Chronic heart pathology

2021-01-28 12:00 AM

Chronic obstructive pulmonary disease is the main cause of chronic pulmonary hypertension and cardiomyopathy. Pulmonary hypertension is mainly secondary to hypoxia


Chronic bronchiectasis is an RV enlargement due to enlargement and or dilatation of the right ventricle secondary to disorders or diseases of the respiratory system. The disease is caused by a disease within the master lung tissue; Some cases may be due to an abnormality of ventilation command, an injury to the chest and or the respiratory muscle system, or possibly due to diseases of the pulmonary circulation. Pulmonary hypertension is always ahead of the chronic heart failure including right heart failure.


It is difficult to determine the frequency of chronic heart waste; From the age of 50, chronic heart disease is the third most common cardiovascular disease after anaemia and hypertension. The disease is usually secondary to chronic obstructive bronchial disease. Indeed, in countries that smoke a lot of cigarettes and have environmental pollution, chronic bronchitis and emphysema have a high frequency and chronic bronchitis accounts for one-third of heart failure cases. Nowadays men suffer more than women, probably because of tobacco.


Chronic obstructive pulmonary disease

Chronic obstructive pulmonary disease is the main cause of chronic pulmonary hypertension and cardiomyopathy. Pulmonary hypertension is mainly secondary to hypoxia due to an abnormal ventilation-perfusion ratio.

Interstitial lung diseases

Interstitial lung disease may be secondary to sarcoidosis, asbestosis, and collodionize, but it may also be of unknown cause. In all of these diseases, there is ventilatory restriction syndrome but no obstructive syndrome. The interstitial infiltrates compress and destroy the wall arteries, increasing the resistance of the pulmonary vessels. Sometimes, these lesions are combined with the closure of the bronchioles by an inflammatory process around the bronchioles.

Decreased bronchial ventilation with normal lungs

Myasthenia gravis, muscular dystrophy; hunchbacked and overweight.

Colloidal diseases

In colloid diseases such as lupus erythematosus often damage the pulmonary blood vessels. Scleroderma and similar diseases such as CREST syndrome also have a high incidence of pulmonary vascular damage and progress to the heart.

Thrombosis - pulmonary artery embolism

Thrombosis causes blockage of the pulmonary arteries and arterioles:

Thrombosis and re-channelization of the small muscular arteries and pulmonary arterioles have been found by biopsy and autopsy in patients with pulmonary hypertension of different etiologic. To account for this local thrombosis, endothelial lesions of the pulmonary microcirculation have been demonstrated, a paroxysmal imbalance between local coagulation and fibrinolysis, and activation Discontinue platelet aggregation in this microcirculation.

Chronic pulmonary artery embolism near the base:

The presence of one or more organized blood clots, clogging the large branches of the pulmonary artery with the gradual formation of the coronary heart. Insufficient local fibrinolysis causes the blood clot to dissolve either frontal or posterior, causing the pulmonary arteries to be blocked near the base, in conjunction with a decrease in the dilation of the central pulmonary vessels.

Pulmonary vein disease

Large pulmonary veins can be blocked by metastases of cancer such as breast or lung cancer, by infections such as tuberculosis or histoplasmoses, by lymphadenopathy such as sarcoidosis or by less common causes such as inflammation. fibrotic mediastinum.

Primary pulmonary hypertension

Primary pulmonary hypertension progressing to the heart of chronic lung is not caused by heart disease or underlying lung disease; also known as unexplained pulmonary hypertension. Primary pulmonary hypertension is a rare disease. It can occur at any age, but the first symptoms usually appear in young people. Recently, an increase in antinuclear antibodies has been established in these patients

Mechanism of pathogenesis

The reduction of PaO 2 is the most important objective disorder known as chronic hypoxaemia when a PaO 2 less than 70 mmHg occurs persistently during the stable period. In fact, chronic hypoxia only becomes ominous from a PaO 2 = 55 mmHg because at that time it can have harmful effects and requires treatment.

The erythropoietic reaction is beneficial by allowing adequate oxygen transport, so oxygen transport is usually not affected much except during acute respiratory failure or during severe hypoxia episodes such as sleep. However, polycythaemia vera is harmful to increase blood viscosity and thus contributes to the increase in pulmonary vascular resistance leading to the development of pulmonary hypertension.

Chronic hypoxia causes neurological and mental abnormalities such as attention and memory disorders, difficulty with abstract thinking, skilful behaviour, and simple movement disorders.

Chronic hypoxia increases pulmonary vascular resistance due to strong spasm; hypertrophy increases smooth muscle in the artery wall, causing pulmonary artery hypertension and right heart burden. The heart compensates for this increase in burden increasing systolic frequency and output to ensure oxygen supply. It should be noted that pulmonary hypertension is an adaptive mechanism, helping to select a number of capillaries for good perfusion, improving the ventilatory / perfusion relationship.

Chronic bronchitis occurs after pulmonary hypertension, the most common cause of increased RV burden is an increase in pulmonary vascular resistance, occurring mainly in the small aperture arteries and arterioles.

The normal pulmonary vascular system is a highly dilated ring, with low resistance, with moderate exertion, the blood flow triples and causes only a slight increase in pulmonary dynamics. However, when the pulmonary vascular reserve is depleted due to a gradual decrease in the area and expansion of the pulmonary vascular system, a slight increase in cardiac output may be sufficient to induce a rise in pressure. clear lungs. Lack of oxygen causes constriction of the small aperture arteries and arterioles. It was found that acidosis (pH <7.2) increased pulmonary vasoconstriction. In chronic hypoxia, the effects of this pulmonary hypertension stimulation are often exacerbated by the increase in blood mucus associated with secondary polycythaemia. As opposed to the consequences of hypoxia, the act of carbon dioxide on the pulmonary circulation mediated by acidosis causes direct vasoconstriction. An increase in carbonic gas reduces the response of the respiratory centres to carbonic stimuli and induces renal bicarbonate reabsorption.



Clinical symptoms of chronic obstructive pulmonary disease: Chronic bronchitis, tobacco-induced emphysema, prolonged bronchial asthma in which poor bronchial recovery, bronchiectasis, often with exacerbations. After each outbreak, the disease worsens.

Pulmonary functional damage in this group of diseases exhibits decreased first-second forced expiratory volume (FEV1), decreased FEV1 / FVC, airway resistance and increased sediment volume (VR).

Symptoms of restrictive lung diseases: such as pulmonary fibrosis, alveolar dilatation, obesity, scoliosis, chest deformity, diffuse pulmonary fibrosis, pleural thickening, pulmonary vascular disease.

The functional impairment of this group of diseases is a reduced vital capacity (FVC).

It is possible to combine the symptoms of the two groups of diseases above.

This progressive stage of chronic lung disease can range from 3 years to 20 years.

Stage of pulmonary hypertension

Clinical symptoms:

Functional symptoms help detect:

Exertional dyspnoea: Always.

Bronchitis syndrome: cough and sputum production.

Excessive liver pain: T is vague.

Physical symptoms:

In addition to the root disease symptoms, the earliest cardiac symptoms were the second strong heartbeat in the pulmonary valve drive, the Harzer's mark was less common, the tachycardia was not very valuable, liver pain may occur with pressure on the right lower rib.

Subclinical symptoms:

Pulmonary film: In addition to the signs of bronchial disease - lung origin, the most common is the pulmonary artery bulging.

Ultrasound: 2-plane ultrasound shows RV dilatation. Colour Doppler ultrasound can assess pulmonary artery pressure above 35mmHg.

Hemodynamic Bilan: Measure central venous pressure, if increased is an early sign of chronic heart-lung.

Right heart failure stage

Clinical symptoms:

Functional symptoms: Increasing dyspnoea from shortness of breath during exertion, to difficulty breathing when climbing uphill or on stairs, to difficulty breathing when travelling fast on a flat road, to difficulty breathing when walking slowly on the road, in the end, it was difficult to breathe when doing light work such as cleaning, undressing, and then having difficulty breathing even when resting.

Physical symptoms:

Peripheral symptoms: Liver enlarged and painful, neck veins raised and pounding, enema, purple, bulging and congested eyes, central venous pressure measurement above 25 cm of water, finger drumstick.

Cardiovascular symptoms: Tachycardia, sometimes complete arrhythmia, signs of Harzer, strong T2 and splits in the pulmonary valve drive. 3 leaves.

Subclinical symptoms:

Pulmonary film: The pulmonary artery body is enlarged; the right ventricular hypertrophy causes the heart to appear angular and in the left anterior tilting film the light behind the sternum is lost. Pleural effusion may occur.

ECG: There is a right atrial thickening (P waste) and right ventricular thickening.

Colour Doppler ultrasound: Measure pulmonary artery pressure above 45mmHg.

Hemodynamic bilan: In the stage of pronounced right ventricular failure, pulmonary artery pressure increases above 45 mmHg.

Measurement of blood gases: PaO2 decreases, PaCO2 increases. Decreased saO2 and decreased blood pH are prone to respiratory prescription infections

Haematology: Polycythaemia vera, haematocrit increased.


Chronic heart failure progresses slowly, damaging the function and structure of the lung leading to partial respiratory failure, total respiratory failure, right heart failure and finally total heart failure. Today, although there are many modern treatment methods, right heart failure still accounts for a very high mortality rate: 60-70% in the first or second right heart failure episode.

The progression of the disease depends on the cause of the disease, and especially on whether the patient discovers his or her disease early or not, when it is discovered, has been treated and monitored regularly or not.

The most common cause of obstructive pulmonary insufficiency is a chronic tobacco-induced obstructive pulmonary disease that can easily lead to a heart attack. The acute exacerbation of chronic obstructive pulmonary disease will aggravate the heart of the heart, in some cases after 3 years there has been a sign of right heart failure. For bronchial asthma, bronchial asthma allergic infections sometimes, after 5 to 10 years, there are signs of right heart failure, whereas allergic bronchial asthma without infection is less likely to lead to chronic heart failure.

For restrictive chronic respiratory failure such as pulmonary fibrosis caused by tuberculosis, but must be diffuse fibrous tuberculosis, it will lead to the heart of chronic bronchitis. Conversely, if there is a small amount of fibrosis it does not lead to the heart, but if it is bronchiectasis is rapidly becoming chronic because of that time, combined chronic respiratory failure. In this case, if there is an accompanying bronchopulmonary infection, it also aggravates the chronic heart.

If the patient is monitored and treated well, the disease can be stable, it can take 10-20 years or longer to have heart failure complications, in some cases, it is possible to live with the patient for life.


Diet and rest

Rest is very necessary, so do light work, when there are signs of heart failure need to reduce or quit strenuous work.

Light, low-salt diet, can eat 1-2 grams of salt / day. In the case of severe heart failure, severe oedema, the diet is stricter; only use 0.5 g of salt per day, but not for long.

Oxygen therapy

One can give oxygen by nasal inhalation, oxygen should be led through a water bottle to moisten, should not give 100% oxygen with a low dose of 1.5-2 litters/minute, to be effective, useless. 12 hours / 24 hours, but the best is 15 - 20 hours / 24 hours. How do people provide oxygen to maintain a PaO2 above 60 mmHg and SaO2 above 90%, if so, it will reduce mortality and provide the patient with a relatively comfortable life.

The drug improves ventilation rate - pulmonary perfusion

Bismesialate d'almitrine (VECTARION) Usage: attack therapy with 50 mg, 1-2 tablets/day for 3 months, then maintenance therapy, after attack treatment, 1-month break, continue treatment 2 months. Currently very little in use.

Treatment of heart failure

In chronic heart failure, there may be total heart failure, but mainly right heart failure, so the main treatment is diuretics, followed by digitale, which can be combined with nitré derivatives.


Furosemide (LASIX): 2-4 tablets of 40 mg/day, divided equally; or 2 to 3 ampoules of 20 mg/day, divided equally.

When using furosemide diuretics must be cautious because it will cause metabolic alkalosis, so there may be a risk of exacerbating respiratory failure due to decreased respiratory stimulation effect of carbon dioxide.

Spironolactone (ALDACTONE): 50 mg - 100 mg (1-2 tablets) / day, in severe cases it may be increased to 6 capsules / day, divided equally. Usually use Aldactazine (Aldactone 50mg + Alizide 15mg) x 2 tablets / day.

Digitale: Often used digoxine, only used in compensated heart failure, for a mild dose of 0.25 mg - 0.50 mg (1-2 tablets) / day, not when using decompensated heart failure.

Nitrite derivatives: As Isosorbide mononitrate (Imdur) 60mg x 1/2 tablet / day.

ACE inhibitors: Such as captopril 6.25mg / day or Lisinopril 2.5mg / day.

Diuretics and digitale, nitrite derivatives or ACE inhibitors, in this case, are not as important as methods to improve alveolar ventilation such as oxygen therapy.


Stable or improved vasodilators occur in up to one-third of patients. The effectiveness of drugs varies from patient to patient.

Calcium inhibitors such as Nifedipine, Diltiazem can be used.

In addition, people also use Hydralazine with the hope of reducing circulation pressure, but this drug works to reduce blood oxygen, due to a disorder of the ratio of ventilation-perfusion.

Endothelin receptor blockers (Bosentan): Endothelin 1 is an endothelial vasoconstrictor that causes pulmonary hypertension,

Bosentan improves exercise and hemodynamic performance in patients with pulmonary hypertension, the drug is given for 12 weeks, the starting dose is 62.5 mg twice daily for the first 4 weeks, and then increases the dose. up to 125 mg twice daily

Prostacyclin continuous intravenous pass.

The drug Sildenafil (Viagra) in the treatment of pulmonary hypertension secondary to pulmonary fibrosis:

Sildenafil selectively increases vasodilation and improves gas exchange in patients with pulmonary fibrosis and pulmonary hypertension.

Epoprostenol is used intravenously or Sildenafil is used orally, after the patient's hemodynamic change returns to normal values, followed by aerosolized Nitric oxide 10-20 ppm, they take 50mg.

Sildenafil or maximum pass Epoprostenol (average 8ng / kg / min). Duration of effect of Sildenafil from 120 150 minutes.

So far, Sildenafil is the best drug of choice in the treatment of pulmonary vasodilation.


Very effective in the treatment of exacerbations, Prednisone oral 5 mg, 4 tablets/day or nebulized dipropionate de beclomethasone, or Depersolone 30 mg intravenously, both anti-inflammatory and anti-allergic and reduce secretion Translate.


Antibiotics are only used when bronchopulmonary superinfection, common bacteria are Streptococcus pneumonia, Haemophilus influenza, Moraxella catarrhalis, Mycoplasma pneumoniae, Legionella pneumophila, Staphylococcus aureus.

If mild, the most commonly used drugs today are:

Azithromycin: 250 mg x 2 tablets/day in 2 divided doses on the first day, then 250 mg x 1 tablet for 4 days.

Cefadroxil (Droxyl, Oracefal): 500 mg, 3 tablets / day, divided into 3 times.

 Ciprofloxacin 500mg x 3 tablets / day in 3 divided doses.

If severe, the drug is usually administered by an injection of meat or vein:

One of the first generation Cephalosporine (Cefapirine: Cefeloject = 2g / day in 2 divided doses) II (Cefuroxime: Zinnat = 750mgx2 or 3 bottles / day divided into 2 or 3 times) III (Cefotaxime: Claforan = 2g / day in 2 divided doses) IV (Axepim = 2g / day in 2 divided doses) can be combined with Aminosides (Amikacine: Amiklin = 15mg / kg / day, 1 or 2 or 3 times) or Fluoroquinolones (Ciprofloxacin: 200mg x 2 vials - 4 vials of static pass vessel).

Motor therapy:

Breathing exercises are very important, increase the expansion of the lungs and chest, increase alveolar ventilation, especially breathing through the diaphragm.

Eliminate irritants:

Must quit smoking, avoid contact with dust, toxic gases.