CHANGES IN CHRONIC BRONCHITIS

In chronic bronchitis, irritants inflame the tracheobronchial tree over time, leading to increased mucus production and a narrowed or blocked airway. As the inflammation continues, goblet and epithelial cells hypertrophy. Because the natural defense mechanisms are blocked, the airways accumulate debris in the respiratory tract. Shown below is a cross section of these changes.

CULTURAL DIVERSITY COPD is more prevalent in an urban versus rural environment, and is also related to occupational factors (mineral or organic dusts).

AGE ALERT Children of parents who smoke are at higher risk for respiratory tract infection that can lead to chronic bronchitis.

Causes

Common causes of chronic bronchitis include:

exposure to irritants cigarette smoking genetic predisposition

exposure to organic or inorganic dusts exposure to noxious gases

respiratory tract infection.

Pathophysiology

Chronic bronchitis occurs when irritants are inhaled for a prolonged time. The irritants inflame the tracheobronchial tree, leading to increased mucus production and a narrowed or blocked airway. As the inflammation continues, changes in the cells lining the respiratory tract result in resistance of the small airways and severe / imbalance, which decreases arterial oxygenation.

Chronic bronchitis results in hypertrophy, hyperplasia of the mucous glands, increased goblet cells, ciliary damage, squamous metaplasia of the columnar epithelium, and chronic leukocytic and lymphocytic infiltration of bronchial walls.

(See Changes in chronic bronchitis.) Hypersecretion of the goblet cells blocks the free movement of the cilia, which normally sweep dust, irritants, and mucus away from the airways. With mucus and debris accumulating in the airway, the defenses are altered, and the individual is prone to respiratory tract infections.

Additional effects include widespread inflammation, airway narrowing, and mucus within the airways. Bronchial walls become inflamed and thickened from edema and accumulation of inflammatory cells, and the effects of smooth muscle bronchospasm further narrow the lumen. Initially, only large bronchi are involved but eventually, all airways are affected.

Airways become obstructed and closure occurs, especially on expiration. The gas is then trapped in the distal portion of the lung. Hypoventilation occurs, leading to a / mismatch and resultant hypoxemia.

Hypoxemia and hypercapnia occur secondary to hypoventilation. Pulmonary vascular resistance (PVR) increases as inflammatory and compensatory vasoconstriction in hypoventilated areas narrows the pulmonary arteries. Increased PVR leads to increased afterload of the right ventricle. With repeated inflammatory episodes, scarring of the airways occurs and permanent structural changes develop. Respiratory infections can trigger acute exacerbations, and respiratory failure can occur.

Patients with chronic bronchitis have a diminished respiratory drive. The resulting chronic hypoxia causes the kidneys to produce erythropoietin, which stimulates excessive red blood cell production and leads to polycythemia. Although

hemoglobin levels are high, the amount of reduced (not fully oxygenated) hemoglobin that is in contact with oxygen is low; therefore, cyanosis occurs.

Signs and symptoms

The following signs and symptoms may occur:

copious gray, white, or yellow sputum due to hypersecretion of goblet cells productive cough to expectorate mucus that is produced by the lungs dyspnea due to obstruction of airflow to the lower tracheobronchial tree

cyanosis related to diminished oxygenation and cellular hypoxia; reduced oxygen is supplied to the tissues use of accessory muscles for breathing due to compensated attempts to supply the cells with increased oxygen tachypnea due to hypoxia

pedal edema due to right-sided heart failure

neck vein distention due to right-sided heart failure weight gain due to edema

wheezing due to air moving through narrowed respiratory passages

prolonged expiratory time due to the body's attempt to keep airways patent rhonchi due to air moving through narrow, mucus-filled passages

pulmonary hypertension caused by involvement of small pulmonary arteries, due to inflammation in the bronchial walls and spasms of pulmonary blood vessels from hypoxia.

Complications

Possible complications of this disorder include:

cor pulmonale (right ventricular hypertrophy with right-sided heart failure) due to increased right ventricular end-diastolic pressure

pulmonary hypertension

heart failure, resulting in increased venous pressure, liver engorgement, and dependent edema acute respiratory failure.

Diagnosis

The following tests help diagnose chronic bronchitis:

Chest X-rays may show hyperinflation and increased bronchovascular markings.

Pulmonary function studies indicate increased residual volume, decreased vital capacity and forced expiratory flow, and normal static compliance and diffusing capacity.

Arterial blood gas analysis reveals decreased PaO₂ and normal or increased PaCO₂. Sputum analysis may reveal many microorganisms and neutrophils.

Electrocardiography may show atrial arrhythmias; peaked P waves in leads II, III, and aV_F; and occasionally, right ventricular hypertrophy.

Treatment

Correcting chronic bronchitis typically involves:

avoidance of air pollutants (most effective) smoking cessation

antibiotics to treat recurring infections

bronchodilators to relieve bronchospasms and facilitate mucociliary clearance adequate hydration to liquefy secretions

chest physiotherapy to mobilize secretions

ultrasonic or mechanical nebulizers to loosen and mobilize secretions corticosteroids to combat inflammation

diuretics to reduce edema oxygen to treat hypoxia.

Chronic obstructive pulmonary disease

Chronic obstructive pulmonary disease (COPD), also called chronic obstructive lung disease (COLD), results from

emphysema, chronic bronchitis, asthma, or a combination of these disorders. Usually, more than one of these underlying conditions coexist; bronchitis and emphysema often occur together. (See “Asthma,” “Chronic bronchitis,” and

“Emphysema” for a review of these conditions.)

COPD is the most common lung disease and affects an estimated 17 million Americans; the incidence is rising. The disease is not always symptomatic and may cause only minimal disability. However, COPD worsens with time.

Causes

Common causes of COPD may include:

cigarette smoking

recurrent or chronic respiratory tract infections air pollution

allergies

familial and hereditary factors such as deficiency of alpha₁-antitrypsin.

Pathophysiology

Smoking, one of the major causes of COPD, impairs ciliary action and macrophage function and causes inflammation in the airways, increased mucus production, destruction of alveolar septa, and peribronchiolar fibrosis. Early inflammatory changes may reverse if the patient stops smoking before lung disease becomes extensive.

The mucus plugs and narrowed airways cause air trapping, as in chronic bronchitis and emphysema. Hyperinflation occurs to the alveoli on expiration. On inspiration, airways enlarge, allowing air to pass beyond the obstruction; on expiration, airways narrow and gas flow is prevented. Air trapping (also called ball valving) occurs commonly in asthma and chronic bronchitis. (See Air trapping in chronic obstructive pulmonary disease.)

Signs and symptoms

The following signs and symptoms may occur:

reduced ability to perform exercises or do strenuous work due to diminished pulmonary reserve productive cough due to stimulation of the reflex by mucus

dyspnea on minimal exertion frequent respiratory tract infections intermittent or continuous hypoxemia

grossly abnormal pulmonary function studies thoracic deformities.

Complications

Possible complications of COPD include:

overwhelming disability cor pulmonale

severe respiratory failure death.