Asthma high blood pressure drug compatibility. Treatment of hypertension in bronchial asthma. Pulmonary hypertension with mitral stenosis and atherosclerosis

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 “pneumogenic” 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" hypertension 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, asthma patients with elevated and normal blood pressure do not differ from each other in the form and severity of asthma, 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 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 noradrenaline 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, the inactivation of serotonin 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 heart cavities and great vessels, it was found that with concomitant hypertension (mainly with a labile course) outside of asthma exacerbation, 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 characteristic of 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 sex, age, hypertension, smoking, and others - do not play a significant role in the development of AD.

However, chlamydial infection may 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 "relaxing factor produced by the endothelium" 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 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 BA patients could not be found in the literature, which is an 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 highly 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 have a significant impact on 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 premature beats, 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 arrhythmias. 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 theophyllines at therapeutic concentrations 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 by at least 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 quite 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 who had arrhythmias was 40 years, and the average age of patients without arrhythmias 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 treatment difficulties in 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.

Along with asthma, other diseases appear: allergies, rhinitis, diseases of the digestive tract and hypertension. Are there special pressure pills for asthmatics, and what can patients drink so as not to provoke respiratory problems? The answer to this question depends on many factors: how the 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.

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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.

Treatment of arterial hypertension in patients with bronchial asthma and COPD

Yaroslav Vladimirovich Marchenkov
Research Institute of Pulmonology, Ministry of Health of the Russian Federation

Management of patients with arterial hypertension
in combination with bronchial asthma (BA) and COPD, is very relevant
problem due to the high prevalence of these diseases in adult
populations.

The root of the problem is that some drugs
reduce blood pressure (BP), can induce asthmatic
seizures, as well as cause other unwanted reactions. For example,
beta-blockers should be used with great caution in patients
patients with asthma and COPD, as well as in patients with bronchoconstriction caused by
physical load. ACE inhibitors and beta blockers can also cause
unwanted effects.

Drugs from the group of beta-blockers can increase
bronchial obstruction in asthmatics, as well as increase the reactivity of the airways
and interfere with the therapeutic action of inhaled and oral sympathomimetics
(albuterol and terbutaline). Although these drugs have
different selectivity for beta-1-adrenergic receptors, none of them
can be regarded as absolutely safe. It should be noted that even
local administration of these drugs in the form of eye drops for glaucoma can
cause exacerbation of AD.

The exact mechanism of beta-blocker-induced bronchospasm is still
unknown. However, there are observations about the role of the parasympathetic nervous system in
this mechanism. Evidence of this fact is the effectiveness of oxitropium
bromide, an anticholinergic drug that inhibits the effect of
inhaled propranolol.

The most well-known side effect of ACE inhibitors is cough,
which worries 20% of patients taking these drugs. Usually cough
dry, persistent, rarely productive, accompanied by irritation of the upper
respiratory tract.

Due to bronchial hyperreactivity, which occurs in
patients taking ACE inhibitors, it has been hypothesized that such
the type of cough may be equivalent to asthma, although this is an uncommon finding. It was
It has been shown that patients with asthma are more likely to cough when taking
ACE inhibitors than non-BA patients.

Recent studies on the effect of ACE inhibitors on
respiratory system, indicate that bronchospasm, shortness of breath and suffocation
observed in 10% of patients. Despite the fact that the exacerbation
broncho-obstructive syndrome while taking ACE inhibitors is not acute
problem of asthmatics, several cases of asthma exacerbation have been described in such
sick.

Today, ACE inhibitors are not among the first-line drugs
in patients suffering from broncho-obstructive diseases. It is important to note that
respiratory diseases are not a contraindication to the appointment of this group
drugs, if the clinician is aware of their characteristic side effects.
However, preference is given to angiotensin II receptor antagonists.

Diuretics can be used quite effectively in patients
with BA, however, there is a risk of developing hypokalemia. This is especially
relevant, given that inhaled beta-2-agonists contribute to
the entry of potassium into the cell (thus, the concentration of potassium ions in
blood plasma decreases to 0.5-1 meq / l), and glucocorticosteroids taken
inside, increase the excretion of potassium in the urine.

Another equally important problem of diuretic therapy of patients
COPD is chronic hypercapnia. Metabolic alkalosis caused by ingestion
diuretics, is able to suppress the respiratory center, increasing hypoxemia.

Thus, patients with asthma and COPD without pronounced edematous
syndrome, it is safer to prescribe low doses of diuretics (12.5–25 mg
hydrochlorothiazide). Therapy with low-dose diuretics is considered more
effective and safer in relation to the development of hypokalemia and
metabolic alkalosis.

Calcium antagonists - especially the dihydropyridine group,
such as nifedipine, nicardipine - are the most optimal means for
treatment of arterial hypertension in patients with asthma. In addition, these drugs
cause relaxation of the muscles of the tracheobronchial tree, inhibit degranulation
mast cells, enhance the bronchodilating effect of beta-2 agonists.

So, nifedipine is able to reduce the bronchoconstrictor effect
antigen, histamine or cold air. During clinical trials
It has been shown that calcium antagonists do not impair external function
breathing in asthmatics.

Thus, the use of calcium antagonists in the form
monotherapy or in combination with thiazide diuretics is optimal
choice for the treatment of hypertension in patients with broncho-obstructive syndrome.

Clonidine and other alpha-blockers (methyldopa) with a large
caution should be used in patients with asthma. Oral doses of these drugs are not
lead to a change in bronchial patency in asthmatics, but they are able to
increase the sensitivity of the bronchi to histamine.

One study showed that an alpha-1 blocker
prazosin can significantly increase dyspnea in patients with asthma, however
changes in the parameters of the function of external respiration were not revealed.

Treatment of bronchial asthma and hypertension

Bronchial asthma and hypertension are dangerous separately for human life, what can we say if they develop in parallel. In fact, this situation is quite common these days. It is difficult to say which disease provokes another. Although doctors note that usually bronchial asthma is preceded by improper use of drugs that should reduce pressure.

Non-compliance with the doctor's recommendations and self-treatment are the reasons that, according to statistics, most often lead to complications and the development of secondary diseases.

Treatment and side effects

Hypertension and asthma should only be treated by a specialist. Firstly, such a doctor will be able to correctly analyze the situation and refer the patient to the necessary examinations. Secondly, focusing on the results, the doctor prescribes drugs to combat hypertension and bronchial asthma.

As for treatment, the following categories of drugs can be used here, which have their own side effects:

beta-blockers;

These drugs can cause bronchial obstruction in asthmatic patients, as well as provoke airway reactivity, which blocks the therapeutic effect of inhalation and oral medications. Beta-blockers are not absolutely safe medicines, so even eye drops from this category can exacerbate asthma or hypertension.

Unfortunately, even despite the achievements of modern medicine, there is still no exact opinion, which is why the use of this group can provoke bronchospasm. Nevertheless, it is believed that in such a situation, disturbances in the parasympathetic system of the body are the main factor.

angiotensin-converting enzyme (ACE) inhibitors;

In terms of side effects, dry cough is the most common, and this symptom usually occurs due to irritation of the upper respiratory tract. According to the observations of doctors, patients with bronchial asthma more often than healthy people have such a consequence as coughing.

In addition, shortness of breath, suffocation and hypertension can be observed, respectively, asthma itself can worsen. To date, specialists rarely prescribe ACE inhibitors to patients with bronchitis, especially obstructive forms. But in fact, any disease of the respiratory system can be treated with this category of drugs, the main thing is that the doctor correctly selects the drug. The patient must be aware of the potential side effects. But still it will be better if the disease is treated with angiotensin II receptor antagonists.

This group is great for asthmatics, but it can provoke the development of hypokalemia. Hypercapnia can also develop, which suppresses the respiratory center, which increases hypoxemia. If, with hypertension, the patient does not have pronounced swelling of the respiratory tract, then diuretics are prescribed in very small doses in order to give the maximum effect without side effects.

With arterial hypertension and asthma, patients are often prescribed nifedipine and nicardipine, which belong to the dihydropyridine group. These drugs help to relax the muscles of the tracheobronchial tree, inhibit the release of granules into the surrounding tissues, and also enhance the bronchodilator effect. According to numerous observations, the treatment of hypertension with calcium antagonists does not give any complications on the respiratory function in patients with asthma. The optimal solution to the problem of hypertension is the use of monotherapy or the dilution of calcium antagonists with diuretics.

These medicines are used very carefully in the treatment of hypertension, especially when the patient has bronchial asthma. If drugs are taken orally, then no changes in bronchial patency will be observed, but instead there may be a problem with the reaction of the bronchi to histamine. Any medicine for hypertension or bronchial asthma should be prescribed by a specialist. Any self-medication can cause health complications, not to mention the fact that there are many possible side effects.

Asthmatic bronchitis and methods of its treatment

It has already been noted above that it is necessary to determine which problem is the main one - hypertension or asthma. In the previous section, attention was paid to the medical treatment of hypertension, now it's time to talk about asthmatic bronchitis.

In order to get rid of such a disease, the following approaches are used:

means for internal use - herbal preparations (extracts), fortified complexes, complexes with microelements, chlorophyllipt, pharmaceutical preparations;
folk medicine - herbal decoctions and tinctures;
drops and syrups for oral administration - can be represented by extracts from medicinal herbs;
means for local action - ointments, rubbing, compresses, microorganics, substances based on plant pigments, vitamins and essential oils, vegetable fats and herbal infusions;
treatment of asthmatic bronchitis is also carried out with the help of vitamin therapy - these funds can be used orally or subcutaneously;
preparations for treating the chest, there is an effect on the skin, so herbal extracts, natural oils with macro-, microelements and monovitamins, chlorophyllipt can be used;
as for external influence, you can still use a talker, which may include herbal infusions, minerals, medications, chlorophyllipt, and apply it not only to the chest, but also to the entire body, especially on the sides;
emulsions and gels - applicable for local effects on the chest, created on the basis of plant pigments and fats, herbal extracts, trace elements, vitamins A and B, monovitamins;
bronchial asthma is also successfully treated with the help of lactotherapy - these are intramuscular injections of extracts from whole cow's milk, to which aloe tree juice is added;
apipuncture - a relatively new method of treatment, helps to reduce the manifestations of not only asthma, but also hypertension;
physiotherapy - this treatment involves the use of ultrasound, UHF, electrophoresis, external laser blood irradiation, magnetotherapy, magnetic laser therapy;
pharmaceuticals - bronchodilators, antihistamines, expectorants, immunomodulators, anti-inflammatory, antitoxic, antiviral, mucolytics, antifungal and other medicines.

As a conclusion

Basically, the effect on bronchial asthma is from the inside, so that all therapeutic components can interact with the entire respiratory system as much as possible, from the airways to the internal organs.

But in order to fully cope with hypertension and asthma, you will need an integrated approach, that is, you should use the methods of traditional and alternative medicine, as well as physiotherapy.

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.

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.

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.

source

elderly age;
obesity;
taking medications that have a side effect in the form of hypertension.

Features of the course of hypertension against the background of bronchial asthma is an increased risk of complications in the form of disorders of cerebral and coronary circulation, cardiopulmonary insufficiency. It is especially dangerous that in asthmatics the pressure at night is not sufficiently reduced, and during an attack, a sharp deterioration in the condition in the form of a hypertensive crisis is possible.

One of the mechanisms that explains the occurrence of systemic hypertension is insufficient oxygen supply due to bronchospasm, which provokes the release of vasoconstrictor compounds into the blood. With a long course of asthma, the arterial wall is damaged. This manifests itself in the form of dysfunction of the inner membrane and increased stiffness of the vessels.

Read more about emergency care for cardiac asthma here.

intense headache, diffuse or limited to the temples and the back of the head;
noise in ears; Signs of high blood pressure
heaviness in the head;
dizziness;
feeling of constant weakness;
fast fatiguability;
nausea;
visual impairment;
insomnia;
increased heart rate;
sweating;
hand trembling;
numbness of the limbs;
pressing pains in the region of the heart.

This accelerates the rhythm of contractions and increases cardiac output. The systolic blood pressure rises and the diastolic pressure falls. High pulse blood pressure, sudden tachycardia and the release of stress hormones during an attack lead to a significant circulatory disorder.

source

Pills for hypertension in asthma. Hypertension and bronchial asthma. What foods can help lower blood pressure

As for treatment, the following categories of drugs can be used here, which have their own side effects:

angiotensin-converting enzyme (ACE) inhibitors;

In order to get rid of such a disease, the following approaches are used:

means for internal use - herbal preparations (extracts), fortified complexes, complexes with microelements, chlorophyllipt, pharmaceutical preparations;
folk medicine - herbal decoctions and tinctures;
drops and syrups for oral administration - can be represented by extracts from medicinal herbs;
means for local action - ointments, rubbing, compresses, microorganics, substances based on plant pigments, vitamins and essential oils, vegetable fats and herbal infusions;
treatment of asthmatic bronchitis is also carried out with the help of vitamin therapy - these funds can be used orally or subcutaneously;
preparations for treating the chest, there is an effect on the skin, so herbal extracts, natural oils with macro-, microelements and monovitamins, chlorophyllipt can be used;
as for external influence, you can still use a talker, which may include herbal infusions, minerals, medications, chlorophyllipt, and apply it not only to the chest, but also to the entire body, especially on the sides;
emulsions and gels - applicable for local effects on the chest, created on the basis of plant pigments and fats, herbal extracts, trace elements, vitamins A and B, monovitamins;
bronchial asthma is also successfully treated with the help of lactotherapy - these are intramuscular injections of extracts from whole cow's milk, to which aloe tree juice is added;
apipuncture - a relatively new method of treatment, helps to reduce the manifestations of not only asthma, but also hypertension;
physiotherapy - this treatment involves the use of ultrasound, UHF, electrophoresis, external laser blood irradiation, magnetotherapy, magnetic laser therapy;
pharmaceuticals - bronchodilators, antihistamines, expectorants, immunomodulators, anti-inflammatory, antitoxic, antiviral, mucolytics, antifungal and other medicines.

As you know, blood pressure in almost every person increases with age. However, for asthmatics, the presence of hypertension is a poor prognostic sign. Such patients need special attention and carefully planned drug therapy.

Doctor/nurse checking blood pressure.

Despite the fact that both diseases are pathogenetically unrelated, it has been found that blood pressure rises quite often in asthma.

Some asthmatics are at high risk of developing hypertension, namely people:

Elderly age.
With increased body weight.
With severe, uncontrolled asthma.
Taking medications that provoke hypertension.

Doctors separately distinguish secondary hypertension. Nominal this form of high blood pressure is more common among patients with bronchial asthma. This is due to the formation of chronic cor pulmonale in patients. This pathological condition develops due to hypertension in the pulmonary circulation, which, in turn, leads to hypoxic vasoconstriction. The latter is a compensatory mechanism of the body, which consists in a smaller supply of blood to the ischemic areas of the lungs towards those areas where gas exchange is intense.

However, bronchial asthma is rarely accompanied by a persistent increase in pressure in the pulmonary arteries and veins. That is why the option of developing secondary hypertension due to chronic cor pulmonale in asthmatics is possible only if they have a concomitant chronic lung disease (for example, obstructive disease).

Rarely, bronchial asthma leads to secondary hypertension due to disturbances in the synthesis of polyunsaturated arachidonic acid. But the most common cause of hypertension in such patients is drugs that are used for a long time to eliminate the symptoms of the underlying disease.

These medications include sympathomimetics and corticosteroids. So, Fenoterol and Salbutamol, which are used quite often, in high doses can increase the heart rate and, accordingly, increase hypoxia by increasing myocardial oxygen demand.

It is worth remembering that an asthma attack can cause a transient increase in pressure. This condition is life-threatening for the patient, because against the background of increased intrathoracic pressure and stagnation in the superior and inferior vena cava, swelling of the cervical veins and a clinical picture similar to pulmonary embolism often develop. Such a condition, especially without prompt medical attention, can lead to death. Also, bronchial asthma, which is accompanied by high blood pressure, is dangerous for the development of disorders in the cerebral and coronary circulation or cardiopulmonary insufficiency.

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(c) Can Stock Photo Inc. / Portokalis If a person suffering from bronchial asthma began to register cases of high blood pressure, you should immediately seek help from a doctor. It is categorically not recommended to choose pills for hypertension on your own, since many of them are contraindicated for asthmatics, because they can only worsen the condition.

Determining the tactics of treatment, the doctor first determines whether there is a connection between asthma attacks and an increase in blood pressure. If both of these conditions are interrelated, then only drugs are prescribed to relieve the symptoms of a pulmonary disease. If not, special medications are selected that eliminate the signs of arterial hypertension. Such medicinal products must:

Possess antithrombotic activity.
Show antioxidant activity.
Maintain potassium levels at the proper level to prevent the development of pulmonary insufficiency.
Do not cause the patient to cough.
Do not interact with bronchodilators.

Preference is given to drugs that exhibit a local rather than a systemic effect on the body. As maintenance therapy, in the presence of chronic hypertension, diuretics (mainly potassium-sparing - Veroshpiron, Triampur), potassium and magnesium preparations can be prescribed by a doctor.

Choosing a medicine for pressure in bronchial asthma should be done carefully, always taking into account side effects. Preference in treatment is given to drugs that do not impair the ventilation capacity of the lungs.

As already mentioned, bronchial asthma can progress against the background of some incorrectly selected antihypertensive drugs.

Beta blockers. A group of drugs that enhances bronchial obstruction, airway reactivity and reduces the therapeutic effect of sympathomimetics. Thus, drugs aggravate the course of bronchial asthma. Currently, it is allowed to use selective beta-blockers (Atenolol, Tenoric) in small doses, but only strictly according to the indications.
Some diuretics. In asthmatics, this group of drugs can cause hypokalemia, which leads to the progression of respiratory failure. It should be noted that the joint use of diuretics with beta-2-agonists and systemic glucocorticosteroids only enhances unwanted potassium excretion. Also, this group of drugs is able to increase blood clotting, cause metabolic alkalosis, as a result of which the respiratory center is inhibited, and gas exchange indicators deteriorate.
ACE inhibitors. The action of these drugs causes changes in the metabolism of bradykinin, increases the content of anti-inflammatory substances in the lung parenchyma (substance P, neurokinin A). This leads to bronchoconstriction and coughing. Despite the fact that this is not an absolute contraindication to the appointment of ACE inhibitors, preference in treatment is still given to another group of medications.

Another group of medicines, when using which care must be taken, is alpha-blockers (Physiotens, Ebrantil). According to studies, they can increase the sensitivity of the bronchi to histamine, as well as increase shortness of breath in patients with bronchial asthma.

What antihypertensive drugs are still allowed to be used in bronchial asthma?

First-line drugs include calcium antagonists. They are divided into non- and dihydropidic. The first group includes Verapamil and Diltiazem, which are used less often in asthmatics in the presence of concomitant congestive heart failure, due to their ability to increase heart rate.

Dihydropyridine calcium antagonists (Nifedipine, Nicardipine, Amlodipine) are the most effective antihypertensive drugs for bronchial asthma. They expand the lumen of the artery, improve the function of its endothelium, and prevent the formation of atherosclerotic plaques in it. On the part of the respiratory system - improve the patency of the bronchi, reduce their reactivity. The best therapeutic effect was achieved when these drugs were combined with thiazide diuretics.

However, in cases where the patient has concomitant severe cardiac arrhythmias (atrioventricular block, severe bradycardia), calcium antagonists are prohibited for use.

Another group of antihypertensive drugs commonly used in asthma are angiotensin II receptor antagonists (Cozaar, Lorista). In their properties, they are similar to ACE inhibitors, however, unlike the latter, they do not affect the metabolism of bradykinin and thus do not cause such an unpleasant symptom as coughing.

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

According to the course of the disease

Secondary (symptomatic)	It appears as a complication of other diseases.
benign	Imperceptible and prolonged development of symptoms.
Malignant	Develops rapidly.
By pressure level	Soft (1st degree)	The disease does not require medical treatment. The patient can only change the way of life.
	Moderate (2nd degree)	Pressure over 160 on 109 indicators. Use of medicinal methods
	Severe (3rd degree)	The readings are above 180 over 110. The pressure is constantly at this level. Possible damage to other organs.

During an attack, there is an increase in blood pressure.

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.

Bronchial asthma is often accompanied by high blood pressure. This combination refers to an unfavorable prognostic sign of the course of both diseases. Most asthma medications worsen the course of hypertension, and reverse reactions are observed, which must be taken into account when conducting therapy.

Bronchial asthma and hypertension do not have common prerequisites for occurrence - different risk factors, patient population, development mechanisms. The frequent joint course of diseases has become an occasion to study the patterns of this phenomenon. Conditions have been found that often increase blood pressure in asthmatics:

elderly age;
obesity;
decompensated asthma;
taking medications that have side effects in the form.

Features of the course of hypertension against the background of bronchial asthma is an increased risk of complications in the form of disorders of cerebral and coronary circulation, cardiopulmonary insufficiency. It is especially dangerous that asthmatics do not have enough pressure at night, and during an attack, a sharp deterioration in their condition is possible.

One of the mechanisms that explains the occurrence of systemic hypertension is due to bronchospasm, which provokes the release of vasoconstrictor compounds into the blood. With a long course of asthma, the arterial wall is damaged. This manifests itself in the form of dysfunction of the inner membrane and increased stiffness of the vessels.

An increase in blood pressure in bronchial asthma can be suspected by the following clinical manifestations:

In the most severe cases, against the background of an asthma attack and a crisis, there is a convulsive syndrome, loss of consciousness. This condition can develop into cerebral edema with fatal consequences for the patient. The second group of complications is associated with the possibility of developing pulmonary edema due to both cardiac and pulmonary decompensation.

The complexity of the treatment of patients with a combination of hypertension and bronchial asthma lies in the fact that most medications for their therapy have side effects that worsen the course of these pathologies.

Long-term use of beta-agonists in asthma causes a steady increase in blood pressure. So, for example, Berotek and Salbutamol, which are very often used by asthmatics, only in low doses have a selective effect on bronchial beta receptors. With an increase in the dose or frequency of inhalation of these aerosols, receptors located in the heart muscle are also stimulated.

This accelerates the rhythm of contractions and increases cardiac output. The diastolic rises and falls. High pulse blood pressure, a sharp release of stress hormones during an attack lead to a significant circulatory disorder.

Hormonal preparations from the group of corticosteroids, which are prescribed for severe bronchial asthma, as well as Eufillin, which leads to heart rhythm disturbances, have a negative effect on hemodynamics.

Therefore, for the treatment of hypertension in the presence of bronchial asthma, drugs of certain groups are prescribed.

The use of diuretics is preferable from the group of loop drugs - Lasix, Uregit, as well as potassium-sparing - Veroshpiron and Triampur.

When prescribing antihypertensive drugs, it should be borne in mind that beta-blockers lead to bronchospasm. This impairs pulmonary ventilation and is manifested by shortness of breath, an increase in shortness of breath. This is especially true for drugs with non-selective action.

Low-dose cardioselective agents for concomitant tachycardia and may be used in patients with asthma. The safest for this category of patients is its analogues.

A frequent complication of taking angiotensin-converting enzyme inhibitors is stubborn dryness. Therefore, although these medications do not directly affect the tone of the bronchi, but attacks of shortness of breath, turning into suffocation, respiratory failure significantly worsen the well-being of patients with asthma.

Formation of "Pulmonary heart"

In severe cases, asthmatics develop a symptom complex called cor pulmonale.. Such patients are prone to severe arrhythmias and should not be treated with calcium antagonists that slow down the heart rate.

In this regard, all patients who take hormonal drugs and use aerosols to relieve an asthma attack are advised to monitor their pulse rate and blood pressure daily. With a steady increase or decrease in them, you need to contact your doctor to correct therapy.

Dry cough is a side effect of antihypertensive drugs from the group of angiotensin-converting enzyme inhibitors. It especially often occurs when using tablets:

first generation - Enap, Captopril;
constantly and in large doses;
in patients with hypersensitivity to allergens;
in old age;
against the background of chronic bronchitis, bronchial asthma;
in smokers.

A hereditary predisposition to such a reaction has also been established. Cough does not cause complications, but significantly worsens the quality of life of patients, forcing them to take drugs to suppress it. They usually do not help much, and a change of medication is necessary to get rid of it. In this case, it would be best to switch to another group.

It has been proven that pressure medications related to sartans, trade names of medicines, practically do not cause coughing:

Tablets for asthmatics to lower blood pressure should not narrow the lumen of the bronchi, for this they choose from the following groups:

source

Have you struggled with HYPERTENSION for many years without success?

Head of the Institute: “You will be amazed at how easy it is to cure hypertension by taking it every day.

Hypertension is a fairly common disease. This disease today affects not only the elderly, but also the youth. This trend is explained quite simply: a large number of chronic diseases, untimely treatment, minimal physical activity, malnutrition - all these are the direct causes of high blood pressure. What pills for high blood pressure should I take? What threatens for each self-medication or uncontrolled intake of drugs?

What is the relationship between diseases?

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

Types of hypertension

Separation type	species name	Some facts
Origin	primary()	It accounts for up to 95% of morbidity cases. The cause of occurrence is heredity.
According to the course of the disease	Secondary (symptomatic)	It appears as a complication of other diseases.
	benign	Imperceptible and prolonged development of symptoms.
	Malignant	Develops rapidly.
By pressure level	Soft (1st degree)	The disease does not require medical treatment. The patient can only change the way of life.
	Moderate (2nd degree)	Pressure over 160 on 109 indicators. Use of medicinal methods
	Severe (3rd degree)	The readings are above 180 over 110. The pressure is constantly at this level. Possible damage to other organs.

Course of the disease

During an attack, there is an increase in blood pressure.

Doctor/nurse checking blood pressure.

Despite the fact that both diseases are pathogenetically unrelated, it has been found that blood pressure rises quite often in asthma.

Some asthmatics are at high risk of developing hypertension, namely people:

Elderly age.
With increased body weight.
With severe, uncontrolled asthma.
Taking medications that provoke hypertension.

Principles of therapy

[File #csp8995671, License #1702849]
Licensed through http://www.canstockphoto.com in accordance with the End User License Agreement (http://www.canstockphoto.com/legal.php)
(c) Can Stock Photo Inc. / Portokalis If a person suffering from bronchial asthma began to register cases of high blood pressure, you should immediately seek help from a doctor. It is categorically not recommended to choose pills for hypertension on your own, since many of them are contraindicated for asthmatics, because they can only worsen the condition.

Possess antithrombotic activity.
Show antioxidant activity.
Maintain potassium levels at the proper level to prevent the development of pulmonary insufficiency.
Do not cause the patient to cough.
Do not interact with bronchodilators.

Choosing a medicine for pressure in bronchial asthma should be done carefully, always taking into account side effects. Preference in treatment is given to drugs that do not impair the ventilation capacity of the lungs.

Unwanted drugs

As already mentioned, bronchial asthma can progress against the background of some incorrectly selected antihypertensive drugs.

These include:

Beta blockers. A group of drugs that enhances bronchial obstruction, airway reactivity and reduces the therapeutic effect of sympathomimetics. Thus, drugs aggravate the course of bronchial asthma. Currently, it is allowed to use selective beta-blockers (Atenolol, Tenoric) in small doses, but only strictly according to the indications.
Some diuretics. In asthmatics, this group of drugs can cause hypokalemia, which leads to the progression of respiratory failure. It should be noted that the joint use of diuretics with beta-2-agonists and systemic glucocorticosteroids only enhances unwanted potassium excretion. Also, this group of drugs is able to increase blood clotting, cause metabolic alkalosis, as a result of which the respiratory center is inhibited, and gas exchange indicators deteriorate.
ACE inhibitors. The action of these drugs causes changes in the metabolism of bradykinin, increases the content of anti-inflammatory substances in the lung parenchyma (substance P, neurokinin A). This leads to bronchoconstriction and coughing. Despite the fact that this is not an absolute contraindication to the appointment of ACE inhibitors, preference in treatment is still given to another group of medications.

Drugs of choice

What antihypertensive drugs are still allowed to be used in bronchial asthma?

However, in cases where the patient has concomitant severe cardiac arrhythmias (atrioventricular block, severe bradycardia), calcium antagonists are prohibited for use.

Hydrostatic (cardiogenic or cardiac) pulmonary edema
It happens during diseases that are characterized by an increase in pressure (hydrostatic) inside the capillaries and further penetration of plasma from them into the pulmonary alveoli. The reasons for this form are: vascular defects, heart; myocardial infarction; acute insufficiency of the left ventricle, myocarditis; stagnation of blood in hypertension, cardiosclerosis; heart defects with the presence of difficulty in heart contractions; emphysema, bronchial asthma.
Non-cardiogenic pulmonary edema, which includes:
iatrogenic	Occurs: at an increased rate of drip injection into a vein of large volumes of saline or plasma without actively forcing urine output; with a low amount of protein in the blood, which is often detected with cirrhosis of the liver, nephrotic kidney syndrome; during a period of prolonged rise in temperature to high numbers; during fasting; with eclampsia of pregnant women (toxicosis of the second half).
Allergic, toxic (membranous)	It is provoked by the action of poisons, toxins that violate the permeability of the walls of the alveoli, when liquid penetrates into them instead of air, filling almost the entire volume. Causes of toxic pulmonary edema in humans: inhalation of toxic substances - glue, gasoline; an overdose of heroin, methadone, cocaine; poisoning with alcohol, arsenic, barbiturates; drug overdose (Fentanyl, Apressin); penetration into the cells of the body of nitric oxide, heavy metals, poisons; extensive deep burns of lung tissue, uremia, diabetic coma, hepatic food allergy, medicinal; radiation damage to the sternum; poisoning with acetylsalicylic acid with prolonged use of aspirin in large doses (more often in adulthood); metal carbonate poisoning. Often passes without characteristic signs. The picture becomes clear only when X-rays are taken.
Infectious	Develops: when an infection enters the bloodstream, causing pneumonia, sepsis; in chronic diseases of the respiratory organs - emphysema, bronchial asthma, pulmonary thromboembolism (blockage of an artery with a platelet clot - an embolus).
aspiration	Occurs when a foreign body enters the lungs, the contents of the stomach.
Traumatic	Occurs with penetrating chest trauma.
Cancer	Occurs due to a malfunction of the functions of the pulmonary lymphatic system with difficulty in the outflow of lymph.
neurogenic	Main reasons: intracranial hemorrhage; intense convulsions; accumulation of exudate in the alveoli after brain surgery.

Severity	Severity of symptoms
1 - on the border of development	Revealed: mild shortness of breath; violation of the heart rate; often there is bronchospasm (a sharp narrowing of the walls of the bronchi, which causes difficulties with the flow of oxygen); anxiety; whistling, individual wheezing; dry skin.
2 - medium	Observed: wheezing that can be heard at a short distance; severe shortness of breath, in which the patient is forced to sit, leaning forward, leaning on outstretched arms; throwing, signs of neurological stress; perspiration appears on the forehead; severe pallor, cyanosis in the lips, fingers.
3 - heavy	Explicit symptoms: bubbling, seething rales are heard; there is a pronounced inspiratory dyspnea with a difficult breath; dry paroxysmal cough; the ability to only sit (because the cough increases in the supine position); constricting pressure pain in the chest caused by oxygen deficiency; the skin on the chest is covered with profuse sweat; pulse at rest reaches 200 beats per minute; intense anxiety, fear.
4 degree - critical	The classic manifestation of a critical condition: severe shortness of breath; cough with copious pink frothy sputum; severe weakness; far audible coarse bubbling rales; painful attacks of suffocation; swollen neck veins; bluish, cold extremities; fear of death; profuse sweat on the skin of the abdomen, chest, loss of consciousness, coma.