Chapter 10 The Respiratory System
Atelectasis refers to incomplete expansion of the lungs or the collapse of previously inflated lung substance (Fig. 10-1). It is a pathologic condition that produces areas of relatively airless pulmonary parenchyma. Severe atelectasis significantly reduces oxygenation and predisposes to infection. Acquired atelectasis is generally encountered in adults and may be divided into the following categories:
Figure 10-1 Atelectasis. Four types of atelectasis are illustrated. Left to right: Obstruction atelectasis involves parts of the lung distal to an obstructed bronchus. Compression atelectasis usually involves the entire lung. The pleural space is filled with fluid compressing the lung, which has retracted toward the hilus. Similar findings can be produced by pneumothorax, except in this case the lung collapses because of entry of air into the pleural space. Patchy atelectasis involves small segments of all lobes. Airless patches of lung parenchyma, which have collapsed because of a deficiency of surfactant, are distributed irregularly and usually are found in both lungs. Contraction atelectasis usually occurs in subpleural areas and is typically caused by interstitial fibrosis, which prevents the expansion of the parenchyma.
Initially, patients may have no pulmonary symptoms. ARDS is heralded by profound dyspnea and tachypnea, but the chest radiograph is initially normal. Subsequently, progressive cyanosis and hypoxemia develop, followed by respiratory failure and the appearance of diffuse bilateral infiltrates on x-ray examination. Hypoxemia can then become unresponsive to oxygen therapy, sometimes resulting in respiratory acidosis. Patients’ lungs can be divided into areas that are infiltrated, consolidated, or collapsed (and thus poorly aerated and poorly compliant) and regions that have almost normal levels of compliance and ventilation.
Therapy of ARDS is extremely demanding, and the disorder is frequently fatal (60%). High concentrations of oxygen, required in therapy for ARDS, can contribute to perpetuation of the damage (oxygen toxicity).
Obstructive diseases (or airway diseases) are characterized by an increase in resistance to airflow due to partial or complete obstruction from the trachea and larger bronchi to the terminal and respiratory bronchioles. Pulmonary function tests in patients with obstructive lung disease always show a decrease in expiratory flow rates. The major obstructive disorders (excluding tumor or inhalation of a foreign body) are:
Restrictive diseases are characterized by reduced expansion of lung parenchyma, with decreased total lung capacity. The hallmark of the restrictive pattern of disease is a decrease in lung volumes. Restrictive diseases occur in the following conditions:
The incidence of COPD has increased dramatically in the past few decades (largely because of cigarette smoking and environmental pollutants) and currently represents a major cause of activity-restricting or bed-confining disability in the United States.
Emphysema is a condition of the lung in which abnormal permanent enlargement of the airspaces distal to the terminal bronchiole is accompanied by destruction of their walls, without obvious fibrosis. There are four main types of emphysema:
Only the first two types cause clinically significant airflow obstruction. Centriacinar emphysema accounts for 95% of all cases and is far more common than the panacinar form or other rare forms of emphysema.
The clinical manifestations of emphysema do not appear until at least one third of the functioning pulmonary parenchyma is incapacitated. Dyspnea is usually the first symptom, but in some patients the main complaints are cough or wheezing. Weight loss is common, and patients are barrel-chested and dyspneic, with an obviously prolonged expiration. Classically, patients sit bending forward in a hunched-over position, attempting to squeeze the air out of the lungs with each expiratory effort. Patients have a pinched face and breathe through pursed lips.
18 What is the difference in clinical presentation between patients with emphysema and those with chronic bronchitis?
In patients with severe emphysema, cough is often slight, but overdistention is severe. They exhibit low diffusing capacity, and blood gas values are relatively normal. Overventilation helps them remain well oxygenated (pink puffers).
Patients with chronic bronchitis often have a history of recurrent infection and abundant purulent sputum, followed by hypercapnia and severe hypoxemia (blue bloaters). The important complication in severe bronchitis, in addition to the respiratory difficulties, is the development of cor pulmonale and eventual congestive heart failure, associated with secondary pulmonary hypertension.
Chronic bronchitis is defined clinically as persistent cough with sputum production for at least 3 months of the year, in at least 2 consecutive years. Clinically there are several forms of chronic bronchitis:
Hyperemia, swelling, and bogginess of the mucous membranes are the main macroscopic features. They are frequently accompanied by excessive mucinous to mucopurulent secretions covering the epithelial surfaces. Heavy casts of secretions and pus occasionally fill the bronchi and bronchioles.
The typical histologic feature of chronic bronchitis is enlargement of the mucus-secreting glands of the trachea and bronchi. Increase in the size of the mucous glands is assessed by the ratio of the thickness of the mucous gland layer to the thickness of the wall between the epithelium and the cartilage (Reid index). The Reid index is normally 0.4. Marked narrowing of bronchioles caused by goblet cell metaplasia also occurs, as do mucous plugging, inflammation, and fibrosis. In the most severe cases, obliteration of lumens (bronchiolitis obliterans) further aggravates the patient’s condition.
Bronchial asthma is a chronic relapsing inflammatory disorder presenting with hyperreactive airways that cause episodic, reversible bronchoconstriction. The reaction is the consequence of increased responsiveness of the tracheobronchial tree to various stimuli. Patients experience unpredictable disabling attacks of severe dyspnea, coughing, and wheezing triggered by sudden episodes of bronchospasm. Between the attacks, virtually no symptoms occur, but in some people, chronic bronchitis or cor pulmonale supervenes. In the most severe form of asthma, status asthmaticus, the severe acute paroxysm persists for days and even weeks, threatening the ventilatory function enough to cause severe cyanosis and even death.
Atopic asthma usually begins in childhood, when it is triggered by environmental antigens, such as dusts, pollens, animal dander, and foods. Patients with this condition usually have a positive family history of atopy, and asthmatic attacks are often preceded by allergic rhinitis, urticaria, or eczema. It is a classic example of type I immunoglobulin E (IgE)-mediated hypersensitivity reaction. In the airways, inhaled antigens (allergens) initiate reactions, which eventually promote IgE production by B cells, growth of mast cells, and growth and activation of eosinophils.
27 Describe the main differences between acute and late-phase reactions in patients with bronchial asthma
Acute (immediate) response is caused by exposure of presensitized IgE-coated mast cells to the same or cross-reacting antigen and occurs within minutes after stimulation. Either directly or via neuronal reflexes, the mediators induce bronchoconstriction and increase vascular permeability (edema), mucus production, and, in extreme instances, hypotension. Mast cells also release cytokines that cause the influx of other leukocytes (particularly eosinophils).
Late-phase response is mediated by mediators released from leukocytes (neutrophils, monocytes, lymphocytes, basophils, and eosinophils), endothelium, and epithelial cells. It occurs 4 to 8 hours after exposure and may persist for 12 to 24 hour or more.