What drugs to take for pressure in bronchial asthma. How are hypertension and asthma related? Bronchial asthma and arterial hypertension

In recent years, the attention of researchers has been increasingly attracted by the problem of multi- and comorbidity. The likelihood of developing comorbidities increases with increasing life expectancy, which can be explained both by age-related changes and by the negative effects of the environment and living conditions for a long time.

The increase in the number of diseases with age reflects, first of all, involutionary processes, and the concept of comorbidity implies the deterministic possibility of their combined course, and the latter has been studied much less.

There are a number of well-known combinations, such as coronary heart disease (CHD) and diabetes mellitus, arterial hypertension (AH) and CAD, hypertension and obesity. But at the same time, there are more and more indications of rarer combinations, for example, peptic ulcer and coronary artery disease, mitral stenosis and rheumatoid arthritis, peptic ulcer and bronchial asthma (BA).

The study of variants of combined pathology can contribute to a deeper understanding of the pathogenesis of diseases and the development of pathogenetically substantiated therapy. This is especially important in relation to widespread and socially significant diseases, which primarily include diseases of the cardiovascular system (AH, IHD) and bronchopulmonary system (BA).

Bronchial asthma and arterial hypertension

The possibility of combining BA and AH was first pointed out in the domestic literature by B.G. Kushelevsky and T.G. Ranev in 1961. They considered this combination as an example of "competing diseases". Further studies have shown that the prevalence of arterial hypertension in patients with bronchial obstruction averages 34.3%.

Such a frequent combination of BA with AH allowed N.M. Mukharlyamov to put forward a hypothesis about symptomatic "pulmonogenic" hypertension, the signs of which are:

increased blood pressure (BP) in patients with chronic nonspecific lung diseases against the background of an exacerbation of the disease, including BA patients with asthma attacks;
decrease in blood pressure as indicators of respiratory function improve against the background of the use of anti-inflammatory and bronchodilator (but not antihypertensive) drugs;
the development of hypertension several years after the onset of lung disease, initially labile, with an increase in blood pressure only during increased obstruction, and then stable.

Situations where AH preceded the onset of BA and was not associated with a worsening of bronchial patency should be regarded as AH.

Studying "pulmonogenic" hypertension in patients with bronchial asthma, D.S. Karimov and A.T. Alimov identified two phases in its course: labile and stable. The labile phase of "pulmonogenic" hypertension, according to the authors, is characterized by the normalization of blood pressure during the treatment of obstructive pulmonary pathology.

The stable phase is characterized by the absence of a correlation between the level of blood pressure and the state of bronchial patency. In addition, the stabilization of hypertension is accompanied by a deterioration in the course of pulmonary pathology, in particular, a decrease in the effectiveness of bronchodilators and an increase in the incidence of asthma.

V.S. Zadionchenko and others agree with the concept of “pulmonogenic” hypertension, who believe that there are pathogenetic prerequisites for isolating this form of symptomatic hypertension, and consider insufficient reduction in blood pressure at night as one of its features.

An indirect, but very strong argument in favor of "pulmonogenic" hypertension are the results of other studies that have proven the role of hypoxia in the development of hypertension in patients with obstructive sleep apnea syndrome.

However, the concept of "pulmonogenic" AH has not yet received universal recognition, and at present, most researchers tend to consider an increase in blood pressure in patients with BA as a manifestation of hypertension (AH).

There are a number of good reasons for this. First, BA patients with elevated and normal BP do not differ from each other in the form and severity of BA, the presence of a hereditary predisposition to it, occupational hazards, and any other features of the underlying disease.

Secondly, the differences between pulmonary and essential hypertension in patients with BA are largely reduced to the lability of the first and the stability of the second. At the same time, the greater dynamics of blood pressure figures and the possibility of their temporary being within the normal range in patients with suspected pulmonary hypertension may be a manifestation of the early stages of GB.

The rise in blood pressure during an asthma attack can be explained by the reaction of the cardiovascular system to a stressful state, which is an asthma attack. At the same time, the majority of BA patients with concomitant hypertension react with an increase in blood pressure not only to the deterioration of airway patency, but also to meteorological and psychoemotional factors.

Thirdly, the recognition of pulmonary hypertension as a separate disease leads to the fact that the prevalence of AH (essential hypertension) among BA patients becomes several times lower than in the general population. This is in conflict with the data on a significant frequency of hereditary predisposition to GB in individuals suffering from BA.

Thus, the question of the genesis of AH in patients with BA has not yet been finally resolved. Most likely, both a combination of BA with GB and a “pulmonogenic” genesis of a persistent increase in blood pressure can take place.

However, the mechanisms responsible for the increase in blood pressure are the same in both cases. One of these mechanisms is a violation of the gas composition of the blood due to a deterioration in the ventilation of the alveolar space due to the presence of broncho-obstructive syndrome. At the same time, an increase in blood pressure acts as a kind of compensatory reaction that contributes to an increase in perfusion and the elimination of oxygen-metabolic deficiency of vital body systems.

At least three mechanisms of the pressor action of hypoxic hypoxia are known. One of them is associated with the activation of the sympathetic-adrenal system, the second - with a decrease in NO synthesis and impaired endothelium-dependent vasodilation, the third - with the activation of the renin-angiotensin-aldosterone system (RAAS), which plays a key role in the regulation of blood pressure.

Hypoxia leads to spasm of the glomerular afferent arterioles, resulting in a decrease in renal blood flow and glomerular filtration. Renal ischemia stimulates the production of renin, which ultimately leads to increased production of angiotensin II (AT-II).

AT-II has a very pronounced vasoconstrictor effect and, in addition, stimulates the production of aldosterone, which retains sodium ions and water in the body. The result of a spasm of resistive vessels and fluid retention in the body is an increase in blood pressure.

Another consequence of RAAS activation in ventilation-induced hypoxic hypoxia should also be noted. The fact is that the angiotensin-converting enzyme is identical to the enzyme kininase-2, which breaks down bradykinin to biologically inactive fragments. Therefore, when the RAAS is activated, there is an increased breakdown of bradykinin, which has a pronounced vasodilating effect and, as a result, an increase in the resistance of resistive vessels.

An analysis of the literature data suggests that the metabolic disorders of biologically active substances characteristic of AD may play an important role in the development of AH. It has been shown, in particular, that already in the early stages of AD, an increase in the level of serotonin in the blood is detected, which, along with bronchoconstrictor, has a weak, but undoubted vasoconstrictor effect.

A certain role in the regulation of vascular tone in patients with AD can be played by prostaglandins, in particular, PGE 2-alpha, which has a vasoconstrictor effect, the concentration of which increases with the progression of the disease.

The role of catecholamines in the development and/or stabilization of hypertension in patients with asthma is beyond doubt, since it has been shown that the excretion of norepinephrine and adrenaline increases during an asthma attack and continues to increase for 6–10 days after its completion.

On the contrary, the question of the role of histamine in the pathogenesis of AH in patients with BA (as well as in the pathogenesis of BA itself) remains a subject of discussion. In any case, V.F. Zhdanov, while studying the concentration of histamine in mixed venous and arterial blood taken from patients with bronchial asthma during catheterization of the heart cavities, did not reveal any differences between groups with normal and elevated blood pressure.

Speaking about the role of metabolic disorders in the development of AH in patients with BA, one should not forget about the so-called non-respiratory lung function. The lungs actively metabolize acetylcholine, serotonin, bradykinin, prostaglandins, to a lesser extent - noradrenaline and practically do not inactivate adrenaline, dopamine, DOPA and histamine.

In addition, the lungs are one of the sources of prostaglandins, serotonin, histamine and kinins. In the lungs, enzymes were found that are necessary for the synthesis of catecholamines, angiotensin-1 is converted into angiotensin-2, the coagulation and fibrinolytic systems, and the surfactant system are regulated.

Pathological situations lead to the fact that the metabolic function of the lungs is impaired. Thus, under conditions of hypoxia, an artificially induced inflammatory process or pulmonary edema, serotonin inactivation decreases and its concentration in the circulatory system increases, and the transition of DOPA to norepinephrine intensifies.

In AD, there was an increase in the concentration of norepinephrine, adrenaline and serotonin in biopsy specimens of the respiratory tract mucosa. When determining the concentration of catecholamines in mixed venous and arterial blood taken from patients with asthma during catheterization of the cavities of the heart and great vessels, it was found that with concomitant hypertension (mainly with a labile course) outside the exacerbation of asthma, the ability of the lungs to metabolize noradrenaline increases, t i.e. to its capture from the blood circulating in the small circle.

Thus, a violation of the non-respiratory function of the lungs in AD can have a rather pronounced effect on the state of systemic hemodynamics, the study of which is devoted to a number of studies.

According to K.F. Selivanova and others, the state of hemodynamics in patients with asthma is influenced by the severity, duration of the disease, the frequency of exacerbations and the severity of organic changes in the bronchopulmonary apparatus.

The restructuring of central hemodynamics according to the hyperkinetic type is noted in the early stages of the disease and in its mild course. As the disease progresses, the value of cardiac output decreases and peripheral vascular resistance increases, which is typical for the hypokinetic variant of central hemodynamics and creates the prerequisites for a persistent increase in blood pressure.

The question of the role of treatment with glucocorticosteroids and sympathomimetics in the development of hypertension in patients with asthma remains open. On the one hand, these drugs appear in the list of causes of the development of iatrogenic hypertension, on the other hand, there is evidence that the use of glucocorticosteroids in therapeutic doses does not lead to a persistent increase in blood pressure in patients with asthma.

Moreover, there is a point of view according to which the treatment of patients with BA and concomitant hypertension with systemic glucocorticosteroids for a long time has not only a bronchodilator, but also a hypotensive effect due to a decrease in the secretion of estradiol, an increase in the concentration of progesterone and restoration of interaction in the "pituitary - cortex" system. adrenals."

Thus, mutual aggravation and progression in the combination of bronchial asthma and arterial hypertension is based on the commonality of some links of pathogenesis (impaired pulmonary and cardiac microcirculation, development of hypoxemia, pulmonary hypertension, etc.). This can lead to progression of heart failure and early development of cardiorespiratory complications.

There is no doubt that in the treatment of arterial hypertension in bronchial asthma, it is justified to prescribe antihypertensive drugs, which should not only effectively reduce blood pressure, but also have a positive effect on endothelial function, reduce pulmonary hypertension, and possibly indirectly reduce the degree of systemic inflammatory reactions in the absence of negative effects. to the respiratory system.

However, recent studies have shown that a high percentage of cardiovascular pathology in such patients opens up a huge problem regarding the prevention and difficulties of therapy with existing bronchial asthma.

Bronchial asthma and coronary heart disease

Ischemic heart disease is one of the most common and severe diseases of the cardiovascular system. More than 10 million working-age population of the Russian Federation suffer from coronary artery disease, 2-3% of them die annually.

The combination of coronary artery disease with lung pathology, in particular with asthma, is not casuistry. Moreover, there is evidence that the prevalence of coronary artery disease is higher in patients with AD than in the general population.

The frequent combination of coronary artery disease and asthma is apparently associated not so much with the presence of common risk factors as with the "crossing" of the pathogenesis and, possibly, the etiology of these diseases. Indeed, the leading risk factors for CHD - dyslipidemia, male gender, age, hypertension, smoking, and others - do not play a significant role in the development of AD.

However, chlamydial infection can be one of the causes of both AD and CHD. It has been shown, in particular, that in a significant percentage of cases, the development of BA is preceded by pneumonia caused by chlamydia. At the same time, there is evidence indicating a relationship between chlamydial infection and atherosclerosis.

In response to chlamydial infection, changes in the immune system occur, leading to the appearance of circulating immune complexes. These complexes damage the vascular wall, interfere with lipid metabolism, increasing the level of cholesterol (Cholesterol), LDL cholesterol and triglycerides.

It has also been shown that the development of myocardial infarction is often associated with an exacerbation of chronic chlamydial infection, in particular bronchopulmonary localization.

Speaking about the "intersection" of the pathogenesis of AD and CHD, one cannot ignore the role of the lungs in lipid metabolism. Lung cells contain systems that are actively involved in lipid metabolism, carrying out the breakdown and synthesis of fatty acids, triacylglycerols and cholesterol.

As a result, the lungs become a kind of filter that reduces the atherogenicity of blood flowing from the abdominal organs. Lung diseases significantly affect the metabolism of lipids in the lung tissue, creating preconditions for the development of atherosclerosis, including coronary atherosclerosis.

However, there is also a directly opposite point of view, according to which chronic nonspecific lung diseases reduce the risk of developing atherosclerosis, or at least slow down its development.

There is evidence that chronic pulmonary pathology is associated with a decrease in the blood levels of total cholesterol (CH) and low-density lipoprotein cholesterol, with an increase in the concentration of high-density lipoprotein cholesterol. These shifts in the lipid spectrum may be due to the fact that, in response to hypoxia, the production of heparin increases, which increases the activity of lipoprotein lipases.

Coronary atherosclerosis is the most important, but not the only factor responsible for the development of CHD. The results of studies of recent decades indicate that increased blood viscosity is an independent risk factor for many diseases, including coronary artery disease.

High blood viscosity is characteristic of angina pectoris, precedes myocardial infarction and largely determines the clinical course of coronary artery disease. Meanwhile, it is well known that in patients with chronic respiratory diseases, in response to arterial hypoxia, erythropoiesis increases compensatory and polycythemia develops with an increase in hematocrit. In addition, with pulmonary pathology, hyperaggregation of blood cells is often observed and, as a result, a violation of microcirculation.

In recent years, much attention has been paid to the study of the role of nitric oxide (NO) in the development of diseases of the cardiovascular and bronchopulmonary systems.

The beginning of the “NO-history” is considered to be the fact, established in 1980, of the disappearance of the vasodilating effect of acetylcholine when the vascular endothelium is damaged, which made it possible to hypothesize the existence of a factor produced by the endothelium, through which the action of acetylcholine and other known vasodilators is realized.

In 1987, it was established that the “endothelial-produced relaxing factor” is nothing more than a nitric oxide molecule. A few years later, it was shown that NO is formed not only in the endothelium, but also in other cells of the body and is one of the main mediators of the cardiovascular, respiratory, nervous, immune, digestive, and genitourinary systems.

To date, three NO synthetases are known, two of which (types I and III) are constitutive, constantly expressed and producing small amounts (picomoles) of NO, and the third (type II) is inducible and is capable of producing large amounts of NO for a long time. (nanomoles) NO.

Constitutive NO synthetases are present in the airway epithelium, nerves, and endothelium, and their activity depends on the presence of calcium ions. Inducible NO synthetase is found in macrophages, neutrophils, endothelium, microglial cells, and astrocytes and is activated by bacterial lipopolysaccharides, interleukin-1β, endotoxins, interferon, and tumor necrosis factor.

Nitric oxide produced by type II NO synthetase acts as one of the components of the body's nonspecific defense against viruses, bacteria, and cancer cells, facilitating their phagocytosis.

Currently, NO is recognized as a reliable marker of inflammation activity in AD, since exacerbation of the disease is accompanied by a parallel increase in the amount of exhaled NO and the activity of inducible NO synthetase, as well as the concentration of highly toxic peroxynitrite, which is an intermediate product of NO metabolism.

Accumulating, toxic free radicals cause the reaction of lipid peroxidation of cell membranes, lead to the expansion of inflammation of the respiratory tract due to an increase in vascular permeability and the appearance of inflammatory edema. This mechanism is called the "dark side" of NO action.

The “bright side” of its action is that NO is a physiological regulator of the tone and lumen of the respiratory tract and, in small concentrations, prevents the development of bronchospasm.

The most important source of nitric oxide is the endothelium, which produces it in response to the so-called "shear stress", i.e. deformation of endothelial cells under the influence of blood flowing through the vessel.

Hemodynamic forces can directly act on the luminal surface of endotheliocytes and cause spatial changes in proteins, some of which are represented by transmembrane integrins that connect elements of the cytoskeleton with the cell surface. As a result, the cytoskeletal architectonics may change with subsequent transmission of information to various intra- and extracellular formations.

The acceleration of blood flow leads to an increase in shear stress on the endothelium, increased production of nitric oxide and expansion of the vessel. This is how the mechanism of endothelium-dependent vasodilation functions - one of the most important mechanisms of blood flow autoregulation. Violation of this mechanism is assigned an important role in the development of a number of diseases of the cardiovascular system, including coronary artery disease.

It is known that the ability of vessels to endothelium-dependent vasodilation is impaired during exacerbation of asthma and is restored during remission. This may be due to a decrease in the ability of endothelial cells to respond to shear stress due to a generalized defect in cell membranes or a violation of intracellular regulatory mechanisms, manifested by a decrease in the expression of inhibitory G-proteins, a decrease in phosphoinositol metabolism, and an increase in protein kinase C activity.

It is possible that an increase in blood viscosity due to an increase in the number of erythrocytes in the blood also plays a role in the impairment of the ability of blood vessels to endothelium-dependent vasodilation during exacerbation of BA, but this issue, judging by the literature, requires further study.

It should be noted that during the period of exacerbation of BA, there is a decrease in the capacity of vessels not only for endothelium-dependent, but also for endothelium-independent vasodilation. The reason may be a decrease in the susceptibility of vascular smooth muscle cells to vasodilating stimuli due to hypoxia due to the progression of ventilation disorders during an exacerbation of the disease.

Reduction of ventilation disturbances and, as a result, normalization of blood gas composition during remission lead to restoration of the sensitivity of vascular smooth muscle cells to the action of vasodilators and restoration of the endothelium-independent ability of blood vessels to dilate.

Another "point of intersection" of the pathogenesis of IHD and AD is pulmonary hypertension. In bronchopulmonary pathology, in particular in BA, pulmonary hypertension is precapillary in nature, since it develops as a result of a generalized spasm of the pulmonary precapillaries in response to a decrease in the partial pressure of oxygen in the alveolar space.

With coronary artery disease, or rather, with the left ventricular failure caused by this disease, postcapillary pulmonary hypertension develops, associated with a violation of the outflow of blood from the pulmonary circulation.

Regardless of the mechanism of its development, pulmonary hypertension increases the load on the right ventricle, which leads to a violation of not only its functional state, but also the functional state of the left ventricle.

In particular, pressure overload of the right ventricle impairs the rate and volume of its diastolic filling, which, in turn, can cause left ventricular diastolic dysfunction. Meanwhile, it is the diastolic dysfunction of the left ventricle that in 50% of cases is the cause of heart failure.

The complexity of the pathogenetic relationship between coronary artery disease and BA predetermines, apparently, the multivariance of the clinical course of these diseases in the case of their combination in the same patient.

As a rule, combined pathologies aggravate each other, an example of which is the development of acute coronary events in patients with coronary artery disease against the background of exacerbation of BA or COPD. However, the results of some studies indicate the possibility of fundamentally different relationships between bronchopulmonary and cardiac pathologies.

So, according to I.A. Sinopalnikova et al., during an exacerbation of BA, there is a regression of the manifestations of concomitant coronary artery disease, both clinical and ECG signs. After relief of exacerbation, there is a return of coronary symptoms, in particular, an increase in episodes of transient myocardial ischemia.

According to the authors, the reason for this may be the development of a functional blockade of the β-adrenergic apparatus due to a decrease in the intracellular concentration of cAMP against the background of exacerbation of AD. The result is an improvement in coronary perfusion and a decrease in myocardial oxygen demand.

As follows from the above, the question of the nature of the interaction between bronchopulmonary and coronary pathology can be considered controversial, but the fact that chronic respiratory diseases can hide the pathology of the cardiovascular system is beyond doubt.

One of the reasons for this is the non-specificity of one of the leading clinical manifestations of AD - shortness of breath. One cannot but agree with the opinion that there are considerable difficulties in the clinical interpretation of the dyspnea syndrome in patients with a long history of chronic diseases of the bronchopulmonary system, combined with coronary artery disease.

Shortness of breath in such patients can be both the equivalent of angina pectoris and a manifestation of broncho-obstructive syndrome. It should be noted that the pathogenesis of broncho-obstructive syndrome in such cases is very complicated, because in addition to primary bronchial obstruction, other mechanisms may also be involved in its genesis, in particular, impaired pulmonary hemodynamics due to left ventricular failure with edema of the pulmonary interstitium and bronchial wall.

According to O.I. Klochkov, patients with BA are much more likely (from 57.2 to 66.7%) than in the general population (from 35 to 40%) to have asymptomatic, in particular painless, forms of coronary artery disease. In such a situation, the role of instrumental methods for diagnosing coronary artery disease, in particular ECG, increases.

However, the interpretation of changes in the terminal part of the ventricular complex in patients with lung pathology causes difficulties, since these changes can be associated not only with coronary pathology, but also with metabolic changes due to hypoxia, hypoxemia, and acid-base disorders.

Similar difficulties arise when interpreting the results of Holter monitoring. Due to its safety and sufficiently high information content, this method has become very widespread for diagnosing coronary artery disease in general and painless myocardial ischemia in particular.

According to A.L. Vertkin and others, episodes of painless myocardial ischemia are detected in 0.5–1.9% of clinically healthy individuals. Data on the prevalence of painless ischemia in patients with BA could not be found in the literature, which is indirect evidence of the complexity of interpreting ECG changes detected in patients with bronchopulmonary pathology.

The interpretation of the latter is complicated by the fact that dystrophic changes in the myocardium caused by pulmonary hypertension and hypoxemia can be observed not only in the right, but also in the left ventricle.

The asymptomatic or atypical course of coronary artery disease causes sudden death in half of all cases in people who have not previously had signs of cardiovascular disease. This fully applies to patients with AD.

According to O.I. Klochkov, in such patients, in 75% of cases, mortality in the elderly and senile age does not occur from diseases of the bronchopulmonary system or their complications. In a number of extrapulmonary causes of death in this category of patients, painless myocardial ischemia accounted for the largest share (40.7%).

The combination of AD with coronary pathology creates serious problems with the medical treatment of both diseases, since drugs that are most effective in the treatment of one of them are either contraindicated or undesirable in the other.

Thus, β-blockers, being the drug of choice in the treatment of coronary artery disease, are contraindicated in patients with BA. Replacing them with blockers of slow calcium channels (verapamil, diltiazem) or blockers of If-channels of the sinus node (ivabradine) does not always achieve the desired effect.

An obligate component of the treatment of coronary artery disease is the appointment of antiplatelet agents, primarily acetylsalicylic acid, the use of which can lead to an exacerbation of asthma. Replacing aspirin with other antiplatelet agents does not reduce the effectiveness of CHD treatment, but significantly increases its cost.

Many drugs needed for the treatment of asthma can have a negative impact on the course of coronary artery disease. Thus, glucocorticosteroids (including inhaled ones) contribute to an increase in the level of LDL cholesterol and the progression of atherosclerosis. Meanwhile, inhaled glucocorticosteroids are the most effective anti-inflammatory drug, and it is almost impossible to refuse to use it in the treatment of patients with BA.

Concomitant coronary artery disease makes the use of theophyllines in the complex therapy of BA extremely undesirable. Theophyllines have not only bronchodilator, immunomodulatory and anti-inflammatory effects, but also have a pronounced effect on the cardiovascular system, increasing myocardial oxygen demand and its ectopic activity. The consequence of this may be the development of severe cardiac arrhythmias, including life-threatening ones.

Refusal to use theophyllines due to the presence of concomitant coronary artery disease in a patient does not significantly affect the effectiveness of asthma treatment, since currently not theophyllines, but β2-agonists are first-line bronchodilators.

As the name implies, β2-agonists have a selective stimulatory effect on β2-adrenergic receptors, resulting in bronchial dilatation, improved mucociliary clearance, reduced vascular permeability, and stabilization of mast cell membranes.

At therapeutic doses, β2-agonists practically do not interact with β1-adrenergic receptors, which allows us to consider them selective. However, the selectivity of β2-agonists is dose-dependent. With an increase in the dose of the drug, along with β2-adrenergic receptors of the bronchi, β1-adrenergic receptors of the heart are also stimulated, which leads to an increase in the strength and frequency of heart contractions and, as a result, to an increase in myocardial oxygen demand.

In addition, stimulation of β1-adrenergic receptors causes an increase in conductivity, automatism and excitability, which ultimately leads to an increase in ectopic activity of the myocardium and the development of arrhythmias.

Bronchial asthma and cardiac arrhythmias

The data presented in the literature indicate that in patients with obstructive pulmonary diseases, almost all types of cardiac arrhythmias, including fatal ones, can be observed.

It is heart rhythm disturbances that often determine the prognosis of the life of such patients. This, apparently, explains the high interest of researchers in the problem of cardiac arrhythmias in patients with pathology of the respiratory system.

The nature of cardiac arrhythmias in patients with BA was analyzed in detail by E.M. share. According to her data, sinus tachycardia, atrial and ventricular extrasystole, atrial mono- and multifocal tachycardia and atrial fibrillation are most common in patients with BA.

The frequency of arrhythmias of atrial and ventricular origin in patients with obstructive pulmonary diseases increases during an exacerbation of the underlying disease, which significantly aggravates its course.

Among the most important factors that can cause cardiac arrhythmias in lung diseases include hypoxemia and associated acid-base and electrolyte imbalances, pulmonary hypertension leading to the development of cor pulmonale, iatrogenic influences and concomitant coronary artery disease.

The role of arterial hypoxemia in the development of cardiac arrhythmias in patients with chronic nonspecific lung diseases was proven in the 1970s. Hypoxemia causes myocardial hypoxia, which leads to its electrical instability and the development of arrhythmias.

Myocardial hypoxia is exacerbated by impaired oxygen transport to tissues associated with an increase in blood viscosity due to secondary erythrocytosis that develops during chronic hypoxia.

In addition, hypoxemia is accompanied by a number of systemic effects, which ultimately also contribute to the appearance of cardiac arrhythmias. One of these effects is the activation of the sympathoadrenal system, accompanied by an increase in the concentration of norepinephrine in the blood plasma due to an increase in its release by nerve endings.

Catecholamines increase the automatism of the cells of the conduction system of the heart, which can lead to the appearance of ectopic pacemakers. Under the influence of catecholamines, the rate of transmission of excitation from Purkinje fibers to myocardiocytes increases, but the rate of conduction through the fibers themselves may decrease, which creates prerequisites for the development of the re-entry mechanism.

Hypercatecholaminemia is accompanied by activation of peroxidation processes, which leads to the appearance of a large number of free radicals that stimulate apoptosis of cardiomyocytes.

In addition, activation of the sympathoadrenal system contributes to the development of hypokalemia, which also creates the preconditions for the onset of arrhythmia. It should be emphasized that the arrhythmogenic effects of catecholamines increase sharply against the background of myocardial hypoxia.

Activation of the sympathoadrenal system during hypoxemia leads to the development of autonomic imbalance, since pronounced vagotonia is characteristic of AD as such. Vegetative imbalance that develops against the background of an exacerbation of the disease may play a role in the development of arrhythmias, especially supraventricular ones.

In addition, vagotonia leads to the accumulation of cGMP and, as a consequence, to the mobilization of intracellular calcium from subcellular structures. An increase in the concentration of free calcium ions can lead to the appearance of ectopic activity, especially against the background of hypokalemia.

An important role in the development of cardiac arrhythmias in patients with obstructive pulmonary pathology is assigned to pulmonary hypertension, leading to hemodynamic overload of the right heart. Acute overload of the right ventricle can cause the development of ectopic arrhythmias due to a change in the slope of phase 4 of the action potential.

Persistent or often recurrent pulmonary hypertension leads to right ventricular hypertrophy, while hypoxemia and toxic effects of inflammatory products contribute to the development of dystrophic changes in the heart muscle. The result is morphological and, as a result, electrophysiological heterogeneity of the myocardium, which creates preconditions for the development of various cardiac arrhythmias.

The most important role in the development of cardiac arrhythmias in patients with asthma is played by iatrogenic factors, primarily the intake of methylxanthines and β-agonists. The arrhythmogenic effects of methylxanthines, in particular eufillin, have long been well studied. It is known that the use of aminophylline leads to an increase in heart rate and can provoke the appearance of supraventricular and ventricular extrasystoles.

Animal experiments have shown that parenteral administration of aminophylline reduces the threshold for the onset of ventricular fibrillation, especially against the background of hypoxemia and respiratory acidosis. Data have been obtained that indicate the ability of aminophylline to cause multifocal ventricular tachycardia, which creates a real threat to the patient's life.

It is generally accepted that at therapeutic concentrations, theophyllines do not cause cardiac arrhythmias, however, there is evidence that arrhythmias can also be provoked by therapeutic doses of aminophylline, especially if the patient has a history of arrhythmias.

In addition, it should be borne in mind that in real clinical practice, an overdose of theophyllines is quite common, since their therapeutic range is very narrow (from about 10 to 20 μg / ml).

Until the early 1960s. theophylline was the most common and effective bronchodilator used in the treatment of patients with asthma. In the 1960s for the relief of bronchospasm, inhaled non-selective adrenomimetics, which have a rapid and pronounced bronchodilator effect, began to be used.

The widespread use of these drugs has been accompanied by a sharp increase in mortality among patients with bronchial asthma in some countries, especially in Australia, New Zealand and the UK. For example, in the UK, during the period from 1959 to 1966, mortality among asthma patients aged 5 to 34 years increased by 3 times, which brought asthma into the top ten leading causes of death.

It is now considered proven that the epidemic of deaths among patients with asthma in the 1960s. was due to the widespread use of non-selective adrenomimetics, an overdose of which provoked the development of fatal arrhythmias.

This is evidenced at least by the fact that the number of deaths among asthma patients increased only in those countries where a single dose of inhaled sympathomimetics exceeded the recommended one (0.08 mg) by several times. In places where less active sympathomimetics were used, for example, in North America, mortality practically did not increase, although sales of these drugs increased by 2-3 times.

The epidemic of deaths described above sharply intensified work on the creation of β2-selective adrenomimetics, which by the end of the 1980s. from the treatment of BA, non-selective adrenomimetics and significantly replaced theophyllines. However, the "change of leader" did not lead to a solution to the problem of iatrogenic arrhythmias in patients with asthma.

It is known that the selectivity of β2-agonists is relative and dose-dependent. It has been shown, for example, that after parenteral administration of 0.5 mg of salbutamol, the heart rate increases by 20 beats per minute, and systolic blood pressure increases by 20 mm Hg. Art. At the same time, the content of the MB-fraction of creatine phosphokinase (CPK) increases in the blood, which indicates the cardiotoxic effect of short-acting β2-agonists.

There is evidence of the effect of β2-agonists on the duration of the QT interval and the duration of low-amplitude signals of the distal part of the QRS complex, which creates prerequisites for the development of ventricular arrhythmias. The development of arrhythmias can also be facilitated by a decrease in the level of potassium in the blood plasma, due to the intake of β2-agonists.

The severity of the proarrhythmic effect of β2-agonists is influenced by a number of factors, ranging from the dose and method of their administration to the presence of comorbidities in the patient, in particular coronary artery disease.

Thus, a number of studies have revealed a significant relationship between the frequency of use of inhaled β-adrenergic agonists and the mortality of patients with BA from fatal arrhythmias. It has also been shown that salbutamol inhalations using a nebulizer in patients with asthma have a significantly stronger proarrhythmic effect than when using a metered dose inhaler.

On the other hand, there is evidence that the ingredients that make up most inhaled drugs, in particular fluoride hydrocarbons (freons), increase the sensitivity of the myocardium to the proarrhythmogenic effect of catecholamines.

The role of coronary artery disease in the development of arrhythmias in patients with BA is, in principle, beyond doubt, however, it is rather difficult to assess its "specific weight" among other arrhythmogenic factors. On the one hand, it is known that the prevalence of arrhythmias in BA patients increases with age, which can be considered indirect evidence of the involvement of coronary artery disease in the development of arrhythmias in patients with obstructive pulmonary disease.

Thus, according to one of the studies, the average age of BA patients in whom arrhythmias were registered was 40 years, and the average age of patients without rhythm disturbances was 24 years. On the other hand, according to I.A. Sinopalnikova, during an exacerbation of BA, there is a regression of the clinical symptoms of coronary artery disease, including cardiac arrhythmias.

It should be noted that the idea of a “protective” role of BA exacerbation in relation to coronary events does not find wide support. Most researchers tend to believe that myocardial ischemia associated with atherosclerosis of the coronary arteries can lead to the development of serious cardiac arrhythmias, including fatal ones.

conclusions

Asthma itself is a serious medical and social problem, but an even more serious problem is the combination of asthma with other diseases, primarily with diseases of the cardiovascular system (arterial hypertension and coronary heart disease).

Mutual aggravation and progression in the combination of bronchial asthma and arterial hypertension is based on the commonality of some links of pathogenesis (impaired pulmonary and cardiac microcirculation, development of hypoxemia, pulmonary hypertension, etc.). This can lead to progression of heart failure and early development of cardiorespiratory complications.

In addition, a high percentage of cardiovascular pathology in such patients opens up a huge problem regarding the prevention and difficulties of therapy with existing bronchial asthma.

Thus, the interaction of diseases, age and drug pathomorphism significantly changes the course of the underlying disease, the nature and severity of complications, worsens the quality of life of the patient, limits or complicates the diagnostic and treatment process.

In medical practice, it is not uncommon for people with a pathology of the respiratory system to experience a significant increase in blood pressure (BP) during an exacerbation of the disease.

The pathologies of the respiratory system, which will be discussed, are collectively denoted by the abbreviation COPD - chronic obstructive pulmonary disease.

This group includes diseases such as chronic obstructive bronchitis, bronchial asthma and emphysema. The phenomenon that causes hypertension in asthma is called pulmonogenic (pulmonary) arterial hypertension.

Many doctors deny the presence of pulmonary hypertension, insisting on the presence of two diseases that are independent of each other.

However, no less number of specialists are convinced of the direct connection between these pathologies. Their confidence is based on the following facts:

about 35% of patients with various forms of COPD suffer from hypertension;
exacerbation of the disease entails an increase in blood pressure;
the period of remission of bronchopulmonary disease is associated with the normalization of blood pressure.

Can bronchial asthma cause complications in the form of hypertension?

Despite the fact that pulmonary hypertension still does not exist as an officially confirmed independently existing disease, an increase in blood pressure in bronchial asthma continues to haunt a huge number of patients.

At the same time, it is necessary to treat high blood pressure with extreme caution, because. many means for normalizing pressure are ways to cause an attack of suffocation in a patient. Such tablets increase the tone of the small bronchi, and therefore their ventilation worsens.

Therefore, the selection of drugs should be carried out with great care.

Usually, if a patient notices an increase in blood pressure only during an asthma attack, it is enough to use only an inhaler (for example, Salbutamol) to stop both symptoms at once - suffocation and increased pressure. Specific treatment for hypertension is not required. The situation is different in a situation where the patient has persistent hypertension that is not associated with the phases of the course of bronchial asthma. In this case, the patient is selected a drug that does not provoke asthma attacks, and courses of treatment for hypertension are carried out as part of complex therapy.

The doctor should also take into account the fact that with a long course of bronchial asthma, a "cor pulmonale syndrome" is formed in a patient, which in practice means a change in the pharmacodynamics of certain drugs, including hypertensive ones. When prescribing a drug to combat high blood pressure, the active substance and dosage should be selected taking into account this feature of the patient's body.

Supporters of the theory of the presence of pulmonary hypertension as an independent disease insist that COPD diseases, including bronchial asthma, can cause persistent hypertension over time. Doctors attribute this to hypoxia, which haunts patients with bronchial asthma. The mechanism by which this relationship occurs is complex and involves CNS neurotransmitters, but can be summarized as follows:

The correctness of this mechanism is partly confirmed by observations of patients in clinical trials.

Patients who do not suffer from COPD, but who experience sleep apnea (periodic breathing stops due to snoring), suffer from high blood pressure in almost 90% of cases!

At the same time, when breathing stops, activation of the sympathetic system is recorded, the mechanism of action of which was described above.

In addition, as mentioned earlier, a long and severe course of bronchial asthma can provoke the development of a symptom complex known as "cor pulmonale". This phrase in practice means the inability of the right ventricle of the heart to properly perform its function.

Cor pulmonale can have different consequences depending on the neglect of the disease and the availability of adequate treatment. One of its most common symptoms is hypertension.

Another reason for the development of arterial hypertension against the background of bronchial asthma is the use of hormonal drugs to stop asthma attacks.

Glucocorticoids, administered as a tablet (oral) or injection (intramuscularly), can cause serious side effects associated with endocrine system disorders. In addition to arterial hypertension, with the frequent use of hormonal drugs for asthma, diabetes mellitus or osteoporosis can develop. However, these side effects are deprived of topical preparations produced in the form of inhalers and nebulizers.

How to treat hypertension in bronchial asthma?

Earlier in the article it was already said that a patient suffering from hypertension with bronchial asthma needs to monitor his condition for some time.

The doctor may even ask the patient to keep a diary, regularly recording blood pressure values, as well as the frequency and intensity of asthma attacks, medications used to relieve symptoms. Based on these data, it can be concluded whether the rise in blood pressure depends only on asthma attacks or pursues the patient constantly.

If blood pressure values exceed the norm only during and after an asthma attack, no special treatment is required. The patient should only choose the right drug, calculate the dosage and time of admission to eliminate the symptoms of asthma. If suffocation can be quickly stopped by inhalation, pressure surges can be avoided without the use of specific drugs.

Choice of drugs

If arterial hypertension is present in the patient constantly, when prescribing the drug, the doctor must solve the following problems. The drug must:

Almost all of these criteria are met by drugs whose action is based on blocking calcium channels. They reduce blood pressure in the lungs, without leading to a decrease in bronchial patency.

Among calcium antagonists, there are two main groups of drugs:

Dihydropyridine;
Non-dihydropyridine.

The main difference lies in the fact that the first group of drugs does not reduce the heart rate, and the second one does, therefore it is not used in case of congestive heart failure.

Dihydropyridine drugs:

felodipine;

Non-dihydropyridine drugs:

Verapamil;
Diltiazem.

The decision to use this or that drug should be made by the doctor, taking into account the patient's condition and the possible risks associated with complications from taking it. You should be especially careful when prescribing a medicine to a patient with cor pulmonale syndrome, ideally, appoint an additional consultation with a cardiologist.

How complicated is the treatment of asthma in hypertension?

Difficulties in the fight against asthma with concomitant hypertension are associated with the same problems as in the selection of a remedy for hypertension in asthma. It is necessary to make sure that the remedies aimed at eliminating both symptoms are compatible with each other - i.e. do not enter into a chemical reaction and do not enhance the side effects of each other. In addition, you should:

In general, with a competent and timely diagnosis of the disease and the appointment of compatible new generation drugs, the patient can live for many years without experiencing severe hypertensive and asthmatic symptoms.

At the same time, it is important to understand one's responsibility for the timely intake of drugs in the correct dosage and, if possible, to minimize the "trigger" factors that provoke asthma attacks or hypertension.

Bronchial asthma with concomitant diseases of various organs- features of the clinical course of bronchial asthma in various concurrent diseases.
The most common in patients with bronchial asthma are allergic rhinitis, allergic rhinosinusopathy, vasomotor rhinitis, nasal and sinus polyposis, arterial hypertension, various endocrine disorders, pathology of the nervous and digestive systems.
The presence of arterial hypertension in patients with bronchial asthma is a generally recognized fact. The frequency of the combination of these diseases is increasing. The main factor in the increase in systemic arterial pressure is central and regional hemodynamic disorders: an increase in peripheral vascular resistance, a decrease in pulse blood filling of the brain, and hemodynamic disturbances in the pulmonary circulation. Hypoxia and hypercapnia accompanying chronic bronchial obstruction, as well as the influence of vasoactive substances (serotonin, catecholamines and their precursors) contribute to an increase in blood pressure. There are two forms of arterial hypertension in bronchial asthma: hypertension (25% of patients), which proceeds benignly and slowly progresses, and symptomatic "pulmogenic" (the predominant form, 75% of patients). In the "pulmogenic" form, blood pressure rises mainly during severe bronchial obstruction (attack, exacerbation), and in some patients it does not reach the norm and increases during exacerbation (stable phase).
Bronchial asthma is often combined with endocrine disorders. There is a known correlation between asthma symptoms and female genital function. In puberty in girls and premenopausal in women, the severity of the disease increases. In women suffering from bronchial asthma, premenstrual asthmatic syndrome often occurs: exacerbation 2-7 days before the onset of menstruation, less often simultaneously with it; with the onset of menstruation comes a significant relief. There are no pronounced fluctuations in bronchial reactivity. Most patients have ovarian dysfunction.
Bronchial asthma is severe when combined with hyperthyroidism, which significantly disrupts the metabolism of glucocorticosteroids. A particularly severe course of bronchial asthma is observed against the background of Addison's disease (a rare combination). Sometimes bronchial asthma is combined with myxedema and diabetes mellitus (about 0.1% of cases).
Bronchial asthma is accompanied by CNS disorders of various nature. In the acute stage, psychotic states with psychomotor agitation, psychoses, and coma are observed. In a chronic course, vegetative dystonia is formed with changes at all levels of the autonomic nervous system. Asthenoneurotic syndrome is manifested by irritability, fatigue, sleep disturbance. Vegetative-vascular dystonia is characterized by a number of signs: hyperhidrosis of the palms and feet, red and white "dermographism", tremor, vegetative crises of the sympathoadrenal type (sudden shortness of breath with a respiratory rate of 34-38 in 1 min, a feeling of heat, tachycardia up to 100-120 in 1 min , rise in blood pressure to 150/80-190/100 mm Hg, frequent profuse urination, urge to defecate). Crises develop in isolation, imitate an asthmatic attack with a subjective feeling of suffocation, but there is no labored exhalation and wheezing in the lungs. Symptoms of autonomic dystonia occur with the onset of bronchial asthma and become more frequent in parallel with its exacerbations. Autonomic dysfunction is manifested by weakness, dizziness, sweating, fainting, and contributes to the lengthening of the period of coughing, asthma attacks, residual symptoms, more rapid progression of the disease and relative resistance to therapy.
Concomitant diseases of the digestive system (pancreatic dysfunction, dysfunction of the liver, intestines), which are found in a third of patients, especially with prolonged glucocorticosteroid therapy, can have a significant impact on the course of bronchial asthma.
Concomitant diseases complicate the course of bronchial asthma, complicate its treatment and require appropriate correction. Therapy of arterial hypertension in bronchial asthma has certain features. "Pulmogenic" arterial hypertension, which is observed only during attacks of suffocation (labile phase), can normalize after the elimination of bronchial obstruction without the use of antihypertensive drugs. In cases of stable arterial hypertension, complex treatment uses hydralazine preparations, ganglion blockers (arpenal, fubromegan, merpanit, temekhin, peitamine), hypothiazide, veroshpiron (has the properties of an aldosterone blocker, corrects electrolyte disturbances) 100-150 mg per day for three weeks . Adrenergic drugs a-blocking, in particular pyrroxane, can be effective, calcium antagonists (corinfar, isoptin) are used.
The neurogenic components of an asthma attack can be influenced by ganglioblockers and anticholinergics (can be used in combination with bronchodilators: arpenal or fubromegan - 0.05 g three times a day; halidor - 0.1 g three times a day; temehin - 0.001 g three times a day day), which are recommended for mild attacks of a reflex or conditioned reflex character, with a combination of bronchial asthma with arterial hypertension and pulmonary hypertension. These drugs must be used under the control of blood pressure; they are contraindicated in hypotension. For the treatment of patients with a predominance of the neurogenic component in the pathogenesis, various options for novocaine blockades are used (subject to the tolerance of novocaine), psychotherapy, hypnosuggestive therapy, electrosleep, reflexology, and physiotherapy. These methods are able to eliminate the state of fear, conditioned reflex mechanisms of seizures, anxious mood.
Treatment of concomitant diabetes is carried out according to the general rules: diet, antidiabetic drugs. At the same time, for the correction of carbohydrate metabolism, it is not recommended to use biguanides, which, due to increased anaerobic glycolysis (the mechanism of hypoglycemic action), can aggravate the clinical picture of the underlying disease.
The presence of esophagitis, gastritis, gastric and duodenal ulcers creates difficulties for glucocorticosteroid therapy. In cases of acute gastrointestinal
bleeding, it is more advisable to use parenteral glucocorticosteroid drugs, an alternative treatment regimen is preferable. The optimal way to treat bronchial asthma complicated by diabetes mellitus and peptic ulcer is the appointment of maintenance inhaled glucocorticosteroid therapy. In hyperthyroidism, there may be a need for increased doses of glucocorticosteroid drugs, since an excess of thyroid hormones significantly increases the rate and changes the metabolic pathways of the latter. Treatment of hyperthyroidism improves the course of bronchial asthma.
In cases of concomitant arterial hypertension, angina pectoris and other cardiovascular diseases, as well as hyperthyroidism, it is necessary to use B-stimulating adrenergic drugs with great care. For persons with impaired function of the digestive glands, it is advisable to prescribe enzyme preparations (festal, digestin, panzinorm), which reduce the absorption of food allergens and can help reduce shortness of breath, especially in the presence of food allergies. Patients with positive tuberculin test results and a history of tuberculosis during long-term glucocorticosteroid therapy are prescribed tuberculostatic drugs (isoniazid) prophylactically.
In elderly patients, the use of adrenergic B-stimulating drugs and methylxanthines is undesirable due to their side effects on the cardiovascular system, especially in coronary atherosclerosis. In addition, the bronchodilating effect of adrenergic drugs decreases with age. With the release of a significant amount of liquid sputum in patients with bronchial asthma of this age group, anticholinergic drugs are useful, which in some cases are more effective than other bronchodilators. There are recommendations on the use of synthetic androgens for elderly men suffering from bronchial asthma with a sharp decrease in the androgenic activity of the gonads (sustanon-250 - 2 ml intramuscularly with an interval of 14-20 days, a course of three to five injections); at the same time, remission is achieved faster and the maintenance dose of glucocorticosteroid drugs is reduced. There are indications of the advisability of using antiplatelet agents, in particular dipyridamole (curantyl) - 250300 mg per day - and acetylsalicylic acid (in the absence of contraindications) - 1.53.0 g per day, especially in elderly patients who have bronchial asthma combined with heart disease. - vascular system. In case of microcirculation disorders and changes in the rheological properties of blood, heparin is used at a dose of 10-20 thousand units per day for 510 days.
Treatment of concomitant pathology of the upper respiratory tract is carried out.

The answer to this question depends on many factors: how seizures proceed, when they begin and what provokes them. It is important to correctly determine all the nuances of the course of diseases in order to prescribe the correct treatment and choose drugs.

What is the relationship between diseases?

Doctors have not found a clear answer to this question. They note: people with respiratory diseases do often face the problem of high blood pressure. But further opinions are divided. Some experts insist on the existence of the phenomenon of pulmonary hypertension, which causes an attack of pressure in asthmatic disease. Other experts deny this fact, saying that asthma and hypertension are two diseases that do not depend on each other and are not related. But the link between diseases is confirmed by the following factors:

35% of people with respiratory diseases suffer from hypertension;
during attacks (exacerbations), the pressure rises, and during the period of remission it normalizes.

Back to index

Types of hypertension

Arterial hypertension is distinguished as a symptom of exacerbation, as well as hypertension, as a disease that occurs in parallel with asthma. Hypertension is of several types. The disease is divided according to the type of origin, the course of the disease, the level:

Course of the disease

Arterial hypertension in bronchial asthma is treated depending on what causes it. Therefore, it is important to understand the course of the disease and what provokes it. The pressure may rise during an asthma attack. In this case, an inhaler will help to remove both symptoms, which stops the asthma attack and relieves pressure. The situation is different if the patient's hypertension is not tied to asthmatic attacks. In this case, the treatment of hypertension should take place as part of a comprehensive course of therapy. Course of the disease

A suitable medicine for pressure is selected by the doctor, taking into account the possibility of the patient developing the syndrome of "cor pulmonale" - a disease in which the right heart ventricle cannot function normally. Hypertension can be provoked by the use of hormonal drugs for asthma. The doctor must track the nature of the course of the disease and prescribe the correct treatment.

Features of the treatment of hypertension in asthma

Bronchial asthma and high blood pressure should be treated under the supervision of a specialist. Only a doctor can prescribe the right drugs for both diseases. After all, every drug can have side effects:

A beta-blocker can cause bronchial obstruction or bronchospasm in an asthmatic, block the effect of the use of anti-asthma drugs and inhalations.
ACE drug provokes dry cough, shortness of breath.
A diuretic can cause hypokalemia or hypercapnia.
calcium antagonists. According to studies, the drugs do not cause complications in the respiratory function.
Alpha blocker. When taken, they can provoke an incorrect reaction of the body to histamine.

Therefore, it is so important for patients with asthma and hypertension to be examined by a specialist to select drugs and ensure correct treatment. Any drug in self-medication can complicate not only current diseases, but also worsen general health. The patient on his own can alleviate the course of bronchial disease, so as not to provoke attacks of suffocation, using folk methods: herbal preparations, tinctures and decoctions, ointments and rubbing. But their choice should also be agreed with the doctor.

Medicines for hypertension in bronchial asthma

How to lower the pressure?

The pressure may rise unexpectedly and quickly. Getting rid of the disease should be prompt - it is dangerous for humans. There are many options for lowering blood pressure, from medications to herbs, foods, and other treatments.

Norms of indicators

For an adult, the normal blood pressure is 120/80. If the indicators deviate up or down by 10 mm Hg, you should not worry. This is also considered a variant of the norm, and many people live with such numbers all the time.

If they rise to 140/90 or more, then hypertension occurs. The condition of the body worsens, it gives a person discomfort. He may experience the following symptoms:

headache;
noise and pulsation in the ears;
dizziness;
weakness;
fainting;
nausea;
palpable heartbeat;
shortness of breath
insomnia and anxiety.

The best way to find out that the pressure has increased is to buy a blood pressure monitor and learn how to use it. If such a pathology is observed in you often, this is an occasion to urgently consult a doctor. There are many modern drugs that effectively fight hypertension. When this happens rarely, you should know how to reduce the pressure yourself.

How to lower high blood pressure

If high blood pressure occurs, there are general recommendations on what to do in such situations. First you need to make sure that the indicators are really overestimated. Measure and evaluate the result. If the increase is insignificant, you can use the people's advice. To normalize the condition, a decoction of herbs is suitable.

If the cause of the jump is an experienced stressful situation, you need to calm down, lie down and stay in that position in silence.

With a strong increase, only medical treatment will help. For such cases, the drugs "Anaprilin", "Nifedipin", "Verapamil" are suitable. It is good to put a dropper with magnesia (magnesium sulfate), if possible.

The tablet may not work right away. No need to increase the dose or try another drug. The effect will manifest itself within an hour, you need to lie down and wait calmly. Too much medication will only make things worse.

After returning to normal levels, exclude provoking factors - do not smoke at least for the first time, do not drink coffee, strong tea and alcohol. If it was not possible to reduce high pressure, call an ambulance.

Medical preparations

The list of drugs that can quickly bring down high blood pressure includes the following drugs:

They are not suitable for frequent use. If you have any chronic disease that causes hypertensive crises, you need to get a doctor's prescription and undergo a course of treatment. How to reduce the pressure of a one-time nature in this case - the specialist will also tell you. Reducing pressure constantly without affecting the cause is dangerous to health.

"Dibazol". The active substance is Bendazole. Available in the form of tablets with a dosage of 20 mg and a solution for injection of 5 or 10 mg. There is also an option for children - tablets of 4 mg.

The drug blocks cationic channels in the muscles of the walls of blood vessels. The action taken is one of the main ways to relieve pressure.

In parallel with this, the active ingredient affects other parts of the body. It increases the production of interferon and antibodies, with which we fight infections, and also increases the excitation of neural connections in the spinal cord.

Apply 1 tablet 2 hours before or after meals. The course of treatment is prescribed by the doctor, based on individual indications. It is forbidden to use in case of hypersensitivity to the components.

"Pentamine". Belongs to the group of ganglion blockers. Release form - 5% solution for injection. It is indicated for hypertensive crisis, vasospasm, renal colic, bronchial asthma, cerebral and pulmonary edema.

Do not use in case of hypotension, the presence of glaucoma, after myocardial infarction, thrombophlebitis, renal or hepatic insufficiency, CNS lesions.

It can be used in two ways - intravenously (with a hypertensive crisis and in other emergency situations) and intramuscularly (with vasospasm). The initial dosage makes 1 ml. solution. The maximum single dose is 3 ml. After the administration of the drug, the patient should lie down for at least 2 hours, as it is possible to relieve the pressure too abruptly and worsen the condition.

Furosemide. This is a diuretic drug. Due to the removal of excess fluid from the body, the load on the walls of blood vessels is reduced, which allows lowering blood pressure.

Release form - tablets of 40 mg of the active substance. Indications: edema in diseases of internal organs (liver, kidneys, heart) and arterial hypertension.

Pressure-reducing tablets for hypertension have contraindications:

kidney or liver failure,
urinary system disorders
low pressure,
pregnancy and lactation,
age up to 3 years,
violation of water-salt metabolism,
hypersensitivity to the components of the drug.

High blood pressure suggests a dosage of mg. This remedy is usually used in combination with other drugs for hypertension. When used together, the dose of another drug is halved.

Anaprilin. The active substance is Propranolol. Produced in the form of tablets of 10 and 40 mg. It belongs to the group of beta-blockers - these are blood pressure lowering and antiarrhythmic drugs. It has concomitant effects on the body - contraction of the uterus, increased tone of the bronchi, a decrease in intraocular pressure.

Apply 40 mg 2 times a day. The maximum dose per day is 320 mg.

"Nifedipine". Dosage form - tablets of 10 mg. Purpose - angina pectoris and hypertension. It belongs to the group of calcium channel blockers. Apply 1 tablet 2 or 3 times a day during or after meals. The daily maximum is 40 mg.

"Verapamil". It is also a calcium channel blocker. They produce tablets of 40 and 80 mg. Indications: angina pectoris, disturbances in the normal rhythm of the heart, arterial hypertension.

Single dose - mg. May be used 3-4 times a day. But usually the number of doses and dosage are calculated individually by the attending physician.

Non-pharmacological ways to solve the problem

How to relieve high blood pressure without resorting to medication? You can use folk recipes, namely, decoctions of herbs. For these purposes, medicinal plants are used, which also have a sedative effect:

All these herbs can be found in any pharmacy. The dosage and the correct method of preparation are indicated on the package. Do not overdose - in large quantities, decoctions from medicinal plants can be harmful to health. The manufacturer's recommendations on how to deal with high blood pressure must be strictly adhered to.

You can brew grass not only for oral administration. Add the decoction to a bath of warm water and soak in it for half an hour. This procedure will calm and help reduce pressure indicators.

What foods can help lower blood pressure

An unusual way to lower blood pressure is to use food. Natural healers include nuts, milk, bananas, garlic. To improve the condition of the body, it is useful to use berries.

Kefir will help to cope with the disease. Pour it into a glass, add a spoonful of cinnamon, mix and drink quickly.

Another product that can reduce blood pressure is beets. In folk medicine, a recipe for a mixture of beetroot juice and honey is known. It will help reset the tonometer a little. You need to mix the products in equal quantities. There are recommendations for the course of taking this natural medicine. Take ½ teaspoon 3 times a day. The duration of treatment is 1 month.

Do not drink freshly squeezed beetroot juice. Let it brew for a day. Otherwise, its action will be the opposite - it will damage the blood vessels.

Fans of folk recipes know how to reduce pressure - with the help of watermelon seeds. They are dried and ground in a blender to a powder state. In this form, take it ½ teaspoon 3 times a day for 3-4 weeks.

There is a recipe for the elderly, which will help not only relieve pressure, but also strengthen the body as a whole. Cut the lemon and orange into pieces and crush to a state of porridge along with the zest. One intake of citrus mixture per day will be enough for a positive result. Before meals, eat one teaspoon of this remedy.

How to quickly bring down the pressure?

If sometimes you feel unwell, and the tonometer readings greatly exceed the norm, you need to remember a few rules on how to lower the pressure without the use of drugs. Here are the main recommendations:

Exposure to a hot stream of water on the back of the head for several minutes.
contrast baths. For half an hour, immerse your feet alternately in hot and cold water with an interval of 2-3 minutes.
Hot baths. We keep our hands in hot water for a minute.
We mix 3 components: half a lemon (can be crushed in a blender), a spoonful of honey and a glass of mineral water. We drink the resulting remedy in one gulp and wait for relief - hypertension decreases after 30 minutes.
Massage. This method will calm and help lower pressure, as a relaxing and sedative remedy. Especially if someone close makes it. But if you want, you can do it yourself. We start with the head, neck, chest. We go down to the abdomen and shoulder blades. After the procedure, you should lie down so as not to feel bad when lowering.
Soak a cloth in apple cider vinegar and apply to your feet. The effect will begin in 15 minutes.
Fresh air. If it is not possible to leave the room and take a walk, be sure to open the windows.
Hold your breath for 2-3 minutes. This is done on the exhale for 8-10 seconds.

If there is an option to reduce blood pressure without medication, use it. When such a jump in pressure is not associated with an internal disease, but is provoked by external factors (stress, weather), alternative methods really help. And they are much more useful and safer than drugs.

There are many answers to the question “how to bring down high blood pressure”. The most common is drugs. But there are many other effective ways. If there is no effect from self-treatment, call a doctor - a long time for the development of pathology can be dangerous. Try to protect yourself from stressful situations. Be more outdoors, do light exercise, eat right, get rid of excess weight and bad habits - hypertension will bypass you.

Pressure drugs that do not cause cough: what to do when taking

Drug treatment of hypertension is necessary, as this will normalize the state of blood pressure and prevent the development of a number of complications, such as heart attack and stroke.

However, drugs for arterial hypertension can be taken only after a doctor's prescription. After all, there are different groups of drugs that have different effects and have a number of side effects, such as dizziness, increased urination, cough, and so on.

You can’t do without drug therapy, because high blood pressure has a slow destructive effect on the entire body. But most often, the kidneys, heart and brain suffer from hypertension.

What should be done to prevent the development of complications? Antihypertensive medications should be taken regularly, because this is the only way to control blood pressure.

All drugs for high blood pressure are divided into groups. They can be used as monotherapy or combined with each other to enhance the effect and reduce side effects.

Types of drugs for pressure

Diuretics. Diuretic drugs can quickly reduce pressure indicators by removing salts and excess fluid from the body. For rapid normalization of blood pressure, the use of potassium-sparing diuretics and saluretics (Dicarb, Hypothiazid, Furosemide, and others) is recommended.

These diuretic drugs remove not only water from the body, but also calcium and sodium salts. However, a deficiency of potassium salts negatively affects the functioning of muscles, including the myocardium.

But what if you need to lower your blood pressure? For these reasons, along with saluretics, preparations containing potassium salts - Asparkam or Panangin should be taken.

Potassium-sparing diuretics for hypertension, such as Triamterene, do not remove potassium. But in case of their illiterate use, they can accumulate in the blood, which also adversely affects the body.

It is worth noting that diuretics do not cause cough, but they can provoke a disorder of the water-salt balance, as a result of which such side effects develop as:

nausea
dizziness;
malaise;
heart problems;
pressure drop, etc.

Popular diuretics are Hydrochlorothiazide, Spironolactone, Indapamide, Triampur, Diuver and others.

Beta blockers. They are used to lower high blood pressure that occurs against the background of heart problems, such as coronary artery disease. The drugs act on the cardiovascular system of adrenaline, they block the beta receptors of adrenaline, which is sensitive to this substance.

At the same time, the vessels, including the coronary ones, expand, as a result of which the heart rhythm normalizes and pressure indicators decrease. As a rule, beta-blockers such as Bisoprolol, Metoprolol, Celiprolol are prescribed to young patients with heart problems.

Due to peripheral vasoconstriction, BB should not be taken by patients with impaired blood circulation in the extremities.

Calcium channel blockers. In addition to lowering blood pressure, such drugs are used for heart disease. CCBs block the entry of calcium into muscle cells, inhibiting their contraction.

With a lack of calcium, the smooth muscles of the walls of blood vessels do not contract as necessary. As a result, the vessels relax, the blood flow inside them is facilitated and the pressure decreases.

Prominent representatives of CCB are the following drugs:

ACE inhibitors. These pills dilate blood vessels. ACE is an enzyme involved in the synthesis of a substance that has a strong vasoconstrictor effect - angiotensin II.

Basically, ACE inhibitors are indicated for hypertension, which develops against the background of heart and kidney diseases. Also, drugs belonging to this group are indicated for high diastolic pressure and in case of increased stress on the heart muscle.

However, with regular use of ACE inhibitors, a dry cough appears. What to do in this case? Often, the doctor prescribes antihypertensive drugs belonging to a different group.

Popular remedies from this group are Ramipril, Perindopril, Enalapril.

Angiotensin II receptor blockers. These drugs control blood pressure for 24 hours. However, in order to achieve a steady decrease in blood pressure, they need to be drunk for at least 3 months.

It is noteworthy that angiotensin 2 receptor blockers have practically no side effects, including they do not cause cough.

Means of central action. Popular representatives of this drug group are Moxonidine, Methyldopa and Albarel. Such drugs bind to receptors in nerve cells, regulating the activity of the SNS and reducing the intensity of vasoconstrictive signals. As a result, vasospasm is removed, and the pressure figures are falling.

It is worth noting that the tablets that have a central effect of the previous generation (Clonidine) are now practically not used in the treatment of hypertension.

What blood pressure medications cause coughing?

Most often, a dry cough develops after taking ACE inhibitors. As a rule, it is this side effect that causes the treatment to be canceled.

It is worth noting that a cough may appear as a result of therapy with any drugs from this group. But most often, such a negative symptom develops during treatment with Enalapril and Captopril. Moreover, cough occurs twice as often after taking Enalapril.

It is worth noting that after taking ACE inhibitors in patients with CHF, such a side effect appears much more often than in hypertensive patients (26% and 15%). Causes of its occurrence include an increase in the concentration of bradykinin, which accumulates in the upper respiratory tract, causing coughing.

In addition, a hereditary predisposition to the appearance of cough after taking ACE inhibitors is assumed. In this case, the patient feels an unpleasant tickling in the back of the throat.

Basically, the cough is paroxysmal, dry, long and hacking. It often worsens when the patient is in the supine position, which can lead to hoarseness and even incontinence and vomiting.

Moreover, these phenomena are not accompanied by hypersensitivity, symptoms of bronchial obstruction or changes in the functioning of the kidneys. What to do to eliminate cough after taking ACE inhibitors? According to some studies, in order to eliminate a cough, it is enough to reduce the dosage of the drug.

The time from the start of therapy with ACE inhibitors and until the onset of an unpleasant symptom can be from 1 day to 1 year. But on average, it appears 14.5 weeks after regular use of the remedy.

It is worth noting that the cough reflex that develops while taking an ACE inhibitor is basically not dangerous for the patient's health, often it just causes discomfort. But it was found that in patients with such a symptom, the quality of life worsens and they are more prone to depressive states.

To establish whether the cough is caused by the use of ACE inhibitors, they must be discontinued for 4 days. As a rule, the symptom disappears after 1-14 days. But if the treatment is resumed, then it can develop again.

What to do and what medications can be used to suppress the cough reflex after taking an ACE inhibitor? To eliminate cough, the following drugs are used:

In addition to ACE inhibitors, cough can develop against the background of lowering blood pressure with beta-blockers. Such drugs affect sensitive receptors located in the vessels, heart and bronchi.

When the blood vessels constrict, a dry, unproductive cough appears. It can also occur with physical activity and a change in body position.

What medications are safest to use for hypertension?

Today, calcium channel blockers are increasingly used in the treatment of hypertension. They have a specific effect on organs and a minimum number of adverse reactions.

New tablets from this group can bind to calcium channels in cell membranes located in the vascular walls and myocardium.

When calcium enters the cell, the following happens:

increased excitability and conductivity;
activation of metabolic processes;
muscle contraction;
increase in oxygen consumption.

However, some modern tablets from this group infringe on such processes. These include the following drugs:

Calcium channel blockers have a number of advantages. So, in addition to lowering pressure, they improve the general well-being of hypertensive patients and are well tolerated in old age. And modern CCBs reduce hypertrophy in the left ventricle and do not suppress physical and mental activity.

In addition, calcium channel blockers do not cause depression and do not increase bronchial tone, which cannot be said about adrenoblockers. Therefore, such drugs are recommended if hypertension is combined with broncho-obstructive diseases.

CCBs also improve the excretory function of the kidneys and have a positive effect on the carbohydrate metabolism of uric acid and lipids. Due to this property, they are superior to thiazide diuretics and adrenoblockers.

In addition to CCB, diuretics are increasingly being used for hypertension, which remove salts and fluid from the body, reducing blood volume, thereby reducing blood pressure. Modern safe diuretics are:

Also, in hypertension, to enhance the effect and reduce adverse reactions, including cough, it is customary to combine antihypertensive drugs.

It is worth noting that with a competent combination, some drugs neutralize the side effects of each other. Therefore, each patient suffering from high blood pressure should know the compatibility of drugs used in the treatment of arterial hypertension.

During treatment with combined drugs, the incidence of hypertensive complications is significantly reduced. Often 2 or 3 are combined. The most effective combinations of 2 drugs are:

ACE inhibitor + diuretic;
Calcium antagonist + receptor blocker;
Receptor blocker + diuretic;
Calcium antagonist + ACE inhibitor;
Calcium antagonist + diuretic.

Such combinations are the optimal solution in the treatment of hypertension. Effective combinations of three drugs are:

ACE inhibitor + AKD + BB;
AKD + BB + diuretic;
BRA + AKD + BB;
BB + ARB + diuretic;
ACE inhibitor + AK + diuretic;
BB + diuretic + ACE inhibitor;
ARB + AK + diuretic.

In addition, there are combination drugs that combine two active ingredients in one tablet at once. These include Enzix duo forte (enalapril and indapamide), Lodoz, Aritel plus (hydrochlorothiazide and bisoprolol), Co-diovan (hydrochlorothiazide and valsartan), and Logimax (metoprolol and felodipine).

Also popular combined agents are Gizaar, Lorista N/ND, Lozap plus (hydrochlorothiazide and losartan), Exforge (amlodipine and valsartan), Atacand plus (hydrochlorothiazide and candesartan), and Tarka (verapamil and trandolapril).

However, absolutely safe means that do not cause any adverse reactions do not exist. But there are modern antihypertensive drugs that have a number of advantages over other drugs. This allows them to have a minimum number of adverse reactions, because new components make such tablets not so dangerous.

Some of the best modern antihypertensive drugs are selective imidazoline receptor agonists. Such drugs rarely provoke the appearance of adverse reactions, quickly normalize blood pressure and they have practically no contraindications. Popular drugs from this group are Monoxidine or Rilmenidine.

In addition, it is worth choosing drugs that have a quick effect and a prolonged effect, which allows you to minimize the risk of adverse reactions. Therefore, it is preferable to choose complex agents that practically do not have adverse reactions, which makes them the best choice in the fight against hypertension.

One of the safest third-generation drugs is Physiotens. After taking it, there is practically no increased drowsiness, coughing and drying of the oral mucosa.

This is a new remedy for high blood pressure without adverse reactions, which does not adversely affect the respiratory function, so Physiotens can be taken even with bronchial asthma. In addition, the drug increases insulin sensitivity, which is important for insulin-dependent patients suffering from diabetes. In detail about the types of tablets, the patients themselves will tell in the video in this article.

What is the electrical axis of the heart?

The electrical axis of the heart is a concept that reflects the total vector of the electrodynamic force of the heart, or its electrical activity, and practically coincides with the anatomical axis. Normally, this organ has a cone-shaped shape, directed with its narrow end down, forward and to the left, and the electrical axis has a semi-vertical position, that is, it is also directed down and to the left, and when projected onto a coordinate system, it can be in the range from +0 to +90 0.

Causes of deviations from the norm
Symptoms
Diagnostics
Treatment

An ECG conclusion is considered normal, which indicates any of the following positions of the axis of the heart: not rejected, has a semi-vertical, semi-horizontal, vertical or horizontal position. Closer to the vertical position, the axis is in thin, tall people of asthenic physique, and to the horizontal position, in strong stocky faces of hypersthenic physique.

The range of position of the electrical axis is normal

For example, in the conclusion of the ECG, the patient may see the following phrase: "sinus rhythm, EOS is not rejected ...", or "the axis of the heart is in a vertical position", which means that the heart is working correctly.

In the case of heart diseases, the electrical axis of the heart, along with the heart rhythm, is one of the first ECG criteria that the doctor pays attention to, and when deciphering the ECG by the attending physician, it is necessary to determine the direction of the electrical axis.

How to determine the position of the electrical axis

Determining the position of the axis of the heart is carried out by a doctor of functional diagnostics, deciphering the ECG, using special tables and diagrams, according to the angle α ("alpha").

The second way to determine the position of the electrical axis is to compare the QRS complexes responsible for the excitation and contraction of the ventricles. So, if the R wave has a greater amplitude in the I chest lead than in the III one, then there is a levogram, or a deviation of the axis to the left. If there is more in III than in I, then a rightogram. Normally, the R wave is higher in lead II.

Causes of deviations from the norm

Axis deviation to the right or to the left is not considered an independent disease, but it can indicate diseases that lead to disruption of the heart.

Deviation of the axis of the heart to the left often develops with left ventricular hypertrophy

Deviation of the axis of the heart to the left can occur normally in healthy individuals who are professionally involved in sports, but more often develops with left ventricular hypertrophy. This is an increase in the mass of the heart muscle with a violation of its contraction and relaxation, necessary for the normal functioning of the whole heart. Hypertrophy can be caused by such diseases:

cardiomyopathy (increase in mass of the myocardium or expansion of the heart chambers) caused by anemia, hormonal disorders in the body, coronary heart disease, postinfarction cardiosclerosis, changes in the structure of the myocardium after myocarditis (inflammatory process in the heart tissue);
long-term arterial hypertension, especially with constantly high pressure figures;
acquired heart defects, in particular stenosis (narrowing) or insufficiency (incomplete closure) of the aortic valve, leading to impaired intracardiac blood flow, and, consequently, increased stress on the left ventricle;
congenital heart defects are often the cause of the deviation of the electrical axis to the left in a child;
violation of conduction along the left leg of the bundle of His - complete or incomplete blockade, leading to impaired contractility of the left ventricle, while the axis is rejected, and the rhythm remains sinus;
atrial fibrillation, then the ECG is characterized not only by axis deviation, but also by the presence of non-sinus rhythm.

In adults, such a deviation, as a rule, is a sign of right ventricular hypertrophy, which develops with such diseases:

diseases of the bronchopulmonary system - prolonged bronchial asthma, severe obstructive bronchitis, pulmonary emphysema, leading to an increase in blood pressure in the pulmonary capillaries and increasing the load on the right ventricle;
heart defects with damage to the tricuspid (tricuspid) valve and the valve of the pulmonary artery extending from the right ventricle.

The greater the degree of ventricular hypertrophy, the more deviated the electrical axis, respectively, sharply to the left and sharply to the right.

Symptoms

The electrical axis of the heart itself does not cause any symptoms in the patient. Disorders of well-being appear in a patient if myocardial hypertrophy leads to severe hemodynamic disturbances and to heart failure.

The disease is characterized by pain in the region of the heart

Of the signs of diseases accompanied by a deviation of the axis of the heart to the left or right, headaches, pains in the region of the heart, swelling of the lower extremities and on the face, shortness of breath, asthma attacks, etc. are characteristic.

If any unpleasant cardiac symptoms appear, you should consult a doctor for an ECG, and if an abnormal position of the electrical axis is found on the cardiogram, an additional examination should be performed to establish the cause of this condition, especially if it is found in a child.

Diagnostics

To determine the cause, if the ECG axis of the heart deviates to the left or right, a cardiologist or therapist may prescribe additional research methods:

Ultrasound of the heart is the most informative method that allows you to evaluate anatomical changes and identify ventricular hypertrophy, as well as determine the degree of violation of their contractile function. This method is especially important for examining a newborn child for congenital heart disease.
ECG with exercise (walking on a treadmill - treadmill test, bicycle ergometry) can detect myocardial ischemia, which can be the cause of deviations of the electrical axis.
24-hour ECG monitoring in the event that not only axis deviation is detected, but also the presence of a rhythm not from the sinus node, that is, there are rhythm disturbances.
Chest X-ray - with severe myocardial hypertrophy, an expansion of the cardiac shadow is characteristic.
Coronary angiography (CAG) is performed to clarify the nature of coronary artery lesions in coronary artery disease a.

Treatment

Directly, the deviation of the electrical axis does not need treatment, since this is not a disease, but a criterion by which it can be assumed that the patient has one or another cardiac pathology. If any disease is detected after the additional examination, it is necessary to begin its treatment as soon as possible.

In conclusion, it should be noted that if the patient sees in the conclusion of the ECG a phrase that the electrical axis of the heart is not in a normal position, this should alert him and prompt him to consult a doctor to find out the cause of such an ECG - a sign, even if there are no symptoms does not occur.

In patients with bronchial asthma, an increase in blood pressure (BP) is often observed, and hypertension occurs. In order to normalize the patient's condition, the doctor must carefully select pressure pills for asthma. Many drugs used to treat hypertension can cause asthma attacks. Therapy should be carried out taking into account two diseases in order to avoid complications.

The causes of asthma and arterial hypertension are different, risk factors, features of the course of diseases do not have common signs. But often, against the background of attacks of bronchial asthma, patients experience an increase in pressure. According to statistics, such cases are frequent, occur regularly.

Does bronchial asthma cause hypertension in patients, or are these two parallel diseases developing independently? Modern medicine has two opposing views on the issue of the relationship of pathologies.

Some doctors talk about the need to establish a separate diagnosis in asthmatics with high blood pressure - pulmonary hypertension.

Doctors point to direct causal relationships between pathologies:

35% of asthmatics develop arterial hypertension;
during an asthma attack, blood pressure rises sharply;
normalization of pressure is accompanied by an improvement in the asthmatic state (absence of attacks).

Adherents of this theory consider asthma to be the main factor in the development of chronic cor pulmonale, which causes a stable increase in pressure. According to statistics, in children with bronchial attacks, such a diagnosis occurs much more often.

The second group of doctors speaks about the absence of dependence and connection between the two diseases. Diseases develop separately from one another, but their presence affects the diagnosis, the effectiveness of treatment, and the safety of drugs.

Regardless of whether there is a relationship between bronchial asthma and hypertension, the presence of pathologies should be taken into account in order to choose the right course of treatment. Many blood pressure pills are contraindicated in asthma patients.

The theory of pulmonary hypertension links the development of hypotension in bronchial asthma with a lack of oxygen (hypoxia) that occurs in asthmatics during attacks. What is the mechanism of occurrence of complications?

Lack of oxygen awakens vascular receptors, which causes an increase in the tone of the autonomic nervous system.
Neurons increase the activity of all processes in the body.
The amount of hormone produced in the adrenal glands (aldosterone) increases.
Aldosterone causes increased stimulation of the artery walls.

This process causes a sharp increase in blood pressure. The data are confirmed by clinical studies conducted during attacks of bronchial asthma.

With a long period of the disease, when asthma is treated with potent drugs, this causes disturbances in the work of the heart. The right ventricle ceases to function normally. This complication is called cor pulmonale syndrome and provokes the development of arterial hypertension.

Hormonal agents used in the treatment of bronchial asthma to help in critical condition also increase the pressure in patients. Injections with glucocorticoids or oral drugs with frequent use disrupt the endocrine system. The result is the development of hypertension, diabetes, osteoporosis.

Bronchial asthma can cause arterial hypertension by itself. The main reason for the development of hypertension are drugs used by asthmatics to relieve attacks.

There are risk factors in which an increase in pressure is more often observed in patients with asthma:

excess weight;
age (after 50 years);
development of asthma without effective treatment;
side effects of drugs.

Some risk factors can be eliminated by making lifestyle changes and following your doctor's recommendations for taking medications.

In order to start treatment of hypertension in time, asthmatics should know the symptoms of high blood pressure:

Strong headache.
Heaviness in the head.
Noise in ears.
Nausea.
General weakness.
Frequent pulse.
Palpitation.
Sweating.
Numbness of hands and feet.
Tremor.
Pain in the chest.

A particularly severe course of the disease is complicated by convulsive syndrome during an asthma attack. The patient loses consciousness, cerebral edema may develop, which can be fatal.

The choice of medicine for hypertension in bronchial asthma depends on what provokes the development of pathology. The doctor conducts a thorough questioning of the patient in order to establish how often asthma attacks occur and when an increase in pressure is observed.

There are two scenarios for the development of events:

BP rises during an asthma attack;
pressure does not depend on seizures, constantly elevated.

The first option does not require specific treatment for hypertension. There is a need to eliminate the attack. To do this, the doctor selects an anti-asthma agent, indicates the dosage and duration of its use. In most cases, inhalation with a spray can stop an attack, reduce pressure.

If the increase in blood pressure does not depend on attacks and remission of bronchial asthma, it is necessary to choose a course of treatment for hypertension. In this case, the drugs should be as neutral as possible in terms of the presence of side effects that do not cause an exacerbation of the underlying disease of asthmatics.

There are several groups of drugs used in the treatment of arterial hypertension. The doctor chooses drugs that do not harm the patient's respiratory system, so as not to complicate the course of bronchial asthma.

After all, different groups of medicines have side effects:

Beta-blockers cause tissue spasm in the bronchi, lung ventilation is disturbed, and shortness of breath increases.
ACE inhibitors (angiotensin-converting enzyme) provoke a dry cough (occurs in 20% of patients taking them), shortness of breath, aggravating the condition of asthmatics.
Diuretics cause a decrease in the level of potassium in the blood serum (hypokalemia), an increase in carbon dioxide in the blood (hypercapnia).
Alpha-blockers increase the sensitivity of the bronchi to histamine. When taken orally, they are practically safe drugs.

In complex treatment, it is important to take into account the effect of drugs that stop an asthmatic attack on the appearance of hypertension. A group of beta-agonists (Berotek, Salbutamol) with prolonged use provoke an increase in blood pressure. Doctors observe this trend after increasing the dose of inhaled aerosol. Under its influence, myocardial muscles are stimulated, which causes an increase in heart rate.

Taking hormonal drugs (Methylprednisolone, Prednisolone) causes a violation of blood flow, increases the pressure of the flow on the walls of blood vessels, which causes sharp jumps in blood pressure. Adenosinergic drugs (Aminophylline, Eufillin) lead to heart rhythm disturbance, causing an increase in pressure.

It is important that drugs that treat hypertension do not aggravate the course of bronchial asthma, and drugs to eliminate an attack do not cause an increase in blood pressure. An integrated approach will ensure effective treatment.

Criteria by which the doctor selects drugs for asthma from pressure:

reduced symptoms of hypertension;
lack of interaction with bronchodilators;
antioxidant characteristics;
decreased ability to form blood clots;
lack of antitussive effect;
the drug should not affect the level of calcium in the blood.

Preparations of the calcium antagonist group meet all the requirements. Studies have shown that these funds do not disrupt the respiratory system, even with regular use. Doctors use calcium channel blockers in complex therapy.

There are two groups of drugs of this action:

dihydropyridine (Felodipine, Nicardipine, Amlodipine);
non-dihydropyridine (Isoptin, Verapamil).

The drugs of the first group are more often used, they do not increase the heart rate, which is an important advantage.

Diuretics (Lasix, Uregit), cardioselective agents (Concor), a potassium-sparing group of drugs (Triampur, Veroshpiron), diuretics (Thiazid) are also used in complex therapy.

The choice of medications, their form, dosage, frequency of use and duration of use can only be carried out by a doctor. Self-treatment threatens the development of serious complications.

It is necessary to carefully select the course of treatment for asthmatics with "cor pulmonale syndrome". The doctor prescribes additional diagnostic methods in order to assess the general condition of the body.

Traditional medicine offers a wide range of methods that help reduce the frequency of asthma attacks, as well as lower blood pressure. Healing collections of herbs, tinctures, rubbing reduce pain during an exacerbation. The use of traditional medicine must also be agreed with the attending physician.

Patients with bronchial asthma can avoid the development of arterial hypertension if they follow the doctor's recommendations regarding treatment and lifestyle:

Relieve asthma attacks with local preparations, reducing the effects of toxins on the entire body.
Conduct regular monitoring of heart rate and blood pressure.
If you experience heart rhythm disturbances or a stable increase in pressure, consult a doctor.
Do a cardiogram twice a year for the timely detection of pathologies.
Take maintenance drugs in case of chronic hypertension.
Avoid increased physical exertion, stress, provoking pressure drops.
Give up bad habits (smoking exacerbates asthma and hypertension).

Bronchial asthma is not a sentence and a direct cause of the development of arterial hypertension. A timely diagnosis, a correct course of treatment that takes into account symptoms, risk factors and side effects, and the prevention of complications will allow patients with asthma to live for many years.