Chronic pulmonary heart

Chronic pulmonary heart

Chronic cor pulmonale – hypertrophy of the right ventricle and right atrium due to chronic pulmonary hypertension caused by obstruction of the vascular bed of the lungs (for example, bronchopulmonary diseases, chest deformity). Frequency – 5-10% of all organic pathology of the heart. The predominant age is over 45 years. The predominant gender is male. Etiology

• • Damage to the bronchial tree and lung parenchyma:
  • COPD
  • Diffuse interstitial lung diseases: pneumoconiosis, silicosis, idiopathic pulmonary fibrosis, radiation fibrosis
  • Granulomatous diseases: pulmonary tuberculosis, sarcoidosis, eosinophilic granuloma
  • bronchiectasis
  • cystic fibrosis
  • Malignant tumors
  • Lung resection
  • Pathology of the pulmonary vessels:
  • Primary pulmonary hypertension
  • Damage to the pulmonary vessels in diffuse connective tissue diseases (rheumatoid arthritis, SLE)
  • Hemoglobinopathies
  • Parasitic diseases of the lungs
  • Restriction of chest excursion:
  • Obesity (Pickwick’s syndrome)
  • Kyphoscoliosis
  • Neuromuscular diseases
  • Thoracoplasty
  • sleep apnea syndrome
  • Chronic hypoxia (for example, with prolonged stay at high altitude). Pathogenesis
  • Mechanisms of pulmonary hypertension
  • hypoxia and acidosis. The vasoconstrictor effect of hypoxia is a strong stimulus for the development of pulmonary hypertension; it can be exacerbated by acidosis, which also has a direct, although less pronounced effect on the pulmonary vessels. The most important aspect of hypoxic vasoconstriction is the likelihood of regression with an increase in the oxygen content in the inhaled air.
  • Obliteration or obstruction of the pulmonary vasculature is a less common mechanism of pulmonary hypertension, occurring in recurrent pulmonary embolism, primary pulmonary hypertension (an infrequent disease of unknown etiology), and pulmonary fibrosis. Significant obstruction of the pulmonary vasculature can also occur with emphysema and lung surgery.
  • Cor pulmonale development
  • Each attack of pulmonary hypertension results in a progressive increase in pressure that persists after the attack.
  • Pulmonary hypertension causes hypertrophy of the SMC of the pulmonary arteries, and then the peripheral pulmonary vessels. As a result, the pulmonary vasculature becomes more rigid and loses its ability to change cardiac output.
  • Changes in the vascular wall disrupt the work of the right ventricle, causing its hypertrophy and insufficiency of the right heart (i.e. cor pulmonale).

Pathomorphology

• • Signs of the underlying disease (see Etiology)
  • Hypertrophied right atrium and ventricle with dilatation of the cavities
  • Enlarged liver.

The clinical picture depends on the underlying disease

• • Shortness of breath, fainting (especially during exercise)
  • Cyanosis
  • Swelling of the neck veins
  • Cough dry or productive
  • Accent II tone over the pulmonary artery
  • Chest pain (pulmonary artery dilatation, myocardial ischemia)
  • Wheezing in the lungs
  • Hepatomegaly and ascites, sometimes – peripheral edema.

Laboratory research

• • Ht is often elevated (secondary erythrocytosis)
  • p02 is reduced.

Special Studies

• ECG
• Sinus tachycardia, possible atrial and ventricular extrasystoles
• EOS deviation to the right (angle a>[+110°])
• Right ventricular hypertrophy – most common in primary pulmonary hypertension
• Right atrial hypertrophy – P-pulmonale (sawtooth P> 2.5 mm in II, III standard leads, aVF)
• Rs or rSR complex in lead V,
• The ratio of the size of the r wave in v6 to the size of the S wave in V6