totally or partially occludes the vessels, leading to myocardial infarctions, cerebral strokes, and blockages in the peripheral arteries.
All these intravascular changes lead to the loss of modulation capacity and the blood circulation to be regulated normally. It is manifested as a decrease in vasodilation and an increase in vasoconstriction. Nitric oxide is inactivated and the production of free radicals is increased by reducing or inactivating the transcription of nitric oxide synthetase. There is also an increase in platelet aggregation, an alteration in plasma activators of tissue factors, thrombomodulin, and proteoglycans.
These changes produced lead to endothelial dysfunction (ET). The endothelium loses its ability to modulate arterial tone, to prevent the inhibition of platelet aggregation, neutrophil adherence, and cell proliferation.
It leads to a loss of local hemostasis with adhesion to the arterial wall of platelets and monocytes. Cell growth factors with proliferation of smooth muscle cells are also released.
The balance between vasodilation, vasoconstriction, and antiplatelet mechanisms is lost. It is accompanied by an increase in plasma C-reactive protein.
Inside there are various physiological stimuli that produce different types of biologically active molecules that fulfill different functions.
The endothelial cells also manufacture other vasodilator substances such as prostacyclins and bradykinin. They also produce powerful vasoconstrictor substances such as endothelin and angiotensin II.
Adinopeptin inhibits the production of adhesion molecules such as integrins and P-selectin. They maintain a balance in the recruitment of inflammatory cells into the arterial wall.
It is a powerful vasodilator and inhibitor of platelet aggregation and adhesion molecules. Stops and prevents abnormal growth of smooth muscle cells in the arteries.
It controls vascular tone, cell proliferation processes and local hemostasis. Nitric oxide and L-citrulline are generated from L-arginine and O2 by the action of L-arginine-NO-guanosine monophosphate synthetase (ONS). Activates K + channels that allow a large amount of calcium to enter the cytoplasm, producing an increase in the enzyme nitric oxide synthetase (ONS), allowing the formation of more nitric oxide
It is released by the frictional pressure of the blood on the endothelium. It is present in all endothelial cells of the arterial tree both in the macro and in the microcirculation. It has a short plasma life (3 to 5 seconds) and due to its low molecular weight and lipophilic structure, it easily penetrates into the arterial wall. Its vasodilation action is achieved by acting on the arterial smooth muscle.
Nitric oxide diffuses into smooth muscle interacting with receptive molecules, especially guanylate cyclase, which degrades guanosine diphosphate. Cyclic GMP, agonist-induced calcium release is increased, and vascular smooth muscle contraction is prevented.
When nitric oxide production decreases, platelet aggregation factors and endothelial growth factors increase. The areas where friction pressure is low increases thrombotic factors and cell proliferation factors. When blood pressure increases, a greater amount of nitric oxide is produced for vasodilation to occur.
It is also known as a flow-mediated endothelial-derived relaxation factor. Its name derives from the place where it is manufactured and what hemodynamic force is exerted on the intra-arterial flow. The various cardiovascular risk factors and especially arterial hypertension reduce its production by reducing the sensitivity of the vascular muscles to nitric oxide. They can also increase their degradation allowing the manufacture of large amounts of superoxides.
Reactive oxygen substances (ROS) are formed within vascular tissue. They are expressed and act within the arterial smooth muscle. Its action has not been demonstrated in another part of the glass. Oxygen free radicals such as superoxide, hydrogen peroxide, peronitrite, and lipid radicals are ROS substances. Xanthine oxidase, NAD (P) H oxidase, endothelial nitric oxide synthetase, and myeloperoxidase are short half-life enzyme systems that act within the vasculature to manufacture ROS substances.
ROS substances are produced by reduction of molecular oxygen and are synthesized from enzyme systems of vascular tissue. A balance occurs in the vascular wall and if the number of oxidizing substances is greater than the antioxidants, oxidative stress occurs.
When there is vascular balance, the formation and degradation of ROS is regulated. When this balance is broken, there is a lot of oxidative activity and little antioxidant activity. Oxygen free radicals such as superoxide form peronitrites that, when they reach high concentrations, are cytotoxic. They produce harmful effects on the function and activity of prostaglandin synthetase, decreasing the production of endothelial prostaglandins.
Hydrogen peroxide and hypochlorous acid are released by neutrophils within the arterial system. When the superoxide is increased it reduces the bioavailability of nitric oxide. Another important source of superoxide comes from the mitochondria of the smooth muscular system.
The increased angiotensin II produces more ROS substances.
This vascular inflammatory condition is known as oxidative stress and is manifested in plasma with an increase in C-reactive protein. Adiponectin is also decreased by increasing the adhesion of monocytes to the vascular endothelium. T and B lymphocytes are found within atheromatous plaques. This stress increases insulin resistance.
Superoxide dismutase, glutathione peroxidase, thiorre-reductase and catalases are enzymatic elements that act as defense within the vascular tissue. They produce the degradation of superoxides formed in excess, reducing their number and avoiding intra-arterial injury.
Its influence is exerted on the oxidative and antioxidant functions of intravascular enzymes. Platelet-derived growth factor, epidermal growth factor, fibroblast growth factor, and insulin growth factor increase the function of NDA (P) oxidase and decrease the action of superoxide-dimintase (SOD ) within vascular smooth muscle.
Interferon gamma, Von Willebrand factor, fibrinogen, interleukin 6 and 8, adiponectin, resistin, homocysteine, and tumor necrosis factor promote oxidation by increasing the levels of NDA (P) oxidase and xanthine– oxidase. They are known as inflammatory markers and effectors.
They form high amounts of superoxides, hydrogen peroxide and peroxynitrates. They accelerate the atherogenesis of the vessels mainly in the noble organs.
Growth factors stimulate the oxidative enzyme system and increase ROS substances.
This endovascular inflammatory state is known as oxidative stress.
RENIN ANGIOTENSIMA ALDOSTERONE SYSTEM. (SRAA)
It is related to the maintenance of arterial tone, the regulation of blood pressure and the hydroelectrolyte balance. They are homeostatic physiological functions related to maintaining correct tissue perfusion.
It is present throughout the body, but mainly within the cardiovascular, renal and adrenal systems.
In the arteries it regulates vasoconstriction and blood volume, acting on the regulation of arterial pressure. In the kidney, it modulates plasma volume or flow and inhibits sodium and water excretion. Increases the excretion of potassium.
In the classic functioning of the system, renal renin splits hepatic angiotensinogen. The pulmonary endothelial angiotensin converting enzyme (ACE) converts angiotensin I to angiotensin II and bradykinin. In the kidney it regulates the excretion of potassium and the reabsorption of water and sodium. These are enzyme systems and substrates that result in different types of angiotensins (I-II-III- and IV) in addition to adrenal aldosterone. Angiotensin I and II migrate through the bloodstream into the target organs where they exert their multiple effects. Angiotensin I and II are produced within cell walls and never within the bloodstream.
It is a protease enzyme that is produced, stored, and freed from within the juxtaglomerular cells of the afferent arteriolar walls in the renal macula dense. It is synthesized from a substance called prorenin. It is poured into the plasma and into the renal interticle where it exerts its action.
Its elaborated quantity helps to evaluate how much angiotensin II may be circulating. It has a short half-life (14 minutes) and its action is exerted on various substrates, but mainly on hepatic angiotensinogen, which it breaks down into angiotensin I.
The kidney is not the only site of synthesis of prorenin and renin because they also appear in the adrenal, salivary, pituitary glands, reproductive system and within the arterial and venous walls. It is also released in different amounts by the action of stimuli that originate from the prisoner and aortic and carotid chemoreceptors.
Four mechanisms are known to intervene in its production.
The first is carried out via the macula densa by chemical signals of change in the concentration of sodium chloride. The second is via the baroreceptors located in the intrarenal afferent arterioles together with the stimuli derived from the carotid and aortic pressoreceptors. The third is via adrenergic B1 and B2 receptors that are stimulated by the release of adrenaline and norepinephrine at the postsynaptic endings of the sympathetic system. The fourth mechanism is through the negative feedback pathway dependent on angiotensin II, potassium, endothelin, and atrial natridiuretic peptide.
All act on juxtaglomerular endothelial cells and increase renin production.
It is the substrate where renin acts, splitting it into angiotensin I.
Its source of formation is the liver, but it is also synthesized by the kidney, the CNS and the vascular cells of the heart. Another important source of production is adipose tissue, especially in abdominal fat. From its formation in the liver it is excreted into plasma and from there to the intacellular space where it is unfolded.
It is increased in arterial hypertension due to the action of RAAS and in gravidic arterial hypertension due to the action of estrogens.
ANGIOTENSIN CONVERSION ENZYME. (ECA)
Angiotensin converting enzyme acts on the substrate, angiotensin I, transforming it into angiotensin II and bradykinin. It is similar to chymase II which subsequently cleaves bradykinin.
ACE is attached to the endothelial cell membrane of the entire organism, but its highest concentration is within the endothelial cells of the pulmonary capillaries. It is also found in high concentration within the brush cells of the renal tubules. Other places where it is found is in the tissues of the prostate, testicles, epididymis, retina and brain in addition to the seminal, amniotic and cerebrospinal fluids.
ACE is not the only enzyme that breaks down angiotensin I and transforms it into angiotensin II since there are several chymases and cathepsins that are known as angiotensin I converters. They are part of the alternative routes of angiotensin II production.
Decreasing the enzyme increases the concentration of angiotensin I and decreases that of angiotensin II. If ACE is permanently blocked, the increase in circulating angiotensin I stimulates renin production and the other enzymatic factors that form angiotensin II are put into operation. The body needs circulating angiotensin II and if there is not enough it makes it synthesize by alternative routes.
By expressing the enzyme within the endothelial tissue forming angiotensin II, it contributes to the regulation of arterial tone.
It is a powerful vasoconstrictor substance and intervenes in the balance of sodium, potassium and water by stimulating the vasoconstriction of the afferent and efferent arterioles in the kidney, as well as promoting the reabsorption of sodium and water in the proximal part of the nephrons. Thus, its loss decreases and potassium excretion increases.
Cardiovascular actions are to increase minute volume and peripheral vasoconstriction through arteriolar smooth muscle. In the adrenals, aldosterone formation increases, intervening in the control of the hydrosaline balance.
Angiotensin II increases the strength of the heart's contraction by opening calcium channels and increasing the heart rate by activating adrenal tone.
On the sympathetic system, the release of adrenal catecholamines increases.
When there is an increase in blood pressure, a baroreceptor reflex is activated that lowers sympathetic tone and increases vagal tone.
Another function is related to the growth of fibroblasts and collagen within the blood vessels and the heart. Activates all cell growth systems causing cardiac myocyte hypetrophy, increase in cell matrix and fibroblasts. There is an increase in muscle mass with subsequent remodeling. It has a short half-life and is cleaved by peptidases into angiotensin III and IV. It is 40 times more powerful vasoconstrictor than adrenaline. It produces permanent vasoconstriction and its elevation is a strong risk factor for causing cardiovascular diseases.
It produces many ROS substances within endothelial cells: it activates NAD (P) H oxidase, favoring the elevation of blood pressure.
Its action is exerted on the cellular receptors AT1-AT2 and AT3 that are located in the vascular smooth muscle, in the heart, in the kidney, in the liver, in the lung and in the adrenal glands where they carry out their transmembrane actions.
AT1 regulates the contraction of the arterial smooth muscle producing vasoconstrictor effects. Due to a dipsogenic action on the CNS, it produces more thirst and the ingested liquid increases blood volume. Diuresis decreases due to increased vasopressin and increases reabsorption at the level of the proximal ankle and increases the concentration of aldosterone in the distal tubule. Increases chronotropism and hypertrophic cell growth producing a gradual increase in blood pressure. The thrombotic state and apoptosis are higher.
These receptors are found in the renal microvasculature, in the loop of Henle, in the conducting ductus, in juxtaglomerular cells and in the cells of the macula densa. Angiotensin II also acts directly within the kidney, producing vasoconstriction, sodium reabsorption (natridiuretic effect), and increased blood pressure.
It produces vasoconstriction of the afferent and efferent arterioles, decreasing renal plasma flow, glomerular filtration, and sodium and water excretion.
The AT2 receptor produces a synthesis of vasodilator substances such as nitric oxide, cyclic GMP and bradykinin. It increases natridiuresis, prevents cell growth, lowers blood pressure and produces antioxidant substances. It has an anti-proliferative, pro-apoptotic and vasodilator effect. They are also abundant in fetal tissues.
The AT3 receptors are found in angiogenesis and in wound healing tissues.
It is a mineralocorticoid hormone that is synthesized in the zona glomerularis of the adrenal cortex.
It is also produced in smaller quantities in the heart, in the brain as well as endothelial cells and arteriolar smooth muscle cells. The substance that most stimulates its production in angiotensin II and acts on the distal renal ankle.
Its main function is to modulate the water and electrolyte balance by retaining sodium and excreting potassium. When there is a high concentration of renin in the adrenal glands there is sodium restriction and increased excretion of potassium. Aldosterone plasma levels are elevated and it produces cellular growth in noble organs with an increase in fibroblasts and collagen deposits in the heart and vascular system.
INSULIN RESISTANCE, OBESITY AND DIABETES.
Abdominal obesity and insulin resistance predispose to hyperglycemia and type II diabetes mellitus. Fat can be in the intraperitoneal or subcutaneous space. The perivisceral is more atherogenic.
This fatty tissue has resistance to insulin, increases the formation of free fatty acids and manufactures different types of adipokines and decreases the number of protective adiponectins.
It is usually accompanied by other cardiovascular risk factors such as dyslipidemia, arterial hypertension and blood hypercoagulability, forming part of the metabolic syndrome.
When they are together, an inflammatory and potrombotic state occurs that increases the risk of suffering from cardiovascular diseases.
Smoking, alcohol, sedentary lifestyle, hormonal disorders, stress, overweight and a diet high in animal fats also contribute. Triglycerides and LDL cholesterol are elevated and HDL cholesterol decreased:
Insulin resistance (IR) produces an increase in fasting blood glucose, an increase in glucose tolerance and glycosylated hemoglobin. It is always present in obesity and is accompanied by genetic factors.
It is seen in tissues designed for glucose homeostasis and its energy use, such as striated muscles, adipose tissue and liver. Produces kidney damage with elevated proteinuria. There is a permanent retention of sodium and an increase in sympathomimetic substances.
There are 30% of hypertensive patients that present the metabolic syndrome and insulin resistance. Obesity is a direct risk factor for insulin resistance and arterial hypertension since when weight is lost, glycemia normalizes and blood pressure drops.
The altered level of glycosylated hemoglobin increases the production of superoxides and oxygen free radicals.
LEFT VENTRICULAR HYPERTROPHY.
A structural transformation occurs in the left ventricle to be able to handle the increased afterload figures. Cardiac myocytes hypertrophy and increase in size, favoring an increase in the ejection fraction due to the continuous elevation of arterial hypertension.
This accommodation of his contractile force lasts for a short time, continuing with a stage of concentric muscular hypertrophy followed by eccentric remodeling. It is accompanied by a dilation of the cavities that alters diastolic filling due to their dilation, reducing systolic cardiac output.
Intracellular oxygen is decreased and ventricular remodeling is increased. This hypoxic muscle cannot expel the required minute volume (systolic overload), which causes an increase in afterload. Areas of necrosis form within the muscle tissue that are replaced by new connective tissue (permanent remodeling) that needs more oxygen to fulfill its functions.
This ventricle then loses its compliance and strength due to the permanent increase in cell growth and subsequent fibrosis. It damages the conduction system giving ventricular arrhythmias. Coronary circulation decreases and myocardial ischemia occurs that progresses to a ventricular morbid state known as congestive heart failure (CHF).
They are thrombotic or hemorrhagic pictures that appear in the course of chronic arterial hypertension. They are called stroke or cerebrovascular accidents (CVA).
Elevated figures both systolic (more than 180 mmHg) and diastolic (more than 110 mmHg) produce a hypertensive emergency that puts the life of the patient at serious risk.
Intra-arterial cell growth with its subsequent fibrosis predisposes to hypertensive encephalopathy and hemorrhage, leading to hypertensive encephalopathy and hemorrhage, leading to silent or not cerebral infarcts culminating in dementia. Atherosclerotic and atherosclerotic lesions occur in the carotid and intracranial circulation. Many vasoactive substances are released and platelet adhesion is increased.
High blood pressure produces microaneurysms that then rupture giving cerebral or cerebellar hemorrhages. Hypertensive encephalopathy produces great edema and cerebral congestion due to an excessive increase in systodiastolic figures.
High blood pressure produces what is known as hypertensive black disease and leads to the condition known as acute or chronic renal failure.
When the systemic pressure in the afferent and efferent glomerular arterioles increases, vasoconstriction increases. Renal flow is decreased by one third because the goal is to avoid glomerular lesions. But the decrease in glomerular arterial perfusion leads to intertitial fibrosis with destruction of the glomeruli and subsequent nephrosclerosis.
The balance between nitric oxide and angiotensin II is lost. Thrombi and microaneurysms form within the renal vessels with a mesangial increase. Many ROS substances are produced that also decrease NO and increase fibrotic material. This nephrosclerosis produces a failure that needs dialysis or eventually a kidney transplant.
There is an increase in uremia, creatinemia, proteinuria, C-reactive protein, and cylindruria.
CLINICAL HISTORY OF THE HYPERTENSIVE PATIENT.
Anamnesis: investigation of the family history of hypertension, the type of hypertension that he presents, since when he knows it, what are his usual figures, where and how he controls it, at what time and place, with what type of equipment, if he is seated, standing or lying down, the times of the measurements, the time it takes to be evaluated, the recent consumption of tobacco, alcohol, coffee or mate, the rush to arrive, stressful situations moments ago or accumulated in time, states of anguish, depression or panic, fever or dehydration, somatic or colic pain, dizziness, lipothymias, seizures, vomiting or diarrhea, tinnitus, cervical or occipital headaches, dyspnea at rest or exertion, typical or atypical chest pain, odynophagia or dysphagia, feeding with excess salt, types of gait, vision, auditions,recent or previous memory, loss of muscle strength and balance, hydration and diet, active gymnastics and sports, work or occupation, work, social, family and economic status, operations and accidents, narcotics, insomnia or drowsiness, changing mood and irritability , sex or erectile dysfunction, drugs you take and your work or family relationship.
Blood pressure must be taken correctly.
The pulse and peripheral pulses will be palpated.
Weight, muscle mass index, abdominal girth and height will be measured.
The cardiac tip shock will be palpated
The cardiac foci, the carotid, renal and peripheral arteries will be auscultated.
The bronchial murmur and the pulmonary vesicular murmur will be auscultated.
The vertex and lung base expansions will be taken.
An eye fundus will be performed.
The tendon reflexes will be taken.
Body temperature will be taken.
The rest of the semiology will be carried out on the whole organism.
Laboratory analysis: complete blood count with platelets, clotting time, prothrombin and blood, HDL cholesterol, LDL cholesterol, triglycerides, blood glucose, uremia, creatinemia, uricaemia, electrophoresis ionogram, fasting urine, 24 hour urine, proteinuria or microalbuminuria, glucose tolerance test, glycolyzed hemoglobin, insulinemia, apolipoprotein, calcium, phosphorus and iron.
Complementary studies : simple electrocardiogram with programmed signal, computerized ergometry, two-dimensional echocardiogram, triggered cardiac spect, coronary angiography and left ventriculogram, color Doppler echo, tilt, test, 3-channel holter, 24-hour ambulatory pressurometry (ABPM), transesophageal echocardiogram, tomography computed cardiac multislice, magnetic resonance of the heart, thyroid ultrasound, arterial and venous vascular Doppler echo, chest radiography and electroencephalogram.