Beginning >> Diseases >> Cardiovascular >> Chronic pulmonary heart



Chronic pulmonary heart

Table of contents
Chronic pulmonary heart
Classification of a pulmonary heart
Clinical picture of a disease
Diagnosis and inspections

Pulmonary heart call secondary increase in a right ventricle (its hypertrophy and/or dilatation) which is caused by the pulmonary arterial hypertension which developed as a result of diseases of bronchial tubes and lungs, defeats of pulmonary vessels or deformation of a thorax.

It is necessary to remember that the increase in a right ventricle caused by dysfunctions and structures of lungs which are caused by primary defeat of the left departments of heart (for example, a stenosis of the left atrioventricular opening, a postinfarction cardiosclerosis, etc.) or inborn heart diseases does not belong to the concept "pulmonary heart".


Data on true prevalence of a pulmonary heart are very inconsistent as diagnosis of this pathological syndrome is complicated, especially when there are no signs of right ventricular insufficiency. According to some data, about 5-10% of all cases of cardiovascular diseases at adults fall to the share of a pulmonary heart. However the weight of evidence suggests that the pulmonary heart belongs to more widespread pathology, especially among men 50 years are aged more senior, and on frequency takes the 3rd place after an ischemic heart disease and AG.


The acute pulmonary heart develops within several hours or days as a result of sudden and substantial increase of pulmonary pressure and practically in all cases is followed by acute right ventricular insufficiency (without the previous hypertrophy of a right ventricle). The thromboembolism of branches of a pulmonary artery is the most frequent reason of an acute pulmonary heart.
The subacute pulmonary heart arises within several weeks, months and is observed at repeated small thromboembolisms, a nodular periarteritis, a carcinomatosis easy, repeated attacks of heavy bronchial asthma, botulism, a myasthenia, a myasthenia
The chronic pulmonary heart is characterized gradual and slow (within several years) by forming of pulmonary arterial hypertension and development of a gipertrofiipravy ventricle (the compensated chronic pulmonary heart). Further in process of increase of pulmonary pressure systolic dysfunction of a right ventricle develops and signs of right ventricular insufficiency (a dekompensirovanny chronic pulmonary heart) appear. Allocate bronchopulmonary (caused by chronic pathological processes in a pulmonary parenchyma and bronchial tubes - 70-80% of cases), vascular (at defeats of vessels of small blood circulation, vasculites, thrombembolias of a pulmonary artery) and torakodiafragmalny (at primary damages of a backbone and thorax with its deformation, at Pikvik's syndrome) forms of a pulmonary heart. There is a set of the reasons leading to forming of a chronic pulmonary heart (see table 1 below).


 Mechanisms of pulmonary arterial hypertension
Gradual forming of the pulmonary arterial hypertension caused by several pathogenetic mechanisms is the cornerstone of development of a chronic pulmonary heart. Though value of each of them variously depending on an etiology of pulmonary hypertensia, nevertheless the main link of its pathogeny in most cases is the alveolar hypoxia arising in the conditions of the increasing irregularity of alveolar ventilation
1.   Hypoxemic pulmonary vasoconstriction. In normally functioning lung there is rather difficult mechanism of regulation of the local blood-groove depending first of all on the partial pressure of oxygen in an alveolar air. This mechanism is known under the name of a reflex of Euler-Lilyestranda. If
in physiological conditions in rather small site of a lung occurs
decrease in partial pressure of oxygen in an alveolar air, in same
site reflex there is local vasoconstriction which leads to adequate restriction of a blood-groove. As a result the local pulmonary blood stream as if adapts to intensity of lung ventilation, and disturbances of ventilating and perfused ratios do not happen
If alveolar hypoventilation is expressed more and extends to extensive sites of pulmonary fabric (for example, at the expressed pneumosclerosis or obstructive diseases of lungs etc.), the generalized increase of a tone of pulmonary arterioles leading to increase of the general pulmonary vascular resistance and pulmonary hypertensia develops.
The mechanism of hypoxemic pulmonary vasoconstriction is up to the end not clear. Possibly, it is implemented with the participation of SAS, and also vasopressor endothelial factors. Endothelins and angiotensin II directly stimulate reduction of smooth muscles of a vascular wall whereas decrease in synthesis of GI2 prostaglandin, the endothelial weakening factor (NO) strengthens these vazokonstriktoriy influences even more.
2. Influence of a hypercapnia. The hypercapnia (increase in concentration of CO2 in blood) also promotes development of pulmonary hypertensia. However high concentration of C2 works not directly with a pas a tone of pulmonary vessels, and indirectly — mainly through the acidosis caused by it (decrease rn less than 7,2).
Besides, the delay of carbon dioxide promotes decrease in sensitivity of a respiratory center to CO2 that reduces ventilation of the lungs even more and promotes pulmonary vasoconstriction.
3. Anatomic changes of a pulmonary vascular bed. In a pathogeny of pulmonary hypertensia structural changes in a vascular bed which treat are of great importance:

  • prelum and zapustevaniye of arterioles and capillaries owing to gradually progressing fibrosis of pulmonary fabric and emphysema of lungs;
  • development of a thickening of a vascular wall at the expense of a hypertrophy of muscle cells of a mussel and emergence of a longitudinal layer of myocytes in an intima that is followed by reduction of a gleam of pulmonary arterioles and promotes increase in expressiveness and duration of vazokonstriktorpy reactions;
  • the multiple microfibrinferments arising in the conditions of chronic disturbance of a blood-groove and the increased aggregation of thrombocytes;
  • recurrent thromboembolisms of small branches of a pulmonary artery;
  • development of a bronkhopulmonalny anastomosis, i.e. anastomosis between branches of the bronchial arteries relating to a big circle of blood circulation and branchings of a pulmonary artery. As pressure in bronchial
    arteries above, than in a small circle of blood circulation, there is a redistribution of blood from system of bronchial arteries in system of branches of a pulmonary artery,
    what significantly increases pulmonary vascular resistance.
  • vasculites (for example, at general diseases of connecting fabric) are also characterized by proliferation of an intima, narrowing and an obliteration of a gleam of vessels.

All listed pathological changes of a vascular bed of lungs naturally lead to the progressing increase in pulmonary vascular resistance and development of pulmonary hypertensia.
4. Disturbances of bronchial passability. The patients having chronic obstructive diseases of lungs (chronic obstructive bronchitis, bronchial asthma) with dominance of signs of obstructive respiratory insufficiency are more subject to development of an alveolar hypoxia and forming of a pulmonary heart ("bluebloaters" — "blue bloated"). These patients differ in the expressed irregularity of lung ventilation that causes considerable disturbances of ventilating and perfused ratios, aggravates an alveolar hypoxia and leads to generalized manifestation of the mechanism of hypoxemic pulmonary vasoconstriction.
At patients with dominance of restrictive disturbances and diffusion damages of lungs the alveolar hypoxia is expressed much less. For example, patients with the expressed diffusion emphysema of lungs { "pinkpuffers" "pink puffing") are much less subject to development of pulmonary hypertensia and a chronic pulmonary heart.
Treat number of the accessory factors influencing forming of pulmonary arterial hypertension:

  • the increased viscosity of blood and aggregation of thrombocytes;
  • increase MVB (minute volume of blood);
  • tachycardia.

The expressed hyperglobulia and the polycythemia characteristic of many bronchopulmonary diseases, are followed by increase in aggregation of erythrocytes and viscosity of blood that complicates a blood stream on a vascular bed of lungs even more, increasing its resistance. Besides, increase of viscosity and delay of a blood-groove promote formation of pristenochny blood clots of small branches of a pulmonary artery.
Increase in cordial emission is caused by tachycardia and a hypervolemia which are very characteristic of patients with a chronic pulmonary heart. One of the possible reasons of a hypervolemia, apparently, is the hypercapnia promoting increase in concentration of Aldosteronum in blood and, respectively, Na delay + and waters.
Thus, the described mechanisms of increase of pulmonary vascular resistance and forming of pulmonary arterial hypertension are closely connected with character and expressiveness of changes in pneumatic ways and a vascular bed of lungs. Therefore any exacerbation of bronchopulmonary diseases, as a rule, is followed by aggravation of pulmonary hypertensia. On the contrary, effective treatment of inflammatory changes in a pulmonary parenchyma or respiratory tracts in most cases is followed by reduction of pressure in system of a small circle.
 Main changes of a hemodynamics
As a result of forming of pulmonary hypertensia develop and gradually a number of hemodynamic changes, the most characteristic of patients with the developed clinical picture of a chronic pulmonary heart progresses:

  • The hypertrophy of a right ventricle (without disturbance of its function) developing in response to the expressed and long increase in an afterload (the compensated pulmonary heart).
  • The gradual decrease in systolic function of a right ventricle which is followed by increase of diastolic pressure in a right ventricle, its dilatation and development of stagnation of blood in a venous bed of a big circle of blood circulation (dekompensirovanny HP).
  • Tendency to increase VCB (the volume of the circulating blood), Na delay + and waters in an organism.
  • At late stages of a disease — decrease in cordial emission and the ABP level as a result of reduction of inflow of blood to a small circle of blood circulation and, respectively
    fillings of LZh (mainly due to critical falling of systolic
    functions of a right ventricle and forming of "the second barrier" in the form of the expressed structural
    changes of a vascular bed of lungs).

"Holt — Oram a syndrome   Ectopic rhythms"