Bronchial asthma is a chronic respiratory system disease of infectious and allergic nature, which manifests itself in bronchial lumen obstructive disorders (that is, simply put – airway lumen narrowing) and many cellular elements of various nature participate in this process, releasing a large number of various mediators – biologically active substances, which are the root cause of all these phenomena, and, as a result, asthma attacks.
Chronic pulmonary heart is a pathological condition characterized by a number of changes in heart and blood vessels (the basic are right ventricular hypertrophy and vascular changes). This is explained by mainly pulmonary circulation hypertension. Also, over time, secondary hypertension appears (i. e., increased blood pressure, which cause is reliably known). Question regarding blood pressure at bronchial asthma, its causes and consequences has always been relevant.
Regarding the fact whether these two diseases are interrelated, there are two diametrically opposite points of view. One group of merited academicians and professors sticks to the opinion that they have never affected one another at all, and will not affect, another group of not less respected people considers that asthma is surely the main causal factor in chronic pulmonary heart development, and as a result – secondary hypertension. That is, according to this theory – all asthmatics will suffer from hypertension in future.
The most interesting is that purely statistical data confirm those scholars theory who see bronchial asthma as cause of secondary hypertension – with age people suffering from asthma observe increased blood pressure. It can be argued – hypertension (also known as essential hypertension) occurs with age at each first. Another point is that increased blood pressure (persistent) occurs at asthmatics much earlier, and this causes higher mortality and disability from vascular events occurrence (myocardial infarction, and hemorrhagic, ischemic stroke).
An important argument in this concept favor is also the fact that chronic pulmonary heart, and as a result secondary hypertension, occurs at children and adolescents suffering from asthma. But is statistics confirmed by physiology? The question is very serious, since, determining true etiology, pathogenesis and relationship of this process with external factors, it is possible to develop optimal treatment regimen.
The most reasonable answer on this occasion was given by Professor V. K. Gavrisuk from National Institute of Tuberculosis and Pulmonology named after Yanovsky. It is important that this scholar is also a practicing physician, and that is why his opinion, which was confirmed by numerous studies, can claim not only hypothesis, but theory. The essence of this theory is set out below.
In order to understand the whole problem, it is necessary to better understand pathogenesis of this process. Chronic pulmonary heart develops only on the background of right ventricular insufficiency, which, in its turn, is formed due to increased blood pressure in pulmonary circulation. Hypertension is caused by hypoxic pulmonary vasoconstriction – compensatory mechanism, the essence of which is to reduce blood supply in ischemic lobes of lungs and direct blood flow to where gas exchange intensively takes place (the so-called Vest areas).
Causes and Effects
It should be noted that for right ventricular failure development with hypertrophy and subsequent chronic pulmonary heart, persistent hypertension must be present. At bronchial asthma, even in most severe form, there is no constant increase of blood pressure in pulmonary artery and vein, and therefore it is wrong to consider this pathological mechanism completely etiological factor for secondary arterial hypertension at bronchial asthma.
In addition, there is a number of very important points. When transient arterial hypertension, caused by bronchial asthma attacks, manifests itself, the crucial role in played by increased intrathoracic pressure. It is a prognostically adverse event, as over time patient can observed expressed neck veins swelling, with all subsequent adverse effects (generally speaking, symptoms of this condition will have a lot in common with pulmonary embolism, because these pathological conditions development mechanisms are very similar to each other).
Due to increased intrathoracic pressure and reduced venous return to heart, stagnation in both inferior and superior vena cava pool occurs. The only adequate help in this state is bronchospasm relief by means that are used for bronchial asthma (beta2-agonists, corticosteroids, methylxanthines) and massive hemodilution (infusion therapy).
From everything said above, it becomes clear that hypertension is not asthma consequence, simply because there is an increased blood pressure in pulmonary circulation is intermittent and does not lead to chronic pulmonary heart disease development.
Another question – other chronic respiratory diseases that cause persistent hypertension in pulmonary circulation. Primarily they include chronic obstructive pulmonary disease (COPD), many other diseases affecting pulmonary parenchyma, like scleroderma or sarcoidosis. In this case – yes, their participation in hypertension occurrence is justified.
An important point is heart tissue lesion due to oxygen starvation, which occurs during asthma attack. In future it can play a role in blood pressure increase (persistent), however, contribution of this process will be very small.
A small amount of people with bronchial asthma (approximately twelve percent) acquires secondary high blood pressure, which, anyway, is interconnected with violation of polyunsaturated arachidonic acid formation, associated with excessive thromboxane-A2, some prostaglandins and leukotrienes release into blood. This phenomenon is caused, again, by oxygen decrease in patient’s blood. However, a more significant reason is continued sympathomimetic agents and corticosteroids use. Fenoterol and salbutamol have extremely negative impact on cardiovascular system at bronchial asthma, because in large doses they significantly not only affect beta2-adrenergic receptors, but also are capable of stimulating beta1-adrenergic receptors, significantly increasing heart rate (cause persistent tachycardia) thereby increasing myocardial oxygen demand, increasing already pronounced hypoxia.
Also methylxanthines (theophylline) have a negative effect on cardiovascular system functioning. At constant use these drugs may lead to severe arrhythmia, and, as a result, cardiac dysfunction and following from this hypertension.
Systematically used glucocorticoids extremely negatively affect vessels and (especially those that are used regularly) – due to their side effects, vasoconstriction.
Patients with bronchial asthma management, which will reduce risk of this kind of complications in the future
The most important thing is strictly adhere to treatment course appointed by pulmonologist for asthma and avoid contact with allergens. Bronchial asthma treatment is carried out according to Gin protocol, developed by world’s leading pulmonologists. It contains proposed rational sequential therapy for this disease. That is, on first stage of this process attacks are observed are very rare, not more than once a week, and they are stopped by taking Ventolin (salbutamol). Generally speaking, provided that patient will adhere to treatment and keep healthy lifestyle, avoid contacts with allergens, the disease won’t progress. From these Ventolin dose hypertension will not appear. But patients, for the most part, are irresponsible people, do not adhere to treatment recommendations, which result in necessity to increase drugs dosage, add other groups of drugs with much more pronounced side effects to treatment regimen due to disease progression. All this then transfers into pressure increase, even at children and adolescents.
It is worth noting that treatment of this kind of hypertension is by many times more complex than classical essential hypertension treatment, because of the fact that it is impossible to apply a lot of effective drugs. The same beta blockers, in spite of their high selectivity, still affect receptors located in lungs and may successfully lead to status asthmaticus (“silent lung”) at which Ventolin will not help, due to absence of sensitivity to it.
Although at chronic obstructive bronchitis all the above effects are much more pronounced and involve much more serious consequences, which are not comparable to those, described in this article. But that’s another story.
From all said above, it is possible to make the following conclusions:
- asthma can cause hypertension, but this happens in a small number of patients, usually because of improper treatment, accompanied by a large number of bronchial obstruction attacks. But still, it will be indirect effect, through myocardial trophic disorders;
- a more serious cause of secondary hypertension are other chronic respiratory tract diseases (chronic obstructive pulmonary disease (COPD), many other diseases affecting pulmonary parenchyma, like scleroderma or sarcoidosis);
- the main reason for hypertension at asthmatics are drugs that treat asthma itself;
- systematic adherence to treatment regimens and other recommendations of attending physician is a guarantee (but not absolute) that the process will not progress, and if it is, it will be much slower. This will allow keeping therapy at a level, which was originally assigned, without prescribing stronger drugs, which side effects will not lead to arterial hypertension in future.