Pulmonary emphysema – treatment and symptoms
The main function of respiration is exchange process. By breathing the oxygen which is contained in air is delivered to red blood cells (RBCs) and in exhalation back is discharged carbon dioxide (emissions). Contact between air and body takes place in the lung sacs (alveoles). Alveoles of the lungs have an internal surface of about seventy square meters, while the skin is only one and a half to two square meters.
Pulmonary emphysema is permanently enlargement of the airspace distal to the terminal bronchioles accompanied by destroying (destruction) of the alveolar barrier. The total volume of the lungs in emphysema increases as the increase at the expense of so – called dead space, which does not participate in gas exchange.
Emphysema begins with the destruction of alveolar walls, where is the exchange of oxygen and carbon dioxide in the blood capillaries. Reduced transport of oxygen is clinically manifested by shortness of breath (dyspnea) and cyanosis.
Types of emphysema:
Panacinar /panlobular/ emphysema
When it affects the entire respiratory unit (lobules). In these cases, emphysema is often due to genetic anomaly – hereditary deficiency of alpha-1 antitrypsin. This substance is a protease inhibitor. Its function is to inhibit the activity of enzymes that destroy elastic fibres in alveolar walls. Alpha-1 antitrypsin is present in serum, body fluids and macrophages and is major inhibitor of proteases secreted by neutrophils (while blood cells) in inflammation. With frequent lung infections (acute bronchitis, pneumonia, chronic bronchitis) due to the increased presence of neutrophil leukocytes increases the amount of proteases and thus leads to increased destruction of elastic fibers in lung parenchyma. The level of alpha -1 antitrypsin can be detected in blood tests.
Central – acinar emphysema
On surface of the lung and cut surface is seen wreath of preserved alveoli around emphysema advanced central areas. Respiratory bronchioles are also involved mainly in the upper lobes. This is emphysema in clinical and experimental smokers. Tobacco smoke induces leukocyte and macrophage chemotaxis (attraction of blood cells), releases of elastase and with incoming oxidants of cigarette smoke inhibits alpha-1 antitrypsin. The consequences are destruction of elastic fibers and the development of emphysema.
From this type of emphysema suffer exceptionally smokers. Of these, however only 15-20% develop emphysema. 95% of patients are over 45 years of age. The distribution by gender is almost equally – 54.8% men and 45.2% women. Smoking leads to:
- Affection in balance between elastase and alpha -1antitrypsin.
- Migration of inflammatory cells from blood capillaries into alveoli.
- Separation of enzymes (elastase, collagenase) from inflammatory cells.
- Oxidants in cigarette smoke inhibit the action of elastase inhibitor (alpha-1 antitrypsin).
Chronic bronchitis and bronchiolitis
These two diseases also lead to emphysema in the so called valve mechanism – in inhalation (inspirium) in the alveolus enters a large amount of air that cannot be discharged after.
Senile emphysema is due to atrophy of the elastic fibers after 70 years of age. There is no destruction of alveolar walls.
Symptoms of pulmonary emphysema
There are two variants of the final clinical version of the pulmonary emphysema, and between them – transitional forms that cover to some extent the spectrum of symptoms.
Pink and puff type – these are people with normal weight or thin, emaciated patients with dry irritating cough without cyanosis (turning blue). They suffer from marked shortness of breath (dyspnea).
Blue and bloated type – these are people who are overweight, with marked cyanosis (bluish skin and visible mucous membranes). Their cough is moist and is accompanied by produce sputum. Do not have dyspnea.
For emphysema patient is typical barrel – shaped thorax with horizontal course of ribs, protruding above the clavicle wells box electricity in the percussion of the lungs dampened breathing and reduced heart tones (due to overlapping heart of bloated lung). The diaphragm is a low standing and pushes down the liver that can lead to erroneous diagnosis “enlarged liver”. X-ray shows increased transparency of the lung fields, with the expansion of the intercostal spaces. Pulmonary function testing (PFT) and blood gas analysis helps to determine precisely the extent of lung destruction.
Complications of emphysema – pneumothorax, pulmonary hypertension with chronic cor pulmonale (pulmonary heart), respiratory failure.
Treatment of pulmonary emphysema
- Stopping smoking, dust – free working environment.
- Timely treatment and prevention of pulmonary infections.
- In tough sputum is recommended mucolytic medication that liquefies bronchial secretions, and in severe cases – corticosteroids and bronchodilators.
- Oxygen treatment.
In patients with pulmonary emphysema are absolutely contraindicated drugs that suppress respiration (morphine, diazepam, barbiturates, hypnotics)!
Treatment with bronchodilators and corticosteroids should be performed only by physicians- specialists!
Treatment with antibiotics is appropriate to take place after microbiological examination of sputum and preparation of antibiogram!
Oxygen supply for breathing requires dosing and constant medical supervision, because too much can lead to depression of the respiratory center and the risk of respiratory arrest.
The technique of breathing, which should absorb the emphysema patient is to breathe with pointed lips (so called “brake on the lips”). Thus avoids the collapse of airways during exhalation – so – called expiratory collapse. Forcing breathing (rapid, hard) should be shunned! This means that patients should be protected from heavy physical efforts and emotional outbursts, leading to increased respiratory movements.