The pulmonary heart, as we said earlier, always on this website, is the
consequence of the alteration of the pulmonary circle, which becomes a
high-resistance circuit and this as a result of diseases that destroy the
physiology of the pulmonary circle. Let's see what are these lung diseases that
subsequently cause the engagement of the right sections of the heart and,
therefore, the hypertension of the pulmonary circle and therefore the pulmonary
heart.
The most frequent cause of pulmonary hypertension: bpco
Because of the high incidence, chronic obstructive pulmonary disease (COPD) is
by far the most frequent cause of chronic pulmonary heart (50-60% of cases). All
chronic bronchial obstruction syndromes can give pulmonary hypertension,
including the same bronchial asthma, if it then becomes chronic and flows into
chronic bronchitis.
They are represented by:
chronic bronchitis
pulmonary emphysema
bronchial asthma
If the bronchitic form prevails, it means that we are dealing with the type of patient called "blue blower" or "blue bloater", ie the obese patient, with the belly , where the chronic respiratory disease causes parallel alterations of perfusion, ie of blood circulation and lung ventilation, ie hypoxia and hypercapnia. In fact, if the poor ventilation of the alveoli due to poor respiratory mechanics and alterations of the parenchyma causes poor oxygenation, it follows that hypoxia causes in turn a diffuse arteriolar vasoconstriction, perhaps due to a physiological mechanism that tends to sort the blood circulation in the most ventilated areas of the lung, which in these clinical conditions practically do not exist in the whole lung. It follows, therefore, constrictive vasculopathy and hypertension of the pulmonary circle, with reduced carbon dioxide exchanges, therefore hypercapnia, and therefore respiratory acidosis (cf. acid-base equilibrium ).
In these subjects there are usually repeated episodes of right-handed failure, which in the initial phases respond well enough to the medical, pharmacological and O2 treatment. b) In the predominantly emphysematous forms (pink puffer) the widespread destruction of the alveolar septa determines the reduction of the surface of respiratory exchange. The vascular pathology is predominantly restrictive; pulmonary arterial pressure is normal or only slightly increased at rest. Blood pressure in the blood can remain normal for longer ventilation: hypoxia is therefore only mild, and there is usually hypocapnia. The onset of the chronic pulmonary heart is late, the right decompensation is not affected by medical treatment and usually represents a terminal event.
Bronchiectasis
It is a chronic inflammatory disease that is characterized by cylindrical and /
or sacciform dilatations of the bronchi, with destruction of the pulmonary
parenchyma. The patient may have bronchial ectasia if he has expectoration of
mucus, pertussis or other infantile infectious diseases. In a small percentage
of cases it is congenital forms (triad of Kartagener).
Cystic fibrosis
Lungs are involved in the majority of patients suffering from this congenital disease that is characterized by thick mucus, with obstructive airway facts, with the formation of areas of atelectasis, pneumonia, bronchiectasis and pulmonary abscess.
This category includes a large number of morbid forms that have in common an evolution towards fibrosis, with loss of part of the functional lung parenchyma and vascular bed restriction. As long as hypoxemia remains within reasonable limits, pulmonary hypertension is modest, but when the respiratory failure goes on, the chronic pulmonary heart develops rapidly. In these fibrotic forms a parallel deterioration occurs between ventilatory mechanics and hemodynamics of the small circle, and only when the vital capacity falls below 50% is established significant pulmonary hypertension.
The spontaneous or secondary fibrotorax with therapeutic pneumothorax, both surgical resections, can severely alter ventilatory mechanics, either directly or through frequent pathological processes involving the residual parenchyma, and thus determine pulmonary hypertension.
Neuromuscular system diseases may also result in poor ventilation, hypoxemia and pulmonary hypertension. We are talking about pathological processes of respiratory muscles resulting from generalized muscular diseases (muscular dystrophies, infiltrative myopathies) or neurological diseases (bone marrow lesions, amyotrophic lateral sclerosis, myasthenia, poliomyelitis, Guillain-Barré syndrome). Diseases of the chest wall, which cause alterations and deformations of the wall of the rib cage, such as kyphoscoliosis.
Hypoventilation from obesity , see apneas .
The association between large obesity and hypoventilation is known as Pickvick's
syndrome. even
today the cause of hypoventilation remains obscure: it may depend partly on the
reduction in the compliance of the rib cage, partly on the respiratory muscle
weakness, partly on the hyposensitivity of the respiratory center to the stimuli
of hypoxemia and hypercapnia. We distinguish nocturnal apnea syndromes
characterized by abnormal changes in respiratory function that occur during
sleep. There were three typical behaviors:
1) central apnea;
2) obstructive apnea;
3) mixed apnea.
Regardless of the mechanism, if apnea periods are prolonged and / or iterative,
alveolar hypoventilation results with hypoxemia and subsequent pulmonary
hypertension.
Primary pulmonary hypertension, form an unknown etiopathogenesis that depends on
an increase in arteriolar resistances that recognizes a variegated
etiopathogenesis:
1) recurrent venous thromboembolism misunderstood;
2) primitive thrombotic phenomena at the pulmonary level;
3) congenital defects of the pulmonary vessels;
4) autoimmune collagen-vascular disease;
5) hypersensitivity to some drugs;
6) effect of female hormones;
7) tendency to phenomena of vasoconstriction from arterial spasm.
To deepen the theme:
Pulmonary heart, related diseases
Pulmonary heart, how to cure it
the pulmonary heart, introduction to the topic